Does Licorice Harm the Kidneys?

Concerns about the potential renal effects of licorice root—derived from the plant Glycyrrhiza glabra—are well-documented in clinical pharmacology. While licorice is widely used in traditional medicine and as a flavoring agent, its active constituent, glycyrrhizin, can exert mineralocorticoid-like activity when consumed in excess or over prolonged periods.

Glycyrrhizin inhibits 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), an enzyme responsible for inactivating cortisol in the kidney’s distal tubules. This inhibition allows cortisol to bind to mineralocorticoid receptors, leading to sodium retention, potassium wasting, hypertension, and—in susceptible individuals—hypokalemic metabolic alkalosis. These electrolyte disturbances may secondarily impair renal perfusion and contribute to acute kidney injury, particularly in patients with preexisting chronic kidney disease, heart failure, or hypertension.

Clinical evidence indicates that nephrotoxicity is not a direct cytotoxic effect of licorice on renal tissue but rather a functional consequence of systemic electrolyte and hemodynamic derangements. Case reports describe reversible renal dysfunction following high-dose or chronic licorice ingestion—often exceeding 100 mg of glycyrrhizin per day for several weeks. Symptoms typically resolve within days to weeks after discontinuation, though monitoring of serum potassium, creatinine, and blood pressure remains essential during recovery.

Regulatory agencies, including the U.S. FDA and European Medicines Agency, advise caution with licorice-containing products, especially in older adults and those with cardiovascular or renal comorbidities. Patients should be counseled to avoid sustained intake of licorice-flavored candies, herbal teas, or supplements without medical supervision—and to read ingredient labels carefully, as glycyrrhizin content is rarely disclosed quantitatively.