Abstract Nearly half a century ago Revers 1 reported that administration of a paste prepared from succus liquiritiae, a dried watery extract of the roots of Glycyrrhiza glabra, resulted in a reduction in abdominal symptoms as well as radiographic evidence of healing in patients suffering from gastric ulcer. Subsequent studies demonstrated that this preparation could prevent the formation of gastric ulcers in experimental animals and confirmed the salutary effects in patients, but found that approximately 20% of patients so treated developed facial and dependent edema, often accompanied by headache, shortness of breath, stiffness, and pain in the upper abdomen 2. Although these symptoms suggested an allergic reaction, they were not accompanied by eosinophilia or relieved by antihistamines. These untoward effects usually subdided with a reduction of dose, although in some patients treatment had to be discontinued entirely. Given this profile of side effects, enthusiansm for licorice as a remedy for peptic ulcer disease soon faded. However, the popularity of licorice flavoring in candy and in other products such as chewing tobacco persists to this day, as do the problems in electrolyte and blood pressure homeostasis that can occasionally occur in individuals ingesting large quantities of licorice-containing products. 3,4 Although the pattern of the renal response suggested that the active ingredients in licorice were acting directly on the mineralocorticoid receptors in the kidney, an even more fascinating explanation for the toxic effects of licorice has emerged in the past decade. This article will review the sequence of observations that led to our current understanding of the mechanism by which licorice affects electrolyte metabolism and will particular attention to the interaction with hormonal system involved in blood pressure homeostasis.