Licorice-Induced Hypermineralocorticoidism

EXCESSIVE ingestion of licorice may result in sodium and water retention, hypertension, hypokalemia, and suppression of the renin-aldosterone system.1 , 2 It was thought for years that licorice produced these effects through the binding of its active components, glycyrrhizic acid and its hydrolytic metabolite glycyrrhetinic acid, to mineralocorticoid receptors. Two findings, however, argue against this proposed mechanism. First, the affinity of glycyrrhetinic acid, the most active component of licorice, for mineralocorticoid receptors is 0.01 percent of that of aldosterone.3 Second, licorice, or glycyrrhetinic acid, does not have mineralocorticoid effects in patients with Addison's disease2 or adrenalectomized rats1 unless cortisone or hydrocortisone is . . .