Text Size

Site Search powered by Ajax

Licorice Root

Licorice Root

Botanical Description & Habitat

Glycyrrhiza glabra


Common names
Italian juice root
Spanish juice root
Sweet licorice
Sweet wood

Indigenous to rich low-lands and river valleys of southern Europe, the Middle East, and northern China; it is cultivated in many parts of the world.

The rootstock is brown, wrinkled, and woody, producing an erect striated stem two to five feet in height. The leaves are alternate, odd-pinnate, and have four to seven pairs of ovate, smooth, dark green leaflets. Purple or yellow-white flowers grow in axillary racemes and bloom from June to August.

Medicinal parts

Rootstock - dried, gathered during autumn

Aerial parts contain an estrogenic principle similar in potency to estrone.

Historical Properties & Uses

Licorice root is one of the most biologically active herbs known. It has found extensive therapeutic use throughout the world and has been the subject of an enormous amount of research. In folklore, licorice root is often used for its estrogenic properties, and about 90% of the available research confirms those characteristics.

The herb can influence the course of ulcers; licorice root derivatives, such as Glycyrrhetinic Acid, Deglycrrhizinated Licorice (DGL), and Carbenoxolone Sodium (CS), are among the best proven anti-ulcer medications available. The anti-inflammatory properties of the root are effective against numerous skin disorders, including eczema, dermatitis, and impetigo, as well as in the treatment of asthma.

In the circulatory system, licorice root and/or its derivatives reduce cholesterol levels; however, overdose can lead to hypertension and sodium retention (please see Toxicity for a discussion). The root and its derivatives have recently demonstrated exciting results as interferon inducers in the immune system, and Glycyrrhetinic Acid holds great promise in the treatment of liver diseases such as hepatitis and cirrhosis.

Licorice appears to both mimic and potentiate the action of the adrenal-corticosteroids, although it also differs in action from these chemicals in several important ways. The herb's antiarthritic, antiphlogistic, antitussive, laxative, and expectorant effects have been experimentally verified; its antipyrectic effects are equal to those of sodium salicylate.

This herb has approval status by the German Commission E for catarrh and ulcers.


Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.


Method of Action

Licorice affects the circulatory system and skin
Glycyrrhetinic Acid affects the heart by increasing blood sodium and decreasing blood potassium. With severe overdose, cardiac failure due to hypokalemia may result.

Glycyrrhetinic Acid stimulates the renal tubules to absorb excessive amounts of water, decrease hemoglobin, and cause rises in venous and arterial pulse pressure. These effects are similar to those of desoxycorticosterone or ACTH.

Licorice sometimes induces arterial hypertension.

Glycyrrhetinic Acid can reduce serum cholesterol levels
In one study, rats were made hypercholesterolemic by feeding them a magnesium-deficient, cholesterol-rich diet. Rats receiving dietary Glycyrrhetinic Acid showed an increase of magnesium concentration in the myocardium, a decrease of magnesium and cholesterol in the serum, and increase of glycerol and phosphorus in the lipid fraction of the serum.

The antipyretic effects of Glycyrrhetinic Acid are equal to those of sodium salicylate. Pyrexia was produced in albino rats by injecting a 15% suspension of dried Brewer's yeast in 2% Gum acacia in normal saline subcutaneously ( 1 ml/100 g body weight). Glycyrrhetinic Acid was injected in a dose of 40 mg/kg intraperitoneally, and temperatures were recorded every 2 hours. In two hours Glycyrrhetinic Acid reduced the rats' temperature from 101.6 to 99.0, a statistically significant result (p < .001).

Glycyrrhetinic Acid and its derivatives have strong anti-inflammatory properties
Participation of the adrenals, but not the pituitary, has been shown.

Two isomers of Glycyrrhetinic Acid are present in licorice root: 18-alpha and 18-beta. Both are anti-inflammatory. Whereas 18-alpha operates both through a steroidal action in the target cell and by inhibition of metabolism of endogenous corticosteroid in the liver, 18-beta's action can be explained by the inhibition of metabolism of endogenous corticosteroid alone.

Several derivatives of Glycyrrhetinic Acid showed a pronounced anti-inflammatory action, inhibited the development of histamine-, serotonin-, bradykinin-, and formalin-induced edemas, blocked the function of an inflammatory focus, lowered vascular permeability, granulemic sac weight and exudate amount. The anti-inflammatory action of the compounds remained unchanged under adrenalectomy. By antiphlogistic activity, the derivatives in question compared very favorably to butadion and hydrocortisone, and are similar to prednisolone.

Glycyrrhetinic Acid and aqueous extracts of licorice have antiarthritic properties
This activity was explained in terms of lowering the activities of serum glutamic-oxaloacetic acid transaminase and serum glutamic-pyruvic transaminase, as well as by uncoupling oxidative phosphorylation in subcutaneous tissue, i.e., it inhibits the mitochondrial biosynthesis of adenosine 5- triphosphate without inhibiting mitochondrial respiration.

GLA, 20 mg/100 gm. orally, is effective against formaldehyde-induced arthritis in adrenalectomized rats. The effect of Glycyrrhetinic Acid is slightly less than hydrocortisone (0.5 mg/100 gm, orally) in those rats. In normal animals, the effect of this dose of Glycyrrhetinic Acid is equal to that of 0.5 mg of hydrocortisone. Such findings strongly suggest the action of Glycyrrhetinic Acid is not mediated through the pituitary-adrenal system. Glycyrrhetinic Acid plus hydrocortisone is more effective than hydrocortisone alone, indicating Glycyrrhetinic Acid potentiates the action of hydrocortisone; this might explain a slight decrease in the potency of Glycyrrhetinic Acid in adrenalectomized rats. Other researchers have found a potentiating action of licorice root and Glycyrrhetinic Acid in Addison's disease and other diseases of suprarenal glands. Hydrocortisone is known to have a beneficial effect on rheumatoid arthritis in man. It is therefore strongly suggested Glycyrrhetinic Acid be given a fair trial, along with hydrocortisone, in the treatment of early cases of rhematoid arthritis and other inflammatory diseases.

Some research supports the use of Glycyrrhetinic Acid to treat wounds, to help in the healing of skin tissue following traumatization.

Glycyrrhetinic Acid is often compared to hydrocortisone for its anti-inflammatory action on various kinds of skin problems
A 2% Glycyrrhetinic Acid ointment compares favorably to hydrocortisone, and is much less expensive. Glycyrrhetinic Acid and hydrocortisone may not act in the same way, and there is evidence they may be complementary; thus hydrocortisone succeeds where Glycyrrhetinic Acid fails, and the reverse is equally true. Among the conditions successfully treated with Glycyrrhetinic Acid are the following: atopic, subacute and chronic ecaematous conditions; itching dermatoses; pruritis; acute impetigo; infantile eczema; flexural eczema; seborrheic, infective, sensitization, contact, neuro-, and exfoliative dermatitis; pustular psoriasis; impetigo; and lichen simplex.

Licorice acts on the liver and urinary tract
Glycyrrhetinic Acid has been shown to inhibit the deposition of liver glycogen by cortisone.

In Chinese medicine, licorice is often used as a remedy for jaundice. To investigate this claim, researchers ligated the common bile duct of rabbits to produce obstructive jaundice. The elevated blood bilirubin level expected from the ligation was strongly inhibited by GL. The effect was more potent than those of glucuronolactone or methionine in vivo.

Glycyrrhetinic Acid displayed a similar effect
In another experiment, ligation of the common bile duct in control animals resulted in a decrease of urinary volume and excretion of bilirubin in the urine; the administration of GL or Glycyrrhetinic Acid increased the urinary volume and markedly increased the excretion of bilirubin. In intact animals, using Buerker's common bile-duct fistula method, GL (in a dose of 1-5 mg/kg) increased bile secretion significantly.

Both GL and Glycyrrhetinic Acid prevent the development of cirrhosis in experimental animals. In CCL4-intoxicated rats, GL significantly impeded the elevation of SGPT. GL decreased the accumulation of triglycerides in the liver. Histopathological investigations revealed that lesions of the liver in GL- and GLA-treated rats were less severe that those of the CCL4 controls. Histochemical observation indicated that the liver glycogen in the DL group was increased significantly. GL and Glycyrrhetinic Acid groups had no effect on collagenolytic activity and collagen resorption.

GL, which is classified as a saponin, has a protective effect against hemolysis induced by other saponins or a cationic surfactant. Saponins are generally classified as hemolytic. In hepatic lysosomal systems, GL induces alteration in membrane fluidity by reacting with the components of the membrane or intercalating its moiety into the membrane structure.

Licorice affects the respiratory tract
The demulcent and expectorant properties of licorice are well accepted.

The antitussive activity of Glycyrrhetinic Acid was investigated using chemical stimulation in the unanaesthetized guinea pig, and electrical stimulation in the lightly anaesthetised cat. Glycyrrhetinic Acid was effective in both tests, indicating a central antitussive effect. It had about the same potency as codeine when given subcutaneously to guinea pigs; one Glycyrrhetinic Acid derivative, dicholin glycyrrhetinic acid hydrogen succinate, exhibited the same degree of activity after oral administration.

There is some evidence the anti-inflammatory properties of licorice and Glycyrrhetinic Acid also have some effect on the course of asthma. Glycyrrhetinic Acid has proven a viable treatment for tuberculosis, where its action was comparable to deoxycorticosterone.

Licorice has an effect on the gastrointestinal tract
Both Glycyrrhetinic Acid and DGL are effective in treating ulcers. The effect is not due simply to the chemicals' anti-inflammatory properties, but also probably involves their ability to inhibit gastric acid secretion with the advantage of being devoid of other anticholinergic properties.

Glycyrrhetinic Acid has a strong spasmolytic effect against induced spasms in isolated guinea pig intestine.

CS (equivalent to GLA) has been the subject of a huge amount of research, most of which has been very positive; so positive, in fact, it is often referred to as the only drug treatment for ulcers having unequivocally been shown effective.

CS potentiated the side effects of pure licorice root extract. This led researchers to search for an improved product, one just as effective, but without the side effects. Surprisingly, such an agent was found in the dross left over after the Glycyrrhetinic Acid was extracted.

This form of licorice root, call deglycyrrhizinated licorice (DGL), from which at least 97% of Glycyrrhetinic Acid is extracted, has powerful healing effects on most forms of ulcers.

In one study comparing CS to DGL, CS was slightly more effective than DGL, but not by a statistically significant amount. In most studies, DGL produces a 75%-80% reduction in ulcerative indexes.

A new solid or liquid dosage form containing DGL has been designed. This form is more suitable for human administration than the form previously used; inactive, irritating ingredients and bulky, ineffective quantities of antacids have been removed. The bitter DGL has been formulated into a unique dosage form that does not need to be chewed, one allowing for complete and rapid disintegration in the stomach.

A recent licorice root extract, FM100, has displayed protective and therapeutic effects on acute and chronic peptic ulceration in rats. It inhibited gastric acid secretion in rats and dogs, despite being devoid of anticholinergic properties. FM100 has no effect on gastric motility, salivary secretion, or bile secretion in rats, but does slightly stimulate pancreatic secretion.

Licorice extracts demonstrate action on the adrenal cortex
Licorice extracts Glycyrrhetinic Acid and CS have an aldosterone effect on the body, causing plasma retention of sodium ions and plasma depletion of potassium ions. This effect is achieved via a two-fold action of licorice products: first, they stimulate the adrenal cortex directly to produce mineral corticoids, glucocorticoids, and adrenal sex hormones; and second, they prevent degradation of these hormones by the liver and kidneys. The end result is a continuous and prolonged activation of the corticoids.

A possible mode of action is suggested by an in vitro study in rat liver, which demonstrated that Glycyrrhetinic Acid and its derivatives inhibit 5 beta-reduction to a much greater extent than 5 alpha-reduction. When Glycyrrhetinic Acid or GL were administered, 5 beta-reductase activity was significantly suppressed. On the contrary, 5 alpha-reductase was markedly increased, though its mechanism needs clarification.

In human beings, 5 beta-reductase is quantitatively the major enzyme and plays an important role in the regulation of cortisol and aldosterone metabolism. Thus it can be presumed the suppression of 5 beta-reductase activity by Glycyrrhetinic Acid or GL administration may delay the clearance of corticosteroids and prolong the biological half-life of cortisol, resulting in the synergism of these steroids and Glycyrrhetinic Acid and GL.

In one study, GL's potentiation and prolongation of hydrocortisone treatment was observed in patients with acute rheumatic fever and lupus erythematosus disseminatus. GL caused increased excretion of free and decreased excretion of conjugated 17-hydroxycorticosteroids (17-OHCS), with a total decrease of steroid excretion. It tended to cause a fall in eosinophil counts. In vitro studies showed GL inhibits the metabolism of corticoids, while Glycyrrhetinic Acid is less effective.

Glycyrrhetinic Acid inhibits the antigranulomatous property of cortisone, without affecting its anti-inflammatory ability.

Glycyrrhetinic Acid stimulates the immunosuppressive property of cortisone, while exhibiting an immunosuppressive action of its own. Through the years, licorice has often been compared to glucocorticoids and said to mimic them in action. However, licorice root differs from the glucocorticoids in several ways: it is antagonistic against a variety of physiological actions of glucocorticoids, such as antigranulomatous action, glycogen depositing effect in the liver, accelerating effect on cholesterol synthesis in the liver, atrophic action on thymus, suppressive effect on ACTH biosynthesis and its secretion; and it increases suppressive effect on antibody production and on stress reaction of glucocorticoids.

Finally, as mentioned elsewhere, it is (as SNMC) effective even on steroid-ineffective chronic active hepatitis. It accelerates the reduction of hepatitis Bs antigen titer, disappearance of HBe antigen, and appearance of antiHBe.

Licorice components exert a positive effect on the course of Addison's disease. There is evidence such an effect depends on the presence of a small amount glucocorticoid. If the disease has advanced to the stage of complete adrenal exhaustion, licorice will be beneficial only if exogenous cortisone is also present.

Licorice compounds have a slight anti-tumor action
Several licorice compounds, including monoammonium glycyrrhizinate, were tested in rats and mice with various experimental tumors, and on Ehrlich ascites tumor cells in vitro. Sodium glycyrrhizinate slightly inhibited the growth of sarcoma 45 and Ehrlich ascites cells. Another component, Compound No. 1, inhibited Ehrlich ascites cells and two sarcomas, even at submaximal doses and after oral administration. In vitro tests with all components weak, inhibition of the catabolism of corticosteroids is thought to be the mechanism of action.

Licorice compounds have estrogenic action
The first report of licorice root's estrogenic property was made in 1950, when a steroid estrogen with an absorption spectra identical to estriol was extracted from it. Since then, several investigators have found estrogenic activity in licorice root. Stigmasterol and Beta-sitosterol have been identified as the probable active components.

Licorice root is highly extrogenic, as shown by the mouse uterine weight method. After 3 doses (25 mg each) of alcohol extract, estrogenic activity was significantly higher than estradiol monobenzoate. A higher dose, 50 mg daily for 3 days, had a lower estrogenic value, which suggests an antihormone factor in the extract. Extracts had an inhibitory action on spontaneous movement of the uterus at diestrus, estrus, and pregnancy.

An extract of licorice was found to have a strong estrogenic effect; it increased uterine development in immature rats and produced vaginal cornification in ovariectomized mature rats. Fifty mg of licorice corresponds to 0.1 microgram of estradiol. In searching for the possible active estrogenic component of licorice, Glycyrrhetinic Acid was separated, examined, and found to be estrogenic. Two mg produced insignificant increases in uterine weight of immature mice, but 5 mg increased it significantly. The mean uterine weight for rats injected with Glycyrrhetinic Acid was 52, as compared with 37 for the control group.

In the next experiment, 5 mg of Glycyrrhetinic Acid was equivalent in effect to 0.1 microgram of estradiol. Moreover, Glycyrrhetinic Acid acted synergistically with estradiol by intensifying its action on uterine development. When 2 mg of Glycyrrhetinic Acid was combined with 0.1 microgram of estradiol, they produced slight increase in uterine weight of immature mice, but 5 mg of Glycyrrhetinic Acid plus 0.1 microgram of estradiol produced large and significant increases in weight (86 as compared to 56 for the controls).

There has been one dissenting voice in the research on the estrogenic properties of licorice root. In this study, Glycyrrhetinic Acid was devoid of estrogenic activity in the absence of endogenous estrogen, and was in fact anti-estrogenic; it antagonized exogenous estrogen in doses which did not interfere with somatic growth or the estrogenic effect on pituitary trophic hormone.

Licorice extracts have antihepatitic effects
GL and to a lesser extent, Glycyrrhetinic Acid were found to induce interferon production in mice. A preparation of GL combined with glycine and cysteine has been widely and successfully used in Japan as an antihepatitis drug. Interferon has also been used to treat hepatitis B patients. Licorice (DL) may be an effective antihepatitis drug because it induces production of interferon. Another study, however, found GL is also effective against alcoholic hepatitis. Therefore, the antihepatitic effect of DL may involve more than just interferon induction.

Stronger Neo-minophagen C (SNMC) is an intravenous solution composed of GL (0.2%), cysteine (0.1%), and glycine (2.0%). When chronic active hepatitis is treated (in a double-blind manner) with SNMC, 40 ml daily for 4 weeks, it accelerates the improvement of serum transaminase; prompt improvement with high statistical significance has been observed, compared with those who received a placebo.

It is doubtful GL mimics glucocorticoid in this action, since it is also effective in cases of chronic active hepatitis in which steroids are ineffective.

In one clinical trial of SNMC, of 134 patients with chronic aggressive hepatitis, 53% improved, 15% showed transition to liver cirrhosis, and 32% were unchanged. It is difficult to evaluate the efficacy of SNMC therapy, because spontaneous transient improvement is common. The main advantage of SNMC is its complete lack of toxicity and side-effects.

Glycyrrhizic acid, at concentrations tolerated well by uninfected cells, inhibits both growth and cytopathic effect of vaccinia, herpes simplex, Newcastle disease, and vesicular stomatitis viruses, while being ineffective on polio virus. Glycyrrhizic acid probably interacts with virus structures (conceivably proteins), producing different effects according to the viral stage affected: extracellular inactivation of free virus particles; prevention of intracellular uncoating of infecting particles; and impairment of the assembling ability of virus structural components.

Ethanolic extracts of commercial powdered licorice root showed reproducible antimicrobial activity in vitro against Staphylococcus aureus, Mycobacterium smegmatis, and Candida albicans.

Drug Interactions & Precautions

Known Interactions

A mixture containing astragalia radix, cinnamon, peony cnidii rhioma, angelica root, ginseng root, and licorice root has been shown to enhance antitumor activity and to decrease toxicity of mitomycin C.

Licorice reduces aspirin absorption and protects gastric mucosa against aspirin toxicity.

Possible Interactions

Licorice may induce interferon production, which in turn may inhibit the antiviral activity of puromycin.

Conversely, the adrenocortical or corticosteroidal action of licorice may be antagonized by the use of heparin.

The presence of corticosteroids in licorice may interact with uterine relaxants, such as ritodrine HCl, to produce pulmonary edema. Because this herb can affect blood serum potassium levels, it may potentiate the hypokalemic property of sodium polystyrene sulfonate.

Adrenocortical responsiveness to licorice may be impaired by the use of amphotericin B. The anti-inflammatory activity of the herb can be seriously inhibited by phenobarbital and certain other sedatives and hypnotics, such as chloral hydrate and meprobamate. This is also true of beta-adrenergic blocking agents, such as propranolol.

The presence of estrogen-like substances in licorice may increase the production of procoagulant factors, which in turn may inhibit the anticoagulant action of heparin or coumarin. These estrogenic constituents may also potentiate oral antidiabetics, folic acid antagonists, and some corticosteroids.

The presence of estrogen in licorice can inhibit antihypercholesterolemics by inducing hyperlipemia, and can inhibit the activity of most parenteral medications by reducing the rate of spreading.

Licorice's estrogenic activity may be inhibited by meprobamate and phenobarbital. Due to the presence of estrogenic substances in this herb, oxytocin may augment the electrical and contractile activity of uterine smooth muscle. The estrogen in licorice may raise blood glucose levels enough to alter insulin requirements in diabetics.

The German Commission E notes the possibility for licorice to increase potassium losses from other drugs e.g. diuretics which can then increase the sensitivity to digitalis glycosides.


To the extent that licorice's action depends on the presence of cholinergic substances, it will be affected by the decrease in cholinergic-receptor stimulation produced by anticholinergics.

The fact rifampin stimulates the metabolism of corticosteroids indicates the drug may lower the mineral and glucocorticoid action of licorice. Oral estrogen supplementation may retard the metabolism of licorice's steroidal hormones.

It should be noted in hypertensive persons, regular consumption of licorice candy or carbenoxolone sodium may induce hypokalemia, subsequently potentiating the toxic effects of cardiac drugs and counteracting hypertensive medication.

Although the coumarin content of this herb is low at normal usage levels, it is important to note coumarins can affect the action of almost any drug. It also inhibits platelet activity.

There is evidence combined use of bactericidal and bacteriostatic agents will lower the effectiveness of the bacteriostatic agent. How this finding applies to herbal anti-infectives is still unknown.


Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.

Safety Factors & Toxicity

Licorice's potential toxicity can be completely counteracted by a high-potassium diet.

The signs and symptoms of licorice-induced pseudo-aldosteronism can be summarized as follows: hypertension, hypokalemic alkalosis, suppressed aldosterone and renin levels, myoglobinuria, paresis, tetany, edema, headache, and weakness. Most victims of this condition have ingested large quantities of candy containing licorice extract, and were under treatment with carbenoxolone, or had pre-existing edematous tendencies which were exacerbated by the licorice candy (NOTE: We are talking about European candies here; American licorice has very little or no real licorice extract in it).

An illustrative case: a 53-year-old man was admitted to the hospital exhibiting several of the lesser symptoms listed above. He was a heavy salt and water user, and he was predisposed to such problems, even though he was in otherwise excellent health for his age. During the nine days prior to admission, he ate 700 grams of licorice candy, which apparently pushed him over the edge into pseudo-aldosteronism. Minimal treatment was required to restore his good health.

The sodium and water-retentive properties of licorice extracts were first noticed in 1946, when a doctor found about 20% of the patients treated with these extracts acquired edema. Since then, it has been found licorice intoxication is able to induce hypertension, with features of primary hypermineralocorticism associated with underproduction of aldosterone. The electrolyte-active principle of licorice is glycyrrhizic acid. Glycyrrhetinic Acid competes very weakly with cytoplasmic mineral corticoid receptors, and thus has a direct mineral corticoid action. Such low affinity is in good agreement with the very high doses required to exhibit its biological and/or toxic activity.

Licorice's toxicity has been greatly exaggerated. Candy flavored with licorice extract has indeed led to poisoning in individuals who habitually consumed 1/2 to 1 pound or more daily, and in individuals who, for one reason or another, are extremely sensitive to the extract (as found in ulcer cures and laxatives). Ingestion of the whole herb, in capsule, tea, or stick form, has not resulted in any significant toxicity.

Pseudo-aldosteronism can easily be prevented by a high-potassium, low-sodium diet. Although no experiments have demonstrated an absolute protective effect, patients on carbenoxolone (even those with pre-existing hypertension and angina), who normally consume high-potassium foods and restrict sodium intake, are reported free from sodium-retaining side effects.

As a general cautionary measure, people with a history of hypertension, renal failure, or who are currently using cardiac glycosides, may wish to avoid the use of licorice root altogether.

This herb has approval status by the German Commission E.

The German Commission E recommends a limited duration for the use of this herb of 4 - 6 weeks, unless specified by a physician.


Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.


Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.

Preparation & Administration

Three times a day
Large doses over a long time may produce hypokalemia

Dried root
1-4 grams

made from 1 tsp of dried root

Fluid extract
1:1 in 25% alcohol, 2-5 ml

Deglycerrhizinated root
250 mg

This herb has approval status by the German Commission E.

Recommended daily dosages in Germany are as follows:

5 - 15 g root or 200 - 600 mg glycyrrhizin.

The German Commission E recommends a limited duration for the use of this herb of 4 - 6 weeks, unless specified by a physician.

100 mg may be safely used as a flavoring agent.


Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.

Note: This Herbal Preparation information is a summary of data from books and articles by various authors. It is not intended to replace the advice or attention of health care professionals.



Abe, N., E. Takusaburo & N. Ishida. 1982. Interferon induction by glycyrrhizin and glycyrrhetinic acid in mice. Micro and Imm, 26(6).

Aburada, M., et.al. 1983. Protective effects of juzentaihoto, dried decoction of 10 chinese herbs mixture, upon the adverse effects of mitomycin C in mice. J of Pharmacobiodynamics, 6(12). pp. 100-104.

Adamson, A.C. & W.G. Tillman. Hydrocortisone. British Medical Journal. Dec 17, 1955, p. 1501.

Albert-Puleo, M. 1980. Fennel and anise as estrogenic agents. Journal of Ethnopharmacology, 2. pp. 337-344.

Aleshenshaya, E.E., Y.A. Aleshkina, et.al. Pharmacology of glycyrrhiza glabra (licorice) preparations. Farmikol. I Toksikol., 27(2), 217-222, 1964.

Amagaya, S., E. Sugishita, et.al. Comparative studies of the stereoisomers of glycyrrhetinic acid on anti-inflammatory activities. Journal Pharm. Dyn., 7, 923-928, 1984.

Am Hospital Formulary Service. Am Soc of Hosp Pharm. Wash, D.C.

Andersson, S. Protective action of deglycyrrhizinised liquorice on occurrence of stomach ulcers. Scandanavian Journal Of Gastroenterology. 6(8), 683-686.

Anderson, D.M. & W.G. Smith. The antitussive activity of glycyrrhetinic acid and its derivatives. Journal Of Pharmacy And Pharmacology, 13, 396-404, 1961.

Anderson, Brany, Caboda, & Mizuno. Protective action of deglycyrrhizinated licorice on the occurrence of stomach ulcers in pylorous-ligated rats. Scandinavian Journal Of Gastroenterology, 6, 683-686, 1971.

Azarnoff, D. & A. Hurwitz. 1970. Drug interactions. Pharmacol Physicians. 4(2). pp. 1-7.

Baron, J., J. Nabarro, J. Slater & R. Tuffley. Metabolic studies, aldosterone secretion rate and plasma renin after carbenoxolone sodium as biogastrone. British Medical Journal, 2, 793-795, 1969.

Berger, H, & H. Hoeller. Zur spasmolytischen wirkung handelsueblicher succus-liquiritiae-sorten. Scientia Pharmaceutica, 23(3), 145-148, 1955.

Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.

Borst, J.G.G., S.P. Holt & L.A. De Vries & J.A. Molhuysen. Synergistic action of liquorice and cortisone in Addison's and Simmond's disease. Lancet, 1, 657-663, 1953.

Bressler, R., M.D. Bogdonoff & G.J. Subak-Sharpe. 1981. The Physicians Drug Manual. Doubleday & Co, Inc. Garden City, NY. 1213 pp.

Brogden, R.N., T.M. Speight & G.S. Avery. Deglycyrrhizinised liquorice: a report of its pharmacolgical properties and therapeutic efficacy in peptic ulcer. Drugs, 8(5), 330-339, 1974.

Buffington, G., et.al. 1976. Interaction of rifampin and glucocorticoids. J of the Am Med Assoc, 236. pp. 1958-1960.

Chamberlain, T.J. 1970. Licorice poisoning, pseudo-aldosteronism, and heart failure. Journal of the Am Medical Assoc, 213. p. 1343.

Chang, L. Preliminary report on using glycyrrhiza in combination with antituberculosis drugs in pulmonary tuberculosis. Jen. Min. Pao Chien, 3, 235-238, 1959.

Clark, T.H., A.H. Conney & B.P. Harpole, et.al. 1967. Drug interactions that can affect your patients. Pat Care, 1(11) p. 33-71.

Cliff, J.M. & G.J. Milton-Thompson. A double blind trial of carbenoxolone capsules in the treatment of duodenal ulcer. Gut, 11, 167-170, 1970.

Colin-Jones, E. Glycyrrhetinic acid. British Med Jnal, Jan 19, 1957.

Committee on Pharmocopaeia of the Am Institute of Homeopathy, The Homeopathic Pharmacopaeia of the United States. 8th ed., Vol 1. Otis Clapp and Son, Agents, Boston, l981.

Conn, J.W., D.R. Rovner & E.L. Chohen. J Of Am Med Assoc, 205, 80, 1968.

Cooke, W.M. & J.H. Baron. Metabolic studies on deglycyrrhizinated licorice in two patients with gastric ulcer. Digestion, 4, 264-268, 1971.

Costello, C.H. & C.L. Butler. 1950. The estrogenic and uterine-stimulating activity of asclepias tuberosa. A preliminary investigation. J of the Am Pharm Assoc, 39. pp. 233-237.

Costello, G.H. & E.V. Lynn. Estrogenic substances from plants: I. Glycyrrhiza. Journ Of The Am Pharm. Association, 39, 177-180, 1950.

Cunitz, G. On the effect of succus liquiritae.: Arzneimittel forschung, 18, 434-435, 1968.

Donomae, I. Gycyrhizzin acid. Nippon Rinsho, 19, 1369-1372, 1960.

Drug package insert (FDA approved official brochure) and other labeling based on sponsored clinical investigations and New Drug Appl. data.

Feldman, H., Gilat, T. A trial of deglycyrrhizinated licorice in the treatment of duodenal ulcer. Gut 12 (1971): 499-45 1.

Fujisawam, Watanabe, & Kimura. Therapeutic approach to chronic active hepatitis with glycyrrhizin. Asian Medical Journal, 23, 745-756, 1980.

Goodman, L.S. & A. Gilman. 1975. Pharm Basis of Thera. MacMillan, NY.

Greenberg, H.B., R.B. Polland, et. al. Effect of human leukocyte interferon on hepatitis B virus infectioin in patients with chronic active hepatitis. New England J Of Medicine, 295, 517-522, 1976.

Groen, J., P.H. Willebrands, et.al. Extract of licorice for the treatment of addison's disease. N Eng J Of Med, 244, 474-475, 1951.

Gujral, S. H. Bhumra & M. Swaroop. Effect of ginger (zingebar officinate roscoe) oleoresin on serum and hepatic cholesterol levels in cholesterol fed rats. Nutri Rprts Inter, 17(2), 183-189, 1978.

Gujral, M.L., K. Sareen, D.P. Phukan & M.K.P. Amma. Antiarthritic activity of glycyrhizin in adrenalectomized rats. Indian Journal Of Medical Science, 15(8), 625-629, 1961.

Hansten, P.D. 1979. Drug Interactions, 4th ed. Lea & Febiger, Phila.

Hart, F.D. Treatment of adrenocortical deficiency states. British Medical Journal, 1, 417-422, 1957.

Hench, P.S., E.C. Kendall, C.H. Slocum & H.P. Polly. Further studies concerning the participation of the adrenal cortex in pathogenesis of arthritis. Proceedings Of Mayo. Clin., 24, 181, 1949.

Hida, T. Ulstrstructural studies of the protective effect of glycyrrhizin for the mouse liver injury caused by ethanol administration. J Of Nagoya City Univ Med Assoc, 30, 333-356, 1979.

Hudson, P.B., A. Mithelman & M. Podherezec. Use of glycyrrhizin after bilateral adrenalectomy. New Eng J Of Med. 251, 641-646, 1954.

Hyde, F.F. British Herbal Pharmacopoeia. British Herbal Medicine Assoc: West Yorks, England, 1983

Ichioka, H. The pharmacological action of glycyrrhizin. III. The effect on the bile secretion in rabbits. Gifu Daigaku Igakubu Kiyo, Gigu University School Of Medicine, 15(3), 810-812, 1968.

Ichioka, H. The pharmacological action of glycyrrhzin. II. The effect on urinary excretion of bilirubin in rabbits' ligated common bile duct. Gifu Daigaku Igakubu Kiyo, Gifu University School Of Medicine, 15(3), 580-589, 1968.

Ichioka, H. The pharmacological action of glycyrrhizin. I. The effect on the blood bilirubin level in rabbits ligated common bile duct. Gifu Daigaku Igakubu Kiyo, Gifu University Schoool Of Medicine, (15(3), 792, 1968.

Inoue, H et al., Inhibitory effect of glycyrrhetinic acid derivatives on lipoxygenase and prostaglanding synthetase. Chem. & Pharm. Bull. 1986, 34:901.

Ishii, Y. & M. Terada. Effect of Fm100, a fraction of licorice root, on exocrine secretion from the rat pancreas. Japanese Journal Of Pharmacology, 29, 66-667, 1979.

Iwamura, K. Ergebnisse der therapie mit dem medikament strong neo-minophagen c der chronischaggressiven hepatitis in japan. Therapiewoche, 30, 5431-5445, 1980.

Kastrup, E.K., ed. 1981. Drug Facts and Comparisons, 1982 edition. Facts and Comparisions Division, J.P. Lippincott Co, Phila(St. Louis).

Kraus, S.D. Glycyrrhetinic acid--a triterpene with antioestrogenic and anti-inflammatory activity. J Of Pharm & Pharm, 12, 300-306, 1960.

Kumagai, A. Effect of glycyrrhizin on cortisone action. Proc. 3 Rd Asia And Oceanic Congress On Endocrinology, 1968, pp. 411-413.

Kumagai, A.S., K. Yano, et.al. An inhibitory effect of glycyrrhizin on the antigranulomatous action of cortisone. Endocrinology, 74(1), 145-148, 1963.

Kumagai, A.S., M. Nishino, et.al. An inhibitory effect of glycyrrhizin on metabolic action of cortisone. Endocrinologica Japonica, 13(4), 416-419, 1966.

Kumagai, A.S., M. Nishino, et.al. Effects of glycyrrhizin on thymolytic and immunosuppressive action of cortisone. Endocrinologica Japonica, 14(1), 39-42, 1967.

Kumagi, A.S., S. Yano, et.al. The corticoid-like action of glycyrrhizin and the mechanism of its action. Endocrinologica Japonica, 4, 17-27, 1957.

Kumagi, A.S. Minophagen Medical Review, 12, 14, 1967.

Kuroyanagi, T. The effect of prednisolone, 6-mercaptopurine and glycyrrhizin on skin homo-transplantation in rats." Arerugi, 16(10), 676-679, 1967.

Leven, W., R.M. Welch & A.H. Coney. Effect of phenobarbital and other drugs on the metabolism and uterotropic action of estradiol-17beta and estrone. J of Pharmacology and Experi Thera, 159. pp. 362-371.

Lewis, J.R. Carbenoxolone sodium in the treatment of peptic ulcer. Journal Of The American Medical Association, 229(4), 460-462, 1974.

List, P. & L. Hoerhammer. 1969-1976. Hagers Hanbuch der Pharmazeutischen Praxis, vols. 2-5. Springer-Verlag, Berlin.

References M-Z

Martin, E.W. 1978. Drug Interactions Index, 1978/79. J.B. Lippincott Company, Philadelphia.

Matsuda, S. & K. Oda. Histochemical studies on the effect of glycyrrhizin on corticoid metabolism. Bisshin Igaku 49, 464-481,1962.

McCallum, D.I. Glycyrrhetinic acid. Brit Med J, Nov 24, 1956. Millar, J.H.D., et. al. British Medical Journal, 1, 765, 1973.

Mitscher, Park, Clark, & Beal. Antimicrobial agents from higher plants. antimicrobial isoflavanoids and related substances from flycyrrhiza glabra L. var. typica. Journal Of Natural Products, 43(2), 259-269, 1980,

Molhuysen, J.A., A.J. Gerbranby, et.al. A licorice extract with deoxycortone-like action. Lancet, 259, 6630, 381-(386, 1950.

Morgan, R.J., et.al. 1983. The protective effect of deglycyrrhinized liquorice against aspirin and aspirin plus bile acid-induced gastric mucosal damage, and its influence on aspirin absorbtion in rats. J of Pharm. Pharmacol. 35(9). pp. 605-607.

Mori, T., Yamamoto, N. A new anti-human immunodeficiency virus substance, glycyrrhizin sulfate: endowment of glycyrrhizin with reverse transcriptase-inhibitory activity by chemical modification. Jpn J Cancer Res (GANN) 78 (1987): 767-77 1.

Murav'ev, I.A. & N. Kononikhina. Estrogenic properties of glycyrrhiza glabra. Rastitel'nye Resursy, 8(4), 490-497, 1972

Nagy, G.S. Evaluation of carbenoxolone sodium in the treatment of duodenal ucler. Gastroenterology, 74, 7-10, 1978.

Nakamura, M.Y., T. Ishiara, et.al. Effects of dietary magnesium and glycyrhizzin on experimental atheromatosis of rats. Japanese Heart J, 7(5), 474-486, 1966.

Nakagawa, K. & M. Asami. Effect of glycyrrhizin on hepatic lysosomal systems. Japanese Journal Of Pharmacology, 31, 849-851, 1981.

Nasyrov, K.M. & D.N. Lazareva. Study of the anti-inflammatory activity glycyrrhizin acid derivatives. Farmakologiia I Toksikologiia, 43(4), 399-404, 1980.

Nelson, D.H., et.al. 1963. Potentiation of the biologic effect of administered cortisol by estrogen treatment. J of Clin Endocrinology and Metabolism, 23(3). pp. 261-265.

Newall CA, Anderson LA, Phillipson JD. Herbal Medicines A Guide for Health-care Professionals. London: The Pharmaceutical Press, 1996:21,45,63,282.

Nikitina, S.S. Data on the mechanism of anti-inflammatory action by glycyrrhizic acid and glycyrrhetic acid from glycyrrhiza. Farmikol. I. Toksikol. 29(1), 67-70, 1966.

Osol, Arthur. 1980. Remington's Pharmaceutical Sciences. Mack Publishing Company, Pennsylvania. 1928 pp.

Osol, A. & R. Pratt. 1973. The United States Dispensatory. J.B. Lippincott Company, Philadelphia. 4000 pp.

Oura, H., N. Shoichi, et. al. Immunosuppressive effect of licorice root extracts. Taisha, 10, 651-658, 1973.

Parmar, S.S., K.K. Tangri, P.K. Seth & K.P. Bhargava. Biochemical basis for anti-inflammatory effects of glycyrrhetic acid and its derivatives. Int. Cong. Biochem., 6(5), 410, 1964.

Patton, F. Two cases of arterial hypertension due to glycyrhizzin poisoning. Lyon Med., 223,721-726, 1970.

Pelner, L. 1969. Licorice and hypertension. J of the Am Med Assoc, 208.

Pelser, H.E., A.F. Willebrands, et. al. Comparative study of the use of glycyrrhizinic and glycyrrhetinic acids in Addison's disease. Metabolism, 2, 322-334, 1953.

Pizzorno, Joseph E., & Murray, Michael T. A Textbook of Natural Medicine. John Bastyr College Publications: Seattle, Wa, 1985

Pointet-guillot, U. Contribution A Petude Chimique Et Pharmacologique De La Reglisse. Thesis, Paris, 1958.

Pompei, R., Fiore, O., Marccialis, M.A., Pani, A., Loddo, B. Glycyrrhizic acid inhibits virus growth and inactivates virus particles. Nature 281 (1979): 689-690.

Pompei, R., A. Pani, O. Flore, M. Marcialis & B. Loddo. Antiviral activity of glycyrrhizic acid. Experientia, 36, 304, 1980.

Rees, W, Rhodes, J., Wright, J., et al. Effect of degiycyrrhizinated liquorice on gastric mucosal damage by aspirin. Scand J Gastroent (I 979): 605-607.

Revers, F.E., T. Nederl. Geneesk, 90, 135, 1946.

Riesterer, L. & R. Jaques. 1968. Interference by beta-adrenergic blocking agents with the antiinflammatory action of various drugs. Helv Physiol Acta, 26. pp. 287-293.

Saxen, R.C. & T.N. Ghalla. Antipyretic effect of glycyrrhetic acid and imipramine. Japanese J Of Pharma, 18(3), 353-355, 1968.

Scientific Committee, British Herbal Pharmocopaeia, British Herbal Med Assoc, Lane House, Cowling, Na Keighley, West Yorks, Bd Bd220lx, l983. Sharaf,a. & Gomaa, N. Medicine And Medicament Courier, 11, 29, 1965.

Sharaf, A. & N. Gomaa. Gycyrrhetic acid as an active oestrogenic substance separated from glycyrrhiza glabra (liquorice). Egyptian Journal Of Pharm. Science, 16(2), 245-251, 1975.

Sheehan MP, Atherton DJ. One-year follow up of children treated with Chinese medical herbs for atopic eczema. Br J Dermatol 1994;130:488—93.

Sheehan MP, Rustin MHA, et al. Efficacy of traditional Chinese herbal therapy in adult atopic dermatitis. Lancet 1992;340:13—17.

Shiata, I. & M. Elghamry. Zbl. Veterinairmed, 10, 155, 1963.

Shihata, I.M. & M.I. Elghamry. Estrogenic activity of glycyrrhiza glabra with its effects on uterine motility at various stages of the sex cycle. Zentr. Mterinaermed., Ser A, 10, 155-162, 1963.

Shiki, Y., Shirae, K., Saito, Y., Yoshida, S., Mori, Y., Wakashin, M. Effect of glycyrrhizin on lysis of hapatocyte membranes induced by anti-liver cell membrane antibody. Journal of Gastroenterology and Hepatology I (1992): 12-16.

Shvarev, I.F., N.K. Konovalova & G.I. Putilova. Effect of triterpenoid compounds from glycyrrhiza glabra on experimental tumors. Voprosy Izuch. Ispol'z. Solodki Sssr, Akad. Nauk Sssr, 1966, pp. 167-170.

Sircus, W. Progress report on carbenoxolone sodium. Gut, 13, 816-824, 1972.

Sommerville, J. Glycyrrhetinic acid. Brit Med J, Feb 2, 1957, p.282-283.

Spangler, A.S., et.al. 1969. Enhancement of the antiinflammatory action of hydrocortisone by esrtogen. J of Clin Endoc, 29(5) p.650-655.

Stuart, D.M. 1968. Drug metabolism Part 2. Drug interactions. PharmIndex, 10(10). pp. 4-16.

Takagi, K., K. Watanabe & Y. Ishii. Peptic ulcer inhibiting activity of licorice root. Proc. Int. Pharmacol. Meeting, 7(2), 1-15, 1965.

Takino, Y., Koshloka, M., Shlokawa, M., et al. Quantitative determination of glycyrrhizic acid in liquorice roots by TLC-densitometry. Studies on the evaluation of crude drugs, VI. Planta Medica 36 (1979): 74-78.

Tamura, Y., T. Nishikawa., et. al. Effects of glycyrrhetinic acid and its derivatives on delta-four-5-alpha- and 5 beta-reductase in rat liver. Arzneimittel-forschung, 29(4), 647-649, 1979.

Tangri, K.K., P.K. Seth, S.S. Parmar & K.P. Bhargava. Biochemical study of the anti-inflammatory and antiarthritic properties of glycyrrhetic acid. Biochem. Pharmacol., 14(8), 1277-1281, 1965.

Tewari, S.N. & A.K. Wilson. Deglycyrrhizinated licorice in duodenal ulcer. Practitioner, 210, 820-823, 1973.

Turpie, A.G.G., J. Runcie & T.J. Thompson. Clinical trial of deglycyrrhizinated liquorice in gastric ulcer. Gut, 10, 299-302, 1969.

Ulmann, A., J. Menard & P. Corvol. Binding of glycyrrhetinic acid to kidney mineralcorticoid and glucocorticoid receptors. Endrocinology, 97(1), 46-51, 1975.

Vah Hulle, C. Ueber die oestrogene wirkung der suessholzwurzel. Pharmazie, 25, 260-261, 1970.

Wanahoshi, M. The influence of glycyrrhizin on the biological action of cortisone. Nippon Naibumpi Gakkai Zasshi, 42(12), 1312-1319, 1967.

Whitehouse, M.W., P.D.G. Dean & T.G. Halshall. Uncoupling of oxidative phosphorylation by glycyrrhetic acid, fusidic acid and some related triterpenoid acids. J Of Pharm & Pharm, 19(8), 533-544, 1967.

Wison, J.A.C. A comparison of carbenoxolone sodium and deglycyrrhizinated liquorice in treatment of gastric ulcer in the ambulant patient. The British J Of Clin Pract, 26, 563-566, 1972.

Yamamoto, S., Y. Maekawa, et. al. Therapeutic effects of stronger neo-minophagen c on chronic hepatitis. Clin Med & Ped, 13, 73-75, 1958.

Yano, S. The corticoid-like actiion of glycyrrhizin. Nippon Nabinpi Gakkai Zasshi, 34, 745-751, 1958.

Zhao, M.Q., D.W. Han, X.H. Ma, Y.C. Zhao, L. Yin & C.M. Li. The preventive and therapeutic actions of glycyrrhizin, glycyrrhetic acid and crude saikosides on experimental cirrhosis in rats. Yao Hsueh Hsueh Pao, 18(5), 325-331, 1983.



Follow Applied Health on FaceBook Follow Applied Health on Twitter Follow Applied Health on Pinterest Follow Applied Health on YouTube

cruelty free - tested only on humans
We test only on humans