Ibogaine is an alkaloid extracted principally from the root bark of the shrub Tabernanthe Iboga, which grows in the West Central African rain forest.
The most used form of Iboga is Ibogaine Hydrochloride. This is the alkaloid Ibogaine, stabilized in the form of salt, taken in capsules. We also use the Total Extract (TA) of numerous alkaloids contained in the root bark of the shrub Tabernathe Iboga. The content of Ibogaine in the TA is around 40% but it may vary. Some of these alkaloids have similar properties to Ibogaine. In combination these 2 formulas provides a psycho-spiritual experience in addition to addiction relief.
Frequently Ibogaine is referred to as a hallucinogen. It is not. It is an oneirophrenic, though we prefer referring to the effect as a “remogen” referring to the REM or Rapid Eye Movement normally occurring for brief periods of time during the sleep/dream state. With Ibogaine you experience this state of REM for hours while fully conscious and aware.
Legal Status of Ibogaine
The legal status differs from country to country. Ibogaine is currently scheduled as an illegal substance in USA, Sweden, Denmark, France, Belgium and Switzerland. Even where Ibogaine is not illegal it is unlikely that it is available to be administered by a physician or in a clinic or hospital for the simple reason that these institutions can use only registered medications, which Ibogaine is not.
Ibogaine treatment providers put themselves at risk each treatment they do, as from a legal point of view they could be held responsible if anything would happen during the treatment. (Perhaps this is one of the reasons why there are so few Ibogaine treatment providers all around the world.)
Ibogaine & Research
There was a head of steam and considerable excitement relating to the world-wide experimental and research efforts regarding psychedelics and their impact on psychotherapy when, in the mid-60s, these efforts were forcefully shut down, de-funded and disparaged. Great promise came to a screeching halt (except, perhaps with the CIA and the like).
While today there are some visible efforts to resurrect some of this investigation, and beyond, the over arching direct experience is left to the efforts of groups like IbogaQuest. We have experienced remarkable results addressing various conditions being talked about on the Internet but know we have just barely touches the tip of the iceberg relating to numerous physical as well as psychological conditions influenced by the Iboga alkaloids. There is no textbook or reference guide* to reach for and so the burden of bringing promise to reality remains our weight to carry, particularly as people reach out regarding conditions as far afield as Parkinson’s, Alzheimer’s and Fibromyalgia etc. etc. Individual results do not provide an answer and they barely scratch the surface for a reasoned response.
Please support research for Iboga and the universe of plant medicine so unattractive to the profit motives of the medical establishment and pharmaceutical industry.
* GITA has recently published “Clinical Guidelines for Ibogaine-Assisted Detoxification”
Current experience and new findings concerning Ibogaine:
Ibogaine, alkaloid of plant origin, is not yet an officially prescribed drug but many experts consider it a perspective agent in drug dependency cure. The assumption is based on a couple of past open trials and virtually accidental uses of single doses of Ibogaine or short-term Ibogaine therapies resulting in long-term drug abstention for several months, and often ongoing. The above-mentioned incredibly promising effect of Ibogaine, as well as its sometimes questioned safety of application in pharmacotherapy, are currently being tested in experimental and clinical trials. The results are interesting and encouraging.
Ibogaine is an alkaloid discovered in the roots of Tabernathe Iboga shrub (of Apocynacae family, Contonae order) as well as in some other species growing in the rain forests of Central and Western Africa around the equator. The aborigines traditionally chewed the roots for treatment of fatigue, hunger and thirst. Higher doses, especially in extracts, changed the state of mind and were used for religious ritual purposes (best-known is the application in the “Bwiti” religion).
The main active agent – the indole alkaloid called Ibogaine – was first extracted from the root of Iboga in 1901. Its exact structure, however, has only been known since 1957 (the first complete synthesis of Ibogaine from nicotine-amide was performed in 1975). Early 20th century psychotherapists recommended Ibogaine as a stimulating agent in treatment of and recovery from neurasthenia. In the 1930’s extracts containing Ibogaine were sold under the names of Lambarene (France) or Alperton, as stimulating agents and muscle tonics without substantial establishment in medicinal practice. When, in 1906, reports of hallucinogenic effects of Ibogaine began to increase in number its application was prohibited in a number of countries (including the U.S.A. in 1970).
A new revival of pharmaceutical interest in Ibogaine was initiated by the incredible news of its effect in treatment of drug dependency. In 1962-1963 H. S. Lotsof, still in the United States, first opened clinical sessions with heroin and cocaine dependent patients, including himself. He reported that a single dose caused long-term disappearance of desire for the drug craving in some of the dependent patients, inhibiting abstention symptoms in heroin-dependent patients.
About twenty years later Lotsof returned to Ibogaine (continuing his research in the Netherlands), trying to introduce it to the pharmaceutical market under the name of Endabus. Lotsof’s Ibogaine-based therapies were patented in stages (1985 – 1992) for treatment of opiate, cocaine, alcohol, nicotine and multiple dependency – U.S. patent, Lotsof – opiates (1985), cocaine (1986), alcohol (1989), nicotine (1991) and multiple dependency (1992).
Application of Ibogaine in controlled studies performed in the Netherlands was supported by NDA International from 1985. The results of the Dutch studies were very promising: Application of a single dose of Ibogaine (20-25 mg/kg of body weight) led to six-month abstention of minimum two-thirds of the patients (out of the total number of 35 heroine and cocaine dependent), two-year or longer abstention of 10% of the patients, and return to the drug after 14 days of only 10% of the patients. Lotsof also reported improved prognoses after repeated Ibogaine sessions (1).
Unfortunately, in the course of one of the studies a young heroine-dependent female patient died by an unlucky coincidence. The legal action against Lotsof discovered no neglect on the part of the therapist, and the applied dose of Ibogaine was also low and usual (the Ibogaine level in the blood of the deceased patient was 0.75 mg/l). It is maintained that the death might have been caused by simultaneous application of Ibogaine and the drug (the patient probably secretly smoked heroin in the course of the session).
This case, however, pointed out lack of scientific and pharmacological knowledge of Ibogaine – mechanisms of its effect, pharmacokinetics etc. Clinical studies in the Netherlands were discontinued and the focus of the research was moved to experimental pre-clinical level.
Preclinical studies confirmed the effect of Ibogaine in inhibition of symptoms of abstention from opiates and inhibition of “autoapplication” of inhibiting and stimulating drugs, including alcohol and nicotine. A number of details increasing accuracy of pharmacokinetic and toxicological information were acquired, including significant contribution of long-term effectiveness of the active metabolite of noribogaine to the effect of ibogaine. Other related metabolites and derivatives of Ibogaine were tested, including 18-MK substance (18-metoxykoronaridine) with minimum toxicity even in high doses etc. Ibogaine was discovered to influence a number of neuromediating and other regulation systems.
At present clinical tests of Ibogaine are continued, for example in cooperation with the Miami University, U.S.A. (Professor D. C. Mash) or the Panama University. Results of clinical study phase 1 – safety and kinetics – have been published, together with results of phase 2 of research – in first patients, and appear promising.
On the basis of current knowledge a preliminary conclusion can be drawn; about the safety of application of Ibogaine and its active metabolite of Noribogaine in drug dependent subjects, its inhibition of opiate withdrawal symptoms after a single dose and inhibition of craving for heroine and cocaine after a single dose, noting the long-term effect in some patients, or extension of the effect by repeated sessions.
Regarding the multiple effect of the substance on various neuromediators and potential effect on different types of dependencies (in animal experiments blocking autoapplication of opiates, amphetamine, cocaine, alcohol, nicotine) Ibogaine may be considered the beginning of a new trend in research into pharmacotherapy of drug dependence. Ibogaine and its derivatives might be applied in treatment of many more dependencies, including the frequent poly-drug dependencies so difficult to deal with. Of course further research will be necessary.
A number of dose-dependent central psychotropic effects of Ibogaine have been reported in humans. Effects of extract from the root of Tabernathe Iboga are more complex and can differ from the effects of Ibogaine itself. The root extract in sufficient doses evokes fantastic visual images, feelings of excitement, drunkenness, mental confusion to hallucination.
The extract from Iboga root is certainly a CNS stimulating agent, high doses being likely to cause spasms, paralysis and eventually apnea. High doses may also cause hearing, visual and taste synaesthesia and moods ranging from deep sorrow to rejoicing euphoria.
Oral application of Ibogaine or root extract may generate subjective effects lasting for about 6 hours. About 50% of Ibogaine treated individuals described confusion, gesture dis-coordination, nausea, vomiting.
Typical symptoms include sleepiness, with the subject unwilling to move, open its eyes, and communicate (even though being able to communicate). Many subjects react with increased sensitivity to light and preference for darkness. Noise and sounds are very irritating. The resulting condition resembles sleep, although the person is conscious.
The subjects have described fantastic images in quick succession, like a quickly projected film or quickly changing slides. The contents of the images have differed, often including typical archetypal contents, personal experience, problems, past decisions and relationships, including images of animals and other people. Although the fantasies can be manipulated by both the subject and the psychotherapist, the quick succession of images is easy to break. That is why the activity of psychotherapist focuses on the period immediately following the session itself. Higher doses of Ibogaine may cause visual and other hallucinations, often combined with fear and evil apprehensions.
Preliminary results of clinical trials phase 2 (39 patients, application of a single dose, 1 month follow up) have so far demonstrated effect of Ibogaine in the course of detoxification of opiate-dependent patients and in short-term stabilization of drug-dependent subjects before or in early stages of therapy. Ibogaine has significantly reduced craving for cocaine and heroine during detoxification. Depressive symptoms in patients (self-assessment) have also been reduced, the improvement as a rule being preserved until the end of the therapeutic program (30 days).
It can be concluded that to-date research has supported the suitability of Ibogaine application, including some of its derivatives, in drug dependency therapies.
In preclinical experiments Ibogaine has reduced auto-application of cocaine, morphine, heroine, nicotine, and alcohol, minimized or even eliminated opiate withdrawal symptoms, blocked conditioned place preference induced by morphine and amphetamine. No trend towards development of dependency or toleration of Ibogaine has been observed.
Ibogaine interacts with a number of neuro-mediating systems of CNS, many of them related to mechanisms of development of desire for drugs – craving (for example Ibogaine non-competitively blocks NMDA receptors, interacts with dopamine transporters and kappa opiate receptors). Reduction of opiate abstention syndromes is ascribed to NMDA receptor blocking.
Anti-craving effect of Ibogaine is probably complex and implemented with participation of multiple mechanisms and various neuro-mediating systems, including effect on the traditional dopamine route. The idea of a very long-term effect of Ibogaine in drug dependent subjects, with a single dose or a short-term therapy sufficient for months or years of abstention, will still need more verification. Short-term effect in the detoxification stage in humans has already been proved. Ibogaine inhibits withdrawal symptoms after opiates and significantly reduces craving for heroine and cocaine.
It is clear that Ibogaine is not of the substitution therapy drug type. Long-term effective contribution of an active metabolite – Noribogaine – to the overall long-term effect of Ibogaine is assumed, but further research is still needed.
The warning reports of toxicity and neurotoxicity of Ibogaine have been tested with the conclusion that the adverse effects are related exclusively to high doses not used in therapy.
Stage 1 clinical study has demonstrated that Ibogaine in effective doses of 10-20 mg/kg p.o. is safe, well tolerated by patients and generating no significant adverse effects (with the exception of nausea and mild shiver at the beginning of the therapeutic period). Ibogaine and/or some of its derivatives therefore represent a promising trend in research into new medicines for drug dependency therapy, currently in progress on the clinical study level.
- LOTSOF, HS., Bull. MAPS, 1995, vol. 5, 6, 3, Appendix 6, page 16-27
- POPIK, P., SKOLNIK P., The Alkaloids, Academic Press, 1999, vol. 52, p. 197-231
- SANCHEZ-RAMOS, J., MASH, DC . MAPS 1994, vol. 4, no. 11
- MASH, DC., et al, Anna N.Y.Academym 1999, p. 394-401.