Ibogaine is a naturally occurring psychoactive substance that has been demonstrated to interrupt substance use disorders, as well as possess other neurological and psychological benefits. It is found naturally in a number of plant sources, principally in a member of the Apocynaceae family known as iboga (usually Tabernanthe iboga), which has been used for centuries by traditional communities in West Africa for ritual and healing purposes.
In lower doses, ibogaine acts as a stimulant, increasing energy and decreasing fatigue in a way that is distinct from other central nervous system stimulants like amphetamines and cocaine.1 In larger doses, ibogaine produces oneirogenic effects, meaning that it stimulates a dream-like state while awake, as well as closed eye imagery and the retrieval of repressed memories.2
Its physical effects can include ataxia, nausea and vomiting, sensitivity to light and sound, tremors, and cardiac effects. In the early 1960’s, the Chilean psychologist Claudio Naranjo conducted 40 ibogaine sessions with his clients and was the first to scientifically describe the experience. He reported that ibogaine helped people to view difficult experiences in an objective way, and that it helped to facilitate closure of unresolved emotional conflicts.3
The occidental use of ibogaine, especially its application in the treatment of substance use disorders, was pioneered by Howard Lotsof. In 1962, 19 year old Lotsof serendipitously found that a single dose of ibogaine not only interrupted his physiological dependence on heroin, it also took away his craving to use, all with no withdrawal symptoms. Lotsof spent the rest of his life advocating for the development of ibogaine as a prescription medicine.
In the early 1990’s, the US National Institute on Drug Abuse (NIDA) began the development of ibogaine by fully funding pre-clinical animal trials as well as Phase 1 safety trials on human subjects. The results confirmed that ibogaine decreases the self-administration of stimulants, opiates and alcohol, as well as a significant reduction in the withdrawal symptoms from opiates.4
Unfortunately, the development research was ended prematurely because of intellectual property disputes, its high cost and complexity relative to NIDA’s existing resources.5
Phase 1 safety trials conducted by NIDA found that ibogaine is not neurotoxic. However, there are a number of fatalities that have been temporally associated with the ingestion of ibogaine. These were attributed to a variety of factors, including pre-existing medical conditions, especially cardiac conditions, as well as seizures resulting from acute withdrawal from alcohol or benzodiazepines, and in other cases the co-administration of one or more drugs of abuse.
One of the causes cited is that ibogaine potentiates the effects of opiates, as well as their lethality if co-administered. It does this not by acting as an opiate agonist or antagonist, but by enhancing opiate signaling.6 Another is that, in addition to attenuating withdrawal symptoms, ibogaine has been shown to reduce developed tolerance to opiates7 and alcohol,8 essentially returning the user to a novice state. Using substances after administration of ibogaine without taking this into consideration presents a significant risk of overdose.
In the late 1980’s, the first regular ibogaine-assisted detox sessions were conducted by the Danish Drug Users Union in Amsterdam. Over the last several decades a global community of ibogaine therapy providers, which has been dubbed a “medical subculture,” has developed to include former drug users and physicians. In 2007 it was estimated that over 3,400 therapy sessions for substance use disorders, as well as for personal and spiritual growth, had been conducted worldwide.9 This number continues to grow annually, as well as the number of clinics.
Ibogaine-assisted detox efficacy has been explored in two recent studies being conducted by the Multidisciplinary Association for Psychedelic Studies (MAPS), attempt to track the long-term efficacy of ibogaine-assisted detox therapy. The studies, in Mexico and New Zealand, have reported preliminary results of between 20% and 50% rate of clients remaining free from their primary substance of abuse for at least 12 months. Factors influencing this range were suggested to be the ease of follow-up in the New Zealand study become of closer proximity, as well as other factors such as plans for continuing care.10 Ibogaine therapy may have promising results in the treatment of other conditions, including Hepatitis C, Parkinson’s disease and Tourette’s syndrome.
“Modification of awake-sleep equilibrium by tabernanthine and some of its derivatives in the cat.” Da Costa L, Sulklaper I, Naquet R. Review of Electroencephalography and Clinical Neurophysiology. 10:105-112. 1980. ↩
Kaplan, C.D., Ketzer, E., de Jong, J. and de Vries, M. Reaching a state of wellness: Multistage explorations in social neuroscience. Social Neuroscience Bulletin, 1993, 6: 6-7. ↩
Popik P, Glick S. Ibogaine, a putatively anti-addictive alkaloid. Drugs of the Future. 1996; 21:pp 1109-1115. ↩
Alper, Kenneth R. M.D., Marina Stajic, Ph.D., and James R. Gill, M.D. Fatalities Temporally Associated with the Ingestion of Ibogaine. Journal of Forensic Sciences, March 2012, Vol. 57, No. 2. ↩
Trujillo KA & Akil H, Inhibition of Morphine Tolerance and Dependence by NMDA Receptor Antagonist MK-801, Science, 2512:85-87, 1991. ↩
Khanna JM, Kalant H, Shah G, Chau A, Effect of D-cycloserine on Rapid Tolerance to Ethanol, Pharmacology Biochemistry & Behavior 45(4):983-986, 1993. ↩
Kenneth R. Alper, Howard S. Lotsof, Charles D. Kaplan. The ibogaine medical subculture. Journal of Ethnopharmacology. 115: 9–24. 2007. ↩