Licorice, Tobacco Chewing, and Hypertension

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Abstract
In some persons, the long-term ingestion of licorice, which contains glycoside derivatives of glycyrrhetinic acid, produces symptoms similar to those of mineralocorticoid excess —namely, hypertension, sodium retention, and hypokalemia.1 , 2 Such ingestion inhibits both hepatic and, more important, renal 11β–hydroxysteroid dehydrogenase (11β–OHSD), the enzyme that converts the Cortisol to cortisone, its inactive 11-dehydro product.3 , 4 In addition, glycyrrhetinic acid also inhibits hepatic △4–5β–steroid-reductase,5 an enzyme that reduces the A ring of steroids and thus inactivates both glucocorticoids and mineralocorticoids. The overall effect of this enzyme inhibition is an accumulation of glucocorticoid and mineralocorticoid hormones, both of which may be involved in the increased mineralocorticoid-like activity associated with licorice ingestion.6 , 7