Licorice

Glycyrrhiza glabra is a herbaceous perennial legume (family Fabaceae) native to southern Europe, the Middle East, and western Asia. The plant grows to roughly 1–1.5 meters tall, producing pinnate leaves with 9–17 leaflets and pale blue to violet flowers arranged in axillary racemes. The medicinally relevant part is the root and stolon system, which develops an extensive network of woody, yellowish-brown underground runners.

Several Glycyrrhiza species are used medicinally worldwide. G. glabra (European/Mediterranean licorice) and G. uralensis (Chinese licorice, gancao) are the most commercially important. G. inflata, the source of the flavonoid licochalcone A, is also used in Chinese medicine. The glycyrrhizin content varies between species and cultivars, typically ranging from 2–12% of dry root weight.

Key phytochemical constituents beyond glycyrrhizin include liquiritigenin and isoliquiritigenin (flavonoids with estrogenic and anti-inflammatory activity), glabridin (an isoflavane with antioxidant properties), and various coumarins and polysaccharides. The complexity of the root’s chemistry means that whole-extract pharmacology cannot be reduced to glycyrrhizin alone, though glycyrrhizin dominates both the therapeutic and toxicological profile of unprocessed root.

Licorice root appears in the Ebers Papyrus (c. 1550 BCE), making it one of the earliest documented medicinal plants. Ancient Egyptian, Greek, and Roman physicians used it for coughs, throat complaints, and thirst. Theophrastus, writing around 300 BCE, described "Scythian root" — almost certainly licorice — as useful for asthma and dry cough.

In traditional Chinese medicine, gancao (G. uralensis) occupies a uniquely central role. Known as "the great harmonizer," it appears in more classical formulas than any other single herb, often serving as a moderating or synergizing ingredient rather than the primary therapeutic agent. The Shennong Ben Cao Jing (c. 200 CE) classified it as a superior herb.

European use intensified in the Middle Ages. Licorice cultivation in England (notably in Pontefract, Yorkshire) dates to at least the 13th century. By the 19th century, licorice extract was a standard ingredient in pharmacopoeias for throat lozenges, cough syrups, and as a flavoring agent to mask bitter medicines.

The modern scientific understanding of licorice’s risks began crystallizing in the 1940s–1960s, when Dutch physician F. E. Revers observed that licorice extract could heal peptic ulcers but also caused edema and hypertension. This led directly to the development of DGL in the 1970s as an attempt to retain the GI benefits while eliminating the mineralocorticoid side effects.

The dominant pharmacological mechanism of glycyrrhizin involves inhibition of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). This enzyme converts active cortisol to inactive cortisone in mineralocorticoid-sensitive tissues (kidneys, colon, salivary glands). When 11β-HSD2 is blocked, cortisol accumulates and activates mineralocorticoid receptors, producing aldosterone-like effects: sodium and water retention, potassium excretion, and blood pressure elevation. This is pseudoaldosteronism — the clinical picture of aldosterone excess without actual aldosterone elevation.

Glycyrrhizin and its aglycone glycyrrhetinic acid also demonstrate direct anti-inflammatory activity through inhibition of phospholipase A2, modulation of arachidonic acid metabolism, and suppression of complement activation. In vitro, glycyrrhizin shows antiviral activity against several viruses, including hepatitis C and some herpesviruses, though clinical translation of these findings remains limited.

The GI-protective effects attributed to DGL appear to involve stimulation of mucus secretion and enhancement of mucosal blood flow, likely mediated by flavonoid and saponin constituents other than glycyrrhizin. Some evidence suggests DGL may increase prostaglandin E2 production in gastric mucosa, supporting the mucosal defense barrier without the systemic mineralocorticoid effects of whole licorice.

Glabridin and other flavonoid components contribute antioxidant, mild phytoestrogenic, and antimicrobial activities. Liquiritigenin acts as a selective estrogen receptor β (ERβ) agonist in preclinical models, which has generated interest in menopausal symptom research, though clinical evidence remains preliminary.

DGL is the licorice product most often used for indigestion and as an add-on in peptic ulcer care. One small randomized trial of a deglycyrrhizinated extract in 50 people with functional dyspepsia found that symptoms improved more than with placebo over 30 days, an encouraging result, though EMA judged the trial too small to establish efficacy. The older ulcer research is mixed: several placebo-controlled DGL trials from the 1970s found no clear benefit on ulcer healing or symptoms, while a few newer small trials reported some benefit when licorice was added to H. pylori eradication therapy. NCCIH notes that it is unclear whether licorice alone affects digestive symptoms. DGL is not a substitute for evidence-based ulcer treatment (test-and-treat for H. pylori, PPI therapy) but may offer complementary mucosal support.

The EMA recognizes glycyrrhizin-containing licorice root as a traditional herbal medicine used as an expectorant in cough associated with a cold. This rests on long-standing traditional use and pharmacological plausibility (demulcent and mild expectorant effects) rather than clinical trial data; EMA found no clinical evidence to support a well-established use. Its second traditional indication is relief of digestive symptoms, including a burning sensation and dyspepsia. NCCIH adds that a licorice gargle or lozenges used before surgery might help prevent or ease sore throat after intubation, and that a licorice mouth rinse might reduce the size and pain of recurrent canker sores.

In Japan, injectable glycyrrhizin (Stronger Neo-Minophagen C) has been used for decades as a hepatoprotective agent in chronic hepatitis, particularly hepatitis C. This is a specific pharmaceutical preparation administered under medical supervision, not comparable to oral supplementation, and is not widely used outside Japan.

Topical licorice extracts (particularly those standardized to glabridin) are used in dermatology and cosmetics for skin-lightening and anti-inflammatory effects. There is early evidence of benefit for melasma and atopic dermatitis, though most studies are small and more research would help.

DGL (deglycyrrhizinated licorice) is available as chewable tablets, capsules, and powders. The traditional recommendation is to chew DGL tablets 15–20 minutes before meals. Typical doses range from 380–760 mg of DGL extract per dose, taken two to three times daily. DGL has most of its glycyrrhizin removed, but the amount left can vary between products, so choose one that declares its glycyrrhizin content. NCCIH notes that oral DGL products might be safe for up to four months.

Glycyrrhizin-containing licorice root is available as dried root (for decoction), powdered root in capsules, fluid extracts, and solid extracts. For cough, EMA’s 2026 monograph gives 1.5–4.5 g of comminuted root in 150 ml of boiling water as an infusion or decoction, two to three times daily (3–13.5 g a day); for digestive symptoms, 1.5–2 g two to four times daily, one cup after meals (3–8 g a day). Both are for adults only; EMA does not recommend licorice root medicines for anyone under 18. Crucially, treat four weeks as the ceiling for any glycyrrhizin-containing preparation: EMA says not to use licorice root for digestive symptoms for more than four weeks, its assessors concluded that short-term use of no more than four weeks is safe, and reported overdoses involved longer use or high intakes. See a doctor if digestive symptoms last longer than two weeks or a cough lasts longer than a week.

Licorice root tea is widely available and popular, but consumers rarely consider glycyrrhizin content. A strong cup of licorice tea can deliver a pharmacologically relevant dose of glycyrrhizin: in a Dutch analysis cited by EMA, teas listing licorice as an ingredient averaged 126 mg of glycyrrhizin per liter and reached 450 mg per liter, so a 250 ml cup averages about 31 mg. Habitual daily consumption has caused documented cases of pseudoaldosteronism.

Standardized extracts vary enormously in glycyrrhizin content. Products may be standardized to glycyrrhizin (typically 10–25% in concentrated extracts) or to other marker compounds. Always check the label for glycyrrhizin content, and if it is not declared, assume the product contains a full glycyrrhizin load.