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Ibogaine
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Revision as of 13:27, 26 June 2018 by >Kenan(Shouldn't be part of the article)
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.
Ibogaine-containing preparations are used for medicinal and ritual purposes within African spiritual traditions of the Bwiti, who claim to have learned it from the Pygmy peoples. Although it was first commonly advertised as having anti-addictive properties in 1962 by Howard Lotsof, its use in the West predates this by at least a century. In France, it was marketed under the trade-name Lambarène and used as a stimulant. Additionally, the U.S. Central Intelligence Agency (CIA) studied the effects of ibogaine in the 1950s.[citation needed]
Ibogaine is obtained either by extraction from the iboga plant or by semi-synthesis from the precursor compound voacangine,[2][3] another plant alkaloid. The total synthesis of ibogaine was described in 1956 and structural elucidation by X-ray crystallography was completed in 1960.[4][5]
Ibogaine is not currently approved for any medical uses in the United States.[1] Preliminary research indicates that it could potentially be used for treatment of addiction;[1] however, there is a lack of data in humans.[1] The use of Ibogaine has been associated with severe adverse effects, at least 12 deaths have been reported since 1990.[1]
Ibogaine or 12-Methoxyibogamine is an indole alkaloid molecule of the tryptamine class. Tryptamines share a core structure comprised 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 atypical to other hallucinogenic tryptamines.
Ibogaine is substituted at R10 of it's 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.
Like with most psychedelic tryptamines, ibogaine is thought to act as a 5-HT2Apartial agonist. The psychedelic effects are believed to come from ibogaine's binding efficacy at the 5-HT2A receptors. However, the role of these interactions and how they result in the psychedelic experience continues to remain elusive.
Ibogaine is metabolized in the human body into noribogaine. Noribogaine functions as a serotoninreuptake inhibitor. It also acts as a moderate κ-opioid receptor agonist[6] and weak µ-opioid receptor agonist[7] or weak partial agonist.[8] It is possible that the action of ibogaine at the kappa opioid receptor may indeed contribute significantly to the psychoactive effects attributed to ibogaine ingestion. 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,[9] 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. [10] After ibogaine ingestion in humans, noribogaine shows higher plasma levels than ibogaine and is detected for a longer period than ibogaine.[11] Noribogaine is also more potent than ibogaine in rat drug discrimination assays when tested for the subjective effects of ibogaine.[12]
This compound is also thought to act as an NMDA receptor antagonist. NMDA receptors, a type of glutamatereceptor, allow for excitatory electrical signals to pass between neurons in the brain and spinal column; for the signals to pass, the receptor must be open. Dissociatives inactivate the NMDA receptors by blocking them. This disconnection of neurons leads to the general loss of bodily sensation, motor coordination, memory recall and eventually this substance's equivalent of the “K-hole.”
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 - This isn’t common 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.
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.
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."[14]
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".[15] Ibogaine has also been reported in multiple small-study cohorts to reduce cravings for methamphetamine.[16]
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;[17] ibogaine has the added benefit of preventing withdrawal effects.[18]
There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:
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 is known to cause fatal heart complications at a high rate, such as QT prolongation. 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 with most psychedelics it is most often thought to be self-regulating.
Legality
Brazil - On January 14, 2016, Ibogaine was legalized for prescription use.[19]
Canada - As of 2009, ibogaine is unregulated.[20][21]
Germany - Ibogaine is unregulated, but for medical use it can be regulated by the pharmacy rules (AMG).
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.[26]
United States - Ibogaine is classified as a Schedule I drug,[27] 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.[28]
In most other countries it remains unregulated and unlicensed.[29][30]
. PMID 25642835. Cite error: Invalid