Scientific Research on Ibogaine

Ibogaine is a psychoactive compound usually extracted from the West African Tabernanthe iboga plant. In animals, a single dose of ibogaine decreases signs of opioid withdrawal and produces sustained reductions in the self-administration of heroin, morphine, cocaine, nicotine and alcohol. Ibogaine is illegal in the U.S., and legal but unregulated in Canada and Mexico. New Zealand, South Africa, and Brazil authorize the use of ibogaine by licensed medical practitioners. While its mechanism of action is not yet fully understood, it differs from that of standard opioid agonist treatments such as methadone and buprenorphine which maintain dependence, and thus may show promise as an innovative pharmacotherapy for opioid addiction.

As one participant in the Mexico study reported: “Iboga could give an opiate addict several months to half a year of freedom from craving, and a period of time in which to get their life together and learn to face things straightforwardly, directly and honestly. Iboga will not do the work for you.”

The New Zealand study, published on April 12, showed that a single ibogaine treatment could reduce opioid withdrawal symptoms and achieve either cessation from opioids or sustained, reduced use for up to 12 months following treatment. The results indicate that ibogaine may have a significant pharmacological effect on opiate withdrawal. All participants in the study described their ibogaine experience in positive terms. The analysis includes data from 14 out of 15 participants enrolled, with one participant disqualified and one who died during treatment while under the supervision of a qualified medical practitioner. The paper is co-authored by Geoffrey E. Noller, Ph.D., (Dunedin School of Medicine); Chris M. Frampton, Ph.D. (University of Otago); and Berra Yazar-Klosinski, Ph.D. (MAPS).

The highly lipophilic ibogaine is subject to extensive biotransformation, primarily by the cytochrome P450 (CYP450) 2D6 enzyme, and disappears fairly rapidly from the bloodstream (half-life = 7.5 hours) (Mash 2001) Significant interindividual differences are evident in the metabolism of ibogaine; clinical studies have classified individuals as extensive or poor metabolizers. Blood levels of noribogaine, an active metabolite, remain elevated 24 hours after a single dose, partially explaining the long duration of action. In addition, ibogaine is stored in fat and a slow release from fat stores has been hypothesized to further contribute to the protracted effects of the drug (Glick 2001)

The pharmacology of ibogaine is complex and is thought to have multiple actions that are reflected in the ability of the drug to treat diverse addictions (Glick 2001) Ibogaine and noribogaine act on several neurotransmitter systems in the brain that may contribute to the ability to suppress autonomic changes, objective signs, and subjective distress associated with opiate withdrawal. Noribogaine binds to numerous sites in the CNS including serotonin, dopamine, and sigma receptors, kappa- and mu-opioid receptors, and the n-methyl-d-aspartate ion channel. Noribogaine elevates serotonin concentrations in the brain, a possible explanation for its antidepressive effects. The sustained presence of noribogaine in the CNS coupled with its agonist activity at opioid receptors may produce the self-tapering effect in opiate-dependent patients following abrupt discontinuation of opiates.

Anecdotal evidence suggests that ibogaine, which is derived from a plant found in the African rainforest, adjusts brain chemistry to the point that a person who otherwise might experience intense withdrawal symptoms for one or two weeks does not go through withdrawal or suffer from cravings. However, scientists exploring the potential of this drug in addiction treatment do not believe ibogaine completely ends addiction; instead, it interrupts the process. (1)

The addiction model of disease describes the condition as chronic due to long-term changes to the reward centers of the brain. When a person takes ibogaine, the drug is converted into a compound called noribogaine, which targets the areas of the brain affected by drug-seeking and addictive behaviors. Noribogaine “rewires” these areas, allowing the brain to restructure itself to a state similar to before addiction was triggered.