VIVO Pathophysiology
Licorice Intoxication and Hypermineralocorticoidism
(Moderation in all things)
A number of reports have documented a syndrome of water and sodium retention coupled with low plasma concentrations of potassium in individuals that ingested excessive licorice.
The basis of this effect is that licorice contains glycyrrhizinic acid, a molecule that inhibits 11-beta-hydroxysteroid dehydrogenase, the enzyme that normally inactivates cortisol in mineralcorticoid target cells. Cortisol has the same affinity as aldosterone for the mineralocorticoid receptor, but is present is several thousand-fold excess over aldosterone. If cortisol is not inactivated, the net effect is similar to aldosterone excess.
In one interesting case report (Farese, et al, New England J Med 325:1223, 1991), a 70 year old man with signs of severe aldosterone excess was revealed to have consumed 150 to 250 grams of licorice candies daily for 4 to 5 years! Discontinuation of the licorice was associated with normalization of fluid and electrolyte balance, as has been seen in other studies.
References and Reviews
- Farese RV, Biglieri EG, Shakleton CHL, Irony I, Gomez-Fontes R. Licorice-Induced Hypermineralocorticoidism. New Engl J Med 1991; 325:1223-1227.
Send comments to Richard.Bowen@colostate.edu