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Glycyrrhizin, glycyrrhizinic acid or glycyrrhizic acid, is the
active principle of liquorice root. It is a powerful sweetener,
3050 times as potent as sucrose (table sugar).
Chemically speaking, glycyrrhizin is a triterpene glycoside with
the systematic name (3-beta,20-beta)-20-carboxy-11-oxo-30-norolean-12-en-3-yl
2-O-beta-D-glucopyranuronosyl-alpha-D-glucopyranosiduronic acid.
The acid form is not particularly water-soluble, but its ammonium
salt is soluble in water at pH greater than 4.5.
Although sweet, the taste of glycyrrhizin is different from that
of sugar. Glycyrrhizin's sweetness has a slower onset than sugar's,
and lingers in the mouth for some time. Additionally, its characteristic
licorice flavor makes it unsuitable as a direct flavor substitute
for sugar. Unlike the artificial sweetener aspartame, glycyrrhizin
maintains its sweetness under heating.
In the United States, glycyrrhizin is Generally Recognized as Safe
as a flavoring agent, although not as a sweetener. Glycyrrhizin
is used as a flavoring in some candies, pharmaceuticals, and tobacco
products.
In Japan, where concern over the safety of artificial sweeteners
during the 1970s led to a shift towards plant-derived sugar substitutes,
glycyrrhizin is a commonly used sweetener, often used in combination
with another plant-based sweetener, stevia. However, glycyrrhizin
appears to have some pharmacological side effects, and the Japanese
government has asked its citizens to limit their consumption to
200 milligrams per day.
Health Effects
Glycyrrhizin and other licorice root products have been used for
numerous medical purposes, particularly treatment of peptic ulcers
and as an expectorant. The triterpene derivative of glycyrrhizin,
glycyrrhetinic acid, is itself effective in treatment of peptic
ulcer. A synthetic analog, carbenoxolone, was developed in Britain.
Both glycyrrhetinic acid and carbenoxolone have a modulatory effect
on neural signaling through gap junction channels.
The most widely reported side effects of glycyrrhizin use are hypertension
and edema (water retention).
Why Hypertension?
Glycyrrhizin inhibits the conversion of cortisol to cortisone by
inhibiting the enzyme 11-Betahydroxysteroid Dehydrogenase. As a
result, cortisol builds up at the collecting duct. Cortisol has
intrinsic mineralocorticoid properties (that is, it acts like aldosterone
and increases sodium reabsorption) that work on ENaC channels in
the collecting duct. Hypertension develops due to this mechanism
of sodium retention. Patients often have high blood pressure with
a low renin and low aldosterone blood level.
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