At a glance: Liquorice root is obtained from several Glycyrrhiza species and contains glycyrrhizin, a triterpene saponin responsible for both important pharmacology and a distinctive toxicity syndrome. Repeated or high exposure can inhibit renal 11β-hydroxysteroid dehydrogenase type 2, allowing cortisol to activate mineralocorticoid receptors and causing sodium retention, hypertension and potassium loss. Severe cases can lead to arrhythmia, paralysis, rhabdomyolysis or coma.[1][2][3]

Botanical profile

  • Medicinal species in the current EMA monograph: Glycyrrhiza glabra L., Glycyrrhiza inflata Bat. and Glycyrrhiza uralensis Fisch.
  • Common name: liquorice / licorice root.
  • Family: Fabaceae.
  • Medicinal part: root and stolon material represented as Liquiritiae radix.
  • EMA herbal drug name: Liquiritiae radix.[1]

The EMA published a revised final EU herbal monograph and assessment report in July 2026, making liquorice one of the freshest regulatory sources in this library.[1]

Major constituent groups

Important constituents include:

  • Glycyrrhizin (glycyrrhizic acid), the characteristic sweet triterpene saponin.
  • Glycyrrhetinic acid, a pharmacologically active metabolite formed after intestinal metabolism of glycyrrhizin.
  • Flavonoids and chalcones, including liquiritin, isoliquiritin and related compounds.
  • Polysaccharides, coumarins and other phenolics in smaller proportions.[4]

The amount of glycyrrhizin matters enormously for safety, which is why ordinary liquorice and deglycyrrhizinated liquorice (DGL) should not be treated as identical products. DGL has had most glycyrrhizin removed and therefore has a different risk and evidence profile.[5]

Traditional use

Liquorice root has been used across European, Middle Eastern and Asian herbal traditions as a soothing demulcent and expectorant for coughs, sore throats and irritated airways. It has also been used for indigestion, gastritis-like discomfort, heartburn and ulcer-type digestive complaints. In Chinese herbal medicine liquorice is frequently included in formulas as a harmonising herb, used to moderate the properties of other ingredients and support the digestive system.

Contemporary herbal practice

Liquorice is widely used by herbalists as both a medicine in its own right and a formulation herb. It may be chosen for an irritated dry cough, inflamed upper digestive mucosa or as a small component of a multi-herb prescription where its demulcent, expectorant and harmonising qualities are useful. Because glycyrrhizin can materially affect blood pressure, potassium and medicine safety, modern practitioners distinguish ordinary liquorice from DGL and pay close attention to dose and duration.

Regulatory use

The EMA monograph concerns liquorice-root preparations within cough/cold and gastrointestinal therapeutic areas.[1] Students should use the current monograph when describing the exact preparations and indications rather than relying on older retail or textbook summaries, because the 2026 revision supersedes earlier versions.

Why liquorice can raise blood pressure

The classic toxicity mechanism is well characterised. Glycyrrhizin is metabolised in the intestine to glycyrrhetinic-acid-related metabolites. These inhibit 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), an enzyme that normally converts cortisol to less active cortisone in mineralocorticoid-sensitive tissues such as the kidney.[2][6]

When 11β-HSD2 is inhibited, cortisol can stimulate mineralocorticoid receptors more strongly. The resulting syndrome resembles excess aldosterone even though renin and aldosterone are often suppressed. Consequences can include:

  • sodium and water retention;
  • increased blood pressure;
  • potassium loss and hypokalaemia;
  • metabolic alkalosis; and
  • in severe cases, cardiac arrhythmia, muscle weakness or paralysis, rhabdomyolysis and neurological complications.[2][3]

How strong is the human evidence for blood-pressure effects?

A 2017 systematic review and meta-analysis found that consistent glycyrrhizic-acid-containing liquorice ingestion increased systolic and diastolic blood pressure and reduced plasma potassium, renin activity and aldosterone. The analysis also reported a dose-response relationship for blood pressure.[7]

This is not merely a theoretical herb–drug interaction. It is a reproducible physiological effect with a substantial clinical case literature.

Why individual susceptibility varies

Not everyone develops toxicity at the same exposure. Dose and duration matter, but individual pharmacokinetics, intestinal microbiota, renal function, baseline blood pressure, electrolyte status and concurrent medicines may modify risk. Recent research has examined circulating glycyrrhizin metabolites to explain why some people develop pseudoaldosteronism at comparatively low intake while others tolerate more.[6][8]

Preparations and food exposure

Liquorice exposure may come from herbal medicines, teas, confectionery, flavourings and combination traditional medicines. Food exposure is clinically relevant because a person may not think of liquorice sweets or drinks as “taking a herb”.

DGL products are specifically processed to remove most glycyrrhizin. Their use cannot be evaluated by simply importing toxicity or efficacy evidence from ordinary liquorice root, because removing glycyrrhizin changes the intervention.[5]

Interactions and high-risk situations

Because glycyrrhizin-containing liquorice can alter blood pressure, fluid balance and potassium, particular caution is warranted when a person uses medicines or has conditions in which those variables matter. Clinically important examples include:

  • diuretics that can lower potassium;
  • digoxin and other medicines whose toxicity is worsened by hypokalaemia;
  • antihypertensive treatment;
  • corticosteroids or medicines affecting mineralocorticoid physiology; and
  • kidney or cardiovascular disease.

The relevant question is not simply “does liquorice interact with drug X?” but whether the herb’s own physiological effects can amplify the risks of the medicine or disease.

Safety signs that require attention

Possible features of excess glycyrrhizin exposure include new or worsening high blood pressure, ankle or generalised swelling, muscle weakness, cramps, fatigue, palpitations or other symptoms consistent with electrolyte disturbance. Severe symptoms require medical assessment rather than simply reducing the herbal dose.

Pregnancy and breastfeeding

Medicinal use in pregnancy or breastfeeding should be approached cautiously and assessed against current product and regulatory information. LactMed notes that glycyrrhizin is metabolised to active glycyrrhetinic acid and distinguishes ordinary liquorice from DGL; scientifically valid evidence for liquorice as a galactagogue is lacking.[5]

Student note: common evidence traps

  • Do not call liquorice-induced pseudoaldosteronism “high aldosterone”: renin and aldosterone are often suppressed.
  • Do not confuse glycyrrhizin with glycyrrhetinic acid; one is metabolised into the other.
  • DGL is not equivalent to ordinary liquorice root.
  • Food exposure can be pharmacologically relevant.
  • Do not reduce toxicity to “may increase blood pressure”: the full syndrome includes hypokalaemia and potentially life-threatening complications.
  • Check the date of regulatory documents—the EMA monograph was revised in July 2026.

References

  1. European Medicines Agency, Committee on Herbal Medicinal Products. Liquiritiae radix — Glycyrrhiza glabra L.; Glycyrrhiza inflata Bat.; Glycyrrhiza uralensis Fisch., radix. Revised EU herbal monograph, assessment report and reference list. EMA. Revision 1 published 20 July 2026.
  2. Ceccuzzi G, et al. Liquorice toxicity: a comprehensive narrative review. Nutrients. 2023;15(18):3866. doi:10.3390/nu15183866. PubMed.
  3. Update on adverse effects of liquorice consumed as food, including apparent mineralocorticoid excess, hypertension and hypokalaemia. 2023. PubMed.
  4. Nazari S, Rameshrad M, Hosseinzadeh H. A review of the pharmacological efficacy and safety of liquorice root from corroborative clinical trial findings. Journal of Medicinal Food. 2020. doi:10.1089/jmf.2019.4459. PubMed.
  5. National Library of Medicine. Licorice. Drugs and Lactation Database (LactMed). Updated June 2026. PubMed / LactMed.
  6. Yoshino T, et al. Clinical risk factors of licorice-induced pseudoaldosteronism based on glycyrrhizin-metabolite concentrations: a narrative review. PubMed.
  7. Penninkilampi R, Eslick EM, Eslick GD. The association between consistent licorice ingestion, hypertension and hypokalaemia: a systematic review and meta-analysis. Journal of Human Hypertension. 2017;31(11):699–707. doi:10.1038/jhh.2017.45. PubMed.
  8. Updated 2026 review of clinical risk factors and pharmacokinetics in liquorice-induced pseudoaldosteronism. Frontiers in Pharmacology. 2026. PubMed.

Additional materia medica sources

  • ESCOP. Liquiritiae radix — Liquorice root, ESCOP Monographs.
  • Blumenthal M, et al., eds. The Complete German Commission E Monographs. American Botanical Council; 1998.
  • British Herbal Medicine Association. British Herbal Pharmacopoeia 1983 and British Herbal Compendium.
  • Hoffmann D. Medical Herbalism. Healing Arts Press; 2003.

Last reviewed: 20 September 2026. Educational reference only; not an individual dosing or prescribing guide.

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