Chemical Abstracts Service Registry Number: 83-74-9 Formal Names: Endabuse, Tabernanthe iboga Informal Names: Bitter Grass, Iboga, Leaf of God Type: Hallucinogen. See page 25 Federal Schedule Listing: Schedule I (DEA no. 7260) USA Availability: Illegal to possess Pregnancy Category: None
Uses. This drug comes from roots of an equatorial African rainforest shrub called Tabernanthe iboga. Traditionally the natural product has been used in low doses as a mild stimulant, rather like coca or areca nut, to fight hunger, thirst, and weariness and also to improve confidence. The natural product's active ingredient ibogaine was found in 1901. Its stimulant qualities gave it a potential role in Western medicine as a means of treating nervous exhaustion and generally helping sick persons recover from worn-down states. The drug was also viewed as a treatment for influenza and for illness caused by microscopic animals called Trypanosmatina protozoa. None of those applications received wide use. Ibogaine is, however, used as an aphrodisiac and has also seen illicit duty as a performance-enhancing substance in athletics.
In strong dosages ibogaine has been a component of African religious life. In that context the substance is used in its natural product format for meditation and to facilitate divine communication. Users may see rainbows around objects, lose barriers between senses (allowing sounds to be tasted, smells to be heard), and experience hallucinations. Fatal overdose is possible.
Drawbacks. Suspicion exists that ibogaine harms brain function in humans. Rat experiments show that high doses of ibogaine can injure some types of brain cells but that lower doses do not cause such damage. High dosage has caused body tremors and heartbeat trouble in rats. Rat experiments also show that the drug can impair emotions, reaction times, and ability to move.
Abuse factors. Some persons trying to break drug addiction claim that ibogaine drastically reduces craving for heroin, cocaine, and other opioids and stimulants. Switching an abuser from one drug to another one is routine in substance abuse treatment, but supposedly just one ingestion of ibogaine is enough to stop another drug's withdrawal symptoms and to diminish craving for it, with no need to keep taking ibogaine. Scientific efforts to verify such claims were under way while this book was being written. Verification would make ibogaine unique in the history of substance abuse treatment and would also challenge much of what is known about why people abuse drugs.
Ibogaine was given to 33 heroin addicts who did not reside in a treatment center; 25 of them exhibited no effort to obtain heroin during the four days of subsequent observation. These 33 experiences were not, however, part of an experimental study but instead were individual instances noted from time to time over a 31-year period, an overall average of about one instance per year. A group of researchers reported that ibogaine not only suppressed desire for heroin and cocaine among residents being weaned off those drugs in a treatment facility but that ibogaine made the people less depressed as well— an improvement in mood that was still present 30 days after release from treatment. In another study 7 opiate addicts received a single dose of ibogaine. Although 1 addict shortly resumed opiate use, 3 avoided further opiate use for several weeks, and 3 avoided further drug abuse for at least 14 weeks. None of the 7 experienced an opiate withdrawal syndrome. Ibogaine reduces intake of alcohol, cocaine, heroin, morphine, nicotine, food, and water by rats. Lowered consumption of food and water raises question about whether ibo-gaine is affecting drug consumption per se or is exerting some broader action. An ibogaine derivative, however, reduces rats' drug intake without reducing water intake.
Results are inconsistent on whether the drug improves or impedes learning in rats, an effect related to memory. One theory holds ibogaine allows humans to remember why they started using drugs, thereby helping abusers to stop. The instant results claimed for ibogaine, however, are inconsistent with the time necessary for memories to liberate persons from other psychiatric afflictions. And the memory theory also assumes that the reason an abuser started using drugs was either invalid in the past or is no longer valid in the present, an assumption inconsistent with much that is known about drug abuse. Nor does the memory theory explain why ibogaine reduces drug consumption in rats. The memory aspect is commonly mentioned by users, however, and some claim to achieve major positive realignment of their lives through ibogaine-induced insights into past experiences and allegorical interpretations of hallucinations. Nonetheless, some heroin addicts who initially announced themselves cured by ibogaine did not find the change permanent and resumed heroin use. One report says the ibogaine cure lasted less than a month for about 25% of heroin addicts who received it, longer for others who received supplemental therapy and who were dedicated to changing their lives.
A curiosity about the use of ibogaine in addiction treatment is that reported doses range from 500 mg to 1,800 mg. One authority says 1,000 mg is typical. An amount of 200 mg is considered sufficient to cause hallucinations. Additional effects of 200 mg are described as nervousness (perhaps bordering on fear), unpleasant feelings in arms and legs, difficulty in muscular coordination, tremors with rapid and repeated contraction and relaxation of muscles, and inability to sleep. Nausea and vomiting are sometimes reported, along with so much uncomfortable sensitivity to light that people cover their eyes. Such unwanted actions might be publicized as substantial drawbacks in a street drug but receive little, if any, mention in reports where ibogaine is administered as an addiction treatment. Individual personality and the circumstance in which a drug is taken can, of course, make a big difference in effects. So perhaps massive doses of ibogaine do not affect addicts in the same way that people are affected outside a therapeutic context.
Drug interactions. In rat experiments alcohol raised ibogaine's effects.
Cancer. Not enough scientific information to report.
Pregnancy. Not enough scientific information to report.
Additional information. "Iboga" is a nickname for MDMA, but they are not the same substance.
Additional scientific information may be found in:
Alper, K.R., D. Beal, and C.D. Kaplan. "A Contemporary History of Ibogaine in the United States and Europe." The Alkaloids. Chemistry and Biology 56 (2001): 249-81.
Mash, D.C., et al. "Ibogaine: Complex Pharmacokinetics, Concerns for Safety, and Preliminary Efficacy Measures." Annals of the New York Academy of Sciences 914 (2000): 394-401.
Mash, D.C., et al. "Medication Development of Ibogaine as a Pharmacotherapy for Drug Dependence." Annals of the New York Academy of Sciences 844 (1998): 274-92.
Popik, P., and S.D. Glick. "Ibogaine." Drugs of the Future 21 (1996): 1109-15. Popik, P., R.T. Layer, and P. Skolnick. "100 Years of Ibogaine: Neurochemical and Pharmacological Actions of a Putative Anti-Addictive Drug." Pharmacological Reviews 47 (1995): 235-53.
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