Re: Licorice allows cortisol to bind to aldosterone receptors

So funny Amber...was reading about this just yesterday and was going to post it but didn't have time :-)

When there is excess cortisol, the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) should convert the excess to cortisone.

Naturally if there is a problem with this enzyme doing this then, as your link suggests, cortisol remains high and binds to it's own and aldosterone receptors.

However, it seems that Licorice, inactivates this enzyme too.
Which is why  many people with low cortisol find licorice helpful as it extends circulating cortisol and prevents it being converted, yet those with the first stages of AF (high cortisol) find licorice too 'stimulating', as suppressing the very enzyme that converts cortisol to cortisone when you have high cortisol will make you feel even worse.

http://www.endotext.org/adrenal/adrenal24/adrenal24.htm  :

"Since cortisol circulates at plasma concentrations several orders of magnitude higher than those of aldosterone does, and since it has a high affinity for the MR, it would be expected to overwhelm this receptor in mineralocorticoid target tissues and cause mineralocorticoid excess. A local enzyme, 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), however, converts active cortisol to inactive cortisone, and protects the MRs from the effects of cortisol (34). 11β-HSD catalyzes the interconvension of hormonally active C11-hydroxylated corticosteroids (cortisol in humans or corticosterone in rodents) and their inactive C11-keto metabolites (cortisone in humans or 11-dehydrocorticosterone in rodents). Two isozymes of 11β-HSD have been identified, 11β-HSD type 1 (11β-HSD1) and 11β-HSD2, which differ in their biological properties and tissue distributions. 11β-HSD2, a potent NAD-dependent 11β-hydrogenase, rapidly inactivates glucocorticoids. The human 11β-HSD2 gene encodes 405 amino acids and its molecular weight is approximately 40-kilodalton (35). 11β-HSD2 has a hydrophilic N-terminal domain that is thought to anchor the protein into membranes (36). 11β-HSD2 is localized as a dimmer in the nucleus and cytoplasm of cells of the cortical collecting duct and colon (36,37). Prednisolone and prednisone are substrates for both 11β-HSD isozymes (38,39) and dexamethosone is metabolized slightly by 11β-HSD2 (40). Licorice derivatives, such as glycyrrhizic acid, and the hemisuccinate derivative carbenoxolone are inhibitors of 11β-HSD2. Inhibition of 11β-HSD2 with such agents derivatives confers mineralocorticoid potency to physiologic concentrations of endogenous glucocorticoids in the kidney and colon (41). Thus, in normal physiology, 11β-HSD2 protects the MR by converting cortisol to the inactive cortisone and allows aldosterone-selective access to the inherently nonselective MR in mineralocorticoid target tissues."

So perhaps taking liqorice is good for low cortisol, but maybe prolonged intake could disrupts the aldosterone balance so perhaps it isn't good after all?

I've never been on licorice except trying it once or twice and found no difference in symptoms a few months ago.