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Ibogaine for treating drug dependence. What is a safe dose?

L J Schep, R J Slaughter, S Galea, D Newcombe

Drug and alcohol dependence September 1, 2016 DOI: 10.1016/j.drugalcdep.2016.07.005 via PubMed

Summary

AI-generated from the abstract

Ibogaine, an alkaloid from the West African shrub Tabernanthe iboga, is used in the West to treat drug dependence, but requires large, hallucination-inducing doses. Case reports describe ataxia, gastrointestinal distress, ventricular arrhythmias, and sudden deaths in patients. High doses affect neurological receptors and transporters, and rodent studies show neuronal injury in Purkinje cells. Lethality in rodents occurs at about 263 mg/kg orally. Applying safety factors for intra- and inter-species variability and susceptible populations, a safer initial human dose is calculated at 0.87 mg/kg, substantially lower than current practice. Morbidities and mortalities will continue unless practitioners reconsider doses.

Study at a glance

Characteristics Review Case report Peer reviewed
Intervention ibogaine
Dose 0.87 mg/kg
Topics Ibogaine
Keywords Drug dependence Qt prolongation Ibogaine treatment ibogaine Current ibogaine doses Effective treatment
Citations 30
Key finding A safer initial human dose of ibogaine is calculated at 0.87 mg/kg, substantially lower than currently administered doses, and morbidities and mortalities will continue unless practitioners reconsider doses.

Abstract

The indole alkaloid ibogaine, present in the root bark of the West African rain forest shrub Tabernanthe iboga, has been adopted in the West as a treatment for drug dependence. Treatment of patients requires large doses of the alkaloid to cause hallucinations, an alleged integral part of the patient's treatment regime. However, case reports and case series continue to describe evidences of ataxia, gastrointestinal distress, ventricular arrhythmias and sudden and unexplained deaths of patients undergoing treatment for drug dependence. High doses of ibogaine act on several classes of neurological receptors and transporters to achieve pharmacological responses associated with drug aversion; limited toxicology research suggests that intraperitoneal doses used to successfully treat rodents, for example, have also been shown to cause neuronal injury (purkinje cells) in the rat cerebellum. Limited research suggests lethality in rodents by the oral route can be achieved at approximately 263mg/kg body weight. To consider an appropriate and safe initial dose for humans, necessary safety factors need to be applied to the animal data; these would include factors such as intra- and inter-species variability and for susceptible people in a population (such as drug users). A calculated initial dose to treat patients could be approximated at 0.87mg/kg body weight, substantially lower than those presently being administered to treat drug users. Morbidities and mortalities will continue to occur unless practitioners reconsider doses being administered to their susceptible patients.

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