How Much Is Too Much? Exploring Pseudohyperaldosteronism in Glycyrrhizic Acid Toxicity From Chronic Licorice Root Consumption

Licorice has been around for centuries and has been commercialized in the food, tobacco, and healthcare industry. Historically, its therapeutic benefits have been reaped in countless ways, including as a thirst sensation suppressor in battlefields, flavoring agent in medicinal preparations, antacid for gastric discomfort and peptic ulcers, and even as an estrogenic agent in postmenopausal women. Licorice and its derivatives are recognized safe by the US Food and Drug Administration (FDA). Though FDA recognized the licorice to be a food additive in certain concentrations, it has issued warnings against its use in at-risk group and in larger amount. However, it is a lesser known fact that glycyrrhizic acid, the active component in licorice, can cause a metabolic syndrome presenting as pseudohyperaldosteronism. Chronic consumption leads to the development of hypertension, metabolic alkalosis, and hypokalemia. We present a patient who developed a sinus pause on telemetry and subsequent syncope after presenting for evaluation of hypertension and hypokalemia. The patient had been ingesting a significant quantity of deglycyrrhizinated licorice for many years to alleviate postprandial epigastric pain. Although seemingly benign electrolyte disturbance, it is crucial to recognize that chronic consumption of licorice without strict regulation can lead to supraventricular and ventricular ectopics and tachyarrhythmias with the potential to develop life-threatening arrhythmias including ventricular tachycardia, ventricular fibrillation, and Torsades de Pointes.