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Ibogaine – Side effects and safety

One of the first noticeable effects of large-dose Ibogaine ingestion is ataxia, a difficulty in coordinating muscle motion which makes standing and walking difficult without assistance. Xerostomia (dry mouth), nausea, and vomiting may follow. These symptoms may be long in duration, ranging from 4 to 24 hours in some cases. Ibogaine is sometimes administered by enema to help the subject avoid vomiting up the dose. Psychiatric medications Psychiatric medications are strongly contraindicated in Ibogaine therapy due to adverse interactions. Some studies also suggest the possibility of adverse interaction with heart conditions. In one study of canine subjects, Ibogaine was observed to increase sinus arrhythmia (the normal change in heart rate during respiration). Ventricular ectopy has been observed in a minority of patients during Ibogaine therapy. It has been proposed that there is a risk of QT-interval prolongation following Ibogaine administration. This risk was further demonstrated by a case reported in the New England Journal of Medicine documenting prolonged QT interval and ventricular tachycardia after initial use. There are 12 documented fatalities that have been loosely associated with Ibogaine ingestion. Exact determinations of the cause of death have proven elusive due to the quasi-legal status of Ibogaine and the unfamiliarity of medical professionals with this relatively rare substance. No autopsy to date has implicated Ibogaine as the sole cause of death. Causes a given range from significant preexisting medical problems to the surreptitious consumption of other drugs with Ibogaine. legal and illegal Many legal and illegal psychoactive drugs and even foods…
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Ibogaine – Therapeutic uses

Treatment for opiate addiction The most-studied therapeutic effect of ibogaine is the reduction or elimination of addiction to opioids. An integral effect is the alleviation of symptoms of opioid withdrawal. Research also 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. Proponents of ibogaine treatment for drug addiction have established formal and informal clinics or self-help groups in Canada, Mexico, the Caribbean, Costa Rica, the Czech Republic, France, Slovenia, the Netherlands, Brazil, South Africa, the United Kingdom and New Zealand, where ibogaine is administered as an experimental compound. There also exist clandestine drug-treatment facilities in the countries where it is illegal. 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 (Lotsof 1995) on the subject of ibogaine therapy detailing the procedure, effects and aftereffects is found in "Ibogaine in the Treatment of Chemical Dependence Disorders: Clinical…
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Ibogaine – Recreational use

Casual use of ibogaine in a social or entertainment context is nearly unknown due to its high cost, constrained availability, long duration of effects, and uncomfortable short-term side effects. In the clandestine markets, ibogaine is typically sought as a drug addiction treatment, for ritual spiritual purposes, or psychological introspection.
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History of Ibogaine

The History of Ibogaine It is uncertain exactly how long iboga has been used in African spiritual practice, but its activity was first observed by French and Belgian explorers in the 19th century. The first botanical description of the Tabernanthe iboga plant was made in 1889. Ibogaine was first isolated from T. iboga in 1901 by Dybowski and Landrin and independently by Haller and Heckel in the same year using T. iboga samples from Gabon. In the 1930s, ibogaine was sold in France in 8 mg tablets under the name "Lambarene". The total synthesis of ibogaine was accomplished by G. Büchi in 1966. Since then, several further totally synthetic routes have been developed. The use of ibogaine in treating substance use disorders in human subjects was first observed by Howard Lotsof in 1962, for which he was later awarded Patent 4,499,096 in 1985. In 1969, Claudio Naranjo was granted a French patent for the use of ibogaine in psychotherapy. Ibogaine was placed in US Schedule 1 in 1967 as part of the US government's strong response to the upswing in popularity of psychedelic substances, though iboga itself was scarcely known at the time. Ibogaine's ability to attenuate opioid withdrawal confirmed in the rat was first published by Dzoljic et al. (1988). Ibogaine's use in diminishing morphine self-administration in preclinical studies was shown by Glick et al. (1991) and ibogaine's capacity to reduce cocaine self-administration in the rat was shown by Cappendijk et al. (1993). Animal model support for ibogaine claims to…
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Ibogaine – Formulations

In Bwiti religious ceremonies, the rootbark is pulverized and swallowed in large amounts to produce intense psychoactive effects. In Africa, iboga rootbark is sometimes chewed, which releases small amounts of ibogaine to produce a stimulant effect. Ibogaine is also available in a total alkaloid extract of the Tabernanthe iboga plant, which also contains all the other iboga alkaloids and thus has only about one-fifth the potency by weight as standardized ibogaine hydrochloride. Total alkaloid extracts of T. iboga are often loosely called "Indra extract". However, that name actually refers to a particular stock of total alkaloid extract produced in Europe in 1981. The fate of that original stock (as well as its original quality) is unknown. Currently, pure crystalline ibogaine hydrochloride is the most standardized formulation. It is typically produced by the semi-synthesis from voacangine in commercial laboratories. Ibogaine has two separate chiral centers which means that there a four different stereoisomers of ibogaine. These four isomers are difficult to resolve. A synthetic derivative of ibogaine, 18-methoxycoronaridine (18-MC), is a selective α3β4 antagonist that was developed collaboratively by the neurologist Stanley D. Glick (Albany) and the chemist Martin E. Kuehne (Vermont). This discovery was stimulated by earlier studies on other naturally occurring analogues of ibogaine such as coronaridine and voacangine that showed these compounds also have anti-addictive properties.
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Ibogaine – Pharmacology

The pharmacology of ibogaine is quite complex, affecting many different neurotransmitter systems of its fairly low potency at any of its target sites, ibogaine is used in doses anywhere from 5 mg/kg of body weight for a minor effect to 30 mg/kg in the cases of strong polysubstance addiction. It is unknown whether doses greater than 30 mg/kg in humans produce effects that are therapeutically beneficial, medically risky, or simply prolonged in duration. In animal neurotoxicity studies, there was no observable neurotoxicity of ibogaine at 25 mg/kg, but at 50 mg/kg, one-third of the rats had developed patches of neurodegeneration, and at doses of 75 mg/kg or above, all rats showed a characteristic pattern of degeneration of Purkinje neurons, mainly in the cerebellum. While caution should be exercised when extrapolating animal studies to humans, these results suggest that neurotoxicity of ibogaine is likely to be minimal when ibogaine is used in the 10–20 mg/kg range typical of drug addiction interruption treatment regimes, and indeed death from the other pharmacological actions of the alkaloids is likely to occur by the time the dose is high enough to produce consistent neurotoxic changes. Pharmacodynamics Ibogaine affects many different neurotransmitter systems simultaneously. Noribogaine is most potent as a serotonin reuptake inhibitor. It acts as a moderate κ-opioid receptor agonist and weak µ-opioid receptor agonist or weak partial ;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, another plant recognized for its strong hallucinogenic properties, contains the chemical salvinorin A, which is a…
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Ibogaine – Pharmacodynamics

Among recent proposals for ibogaine mechanisms of action is activation of the glial cell line-derived neurotrophic factor (GDNF) pathway in the ventral tegmental area (VTA) of the brain. The work has principally been accomplished in preclinical ethanol research, where 40 mg/kg of ibogaine caused increases of RNA expression of GDNF in keeping with reduction of ethanol intake in the rat, absent neurotoxicity or cell death. Ibogaine is a noncompetitive antagonist at α3β4 nicotinic receptors, binding with moderate affinity. Several other α3β4 antagonists are known, and some of these, such as bupropion (Wellbutrin or Zyban), and mecamylamine, have been used for treating nicotine addiction. This α3β4 antagonism correlates quite well with the observed effect of interrupting addiction. Co-administration of ibogaine with other α3β4 antagonists such as 18-MC, dextromethorphan or mecamylamine had a stronger anti-addictive effect than when it was administered alone. Since α3β4 channels and NMDA channels are related to each other and their binding sites within the lumen bind a range of same ligands ( DXM, PCP), some older sources suggested that ibogaine's anti-addictive properties may be (partly) due to it being an NMDA receptor antagonist. However, ligands, like 18-MC, selective for α3β4- vs. NMDA-channels showed no drop-off in activity. It is suspected that ibogaine's actions on the opioid and glutamatergic systems are also involved in its anti-addictive effects. Persons treated with ibogaine report a cessation of opioid withdrawal signs generally within an hour of administration. Ibogaine is a weak 5HT2A receptor agonist, and although it is unclear how significant this…
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Ibogaine Binding profile

Ibogaine Binding profile Ibogaine has affinity (Ki) for the following sites in decreasing order of potency: σ2 (206 nM) > SERT ( nM) > DAT (1,980 nM) > NMDA (2,001 nM) > κ-opioid (2,717 nM) > µ-opioid (4,362 nM) > σ1 (5,839 nM) > M3 (12,500 nM) > 5-HT2A (14,142 nM) > M1 (22,486 nM) > M2 (39,409 nM) > D3 (70,000 nM). It also has affinity for VMAT and the nACh receptors, among other targets
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Ibogaine – Metabolites

Ibogaine Metabolites Ibogaine is metabolized in the human body by cytochrome P450 2D6, and the major metabolite is noribogaine (12-hydroxyibogamine). Noribogaine is most potent as a serotonin reuptake inhibitor and acts as a moderate κ- and weak µ-opioid receptor full agonist and therefore, also has an aspect of an opiate replacement similar to compounds like methadone. It is possible that this action of noribogaine at the kappa opioid receptor may indeed contribute significantly to the psychoactive effects attributed to ibogaine ingestion; salvia divinorum, another plant recognized for its strong hallucinogenic properties, contains the chemical salvinorin-A which is a highly selective kappa opioid agonist. Both ibogaine and noribogaine have a plasma half-life of around two hours in the rat, although the half-life of noribogaine is slightly longer than the parent compound. It is proposed that ibogaine is deposited in fat and metabolized into noribogaine as it is shows higher plasma levels than ibogaine and may therefore be detected for longer periods of time than ibogaine. Noribogaine is also more potent than ibogaine in rat drug discrimination assays when tested for the subjective effects of ibogaine. The Noribogaine differs from ibogaine in that it contains a hydroxy instead of a methoxy group at the 12 position
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Ibogaine – Research

An ibogaine research project was funded by the US National Institute on Drug Abuse in the early 1990s. The National Institute on Drug Abuse (NIDA) abandoned efforts to continue this project into clinical studies in 1995, citing other reports that suggested a risk of brain damage with extremely high doses and fatal heart arrhythmia in patients having a history of health problems, as well as inadequate funding for ibogaine development within their budget. However, NIDA funding for ibogaine research continues in indirect grants often cited in peer-reviewed ibogaine publications. In addition, after years of work and a number of significant changes to the original protocol, on August 17, 2006, a MAPS-sponsored research team received "unconditional approval" from a Canadian Institutional Review Board (IRB) to proceed with a long-term observational case study that will examine changes in substance use in 20 consecutive people seeking ibogaine-based therapy for opiate dependence at the Iboga Therapy House in British Columbia, Canada. Addiction treatment The most-studied therapeutic effect of ibogaine is the reduction or elimination of addiction to opioids. An integral effect is the alleviation of symptoms of opioid withdrawal. Research also 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." Many users of ibogaine report experiencing visual phenomena during a waking dream state, such as instructive replays of life events that led to…
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