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Licorice Poisoning

  • Author: Seth Schonwald, MD, FACEP; Chief Editor: Asim Tarabar, MD  more...
Updated: Jan 13, 2014


Licorice (or liquorice) is a plant of ancient origin and steeped in history. Natural licorice is an extract from the root of Glycyrrhiza glabra, a 4- to 5-foot woody shrub that contains glycyrrhizic acid (GZA) and grows in subtropical climates in Europe, the Middle East, and Western Asia.

Licorice extracts and its principal component, glycyrrhizin, have extensive use in foods, tobacco products, and snuff, and in traditional and herbal medicine. Licorice extract (block, powder, or liquid) may be applied to cigarette tobacco at levels of about 1-4% to enhance and harmonize the flavor characteristics of smoke, improve moisture-holding characteristics of tobacco, and act as a surface-active agent for ingredient application.[1]

Licorice flavor is found in a wide variety of licorice candies. Licorice is also found in some soft drinks (eg, root beer) and is in some herbal teas where it provides a sweet aftertaste. As a result of these extensive applications, estimated consumption of licorice and glycyrrhizin in the United States is high—0.027-3.6 mg glycyrrhizin per kilograms per day.[2]

Licorice has also been used as a medicinal agent in a number of cultures,[3] dating back to ancient Egypt and China. Medicinal uses have included cough suppression,[4] gastric ulcer treatment,[5] treatment of early Addison disease,[6, 7] treatment of liver disease,[8, 9] and as a laxative.



Natural licorice possesses both mineralocorticoid properties and glucocorticoid properties. Most licorice-flavored foods available in the United States do not contain GZA, and they do not produce the hypermineralocorticoid syndromes observed with the long-term consumption of moderate-to-significant amounts of natural licorice.

Consumption of large doses of GZA in licorice extract can lead to hypokalemia and serious hypertension, a syndrome known as hypermineralocorticoidism.[10, 11] Biochemical studies indicate that glycyrrhizinates inhibit 11-beta-hydroxysteroid dehydrogenase (type 2), the enzyme responsible for inactivating cortisol. As a result, a continuous, high-level exposure to glycyrrhizin compounds can produce hypermineralocorticoid-like effects in both animals and humans. These effects are reversible upon withdrawal of licorice or glycyrrhizin.[2]

In the kidney, cortisol activation of mineralocorticoid receptors alters renal tubular exchange of sodium (retained), potassium (excreted), and hydrogen ions (excreted); producing an increased extracellular volume (hypertension,[12] edema), hypokalemia (weakness, muscle spasm),[13] and metabolic alkalosis.[14]

Pseudoprimary aldosteronism from chronic licorice ingestion is characterized by low serum and urinary aldosterone levels and decreased serum renin activity. This differs from true primary hyperaldosteronism caused by aldosterone-producing adenomas or primary adrenal hyperplasia, which is characterized by elevated urine and serum aldosterone levels.

Licorice can reduce the serum testosterone level, probably by blocking 17-hydroxysteroid dehydrogenase and 17,20 lyase.[15] Licorice has therefore been considered an adjuvant therapy of hirsutism and polycystic ovary syndrome.[16]

The exact amount of ingested GZA that produces mineralocorticoid toxicity is unclear. Avoiding ingestion of natural licorice in the setting of hypertension, diuretic use, sexual dysfunction, or pregnancy is probably wise.



Patients generally fully recover with discontinuation of exposure. After licorice exposure is discontinued, spontaneous correction of hypertension and hypokalemia generally occur within several weeks; however, months may pass before the renin-aldosterone system becomes active again.[17] Muscle weakness/paralysis may resolve within days of potassium replacement.

Contributor Information and Disclosures

Seth Schonwald, MD, FACEP Attending Physician, Department of Emergency Medicine, Boston Veterans Affairs Medical Center

Seth Schonwald, MD, FACEP is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Massachusetts Medical Society, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.


B Zane Horowitz, MD, FACMT Professor, Department of Emergency Medicine, Oregon Health and Sciences University; Medical Director, Oregon Poison Center; Medical Director, Alaska Poison Control System

B Zane Horowitz, MD, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Medical Toxicology

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

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