Synopsis

Source of validity: Scientific
Rating (out of 5): 2

Licorice (Glycyrrhiza glabra) has been historically and scientifically considered in the supportive management of Addison’s Disease, though it should not be regarded as a primary therapy. The rationale is rooted in the pharmacological activity of glycyrrhizin, a constituent found in licorice root. Glycyrrhizin inhibits the enzyme 11β-hydroxysteroid dehydrogenase type 2, which is responsible for converting active cortisol to its inactive form, cortisone. By inhibiting this enzyme, licorice can increase the half-life and activity of endogenous or exogenously administered cortisol, thereby potentially augmenting glucocorticoid effects in patients with adrenal insufficiency.

Historically, licorice was used for "adrenal fatigue" and related conditions before the mechanisms of Addison’s Disease were fully understood. In modern times, a few clinical and preclinical studies have explored licorice’s mineralocorticoid-like effects, which can assist with sodium retention and potassium excretion—similar to aldosterone, the hormone deficient in Addison’s Disease. However, the risk of pseudoaldosteronism (hypertension, hypokalemia, edema) with licorice use is significant, and its benefits are modest compared to standard hormone replacement therapy. Major medical guidelines do not recommend licorice as a standard treatment for Addison’s Disease, but its use is scientifically plausible as an adjunct in select, carefully monitored cases. The overall clinical evidence is limited, and the potential for harm restricts its use.

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