Licorice is a perennial herb native to the Mediterranean region, central to southern Russia, and Asia Minor to Iran, now widely cultivated throughout Europe, the Middle East, and Asia. The material of commerce comes from wild plants and "semiwild" plants cultivated in the former U.S.S.R., Turkey, Greece, Iran, China, India, Pakistan, Afghanistan, Syria, Italy, and Spain (Bruneton, 1995; Karnick, 1994; Leung and Foster, 1996; Wichtl and Bisset, 1994). In the Chinese pharmacopeia, Glycyrrhiza glabra, G. uralensis, and G. inflata are officially recognized and are the species usually employed in commerce (Tu, 1992). Licorice is one of the most widely used medicinal herbs and is found in numerous traditional formulas (Leung and Foster, 1996). Until about 1000 c.e, licorice was collected in the wild. Its cultivation was first recorded by Piero de Cresenzi of Bologna in the thirteenth century. Cultivated roots are harvested after three to four years of growth. Its genus name, Glycyrrhiza, given by first century Greek physician Dioscorides, comes from glukos (sweet) and riza (root) (Foster and Yue, 1992; Grieve, 1979).
Licorice is one of the most extensively researched medicinal and food plants (Chandler, 1997). The roots and stolons contain glycyrrhizin (also knows as glycyrrhizic or glycyrrhizinic acid, about 59% by weight), a compound that is about 50 times sweeter than sucrose. Commercial extracts usually contain gycyrrhizin in its ammonium salt form. The sweet taste is reduced or lost in an acidic medium (Leung and Foster, 1996; Foster and Tyler, 1999). Licorice extracts are widely used to flavor food and liqueurs. Millions of pounds of licorice are imported into the United States each year, about 90% for use in flavoring tobacco products (Foster and Tyler, 1999).
Licorice root has been used therapeutically for several thousand years in both Western and Eastern systems of medicine (Bradley, 1992; Leung and Foster, 1996). A chronological, documented summary of its medical uses since 2100 B.C.E. to the present, with correlations to modern pharmacological research, has been published (Gibson, 1978). Its use is first documented in Assyrian clay tablets (ca. 2500 B.C.E.) and Egyptian papyri. It was used in ancient Arabia to treat coughs and to relieve the unwanted effects of laxatives (Bruneton, 1995). Its use in ancient Scythia spread to Greece. Greek natural scientist Theophrastus (ca. 372287 B.C.E.) reported its use for dry cough, asthma, and all pectoral diseases (Grieve, 1979). Pliny the Elder (ca. 2379 C.E.) reported licorice cleared the voice and had expectorant and carminative actions (Der Marderosian, 1999). In China, licorice is first mentioned in the Shen Nong Ben Cao Jing (ca. 25 C.E.), reconstructed "materia medica" from lost text attributed to Shen Nong Shi (ca. 3000 B.C.E.) (Foster and Yue, 1992). According to the Chinese pharmacopeia, licorice, either aqueous dry extract or hydroalcoholic fluidextract, is an abirritant, often used in combination with expectorants and antitussives to diminish irritation of the mucous membrane of the pharynx. It also relieves spasms of the gastrointestinal smooth muscle and shows desoxycorticosterone-like action (Tu, 1992). In India, licorice is used in traditional Ayurvedic, Siddha, and Unani medicines (Nadkarni, 1976). The present-day Ayurvedic Pharmacopoeia reports it is expectorant, demulcent, spasmolytic, antinflammatory, an adrenal agent, and a mild laxative (Karnick, 1994). It is also official in the Indian Pharmacopoeia as a demulcent (IP, 1996).
In Germany, licorice root is licensed as a standard medicinal tea for bronchitis and for chronic gastritis. It is also used in bronchial teas, stomach teas, and laxative teas available only in the pharmacy. Aqueous and alcoholic extracts of licorice root are used in many bronchial, gastrointestinal, liver and bile, and urological preparations. In the United States, licorice root is often a component of demulcent, expectorant, or laxative preparations (dietary supplement and OTC drug) in aqueous infusion, hydroalcoholic fluidextract and tincture, and solid dosage forms. Licorice root and extracts, fluid and solid, are official in the U.S. National Formulary (NF, 1985).
Many of the modern therapeutic uses of licorice were known in earlier times. Early claims for a broad spectrum of uses for licorice appear to be borne out by modern research (Gibson, 1978). Human studies have investigated efficacy in subacute hepatic failure (Acharya et al., 1993), chronic hepatitis C (Arase et al., 1997), infectious hepatitis (Chang and But, 1986), hemophilia with HIV-1 infection (Mori et al., 1990), and inhibition of HIV replication in patients with AIDS (Hattori et al., 1989). Studies have investigated its effects, in its traditional context as a component of multi-herb formulas, on testosterone secretion in patients with polycystic ovary syndrome (Takahashi et al., 1988), on treating anxiety (Chen et al., 1985), and on gastric and duodenal ulcer (Chang and But, 1986), among others. However, its use in combination formulas cannot determine definitively that the outcome of studies might not also be the result of the effects of other herbs in the formulas, and not attributable to the presence of the licorice alone.
Licorice preparations have been studied for possible benefits in treating digestive tract ulcers. In one clinical study, licorice root fluidextract was used to treat 100 patients with early peptic ulcer, of which 86 cases had been unresponsive to conventional treatment, at a dose of 15 ml four times daily for six weeks. Positive effects were reported in 90% of the cases, in 22 of which ulcer craters disappeared by X-ray examination and 28 others showed improvement. In subsequent studies, researchers reported that licorice powder at a dosage of 2.55.0 g three times daily was more effective than the fluidextract (Chang and But, 1986).
Reports in the literature of adverse effects of the consumption of excessive amounts of licorice (more than 20 g per day) have raised concerns about the potential for glycyrrhizin in licorice to produce pseudoaldesteronism (excessive levels of aldesterone, a hormone produced by the adrenalcortex) and resulting risks (headache, lethargy, sodium and water retention, hypertension, potassium loss that upsets the sodium-potassium balance, possibly resulting in cardiac problems, including cardiac arrest). The therapeutic uses and risks of licorice has been reviewed by Chandler (1997) and Stormer et al. (1993).
A deglycyrrhizinated licorice (DGL) preparation has been developed to provide some of the therapeutic benefits of licorice while reducing risk. A DGL preparation efficacy in treating duodenal and gastric ulcers in clinical trials (D'Imperio et al., 1978; Morgan et al., 1982). DGL may be useful in maintenance therapy for patients with gastric ulcers, although its superiority compared to conventional drugs has been questioned. In a two-year comparison study of a DGL product (CavedS® tablets; two twice per day) and cimetidine, 400 mg at night, 12% (4 of 34) of the DGL subjects had ulcer recurrence compared with 10% (4 of 41) of the drug group in the first year of treatment; in the second year, 29% (9 of 31) for DGL and 25% (8 of 32) for cimetidine (Morgan et al., 1982). After termination of treatment in two years, ulcers recurred rapidly: 2 of 22 DGL patients and 7 of 23 cimetidine patients. The study concluded that long-term maintenance therapy was safe and reasonably effective.
DGL has shown success in treating duodenal gastric ulcers in clinical trials (D'Imperio et al., 1978; Morgan et al., 1982) although its superiority, compared to conventional drugs like cimetidine, has not been confirmed.
Glycyrrhizin itself, in a controlled dosage form with other natural products, has been investigated as a therapy for patients with human immuno-deficiency virus (HIV). One clinical study investigated the effects of glycyrrhizin (SNMC: stronger neo-minophagen C) in 42 hemophilia patients with HIV-1 infection. SNMC is made of 0.2% glycyrrhizin, 0.1% cysteine, and 2.0% glycine dissolved in a saline solution. Patients showed improvement in their clinical symptoms (oral candidiasis, lymph node swelling, rash), immunological functions, and liver functions (Mori et al., 1990). A subsequent study investigated the long-term efficacy of SNMC in 84 patients with chronic hepatitis C. Patients received 100 ml intravenously daily for eight weeks and then two to seven times a week for 2 to 16 years. A reduction in serum alanine aminotransferase (ALT) levels was reported in 34 of the 84 patients (35.7%). This trend toward stabilization of ALT levels was statistically significant. Hepatocellular carcinoma (HCC) in 30 patients with normal ALT levels was slightly lower than the 54 remaining patients with higher ALT scores (p=0.08). An increase in blood pressure was noted in 3 of the 84 patients. The authors concluded that the long-term administration of SNMC for chronic HCC is effective in reducing the risk of liver carcinogenesis (Arase et al., 1997).
The modern therapeutic applications for licorice root are supportable based on its use in well established systems of traditional medicine, on well documented phytochemical investigations, on pharmacological actions reported from in vitro and in vivo studies in animals, and on human clinical studies.
Pharmacopeial grade licorice root must contain not less than 4% glycyrrhizic acid, calculated on the dried root, and must pass a thin-layer chromatography (TLC) assay to show the presence of glycyrrhetic acid. Its water-soluble extractive content must be not less than 20% (Bruneton, 1995; IP, 1996; Ph.Eur.3, 1998; Ph.Fr.X., 1990; Wichtl and Bisset, 1994). The Japanese Pharmacopoeia also requires not less than 25% dilute ethanol-soluble extractive (JP XII, 1993).
Licorice root consists of unpeeled, dried roots and stolons of Glycyrrhiza glabra L. [Fam. Fabaceae], and their preparations in effective dosage. The unpeeled roots contain at least 4% glycyrrhizic acid and 25% water-soluble matter. Licorice root also consists of the peeled, dried roots and stolons of G. glabra and their preparations in effective dosage. The peeled roots contain at least 20% water-soluble matter. The root contains flavanone and isoflavanone derivatives, potassium and calcium salts of glycyrrhizic acid, phytosterols, and coumarins.
Licorice root contains triterpenoid saponins (424%), mostly glycyrrhizin, a mixture of the potassium and calcium salts of glycyrrhizic acid; flavonoids (1%), mainly the flavanones liquiritin and liquiritigenin, chalcones isoliquiritin, isoliquiritigenin and isoflavonoids (formononetin); amines (12%) asparagine, betaine, and choline; amino acids; 315% glucose and sucrose; starch (230%); polysaccharides (arabinogalactans); sterols (b-sitosterol); coumarins (glycerin); resin; and volatile oils (0.047%) (Bruneton, 1995; Bradley, 1992; Budavari, 1996; Leung and Foster, 1996; List and Hrhammer, 19731979; Newall et al., 1996; Wichtl and Bisset, 1994). An extensive review of licorice chemistry has been published recently (Tang and Eisenbrand, 1992).
The Commission E reported that, according to controlled clinical studies, glycyrrhizic acid and the aglycone of glycyrrhizic acid accelerate the healing of gastric ulcers. Secretolytic and expectorant effects have been confirmed in tests on rabbits. In the isolated rabbit ileum, an antispasmodic action has been observed at concentrations of 1:25001:5000.
The British Herbal Compendium reported its actions as anti-inflammatory, expectorant, demulcent, and adrenocorticotropic (Bradley, 1992).
The pseudo-aldesterone-like effects are generally attributed to the glycyrrhizic acid. New research suggests that the glycyrrhetenic acid, the hydrolytic metabolite of glycyrrhizic acid, is the primary active component that causes inhibition of peripheral metabolism of corticol, which binds to mineralocorticoid receptors in the same way as aldosterone (Heikens et al., 1995).
Research suggests two hypotheses for licorice's mechanism of action: binding of glycyrretinic acid to mineralocorticoid receptors and blocking the action of 11-beta-hydroxysteroid dehydrogenase. Recent publications suggest that both may be involved, especially with the confirmation that the blocking of the 11-beta-hydroxysteroid dehydrogenase is temporary and that after this occurs, the pseudoaldesteronism is directly related to increased plasma concentration of licorice metabolites and their binding to mineralocorticoid receptors. Glucocorticoids are usually rapidly metabolized into inactive compounds by 11-beta-hydroxysteroid dehydrogenase, thus controlling glucocorticoid access to mineralocorticoid and glucocorticoid receptors. When licorice prevents the inactivation of hydrocortisone, the result is increased glucocorticoid concentration in mineralocorticoid-responsive tissues, thus resulting in glucocorticoids' occupying mineralocorticoid receptors and producing a mineralocorticoid response, as shown by increased sodium retention and hypertension (Chandler, 1997).
The Commission E approved the internal use of licorice root for catarrhs of the upper respiratory tract and gastric or duodenal ulcers.
The British Herbal Compendium indicates its use for bronchitis, peptic ulcer, chronic gastritis, rheumatism and arthritis, and adrenocorticoid insufficiency (Bradley, 1992). The German Standard License approves licorice root infusions for loosening mucus, alleviating discharge in bronchitis, and as an adjuvant in treating spasmodic pains of chronic gastritis (Bradley, 1992; Braun et al., 1997; Wichtl and Bisset, 1994). In France, licorice preparations may be used to treat epigastric bloating, impaired digestion, and flatulence (Bruneton, 1995).
The World Health Organization recognizes no uses for licorice as being supported by clinical data; WHO recognizes the following uses as being described in pharmacopeias and in traditional systems of medicine: demulcent for sore throats; expectorant in treatment of coughs and bronchial catarrh; prophylaxis and treatment of gastric and duodenal ulcers; used in dyspepsia; anti-inflammatory in treating allergic reactions, rheumatism, and arthritis; to prevent liver toxicity; and to treat tuberculosis and adrenocorticoid insufficiency (WHO, 1999).
Cholestatic liver disorders, liver cirrhosis, hypertonia, hypokalemia, severe kidney insufficiency.
Potassium loss due to other drugs, e.g., thiazide diuretics, can be increased. With potassium loss, sensitivity to digitalis glycosides increases.
On prolonged use and with higher doses, sodium and water retention and potassium loss may occur, accompanied by hypertension, edema, hypokalemia, and, in rare cases, myoglobinuria.
[Ed. Note: Within several weeks of discontinuing use, any symptoms of hyperaldosteronism disappear (Mantero, 1981).]
Not recommended during pregnancy (McGuffin et al., 1997). No restrictions known during lactation.
Unless otherwise prescribed: About 5-15 g per day of cut or powdered root, or dry extracts equivalent to 200-600 mg of glycyrrhizin.
Succus liquiritiae: 0.5-1.0 ml for catarrhs of the upper respiratory tract, 1.5-3.0 ml for gastric or duodenal ulcers.
Infusion or decoction: 2-4 g in 150 ml water, after meals three times daily.
Fluidextract 1:1 (g/ml): 2-4 ml, after meals three times daily.
Native dry extract 5-6:1 (w/w): 0.33-0.8 g, after meals three times daily.
DGL tablets (380 mg DGL 4:1): acute cases (gastric or duodenal ulcers): chew 2-4 tablets before each meal; chronic cases: chew 1-2 tablets before meals (Murray and Pizzorno, 1998).
Duration of administration: Not longer than four to six weeks without medical advice. There is no objection to using licorice root as a flavoring agent up to a maximum daily dosage equivalent to 100 mg glycyrrhizin.
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- This material was adapted from The Complete German Commission E MonographsTherapeutic Guide to Herbal Medicines. M. Blumenthal, W.R. Busse, A. Goldberg, J. Gruenwald, T. Hall, C.W. Riggins, R.S. Rister (eds.) S. Klein and R.S. Rister (trans.). 1998. Austin: American Botanical Council; Boston: Integrative Medicine Communications.
- 1) The Overview section is new information.
- 2) Description, Chemistry and Pharmacology, Uses, Contraindications, Side Effects, Interactions with Other Drugs, and Dosage sections have been drawn from the original work. Additional information has been added in some or all of these sections, as noted with references.
- 3) The dosage for equivalent preparations (tea infusion, fluidextract, and tincture) have been provided based on the following example:
- Unless otherwise prescribed: 2 g per day of [powdered, crushed, cut or whole] [plant part]
- Infusion: 2 g in 150 ml of water
- Fluidextract 1:1 (g/ml): 2 ml
- Tincture 1:5 (g/ml): 10 ml
- 4) The References and Additional Resources sections are new sections. Additional Resources are not cited in the monograph but are included for research purposes.
- This monograph, published by the Commission E in 1994, was modified based on new scientific research. It contains more extensive pharmacological and therapeutic information taken directly from the Commission E.