Black licorice can cause hypokalemia, which potentiates digoxin toxicity and increases the risk of serious cardiac arrhythmias.
Even small amounts of black licorice can cause significant potassium depletion in susceptible individuals.
Elderly patients or those with renal impairment are at higher risk.
Symptoms of interaction may mimic digoxin toxicity; check digoxin levels promptly.
Opt for deglycyrrhizinated licorice (DGL) products, which lack glycyrrhizin.
Black licorice contains glycyrrhizin, which inhibits 11-beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2), leading to accumulation of cortisol that mimics aldosterone. This results in sodium retention, potassium loss (hypokalemia), and hypertension. Hypokalemia reduces the renal clearance of digoxin and sensitizes myocardial cells to its effects, enhancing toxicity.
Increased risk of digoxin-induced arrhythmias (e.g., ventricular tachycardia, AV block), gastrointestinal symptoms (nausea, vomiting), neurological effects (confusion, visual disturbances), and potentially fatal cardiac events, especially in patients with heart failure or renal impairment.
Avoid or strictly limit black licorice consumption (e.g., <2 oz/day or occasional small amounts of licorice-free alternatives). Monitor serum potassium levels regularly, adjust digoxin dose if needed, and consult a healthcare provider. Consider potassium supplementation if hypokalemia develops.
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