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Ibogaine can cause life-threatening heart complications.[1]
It is strongly discouraged to use this substance in high doses or for multiple days in a row. Additionally, a trip sitter with proper medical training and equipment must be present. Please see this section for more details.
WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.
DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.
In West Central Africa, low dosages of Tabernanthe iboga extracts have been used by indigenous people against fatigue, hunger and thirst. Higher dosages capable of inducing visionary states are used for initiation rituals during religious ceremonies.[1] Ibogaine's medical history in the West began in the early 1900s when it was indicated for use as a neuromuscular stimulant.[3] In the 1940s and 1950s, its suitability as potential cardiovascular drug was studied.[4] Later in the 1960s, the substance received much attention because of its potential applicability as an anti-addiction medication.
The pharmacology of ibogaine is complex and poorly understood. While largely behaving as a serotonergic psychedelic, ibogaine interacts with numerous brain systems including transporters, opioid receptors, sigma receptors, glutamate receptors, and nicotinic receptors.[5] Ibogaine’s complex pharmacology entails a significant potential to generate adverse effects, particularly on the cardiovascular system. Its use has been associated with at least 12 deaths since 1990.[1]
Ibogaine is not currently approved for any medical uses in the United States.[1] Preliminary research in animals indicates that it could potentially be used for treatment of addiction;[1] however, there is a lack of non-anecdotal data in humans.[1] Although not licensed as therapeutic drug and despite safety concerns, ibogaine is currently used as an anti-addiction medication in dozens of clinics worldwide.[1]
As a result, it may contain incomplete or wrong information. You can help by expanding it.
The Iboga tree is the central pillar of the Bwiti religion practiced in West-Central Africa, mainly Gabon, Cameroon, and the Republic of the Congo, which uses the alkaloid-containing roots of the plant for its psychoactive properties in a number of ceremonies. Ibogaine is also used by indigenous peoples in low doses to combat fatigue, hunger, and thirst.[5]
Research of ibogaine started in late 19th century. A published description of the ceremonial use of T. iboga in Gabon appears in 1885. Ibogaine was first extracted and crystallized from the T. iboga root in 1901.[5] The total synthesis of ibogaine was described in 1956 and structural elucidation by X-ray crystallography was completed in 1960.[6][7]
Chemistry
Ibogaine, or 12-methoxyibogamine, is an indole alkaloid molecule of the tryptamine chemical class. Tryptamines share a core structure composed of a bicyclic indole heterocycle attached at R3 to an amino group via an ethyl side chain. While ibogaine contains a tryptamine backbone, the structure features substitutions distinct from other hallucinogenic tryptamines.
Ibogaine is substituted at R10 of its structure with a methoxy group. The location of this substitution is identical to other R5 substituted tryptamines, notably 5-MeO-DMT. The traditional amino attached ethyl chain of tryptamine is incorporated into a seven member nitrogenous azepine ring. The azepine ring is fused to three interlocked cyclohexane rings, attached at the integrated tryptamine nitrogen of azepine and two carbons over. Attached to the fusion of cyclohexane rings is an ethyl chain at R7.
Ibogaine is obtained either by extraction from the iboga plant or by semi-synthesis from the precursor compound voacangine,[8] another plant alkaloid.
Ibogaine is believed to produce its psychedelic effects from its binding efficacy at the 5-HT2A receptor. However, the role of these interactions and how they result in the psychedelic experience continues to remain elusive.
Ibogaine is rapidly metabolized in the human body into noribogaine. Noribogaine acts as a serotoninreuptake inhibitor. It also acts as a moderate κ-opioidreceptoragonist[9] and weak µ-opioid receptor agonist[9] or weak partial agonist.[10] It is possible that the action of ibogaine at the kappa opioid receptor may contribute significantly to the psychoactive effects. Salvia divinorum is another plant recognized for its strong hallucinogenic properties; it contains the chemical salvinorin A which is also a highly selective kappa opioid agonist.
Both ibogaine and noribogaine have a plasma half-life of around two hours in rats,[11] although the half-life of noribogaine is slightly longer than that of the parent compound. It is proposed that ibogaine is deposited in fat and metabolized into noribogaine as it is released. [12] After ibogaine ingestion in humans, noribogaine shows higher plasma levels than ibogaine and is detected for a longer period than ibogaine.[13] Noribogaine is also more potent than ibogaine in rat drug discrimination assays when tested for the subjective effects of ibogaine.[14]
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWikicontributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
Physical effects
Stimulation - This effect is exclusively produced at low doses.
Abnormal heartbeat - Abnormal heartbeat is an uncommon effect and typically only occurs when the individual has preexisting health concerns relating to the cardiovascular system. This effect usually only comes about in high dosages due to inhibition of the hERG channels in the heart which affect repolarization (relaxing of the atria) leading to a change in cardiac activity. It is strongly recommended that one go through a physical health evaluation or screening prior to using this substance.
Spatial disorientation - This effect differs from most other dissociatives in that the user is still fairly lucid but physically feels disoriented, off-balance and dizzy.
Withdrawal Suppression - Ibogaine has been shown to reduce withdrawal symptoms of substances. This effect is most prevalent in opioid withdrawal. [16]
Despite typically being classed as a psychedelictryptamine, this compound also presents dissociative-like effects due to its properties as an NMDA receptor antagonist.
Wakefulness - This effect is due to its powerful stimulant and hallucinogenic effects that can last well over 24 hours, this is often capable of keeping the user awake for up to several days with traditional doses.
Rejuvenation - This effect is not usually felt as immediately as it is with ayahuasca or mushrooms, and can often take 2 to 4 full nights of sleep to become fully manifested.
There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:
Research suggests that ibogaine may be useful in treating dependence on other substances such as alcohol, methamphetamine, and nicotine and may affect compulsive behavioral patterns not involving substance abuse or chemical dependence. Researchers note that there remains a "need for systematic investigation in a conventional clinical research setting."[18]
Many users of ibogaine report experiencing visual phenomena during a waking dream state, such as instructive replays of life events that led to their addiction, while others report therapeutic shamanic visions that help them conquer the fears and negative emotions that might drive their addiction. It is proposed that intensive counseling, therapy and aftercare during the interruption period following treatment is of significant value. Some individuals require a second or third treatment session with ibogaine over the course of the next 12 to 18 months. A minority of individuals relapse completely into opiate addiction within days or weeks. A comprehensive article on the subject of ibogaine therapy detailing the procedure, effects and aftereffects is found in "Ibogaine in the Treatment of Chemical Dependence Disorders: Clinical Perspectives".[17] Ibogaine has also been reported in multiple small-study cohorts to reduce cravings for methamphetamine.[19]
There is also evidence that this type of treatment works with LSD, which has been shown to have a therapeutic effect on alcoholism. Both ibogaine and LSD appear to be effective for encouraging introspection and giving the user occasion to reflect on the sources of their addiction, while also producing an intense, transformative experience that can put established patterns of behaviour into perspective;[20] ibogaine has the added benefit of preventing withdrawal effects.[18]
Neuroplasticity
In 2018, a study demonstrated neuroplasticity induced by noribogaine, an active metabolite of ibogaine, and other psychedelics through TrkB, mTOR, and 5-HT2A signaling.[21]
Toxicity and harm potential
This toxicity and harm potential section is a stub.
As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it. Note: Always conduct independent research and use harm reduction practices if using this substance.
Ibogaine has been associated with life-threatening heart complications, such as QT prolongation.[22] It can be taken safely, but only under the supervision of trained medical professionals.
Tolerance and addiction potential
Ibogaine is not habit-forming, and the desire to use it can actually decrease with regular consumption. Like most psychedelics, it is most often thought to be self-regulating.
Legal status
Ibogaine is unregulated and unlicensed in most countries.[23][24] Some exceptions are listed below.
Brazil: On January 14, 2016, Ibogaine was legalized for prescription use.[25]
Canada: Ibogaine is prescription drug since 2017.[26]
Germany: Ibogaine is not a controlled substance under the BtMG[27] (Narcotics Act) or the NpSG[28] (New Psychoactive Substances Act). Technically it would fall under the definition of a medicine by §2 AMG (Medicines Act) because it induces a pharmacological effect.[29] By a decision of the European Court of Justice, this definition was declared ineffective because it was not compatible with EU law.[30] Ibogaine can be considered unregulated.
Switzerland: Ibogaine is a controlled substance specifically named under Verzeichnis D.[35]
United Kingdom: It is illegal to produce, supply, or import this drug under the Psychoactive Substance Act, which came into effect on May 26th, 2016.[36]
United States: Ibogaine is classified as a Schedule I drug,[37] and is not currently approved for addiction treatment (or any other therapeutic use) because of its hallucinogenic, cardiovascular and possibly neurotoxic side effects, as well as the scarcity of safety and efficacy data in human subjects.[38]
Mačiulaitis, R., Kontrimavičiūtė, V., Bressolle, F. M. M., & Briedis, V. (2008). Ibogaine, an anti-addictive drug: pharmacology and time to go further in development. A narrative review. Human & experimental toxicology, 27(3), 181-194. https://doi.org/10.1177/0960327107087802.
Koenig, X., & Hilber, K. (2015). The anti-addiction drug ibogaine and the heart: a delicate relation. Molecules, 20(2), 2208-2228. https://doi.org/10.3390/molecules20022208
↑Schneider, J. A.; Rinehart, R. K. (1957). "Analysis of the cardiovascular action of ibogaine hydrochlorid". Archives internationales de Pharmacodynamie et de Thérapie. 110: 92–102. ISSN0003-9780. OCLC5806034. PMID13425751.
↑Soriano-García, M.; Walls, F.; Rodríguez, A.; López Celis, I. (1988). "Crystal and molecular structure of ibogaine: An alkaloid from Stemmadenia galeottiana". Journal of Crystallographic and Spectroscopic Research. 18: 197–206. doi:10.1007/BF01181911. eISSN1572-8854. ISSN1074-1542. OCLC43954962.
↑Baumann, M. H.; Rothman, R. B.; Pablo, J. P.; Mash, D. C. (2001). "In vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in rats". Journal of Pharmacology and Experimental Therapeutics. 297 (2): 531–539. eISSN1521-0103. ISSN0022-3565. OCLC1606914. PMID11303040.
↑Hough, L. B.; Bagal, A. A.; Glick, S. D. (2000). "Pharmacokinetic characterization of the indole alkaloid ibogaine in rats". Methods and Findings in Experimental and Clinical Pharmacology. 22 (2): 77–81. doi:10.1358/mf.2000.22.2.796066. ISSN0379-0355. OCLC5586831. PMID10849889.
↑Mash, D. C.; Kovera, C. A.; Pablo, J.; Tyndale, R. F.; Ervin, F. D.; Williams, I. C.; Singleton, E. G.; Mayor, M. (2000). "Ibogaine: Complex Pharmacokinetics, Concerns for Safety, and Preliminary Efficacy Measures". Annals of the New York Academy of Sciences. 914 (1): 394–401. doi:10.1111/j.1749-6632.2000.tb05213.x. eISSN1749-6632. ISSN0077-8923. OCLC01306678. PMID11085338.
↑A. James Giannini (1997). Drugs of Abuse (2 ed.). California, United States: Practice Management Information Corporation. ISBN1-57066-053-0. OCLC34906127.
. PMID 25642835.