A case series of ibogaine toxicity reported to the United Kingdom National Poisons Information Service (NPIS) over a 10-year period.
Ella P Edwards, Laurence A Gray, Muhammad E M O Elamin, Aravindan Veiraiah, Ruben H K Thanacoody, James M Coulson
Clinical toxicology (Philadelphia, Pa.) March 1, 2025 DOI: 10.1080/15563650.2024.2447500 via PubMed
Summary
AI-generated from the abstractIbogaine, a psychoactive alkaloid from the West African shrub Tabernanthe iboga, is not licensed in the UK but is used by individuals to self-treat drug or alcohol use. A retrospective analysis of telephone enquiries to the UK National Poisons Information Service from 2012 to 2022 identified eleven enquiries about seven patients, all symptomatic and using ibogaine recreationally. Doses ranged from 5g to 34g. Seven patients had neurological symptoms and six had cardiotoxicity, including cardiac arrest, hypoxia, torsade de pointes, and QT prolongation. The findings indicate that ibogaine can cause severe cardiotoxicity and neurological harm, especially when used in variable, unregulated doses.
Study at a glance
| Characteristics | Retrospective analysis Case report Peer reviewed |
|---|---|
| Sample size | 7 |
| Population | Patients who used ibogaine and were reported to the UK National Poisons Information Service |
| Intervention | Ibogaine |
| Dose | 5g to 34g |
| Topics | Ibogaine |
| Keywords | Cardiotoxicity Neurotoxicity Ibogaine toxicity: ibogaine Ibogaine risks |
| Citations | 2 |
| Key finding | Ibogaine use is associated with severe cardiotoxicity, including ventricular tachyarrhythmias and cardiac arrest, as well as neurological symptoms. |
Abstract
Ibogaine is a psychoactive alkaloid derived from the root bark of the West African shrub Tabernanthe iboga. It is not licensed in the United Kingdom but is used by individuals to alleviate drug or alcohol use. A retrospective analysis of telephone enquiries involving ibogaine between 1 January 2012 and 31 December 2022 to the United Kingdom National Poisons Information Service was performed. Eleven enquiries relating to seven patients were made to the United Kingdom National Poisons Information Service in this period. Five of these patients were male (71%) with the majority in the age category 31-40 years (57%). All patients presented symptomatically. The circumstances for all seven cases were recorded as "recreational abuse." The exact indication was not specified in three cases but in two cases it was being used to alleviate diacetylmorphine (heroin) use and in another two cases it was being used for relief from insomnia. Three sources of ibogaine were reported - in one case it was bought online, in one case by a dealer and in two cases it was bought from a shaman. When reported, the dose ingested ranged from 5g to 34g. Two patients took it in tablet form and four patients ingested the root bark. The time since exposure, when reported, ranged from 16 h to 1 month. Seven patients experienced neurological symptoms and six displayed features of cardiotoxicity. The most frequently reported features included cardiac arrest, hypoxia, torsade de pointes, QT interval prolongation, coma, convulsions, stupor, bradycardia, vomiting and anxiety. Our cases are consistent with other case reports that demon-strate ibogaine can cause severe cardiotoxicity, including ventricular tachyarrhythmias, prolonged QT interval, and tor-sade de pointes; which can lead to loss of cardiac output and arrest. Individuals using ibogaine in variable doses to self-treat for drug use are at risk of developing severe cardiotoxicity and neurological symptoms. Further studies to quantify dose-response relationship and to further improve knowledge of its pharmacokinetics are required.