Ibogaine is an indole alkaloid derived from the root bark of the rain-forest African shrub Tabernan the iboga. It has been used by indigenous peoples in low doses to combat fatigue, hunger and thirst, and in higher doses as a sacrament in religious rituals. Ibogaine is an hallucinogen which can cause tremors. Some addict self-help groups promote it as a treatment for heroin, cocaine, and methamphetamine addition.

Since Ibogaine is a natural substance, it cannot be patented.  This results in less funding being available to explore the claims of some of it being of benefit.  There appears never to have been a single controlled study of its use in treatment.  Some animal research has found that, in somewhat higher doses than normalled used in treatment, ibogaine causes significant damage to Purkinje cells in the cerebellum, probably the cause of the tremors.  Ibogaine appears to block some of the effects of narcotic withdrawal.

In view of ibogaine being a hallocinogen and having definitely neurological toxicity at only 2 1/2 times the estimated therapeutic dose, its value for treating substance abuse does not seem promising.

Purkinje Cell Damage in Rats: Administered systemically, it produces degeneration of a subset of Purkinje cells in the cerebellum, primarily within the vermis. Ablation of the inferior olive affords protection against ibogaine-induced neurotoxicity leading to the interpretation that ibogaine itself is not directly toxic to Purkinje cells. In a rat study, co-administration of GYKI-52466 with ibogaine produces increased toxicity evidenced by more extensive Purkinje cell degeneration. The results show that a non-NMDA antagonist can produce increased excitotoxic injury under some conditions.  Administration of a non-NMDA antagonist, GYKI 52466, increases excitotoxic Purkinje cell degeneration caused by ibogaine. O-Hearn E, et al. Johns Hopkins. . Neurosci 2004;127(2):373-83.

Ibogaine Given for 30 Days to Humans: Ibogaine is from a rain forest shrub of western Africa. It has been used by indigenous peoples in low doses to combat fatigue, hunger and thirst, and in higher doses as a sacrament in religious rituals. Members of American and European addict self-help groups have claimed that ibogaine promotes long-term drug abstinence from addictive substances, including psychostimulants and opiates. Ibogaine is changed via CYP2D6, including the O-demethylation of ibogaine, to 12-hydroxyibogamine (noribogaine). Blood concentration-time effect profiles of ibogaine and noribogaine obtained for individual subjects after single oral dose administrations demonstrate complex pharmacokinetic profiles. Ibogaine has shown preliminary efficacy for opiate detoxification and for short-term stabilization of drug-dependent persons as they prepare to enter substance abuse treatment. Authors report their experience is that ibogaine significantly decreased craving for cocaine and heroin during inpatient detoxification. Self-reports of depressive symptoms were also significantly lower after ibogaine treatment and at 30 days after program discharge. Because ibogaine is cleared rapidly from the blood, the beneficial aftereffects of the drug on craving and depressed mood may be related to the effects of noribogaine on the central nervous system. Ibogaine: complex pharmacokinetics, concerns for safety, and preliminary efficacy measures. Mash DC, et al. University of Miami. . Ann NY Acad Sci 2000 Sep;914:394-401. Ed: This type of study seems irresponsible.  If humans are going to be exposed to a potentially toxic drug, it makes sense to do it in a double-blind study so as to at least minimize the number of humans who have to be exposed to determine if it is of any value.

Ibogaine Used in Detox: One Fatality: In a non-scientific report of 33 adults in opioid detoxification in non-medical settings under open label conditions given ibogaine, resolution of the signs of opioid withdrawal without further drug seeking behavior was observed within 24 hours in 25 patients and was sustained throughout the 72-hour period of posttreatment observation. Other outcomes included drug seeking behavior without withdrawal signs (4 patients), drug abstinence with attenuated withdrawal signs (2 patients), drug seeking behavior with continued withdrawal signs (1 patient), and one fatality possibly involving surreptitious heroin use. Treatment of acute opioid withdrawal with ibogaine. Alper KR, et al. New York University. . Am J Addict 1999 Summer;8(3):234-42. Ed: Another irresponsible study.  It should have been double-blind with maximum safeguards, if done at all.

Purkinje Cell Damage May be Dose Dependent: Cerebellar responses to the high doses of ibogaine used by O'Hearn and Molliver (100 mg/kg or 3 x 100 mg/kg) caused Purkinje cell degeneration in 100% of rats. At a lower dose (40 mg/kg), one effective in reducing morphine and cocaine self-administration, ibogaine displayed no degeneration above the level seen in saline-treated animals. Ibogaine neurotoxicity: a re-evaluation. Molinari HH, et al. Albany Medical College, NY. Brain Res 1996 Oct 21;737(1-2):255-62.

Ibogaine Has Some Effect on Mu Opioid Receptor: Ibogaine potentiates morphine-induced analgesia in mice and reduces certain naltrexone-precipitated withdrawal signs in morphine-dependent rats. Although these results might suggest ibogaine interaction with opioid receptors, previous receptor binding studies (Brain Res. 571:242-247, 1980) found that ibogaine had a Ki value of only 2 microM for the kappa opioid receptor and was virtually inactive in blocking mu and delta receptor binding (Ki > 100 microM). The present investigation of ibogaine interaction with the mu opioid receptor from mouse forebrain labeled with [3H]-naloxone, however, yielded significantly more potent mu opioid Ki values. LIGAND analysis indicated that the data were best fit by a two site binding model, with Ki values of about 130 nM and 4 microM, reflecting ibogaine recognition of different agonist affinity states of the receptor. Inclusion of 100 mM NaCl in the assay to induce the agonist low affinity state of the receptor, reduced ibogaine's inhibition of [3H]-naloxone binding. These results suggest that ibogaine is an agonist at the mu opioid receptor with a Ki value of about 130 nM, potentially explaining ibogaine's antinociceptive effects as well as its reported reduction of opioid withdrawal symptoms and attenuation of drug seeking behavior. High affinity ibogaine binding to a mu opioid agonist site. Codd EE. R. W. Johnson Pharmaceutical Research Institute, Spring House, PA. Life Sci 1995;57(20):PL315-20.