Does Licorice Increase Intraocular Pressure? I attempted to answer this question in 2009 and it came up again in our email discussion group a few years ago.
Immediately below is the information I gathered last time I looked at this question. (NOTE: Below this post, in a reply, is a newer, 2025, update.)
Glycyrrhizin is the main sweet tasting compound from liquorice root.
A derivative of glycyrrhizin is glycyrrhetinic acid.
Glycyrrhetinic acid inhibits 11β-HSD1 (11β-hydroxysteroid dehydrogenase type 1)
11β-HSD1 is an NADPH-dependent enzyme highly expressed in the liver and adipose tissue.
Selective and topical inhibitors of 11ß-HSD1 could provide a novel treatment for patients with glaucoma due to their ability to lower intraocular pressure. (See below.)
Licorice can increase blood pressure, but so far I have found no published studies that indicate licorice can increase intraocular pressure. (If you know of such information, please post an answer here.)
Is it possible that licorice compounds or derivatives could lower intraocular pressure? It appears that some researchers are attempting to answer a closely related question. See the abstract below.
Q J Med 2003; 96: 481-490
Inhibition of 11ß-hydroxysteroid dehydrogenase type 1 lowers intraocular pressure in patients with ocular hypertension
Authors: S. Rauz1,2, C.M.G. Cheung1, P.J. Wood3, M. Coca-Prados4, E.A. Walker2, P.I. Murray1 and P.M. Stewart2
Background:
Intraocular pressure (IOP) is maintained by a balance between aqueous humour (AH) production (dependent on sodium transport across a ciliary epithelial bi-layer) and drainage (predominantly through the trabecular meshwork). In peripheral epithelial tissues, sodium and water transport is regulated by corticosteroids and the 11ß-hydroxysteroid dehydrogenase (11ß-HSD) isozymes (11ß-HSD1 activating cortisol from cortisone, 11ß-HSD2 inactivating cortisol to cortisone).
Aim:
To analyse expression of 11ß-HSD in the human eye and investigate its putative role in AH formation.
Design:
Multipart prospective study, including a randomized controlled clinical trial.
Methods:
The expression of 11ß-HSD1 in normal human anterior segments was evaluated by in situ hybridization (ISH). RT-PCR for 11ß-HSDs, glucocorticoid and mineralocorticoid receptors (GR, MR) was performed on human ciliary body tissue. AH cortisol and cortisone concentrations were measured by radioimmunoassay on specimens taken from patients with primary open-angle glaucoma (POAG) and age-matched controls. Randomized, placebo-controlled studies of healthy volunteers and patients with ocular hypertension (OHT, raised IOP but no optic neuropathy) assessed the effect of oral carbenoxolone (CBX, an inhibitor of 11ß-HSD) on IOP.
Results:
ISH defined expression of 11ß-HSD1 in the ciliary epithelium, while RT-PCR analysis of ciliary body tissue confirmed expression of 11ß-HSD1, with additional GR and MR, but not 11ß-HSD2 expression. In both POAG patients and controls, AH concentrations of cortisol exceeded those of cortisone. The CBX-treated healthy volunteers who demonstrated the largest change in urinary cortisol metabolites, indicative of 11ß-HSD1 inhibition, had the greatest fall in IOP. Patients with OHT showed an overall reduction of IOP by 10% following CBX administration, compared to baseline (p<0.0001).
Discussion:
CBX lowers IOP in patients with ocular hypertension. Our data suggest that this is mediated through inhibition of 11ß-HSD1 in the ciliary epithelium. Selective and topical inhibitors of 11ß-HSD1 could provide a novel treatment for patients with glaucoma.