Ibogaine

12-methoxyibogamine, C20H28N2O (mol. wt. 312.45)

Ibogaine_2D_Structure

 

IBOGAINE – 12-METHOXYIBOGAMINE

SYNTHESIS : There have been three total syntheses of ibogaine reported in the chemical literature. The first of these was a thirteen step process published about 30 years ago. The chemistry lab can serve a fine function for both isolation and purification of ibogaine from plant sources, but in the real world, there is no practical way to start from a bottle of nicotinic acid and actually prepare useful amounts. The parent ring system contains two chiral centers, neither of which is amenable to easy manipulation. Because of these two separate and largely inaccessible chiral centers there are, in theory, four distinct isomers of ibogaine which are difficult to resolve. When the term "synthetic" is used in regard to ibogaine in the scientific journals, it usually applies to the resynthesis of the parent alkaloid from the demethylated metabolite. For reference purposes, here are the finger print number from the infrared spectra: For the free base: IR (in cm-1): 741, 799, 830, 1037, 1111, 1148; mp 152-153 °C. For the hydrochloride salt: IR (in cm-1): 638, 810, 832, 925, 1031, 1149; mp 299-300 °C (dec).
DOSAGE : (from hundreds of milligrams up to a gram or more)
DURATION : (quite long)
EXTENSIONS AND COMMENTARY : Here is an example of a most remarkable material that has allowed people to have some rather complex and dramatic experiences. Any effort to present a fair overview of its action, through a selection of individual responses in the "extension and commentary" format would fail, as it would ignore the impact of the set and setting on the subject. Here I will mention a few of these different sets, and a leading author to search out more detail.
There is a well studied history of the use of the iboga plant in the religious rituals in Gabon and its neighboring countries, from the early part of the 19th century. The Buiti religion calls for the use of the root bark of Tabernanthe iboga as a sacrament in its religion, and the reports of its psychopharmacological effectiveness reflects these needs (see Samorini).
Another area of reports that can be called upon reflect the exploration of the isolate from this plant, or the isolated active component ibogaine itself, in the study of its use in connection with psychotherapy. Here the reports reflect the physician/patient interaction with an emphasis on early memory and the reliving of past experiences (see Naranjo). In clinical studies such as these, a typical dose would be four hundred milligrams of the chemical, twice this weight of the crude isolate, and perhaps ten times again this weight again if the actual root bark is used.
Yet another source of reports is to be found in some studies that are exploring ibogaine as a treatment for heroin dependency (see De Rienzo and Beal). This end-goal of searching for evidence of addiction confrontation and addiction control certainly can color any published reports in its own way. Here, its the chemical ibogaine only that is used, and typical dosages are at or above 1000 milligrams.
There is no question but that ibogaine is a rough trip, physically as well as mentally. Here is one report that shows the body aspects of its use.
(with 200 mg, orally) "Subjectively, the most unpleasant symptoms were the anxiety, the extreme apprehension, and the unfamiliar mood associated with visual and bodily hallucinations. The visual hallucinations appeared only in the dark and consisted of blue disks dancing up and down the walls. Dysesthesia of the extremities. a feeling of light-weightedness, and hyperacusis were other symptoms noted. Autonomic signs, such as dryness of the mouth, increased perspiration, slight pupillary dilation, and increase in pulse rate, as well as extrapyramidal syndromes (fine tremors, slight ataxia, enhanced tendon reflexes and clonus) were also present. The peak effect was reached at about 2 hours after swallowing the drug; it subsided gradually, leaving as a residue complete insomnia. No undesirable after-effects, such as exhaustion or depression occurred."
As was pointed out in a pharmacological review (see Popik et al.), as the hallucinogenic dose appears to be several times higher than the stimulant dose, the user must endure intense and unpleasant central stimulation in order to experience the hallucinogenic effects.
But as fascinating as the pharmacology of ibogaine, it is the chemistry of this alkaloid that is overwhelmingly awesome. The presence of four isomers was mentioned in the chemistry section above, but this fact was not appreciated until the 1960’s and even then, a coupe of troublesome errors were made that confused the absolute configuration picture quite badly. The story has been accurately told in a (almost) hundred page review chapter (see Cordell) which is a "must" for anyone who wants to risk understanding some pretty far out chemistry. Oh my, there are a lot of closely related alkaloids. As to indolic alkaloids in general, there are well over two thousand of them, with a few dozen being added every year. And most of these are kosher tryptamines in that they carry the tryptamine structural skeleton. And, in turn, a great number of the tryptamine alkaloids are found in the remarkable family Apocynaceae, which is the ultimate treasure-trove of alkaloids, probably the richest single source of pharmacologically active compounds in the entire plant kingdom. It is made up, largely, of tropical shrubs of the dog bane group, which almost always ooze out a sticky sap when you break off a twig, which have showy flowers, and which have the reputation of being very poisonous.
And this all leads smoothly to the botany, which is almost as convoluted as the chemistry. Here, let me list the plants that contain ibogaine, or that should contain it. Allow me a brief run-down of binomials. There is a number of species that are, or have been, classified as belonging to the Tabernanthe genus and which are reasonable sources of ibogaine, and which are logical alternatives, psychopharmacologically, to the iboga plant itself.

Tabernanthe iboga. This is the major source of ibogaine and is found in Gabon, mentioned above.
Tabernanthe orientalis. This plant is now called Ervatamia orientalis, and is found in Western Australia. The leaves contain ibogaine, along with six minor alkaloids that are closely related, structurally.
Tabernanthe pubescens. This is found in Zaire, and contains a number of alkaloids closely related to ibogaine in structure, as well as ibogaine itself.
Tabernaemontana spp. This genus is from a tribe within the family Apocynaceae that is called the Tabernaemontaneae. As an official sub-family it would be called Tabernaemontanoideae. It is because of the casual use of names such as these that botanical binomialists are rarely invited to social functions. It (this Genus, that is) contains several dozen species, some with ibogaine, many with analgesic or sedative action in experimental animals, and some with a quite a history of native usage either in Africa or Southeast Asia.

And there are many plants in the Apocynaceae family that carry fascinating alkaloids that are closely related in structure to ibogaine and which, potentially, might have a similar psychopharmacology. In most of these, ibogaine is present in very small amounts, if any at all.

Anacampta spp. have usually been published as Tabernaemontana spp., as have been species originally published as part of the Genera Bonafousia, Capuronetta (which has become the species capuronni under this Genus),Conopharyngia, Ervatamia, Gabunia, Hazunta, Muntafara, Pagiantha, Pandaca, Peschiera, Phrissocarpus, and Stenosolen, All of these contain alkaloids related to Ibogaine.
Callichilia barteri has appeared as Hedranthera barteri, but C. subsessilis demands the name Tabernaemontana subsessilis in the presentation of its alkaloid content.
Creoceras, Rejoua, Schzozygia, Stemmadenia and Voacanga, have, with all their species, remained intact with their original names.
Peschiera echinata. This is one of some ten species within the Tabernaemontaneae classification, with some 2% alkaloid content in its leaves. Ibogaine is present.
Voacanga schweinfurthii var. puberula (known in the older literature as Voacanga puberula) contains some ten related alkaloids, the major one of which is found in the seeds, and is tabersonine present at a rather remarkable 3.5 %. Ibogaine is present in the root bark but, at a concentration of 200 mg/Kg (0.02%), it is truly a minor constituent.

ibogaine_summary1

Extracting Ibogaine from Tabernanthe iboga and Trachelospermum jasminoides

A guide to extracting Ibogaine from J Amer. Chem. soc #80: 123, 1958


Isolation of Ibogaine from Tabernanthe iboga

from J Amer. Chem. soc #80: 123, 1958.

In this case it was for the root/root bark of tabernanthe iboga used as the plant material, which may contain up to 2.5 % or 6 % alkaloids respectively. The plant material was extracted with methanol four times, filtered and the methanol reduced to a small volume. An equal amount of water and acetic acid solution is added and shaken with petroleum naphtha, which is then separated and backwashed with acetic acid solution.

All the aqueous phases are combined. The aqueous phases are reduced in volume, then basified with ammonia hydroxide. This is then extracted four times with ethylene dichloride (possibly chloroform too). The solvent is washed with water, dried and concentrated. An equal amount of ethanol is added and the whole reduced to the original volume, then about twice the amount of ethanol is added. After chilling in the fridge for two days or so, ibogaine crystallises out, and can be collected by filtration. The remaining liquid was again reduced in volume and re-chilled for a second crop of ibogaine.

Evaporation to dryness of the liquid yielded other alkaloids and residual ibogaine, which can be separated by chromatography, though can be laborious. To purify the ibogaine 100 mg of the crude ibogaine, as obtained above, was dissolved in 1 l of acetone, then 53.1 ml of 1:1 HCl was added, with ibogaine HCl precipitating (108 mg in this case) out straight away, this compound being relatively insoluble in acetone, compared to the base. Isolated by filtration.

ibogaine mp 151-153* C sol – ethanol, ether, chloroform, acetone

ibogaine HCl mp 299-300* C.

In tabernanthe iboga, ibogaine seems to be the most active and prominent alkaloid. In other species that are recorded as containing ibogaine, other alkaloids sometimes make up the majority of the alkaloids, with ibogaine being a minor component. Many related alkaloids however have a similar but not such strong action as ibogaine. The isolation of ibogaine from more complex mixtures of alkaloids may be a bit more tricky, especially if ibogaine is not a major component of the alkaloids.
Ibogaine from Trachelospermum jasminoides
(Star Jasmine)

"Leaves and stems (50 kg) were dried in the shade and extracted with ethanol. The crude alcoholic extracts were concentrated and partitioned between 10% hydrochloric acid and chloroform (pH 1). The chloroform layer was dried with anhydrous sodium sulfate and concentrated to a gum (25 g, F1). The aqueous acidic layer was basified with aqueous ammonia and extracted into chloroform at various pH values (5, 7, 9, and 11). The fraction obtained at pH-5 (20 g, F2) was found to contain major alkaloids. We have recently reported five indole alkaloids from this plant (2)."

"The crude alkaloidal fraction (F1, 25 g) was subjected to flash chromatography. […] The alkaloid isolated was identified as voacangine-7-hydroxyindolenine by comparison of its spectral data with those reported in the literature (3). […] Voacangine-7-hydroxyindolenine may have been formed by air oxidation during the extraction and isolation process."

"Fraction F2 (20 g) was also loaded on a silica column (750 g) and was eluted with increasing polarities of mixtures of petroleum ether, chloroform, ethyl acetate, and methanol." "The fraction obtained on elution with chloroform:ethyl acetate (3:1) consisted of a mixture of four alkaloids. This fraction was subjected to a flash chromatography which was eluted with increasing polarities of mixtures of petroleum ether in acetone. The fraction obtained on elution with 70% petroleum ether in acetone was found to contain two major alkaloids. These alkaloids were separated by preparative TLC on silica gel (petroleum ether:acetone:ammonia, 6:3.95:0.05). The faster moving alkaloid was identified as ibogaine by comparison of its spectral data with those reported in the literature (7) while the slower moving alkaloid was identified as tabernaemontanine (8)."

"Further elution of the same column with 60% petroleum ether in acetone afforded another alkaloid which was further purified by preparative TLC on silica gel (petroleum ether:acetone:ammonia, 1:1:0

Created 7/31/2001 4:08:23
Modified 7/31/2001 4:11:12
Leda version 1.4.3

Tihkal #25. This indole alkaloid with a distinctive (and synthetically difficult) seven-membered ring is under investigation as a cure for addiction.

From "Psychedelic Drugs Reconsidered" by Grinspoon and Bakalar:

Psychological effects: Little is known, but the available reports suggest that it is like harmaline, but less purely visual and symbolic. The images are often of fountains, tubes, marshy creatures, white and blue light, and rotating motion. Explosions of rage directed agains the images of persons and situations from the past are reported. Childhood fantasies are reenacted, and a sense of insight and heightened emotion often accompany the images. The drug taker concentrates on his inner world and personal past. The effect is easily distinguishable from LSD.

CAS
83-74-9


Dosage:
  • Oral

    200-400 mg. Effects last 8-12 hours.

Tabernanthe iboga

Eboka

West african shrub, used as a stimulant and entheogen by the Bwiti cult.

This entheogen is sacred to the syncretic Christian Bwiti cult of the Fang people of Gabon. It is also used at lower doses as a stimulant and aphrodisiac. Adherents to the cult believe use of eboka allows them to contact their ancestors. Initiation into the cult involves consuming large quantities of the drug (which in a few cases has lead to death), for the purposes of "breaking open the head"

From "Medical Botany" by Walter H. Lewis:

Among a dozen or so of the complex indole alkaloids derived from tryptamine and found in Tabernanthe iboga (Apocynacea) ibogaine is the most important hallucinogen, not only in iboga, but perhaps of all those species indigenous to to the African continent.

Found in Gabon, the Republic of the Congo, a large area of Zaire,and also cultivated in west Africa beyond this natural range, iboga is an important element of life, not only for its hallucinogenic powers but also as an aphroidisiac prized more by the natives for this purpose than the famous African yohimbine. The use may be justified, for the stimulating properties of this drug may well increase confidence and stave off fatigure. Iboga is also taken during religious festivals and rites, esp. by shamans to enhance their psychic powers, increase inspiration and assist in contemplation.

Botanical Suffix
Baillon

Ibogaine FAQ

by ibog@aol.com, originally posted to alt.psychoactives, 1995. Includes a useful bibliography.


IBOGAINE:

Ibogaine is not a substitute for narcotics or stimulants, is not addicting and is given in a single administration modality (SAM). It is a chemical dependence interrupter. Retreatment may occasionally be needed until the person being treated with Ibogaine is able to extinguish certain conditioned responses related to drugs they abuse. Early data suggests that a period of approximately two years of intermittent treatments may be required to attain the goal of long-term abstinence from narcotics and stimulants for many patients. The majority of patients treated with Ibogaine remain free from chemical dependence for a period of three to six months after a single dose. Approximately ten percent of patients treated with Ibogaine remain free of chemical dependence for two or more years from a single treatment and an equal percentage return to drug use within two weeks after treatment. Multiple administrations of Ibogaine over a period of time are generally more effective in extending periods of abstinence.

A BRIEF HISTORY

Ibogaine, a naturally occurring alkaloid found in Tabernanthe iboga and other plant species of Central West Africa, was first reported to be effective in interrupting opiate narcotic dependence disorders in U.S. patent 4,499,096 (Lotsof, 1985); cocaine dependence disorders in U.S. patent 4.587,243 (Lotsof, 1986) and poly-drug dependence disorders in U.S. patent 5,152,994 (Lotsof, 1992). The initial studies demonstrating Ibogaine’s effects on cocaine and heroin dependence were accomplished in a series of focus group experiments by H. S. Lotsof in 1962 and 1963. Additional data on the clinical aspects of Ibogaine in the treatment of chemical dependence were reported by Kaplan (1993), Sisko (1993), Sanchez-Ramos & Mash (1994), and Sheppard (1994).

Prior to Ibogaine’s evaluation for the interruption of various chemical dependencies, the use of Ibogaine was reported in psychotherapy by Naranjo (1969, 1973) and at the First International Ibogaine Conference held in Paris (Zeff, 1987). The use of Ibogaine-containing plants has been reported for centuries in West Africa in both religious practice and in traditional medicine (Fernandez, 1982; Gollnhofer & Sillans 1983, 1985) An overview of the history of Ibogaine research and use was published by Goutarel et al. (1993).

Claims of efficacy in treating dependencies to opiates, cocaine, and alcohol in human subjects were supported in preclinical studies by researchers in the United States, the Netherlands and Canada. Dzoljic et al. (1988) were the first researchers to publish Ibogaine’s ability to attenuate narcotic withdrawal. Stanley D. Glick et al. (1992) at Albany Medical College published original research and a review of the field concerning the attenuation of narcotic withdrawal. Maisonneuve et al. (1991) determined the pharmacological interactions between Ibogaine and morphine, and Glick et al. (1992) reported Ibogaine’s ability to reduce or interrupt morphine self-administration in the rat. Woods et al. (1990) found that Ibogaine did not act as an opiate, and Aceto et al. (1991) established that Ibogaine did not precipitate withdrawal signs or cause dependence.

Cappendijk and Dzoljic (1993) published Ibogaine’s effect in reducing cocaine self-administration in the rat. Broderick et al. (1992) first published Ibogaine’s ability to reverse cocaine-induced dopamine increases and later, on Ibogaine’s reduction of cocaine-induced motor activity and other effects (1994). Broderick et al.’s research supported the findings of Sershen et al. (1992), that Ibogaine reduced cocaine-induced motor stimulation in the mouse. Sershen (1993) also demonstrated that Ibogaine reduced the consumption of cocaine in mice. Glick (1992) and Cappendijk (1993) discovered in the animal model that multiple administrations of Ibogaine over time were more effective than a single dose in interrupting or attenuating the self-administration of morphine and cocaine, supporting Lotsof’s findings in human subjects (1985).

Popik et al. (1994) determined Ibogaine to be a competitive inhibitor of MK-801 binding to the NMDA receptor complex. MK-801 has been shown to attenuate tolerance to opiates (Trujillo & Akil 1991) and alcohol (Khanna et al. 1993). MK-801 has also shown a blockade of "reverse tolerance" of stimulants (Karler et al. 1989). Ibogaine’s effects on dopamine, a substance hypothesized to be responsible for reinforcing pleasurable effects of drugs of abuse, and the dopamine system were found by Maisonneuve et al. (1991), Broderick et al. (1992) and Sershen et al. (1992). Ibogaine binding to the kappa opiate receptor was reported by Deecher et al. (1992). Thus we begin to see a broad spectrum of mechanisms by which Ibogaine may moderate use of substances so diverse as opiate narcotics, stimulants and alcohol.

Ibogaine is currently under review by the National Institute on Drug Abuse. On March 8, 1995 an Ibogaine Review meeting was held to determine if the Medications Development Division of NIDA would proceed to multi-site clinical studies. That decision is now being awaited.

The FDA has already approved one human Ibogaine research project and is considering changes that may allow the research to move more quickly. Additionally the National Institute on Drug Abuse may proceed to multi-site human studies to determine if Ibogaine is effective in treating cocaine dependency. The ministry of Health in the Republic of Panama has approved experimental Ibogaine treatments at therapeuic doses which puts it about two years head of the United States. Researchers in Israel and Turkey are also considering human trials for opiates and alcoholism.

Ibogaine is not an LSD-like drug and appears according to early reports to be effective in the treatment of various forms of chemical dependence including opiates, stimulants, alcohol, nicotine or combinations of the above. The real surprise seemed to come when prelimiary treatment of methadone dependent persons also appeared to be effective in the same two to four day Lotsof procedure for the treatment of addiction. The substance has a psycho/pharmacological effects including both Freudian and Jungian perceptions in addition to its ability to diminish narcotic withdrawal.

Ibogaine’s actions breaks down into three component parts. The first is a four to six hour period emulating dreaming in which either visual presentations or thoughts dealing with past events are experienced. The second is a cognitive or intellectual period in which those experiences are evaluated and the third is a period of residual stimulation eventually resulting in sleep. It is after the patient awakes that the effects are principally noticed in a lack of a desire in the majority of patients to seek or use the drugs they were abusing. However, it should be noted that the responses to the drug are very individual just as the patient has individual characteristics.


IBOGAINE, PSYCHOTHERAPY, AND THE TREATMENT OF SUBSTANCE-RELATED DISORDERS

by Barbara E. Judd, CSW

Presented at
The Eighth International Conference on Drug Related Harm
Washington, DC
November 19, 1994


Introduction

I have been working with chemically dependent patients, some having dual diagnoses, for twelve years in outpatient settings. My observations have been that the earliest phase of recovery, the first ninety days, is the most difficult for the therapist and the patient. I would like to compare and contrast certain issues seen as obstacles by patients, some of whom were treated with the Lotsof method and some treated in traditional outpatient settings.

My observations are based on a small sample of patients seen in the U.S. and overseas. These observations are inconclusive and my work is ongoing.

My involvement with Ibogaine began in June 1993, when I was approached by the International Coalition for Addict Self-Help (ICASH) and requested to provide aftercare for five patients who were treated with Ibogaine and were eager to share their experience and struggles. Four of the group were white males ranging in age from early thirties to mid forties. One was a female in her thirties. Their dependencies were to heroin, Methadone and/or cocaine. Additional substance use included marijuana, alcohol and psychedelics. This group met once a week for the duration of one year.

Concurrent treatment was provided to one member of this group on an individual basis. This patient, who we will refer to as "M" is still presently under my care. "M" is thirty-three years old and formally heroin/methadone/cocaine dependent. He has been using drugs since the age of fourteen.

My most recent involvement with Ibogaine has been with NDA International, Inc. when I participated in the treatment of three patients using the Lotsof method in Panama. All three patients were white males in the thirty to forty age range. Two of the patient’s major drug of choice was cocaine which was taken, orally, nasally or by IV injection by one patient; the other by oral or nasal administration only. The third patient was heroin/cocaine dependent and occasionally used methadone in attempts to curb his habit. All patients had used drugs from six to sixteen years.

One of the most difficult aspects of treatment is getting the patient to enter treatment. The three major obstacles are the fear of detoxification, lack of insight, and the inability of patients to control their urges to use drugs. These are the areas where I have observed the benefits of Ibogaine treatment versus traditional methods.

Fear of Detoxification

Across the board, addicts who enter outpatient treatment programs report that their fear of detoxing from drugs has prevented them from attending treatment. Although withdrawal from cocaine is not as severe or obvious as that from opiate narcotics, there is a fear of the psychological pain of never being able to use again. There is also a dread that once drug free, feelings that have been blocked by self-medicating will surface and be too overwhelming for the patient to handle.

Most heroin addicts are petrified of withdrawal symptoms and are afraid of hospital detoxification. Outpatient clients have stated to me that they have delayed treatment to avoid this anticipated discomfort.

My observations with Ibogaine treated patients have been that patients are eager to be treated when they know that Ibogaine promises to eliminate painful withdrawal, takes one administration with up to seventy-two hours of supervised care, and promises to interrupt their urges to use drugs.

Three patients: Panama
  • Patient "1" had used approximately $100 each per day of heroin and cocaine by IV administration for twenty of the thirty days prior to Ibogaine treatment.
  • Patient "2", prior to treatment was using $80 per day of cocaine and alcohol.
  • Patient "3" was using $50 of cocaine on a daily basis via IV injection and smoking. He had previously been heroin dependent.

I observed during treatment with the Lotsof method, all of the three patients treated appeared calm and comfortable and exhibited no signs of withdrawal. This is significant considering the extent of the level of their drug use prior to treatment with Ibogaine.

For these patients to have had little discomfort during withdrawal, speaks to the importance of the use of Ibogaine in the beginning of the recovery process. As patient "M" had stated, "Ibogaine is a much more humane and dignified approach to detox".

Obstacles Within Traditional Treatment

Returning to the obstacles of treatment, the second being the patients’ lack of insight. Insight is necessary for patients to be able to focus and develop goals while in recovery.

Patients in traditional outpatient groups who have less than ninety days clean, spend more time struggling with their urges to use and dealing with their defenses, specifically denial. They do develop insight into their problems, however, it takes at least one year of group treatment meetings one or two times a week on a regular basis.

In contrast, my involvement with providing aftercare for the Ibogaine treated group showed these patients as having tremendous insight into their own issues, their feelings, and what might have caused them to use in the first place.

After their Ibogaine treatment, patients began to see their drug use as destructive. This realization, coupled with psychotherapy, has allowed these patients to work on how to stay clean and to focus on what they must do to maintain a less destructive lifestyle.

The reason for this insight developed by these patients appears to be the release of repressed material during the visualization stage of Ibogaine treatment. This material includes both images and racing thoughts, which somehow get processed to allow patients to have a better understanding of their emotional histories.

The urge to use drugs again, is the highest cause for people to drop out of traditional treatment. Relapse, I think, is clearly inherent in the definition of substance-related disorders. In working with people treated with or without Ibogaine, my observations have been that relapse at some point is certain.

However, according to members in the Ibogaine group, Ibogaine had reduced their urges to use, anywhere from two months to more than one year. This advantage allowed these patients to get a head start in their recovery, whereas clients in traditional outpatient treatment have a great deal of confusion around how to control their urges. Consequently, those patients have to learn very basic and concrete ways to stay clean as taught by self-help meetings, and emphasized in psychotherapy. The Ibogaine aftercare group did not appear to need self-help type assistance to reduce their urges, but seemed to benefit well from psychotherapy.

Conclusion

In conclusion, there is difficulty treating the drug addicted patient, particularly in the early stages of recovery, because of their fear of detox, their lack of insight, and their urges to relapse.

Thus far, there is no opportunity for Ibogaine treatment within the United States. It is my recommendation that there be future research done with Ibogaine, so that some of the above mentioned observations are supported by more conclusive data.

The prospects for a painless withdrawal method makes Ibogaine an attractive alternative to traditional treatment methods. Because Ibogaine interrupts substance related disorders, it gives patients a head start in their recovery. It also increases the patients’ receptiveness to psychotherapy, which is a necessary component to the recovery process.

Brief Ibogaine Bibliography
  1. Aceto MD, Bowman E, Harris LS, Dependence studies of new compounds in the rhesus monkey, rat and mouse, NIDA Research Monograph, 95:578,607, 1990.
  2. Broderick PA, Phelan FT, Berger SP, Ibogaine alters cocaine induced biogenic amine and psychostimulant dysfunction but not [3H] GBR-12935 binding to the dopamine transporter protein, NIDA Research Monograph, 119:285, 1992.
  3. Broderick PA, Phelan FT, Eng F, Wechsler RT, Ibogaine Modulates Cocaine Responses Which Are Altered Due to Environmental Habituation: In Vivo Microvoltammetric and Behavioral Studies, Pharmacology Biochemistry and Behavior, 49(3):711-728, 1994.
  4. Cappendijk SLT, Dzoljic MR, Inhibitory effects of ibogaine on cocaine self-administration in rats, European Journal of Pharmacology, 241:261-265, 1993.
  5. Cappendijk, SLT, Fekkes D, Dzoljic MR, The inhibitory effects of norharman on morphine withdrawal syndrome in rats: comparison with ibogaine, Behavioural Brain Research, 65:117-119, 1994.
  6. Deecher DC, Teitler M, Soderland DM, Bornmann WG, Kuehne MR, Glick SD, Mechanisms of action of ibogaine and harmaline congeners based on radioligand binding studies, Brain Research, 571:242-247, 1992.7.
  7. Depoortere H, Neocortical Rhythmic Slow Activity during Wakefulness and Paradoxical Sleep in Rats, Neuropsychobiology, 18:160-168, 1987.
  8. Dhahir HI, A Comparative Study of the Toxicity of Ibogaine and Serotonin (Doctoral Dissertation, Indiana University) University Microfilms International, 71-25-341, 1971.
  9. Dzoljic ED, Kaplan CD, Dzoljic MR, Effects of Ibogaine on Naloxone-Precepitated Withdrawal Syndrome in Chronic Morphine-Dependent Rats, Archive of International Pharmacodynamics, 294:64-70, 1988.
  10. Glick SD, Rossman K, Steindorf S, Maisonneuve IM, Carlson JN, Effects and aftereffects of ibogaine on morphine self-administration in rats, European Journal of Pharmacology, 195:341-345, 1991.
  11. Glick SD, Rossman K, Rao NC, Maisonneuve IM, Carlson JN, Effects of Ibogaine on Acute Signs of Morphine Withdrawal in Rats: Independence from Tremor, Neuropharmacology, 31(5):497-500, 1992.
  12. Glick SD, Gallagher CA, Hough LB, Rossman KL, Maisonneuve IM, Differential effects of ibogaine pretreatment on brain levels of morphine and (+) – amphetamine, Brain Research, 588:173-176, 1992.
  13. Glick SD, Kuehne ME, Raucci J, Wilson TE, Larson E, Keller, Jr. RW, Carlson JN, Effects of iboga alkaloids on morphine and cocaine self-administration in rats: relationship to tremorgenic effects and to effects on dopamine release in nucleus accumbens and striatum, Brain Research, 657:14-22, 1994.
  14. a. Goutarel R, Gollnhofer O, Sillans R, Pharmacodynamics and Therapeutic Applications of Iboga and Ibogaine, Psychedelic Monographs and Essays, vol. 6, 1993.
    b. Goutarel R, Gollnhofer O, Sillans R, L’IBOGA CONTRE LA DEPENDENCE AUX STUPEFIANTS. PHARMACODYNAMIE ET APPLICATIONS PSYCHOTHERAPEAUTIQUES, Psychotropes, 3(3):63-86, 1993.
  15. Harsing LG, Sershen H, Lajtha A, Evidence that ibogaine releases dopamine from the cytoplasmic pool in isolated mouse striatum, Journal of Neural Transmission, 96:215-225, 1994.
  16. Jacobson AE, Biological Evaluation of Compounds for Their Physical Dependence Potential and Abuse Liability. XIII. Drug Tersting Program of the Committee on Problems of Drug Dependence, Inc., NIDA Research Monograph, 95:563, 1990.
  17. Kaplan CD, Ketzer E, de Jong J, de Vries M, Reaching a State of Wellness: Multistage Explorations in Social Neuroscience, Social Neuroscience Bulletin, 6(1):6-7, 1993.
  18. Keefner SM, Glick SD, Ibogaine Antagonism of Morphine-Induced Hyperactivity: Enhancement by Prior Morphine Exposure and Role of Kappa Opioid Receptors, Society of Neuroscience Abstracts, 20:502.5, 1994.
  19. Lotsof HS, U.S. patent 4,499,096; Rapid Method for Interrupting the Narcotic Addiction Syndrome, 1985.
  20. Lotsof HS, U.S. patent 4,587,243; Rapid Method for Interrupting the Cocaine and Amphetamine Abuse Syndrome, 1986.
  21. Lotsof HS, U.S. patent 4,857,523; Rapid Method for Attenuating The Alcohol Dependency Syndrome, 1989.
  22. Lotsof HS, U.S. Patent 5,026,697, Rapid Method for Interrupting or Attenuating The Nicotine/Tobacco Dependency Syndrome., 1991.
  23. Lotsof HS, U.S. patent 5,124,994; Rapid Method for Interrupting or Attenuating Poly- drug Dependency Syndromes, 1992.
  24. Lotsof HS, Ibogaine in the Treatment of Chemical Dependence Disorders: Clinical Perspectives (A Preliminary Review), Bull. MAPS, 5(3), 1995.
  25. Mash DC, Douyon R, Hearn WL, Sambol NC & Sanchez-Ramos J, A Preliminary Report on the Safety and Pharmacokinetics of Ibogaine, Biological Psychiatry, 1995 In Press.
  26. Maisonneuve IM, Keller RW, Glick SD, Interactions between ibogaine, a potential anti- addictive agent and morphine: an in vivo microdialysis study, European Journal of Pharmacology, 199:35-42, 1991.
  27. Maisonneuve IM, Glick SD, Interactions between ibogaine and cocaine in rats: in vivo microdialysis and motor behavior, European Journal of Pharmacology, 212:263- 266, 1992.
  28. Maisonneuve IM, Rossman KL, Keller Jr. RW, Glick SD, Acute and prolonged effects of ibogaine on brain dopamine metabolism and morphine-induced locomotor activity in rats, Brain Research, 574:69-73, 1992.
  29. Maisonneuve IM, Keller Jr. RW, lick, SD, Interactions of ibogaine and D-amphetamine: in vivo microdialysis and motor behavior in rats, Brain Research, 579:87-92, 1992.
  30. Molinan HH, Maisonneuve IM, Glick SD, Dose Dependence of Ibogaine Neurotoxicity, Society for Neuroscience Abstracts, 20:504.4, 1994.
  31. Naranjo C, Psychotherapeutic Possibilities New Fantasy Enhancing Drugs, Clinical Toxicology, 2(2):209-224, 1969.
  32. Naranjo C, The Healing Journey, Pantheon Books, Div. Random House, NY, 174-228, 1973.
  33. O’Hearn E, Long DB, Molliver MR, Ibogaine induces glial activation in parasagittal zones of the cerebellum, Neuropharmacology and Neurotoxicology, NeuroReport 4:299- 302, 1993.
  34. O’Hearn E, Molliver ME, Degeneration of Purkinje Cells in Parasagittal Zones of the Cerebellar Vermis After Treatment with Ibogaine or Harmaline, Neuroscience, 55(2):303-310, 1993.
  35. Popik P, Layer RT, Skolnick P, The Putative anti-addictive drug ibogaine is a competitive inhibitor of [3H]MK-801 binding to the NMDA receptor complex, Psychopharmacology, 114:672-674, 1994.
  36. Sanchez-Ramos J, Mash DC, Ibogaine Research Update: Phase I Human Study, MAPS, IV(4):11, 1994.
  37. Schechter MD, Gordon TL, Comparison of the behavioral effects of ibogaine from three sources: mediation of discrimintive activity, European Journal of Pharmacology 249:70-84, 1993.
  38. Schneider JA, McArthur M, Potentiation Action of Ibogaine (Bogadin TM) on Morphine Analgesia, Experientia, XII(8):323-324, 1956.
  39. Schneider JA, Sigg EB, Neuropharmacological Studies of Ibogaine, An Indole Alkaloid with Central Stimulant Properties, Annals New York Academy of Sciences, 66:765-776, 1957.
  40. Schneider, JA, Rinehart RK, Analysis of the Cardiovascular Action of Ibogaine Hydrochloride, Archive of International Pharmacodynamics, CX(1):92-102, 1957.
  41. Sershen H, Hashim A, Harsing L, Lajtha A, Ibogaine Antagonizes Cocaine Induced Locomotor Stimulation in Mice, Life Sciences, 50:1079-1086, 1992.
  42. Sershen H, Harsing LG, Hashim A, Lajtha A, Ibogaine Reduces Amphetamine-Induced Locomotor Stimulation C57L/6By Mice, but Stimulates Locomotor Activity in Rats, Life Sciences, 51:10003-1011, 1992.
  43. Sershen H, Hashim A, Lajtha A, Ibogaine Reduces Preference for Cocaine Consumption in C57BL/6By Mice, Pharmacology Biochemistry and Behavior. 46:942-948, 1993.
  44. Sershen H, Hashim A, Lajtha A, Effects of Ibogaine on Serotonergic and Dopaminergic Interactions in Striatum of Mice and Rats, Neurochemical Research, 19(11):1463- 1465, 1994 In Press .
  45. Sershen H, Hashim A, Lajtha A, The Effects of Kappa-Opioid and 5-HT3-Induced Changes in Stimulation-Evoked Dopamine Release in Vitro from Striatum of C57BL/By Mice, Brain Research , 1994, In Press.
  46. Sharpe LG, Jaffe JH, Ibogaine Fails to Reduce Naloxone-Precipitated Withdrawal in the Morphine-Dependent Rat, Neuropharmacology and Neurotoxicology (NeuroReport), 1:17-19, 1990.
  47. Sheppard SG, A Preliminary Investigation of Ibogaine: Case Reports and Recommendations for Further Study, Journal of Substance Abuse Treatment, 11(4):379-385, 1994.
  48. Sisko B, Interrupting Drug Dependency: A Summary of 4 Case Histories, MAPS 4(2):15- 23, 1994.
  49. Woods JH, Medzihdsky F, Smith CB, Winger GD, France CP, 1989 Annual Report, Evaluation of New Compounds for Opioid Activity, NIDA Research Monographs, 95:655-656, 1990.

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Ibogaine — The End Of Heroin Withdrawl?

by Alexander Highcrest. From "eye WEEKLY", August 4, 1994, Toronto.


Depending upon who is collecting the statistics, there are anywhere between 5,000 to 25,000 regular heroin users in Toronto. Most of these people have one thing in common — they’ve thought about kicking the habit. They may even have tried a couple of times.

Others, like myself, were motivated enough to break the habit on the first try.

There are basically two ways to break a heroin addiction. The user can just stop — go cold turkey — and suffer the physical and emotional hell of withdrawal, or the user can get into a methadone program and swap the heroin habit for a methadone habit. Ibogaine, a non-narcotic, non-addictive drug, could offer up a third option.

Ibogaine comes from a shrub found in the rainforests of western Africa. The people there have used ibogaine for centuries as an upper to help them stay alert when hunting, or for inducing visions during initiation rites. Among the secret societies of Gabon and the Congo, ibogaine is closely associated with death. The plant that produces the drug is often described as a supernatural being which can carry someone away to the realm of the dead. Actual death by overdose is possible, but heavy users usually just slide into a semi-coma while gazing off into space. West African cultists who use the drug believe that during this almost comatose experience the soul leaves the body and wanders around in the land of the dead.

In the early ’60s the drug was introduced to the West as a psychoanalytic tool. Ibogaine is characterized as a hallucinogen, but it doesn’t cause LSD-like hallucinations. Users of the drug claim that they "see" their lives appear as if on a movie screen on their eyelids, or on any surface they focus on. In 1967 ibogaine was officially made illegal in the U.S.

Howard Lotsof, an American heroin addict looking for a new drug experience, tried ibogaine in 1962. Although his first ibogaine high lasted longer than his usual heroin injection interval, he didn’t suffer any withdrawal symptoms. Instead, Lotsof’s craving for heroin disappeared completely. Lotsof gave ibogaine to seven other heroin addicts and five of them quit using heroin after their first ibogaine experience. At the time neither Lotsof nor any of his friends were planning to quit.

Based on his personal experiences, Lotsof decided to promote ibogaine as a potential addiction therapy. He founded NDA (New Drug Application) International and between 1985 and 1989 obtained three patents for drug addiction treatment methods based on ibogaine. NDA claims that ibogaine can beat an addiction in three steps. (Warning! The following is in psych-speak.)

First, the addict’s repressed memories are released. Then the memories are intellectually re-evaluated. Finally, a new understanding of the memories is integrated into the client. Former addicts who have successfully used ibogaine say that they came to understand their drug use patterns and then reached a point when they felt they could choose whether or not to use drugs.

The U.S. government hasn’t pursued ibogaine as a treatment for addiction with much enthusiasm, despite the urgings of AIDS activists, rainforest conservationists, drug policy reformers and drug user advocates. In August, 1993, the U.S. Food and Drug Administration finally gave the University of Miami the go-ahead to conduct clinical trials on volunteer patients. This decision made ibogaine the second psychoactive drug to begin the journey toward FDA approval. MDMA was the first. One surprising thing about the FDA decision is that it followed on the heels of a study conducted by the John Hopkins University in Baltimore, which indicated that high doses of ibogaine can cause brain damage in rats.

The situation is no better in Canada. A spokesperson for Toronto’s Addiction Research Foundation told eye that they weren’t currently investigating ibogaine because there were "other research priorities." To his knowledge no one was researching ibogaine in Canada.

Ibogaine treatment is available overseas. The International Coalition for Addict Self-Help (ICASH) has developed an "underground railroad" to assist addicts in getting ibogaine treatment in Europe, primarily in the Netherlands. There, ibogaine reportedly has been successful in breaking addictions to heroin, cocaine, nicotine and alcohol. Nearly one-quarter of all the treated addicts stayed drug- free for at least six months. Another 40 per cent to50 per cent kicked their habits, but needed help from other support programs to stay on the wagon. Some 20 per cent to 30 per cent went back to using their drugs of choice within a month following ibogaine treatment, while roughly 10 per cent decided they needed further ibogaine treatments to stave off their old cravings. The Dutch experience has also had its share of setbacks. One woman died of a heroin overdose while taking ibogaine and the controversial drug may be linked to other deaths.

Ibogaine has been around for 30 years and there’s plenty of evidence to suggest it could be useful in helping people overcome addictions. Why has our government paid so little attention to the drug? Canadian and American national drug strategies have always placed more emphasis on a law enforcement approach rather than on treatment and prevention. Our drug war mentality has made it difficult to imagine a mind-altering drug as being a good thing; just try getting marijuana for medical reasons. It could be that large drug companies don’t see much profit potential in ibogaine. And, as always, there is such a stigma attached to drug addiction that the people with the money and power are reluctant to listen to others with real, front-line experience — the addicts.

There should be a variety of treatment options available to addicts who decide to kick their habits. There may be a place for ibogaine in treatment methodology, but I doubt it’s the magic bullet to end all addictions. When I broke my own heroin habit back in 1991, I went through what treatment experts called "spontaneous recovery." Everybody else called it going cold turkey. I know other former users who are joined at the hip to doctors and clinics because they’ve succeeded in getting onto a methadone program.

Earlier this year I met Bob Sisko, an activist from New York involved in ICASH. He spoke about ibogaine like a TV evangelist talks about Jee-Zus. He told me that ibogaine doesn’t cure addiction, but puts it in remission. He went on to say that detoxification is the first step in any drug treatment program, and ibogaine allows the addict to detoxify with dignity.

In Toronto it is virtually impossible to kick a drug habit with any dignity. This city, with its thousands of heroin addicts, only has room for about 200 people in its handful of methadone programs. Alcohol detox centres are overcrowded. Barring bad-tasting chewing gum or odd little patches, there’s nothing available to help those who want to quit smoking. People addicted to crack, this decade’s big evil, pretty well have to go it alone when they want to stop using. This is a disgrace.

Sure, there have been problems with ibogaine — it’s probably not the wonder cure. But isn’t it worse to ignore the possibility that a non- narcotic, non-addictive drug like ibogaine could help to eliminate the belief that it’s really a waste of time trying to help an addict? The drug could prove to be an important part of a rational, humane approach to treating the problem of drug abuse. It’s certainly worth trying to find out.

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Leda version 1.4.3

Ibogaine Info

by Shecky Green, from alt.psychoactives


Ibogaine is the primary psychoactive alkaloid found in the African shrub Tabernanthe iboga. Ibogaine is one of at least 12 alkaloids found in the plant, and is in highest concentration in the root bark.

The T. iboga bush grows only in the equatorial rainforests of Gabon, westernmost Congo, and portions of Zaire on the west coast of Africa. It grows to about five feet in height, and is cultiavted by villagers as a decorative shrub near their homes. There are at least seven other species in its genus, but only one other plant is known to be psychoactive (Tabernanthe manii).

T. iboga is traditionally known by any of number of variations on the word "eboka". It has been used for centuries as a ceremonial sacrament in the rituals and initiation ceremonies of several West African religions. The two "cults" which have been most extensively covered in western literature are the Bwiti and the MBiri. Both "cults" are practiced among the Fang.

These tradtional religions which use eboka have been gaining in popularity in recent years. They have even hampered the spread of Christianity and Islam.

CHEMISTRY/TOXICITY

Ibogaine is a choline-esterase inhibitor, a stimulant which affects the central nervous system. The molecule exhibits the two-ring indole nucleaus structure common to most hallucinogens. It’s stereochemirty was established in the late 1960s.

In small doses, much like coca leaves in South America, eboka is eaten to stay awake and alert long hunts and canoe trips, which can last two days or more. It is also reported to have aphrodisiacal properties. (The olive-sized yellowish-orange fruits of T. iboga, while not psychoactive, are sometimes used "for barrenness in women".)

In larger amounts, ibogaine acts as a hallucinogen. It causes nausea and vomiting, much like peyote. At this level, it puts the user in an intense, deep trance state in which physical movement is all but impossible. The trance is intensely visual, and ususally manifests as a long journey.

At excessive levels, ibogaine causes convulsions, paralysis and death by arrested respiration. Toxicity levels are weight-related.

Traditionally, the root bark is scraped and dried to a yellowish-brown powder. Sometimes it is mixed with water and drunk, but it is said to be strongest when fresh. Usually it is taken by itself, although some sects use it with marijuana (which is called "yama" or "nkot alok"). The smoke represents the soul leaving the body and traveling to mix with the ancestors’.

"First tier" dosage (for stimulant, nonpsychedelic effects) average around two to three teaspoons for women and three to five teaspoons for men.

WESTERN MEDICINE

The earliest record of Western scientists studying T. iboga is in 1864, when Griffon du Bellay took specimens to Europe. His writings clearly show that he was aware of the plants psychoactive effects.

Around the 1880s, the colonizing Germans "permitted and possibly encouraged" eboka use for stamina by the African slaves working on the Douala-Yaounde railroad and other colonial projects.

The first botanical description of T. iboga was made in 1889. In 1901, two teams of chemists isolated the major alkaloid, ibogaine. There followed a flurry of French and Belgian studies.

In 1905, a Dr. Huchard used doses of 10 to 30 mg. of ibogaine for the treatment of influenza, neurathenia, and depresssion, as well as some cardiac disorders. Huchard reported that he observed improved appetites, muscle tone, and generally improved raates of recovery.

Huchard and a M.C. Phisalex were apparently the only Westerners to use ibogaine medically, and neither of them used it for its psychoactive properties. It was for another 50+ years until this was explored.

PSYCHOTHERAPEUTIC EXPLORATION

The first Westerner to explore the psychoactive properties of ibogaine was Chilean psychiatrist Claudio Naranjo. In his book, "The Healing Journey" (1973), Naranjo cites extensive case notes from 40 therapeutic sessions with 30 patients in which he used either ibogaine or total iboga extract. He also describes 10 sessions with a different group in which he used iboga extract with another amphetamine.

(Naranjo was a pioneer in psycholytic therapy–psychotherapy using psychedelics as an adjunctive tool. He did important early research on LSD, MDA, yage/ayahuasca, and other psychededlics, much of it the first in the literature. He even exchanged LSD for ayahuasca with Amazonian shamans.)

In his book, Naranjo writes that "Ibogaine is most suited to the exploration of the past, in contrast to MDMA, which is most adequate for the clarification of the present…[T]he reaction to ibogaine is noteworthy for its emphasis on symbols, and only by means of symbols–conceptual or visual–can we deal with a reality which is not present…Parental images evoked by means of ibogaine probably correspond to the child’s conception of his parents, which still lies in the subconscious of the adult–but these do not necessarily match the patient’s reality. The therapeutic process with ibogaine may be depicted as that of seeing such constructions for what they are and being freed through confrontation with them…."

In short, ibogaine permits unusual access to past memories and feelings, while simultaneously allowing an extraordinary degree of symbolic objectivity. Such objectivity permits the subject to place these events and feelings in their appropriate context, and thus make progress which would take months or years under traditional therapeutic techniques.

Naranjo’s work dates to at least 1966, when he presented a paper on his preliminary work with 15 cases to a psychedelic conference in San Francisco.

ADDICTION CURE?

In 1962, Howard Lotsof, a 19-year-old junkie from the Bronx, somehow got hold of a dose of ibogaine and took it. The trip itself was apparently quite remarkable. Far more incredible was the fact that when he came down, he no longer had any desire to take heroin. He evetually took ibogaine on five occasions, one week apart, in a dose-increasing regimen. From this self-administered treatment, Lotsof stayed clean for three and a half years. Later his urge to take heroin returned, but he was unable to obtain ibogaine. He became readdicted for a year and a hlaf, eventually entered a methadone program. Realizing he was still trapped in a vicious circle, he was able to detox from methadone largely due to the experiences he’d had years previously with ibogaine.

In 1980, after his life had stabilized, Lotsof began to work toward making ibogaine available to the public as an addiction interrupter. (Such a treatment modality is completely new; the usual methods are either cold-turkey withdrawl or replacement addiction –e.g.-methadone, which is an opiate just like heroin.) In 1986 he opened NDA International, INc. a company based in Staten Island, NY to promote research into the substance, and ultimately to market ibogaine under the tradename Endabuse. (He is still forbidden by law from doing so.)

Lotsof has also been awarded five US Patents for various ibogaine treatments. This is despite the fact that ibogaine is illegal: somehow it would up a Schedule I substance, right alongside LSD, heroin, marijuana, psilocybin, etc. Paradoxically, ibogaine is all but impossible to obtain in the US: one source reports that less than 4 grams have been seized in over 20 years.

What is especially remarkable about ibogaine as an addiction interupter is that it not only blocks the addiction drive for approximately six months, but it also nearly totally nullifies withdrawl symptoms. Withdrawl is a debilitating experience for addicts, and can even be fatal in extreme cases. Ibogaine is so effective in this regard that junkies undergoing ibogaine treatment will even request and eat sizeable meals 24-36 hours after their last fix, something unimagineable in normal circumstances.

But this unexplained chemical process is but one aspect of the ibogaine treatment. Crucial to recovery is the trip experience itself. As Naranjo noted in his research, the experience allows the addict to come to terms with life experiences which lead them to manifest addictive behavior. As any recovery specialist will tell you, it is this which must be addressed to truly effect recovery on a long-term basis.

Lotsof’s findings were replicated in 1990, when the International Coalition for Addict Self-Help (ICASH) reported their findings relative to nine individuals treated with ibogaine for drug dependency. Since then, that body of work has been elaborated on to include 21 case histories of treatments conducted over the last five years.

ICASH has pioneered the paraclinical application of ibogaine by addicts for addicts, using treatment methodology acquired from Dutch counterparts who formed guerilla treatment programs under the banner of DASH (Ducth Addict Self-Help).

These and other studies have confirmed that ibogaine is an effective addiction interupter for a wide range of addictive disorder including heroin, methadone, cocaine and amphetamine, alcohol, nicotine, and even poly-drug dependency.

RECENT DEVELOPMENTS

This past year, NDA International (Lotsof’s organization) sponsored the First International Ibogaine Treatment Symposium, which was held just outside the town of Leiden in the Netherlands. Researchers from Holland, Germany, Israel and the US were present. During the three-week seminar, participants were able to observe the treatment of patients by the world-renowned Dutch psychiatrist Prof. Dr. Jan Bastiaans, widely know for his work treating Holocaust survivors and victims of trauma with LSD-assisted psychotherapy. In all six addicts received successful treatment.

A second such symposium is planned for late 1993 or early 1994. (For additional information about the symposium, including case histories, see the journal of the Multidisciplinary Assoc. for Psychedelic Studies, Summer 1993 edition.)

After some considerable foot-dragging by the National Institute for Drug Addiction (NIDA), the FDA has finally just approved ibogaine for human testing to determin its efficacy in addiction interuption. Phase I studies (determining toxicity, etc.) will begin shortly. The study will be conducted at the University of Miami under the direction of Dr. Deborah Mash, along with Dr. J. Sanchos Ramos. Both were present at the International Treatment Symposium.

Thus, ibogaine joins LSD, MDMA, psilocybin, and DMT as substances which have been approved by the FDA (with the permission of the DEA and the Drug Czar’s office) for human testing for therapeutic applications.

SELECTED BIBLIOGRAPHY

"Psychedelic Monographs and Essays" vol. 6 (1993), ed. by Thomas Lyttle; pp. 71-111: R. Goutarel, et al.: "Pharmacodynamics and Therapeutic Applications og Iboga and Ibogaine". Probably the best overview of ibogaine I have come across yet. Goutarel isolated several of the alkaloids in T. iboga, and is considered one of the world’s experts on it. This superb article gives historic background, details traditional use incl. a full account of initiation rites, plus gives an extensive examination of modern ibogaine treatment, incl. a breakdown of the various stages of the ibogaine trip.

"Ibogaine: Howard Lotsof Taking Aim at Addiction" interview by Peter Gorman, High Times, Nov. 1993; pp. 50-55. Excellent.

"Psychedelics Encyclopedia" by Peter Stafford; Berekely, CA: Ronin Publishing; pp. 358-367. Not as thorough as PM&E’s article, but an excellent place to start.

Bob Sisko [dir. ICASH]: "Ibogaine and Substance Abusers: Follow-up on Four Case Histories", MAPS (journal of the Multidisciplinary Assoc. for Psychedelic Studies), vol. IV no. 2 (Summer 1993); pp. 15-24.

"Flesh of the Gods: The Ritual Use of Hallucinogens" ed. by Peter T. Furst; NY: Praeger, 1972; pp. 237-260: James W. Fernandez: "Tabernathe Iboga: Narcotic [sic] Ecstasis and the Work of the Ancestors." Good ethnographic/ethnobotanical study by an expert on the Fang. Recommend the rest of the book, too, for that matter…

Max Cantor: "Miracle Cure? Advocates Say Ibogaine Ends the Craving for Dope", Village Voice; June 5, 1990

"The Healing Journey: New Approaches to Consciousness" by Claudio Naranjo; NY: Pantheon Books, 1973; pp. 171-224. Alas, out-of-print; but this excerpt along with other choice articles on ibogaine can be obtained from Rosetta. See below.

LOTSOF’S PATENTS:

1985: US Patent No. 4,499,096
1986: US Patent No. 4,587,243
1989: US Patent No. 4,857,523
1991: US Patent No. 5,026,697
(missing one)

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Leda version 1.4.3

Ibogaine — The End Of Heroin Withdrawl?

by Alexander Highcrest. From "eye WEEKLY", August 4, 1994, Toronto.


Depending upon who is collecting the statistics, there are anywhere between 5,000 to 25,000 regular heroin users in Toronto. Most of these people have one thing in common — they’ve thought about kicking the habit. They may even have tried a couple of times.

Others, like myself, were motivated enough to break the habit on the first try.

There are basically two ways to break a heroin addiction. The user can just stop — go cold turkey — and suffer the physical and emotional hell of withdrawal, or the user can get into a methadone program and swap the heroin habit for a methadone habit. Ibogaine, a non-narcotic, non-addictive drug, could offer up a third option.

Ibogaine comes from a shrub found in the rainforests of western Africa. The people there have used ibogaine for centuries as an upper to help them stay alert when hunting, or for inducing visions during initiation rites. Among the secret societies of Gabon and the Congo, ibogaine is closely associated with death. The plant that produces the drug is often described as a supernatural being which can carry someone away to the realm of the dead. Actual death by overdose is possible, but heavy users usually just slide into a semi-coma while gazing off into space. West African cultists who use the drug believe that during this almost comatose experience the soul leaves the body and wanders around in the land of the dead.

In the early ’60s the drug was introduced to the West as a psychoanalytic tool. Ibogaine is characterized as a hallucinogen, but it doesn’t cause LSD-like hallucinations. Users of the drug claim that they "see" their lives appear as if on a movie screen on their eyelids, or on any surface they focus on. In 1967 ibogaine was officially made illegal in the U.S.

Howard Lotsof, an American heroin addict looking for a new drug experience, tried ibogaine in 1962. Although his first ibogaine high lasted longer than his usual heroin injection interval, he didn’t suffer any withdrawal symptoms. Instead, Lotsof’s craving for heroin disappeared completely. Lotsof gave ibogaine to seven other heroin addicts and five of them quit using heroin after their first ibogaine experience. At the time neither Lotsof nor any of his friends were planning to quit.

Based on his personal experiences, Lotsof decided to promote ibogaine as a potential addiction therapy. He founded NDA (New Drug Application) International and between 1985 and 1989 obtained three patents for drug addiction treatment methods based on ibogaine. NDA claims that ibogaine can beat an addiction in three steps. (Warning! The following is in psych-speak.)

First, the addict’s repressed memories are released. Then the memories are intellectually re-evaluated. Finally, a new understanding of the memories is integrated into the client. Former addicts who have successfully used ibogaine say that they came to understand their drug use patterns and then reached a point when they felt they could choose whether or not to use drugs.

The U.S. government hasn’t pursued ibogaine as a treatment for addiction with much enthusiasm, despite the urgings of AIDS activists, rainforest conservationists, drug policy reformers and drug user advocates. In August, 1993, the U.S. Food and Drug Administration finally gave the University of Miami the go-ahead to conduct clinical trials on volunteer patients. This decision made ibogaine the second psychoactive drug to begin the journey toward FDA approval. MDMA was the first. One surprising thing about the FDA decision is that it followed on the heels of a study conducted by the John Hopkins University in Baltimore, which indicated that high doses of ibogaine can cause brain damage in rats.

The situation is no better in Canada. A spokesperson for Toronto’s Addiction Research Foundation told eye that they weren’t currently investigating ibogaine because there were "other research priorities." To his knowledge no one was researching ibogaine in Canada.

Ibogaine treatment is available overseas. The International Coalition for Addict Self-Help (ICASH) has developed an "underground railroad" to assist addicts in getting ibogaine treatment in Europe, primarily in the Netherlands. There, ibogaine reportedly has been successful in breaking addictions to heroin, cocaine, nicotine and alcohol. Nearly one-quarter of all the treated addicts stayed drug- free for at least six months. Another 40 per cent to50 per cent kicked their habits, but needed help from other support programs to stay on the wagon. Some 20 per cent to 30 per cent went back to using their drugs of choice within a month following ibogaine treatment, while roughly 10 per cent decided they needed further ibogaine treatments to stave off their old cravings. The Dutch experience has also had its share of setbacks. One woman died of a heroin overdose while taking ibogaine and the controversial drug may be linked to other deaths.

Ibogaine has been around for 30 years and there’s plenty of evidence to suggest it could be useful in helping people overcome addictions. Why has our government paid so little attention to the drug? Canadian and American national drug strategies have always placed more emphasis on a law enforcement approach rather than on treatment and prevention. Our drug war mentality has made it difficult to imagine a mind-altering drug as being a good thing; just try getting marijuana for medical reasons. It could be that large drug companies don’t see much profit potential in ibogaine. And, as always, there is such a stigma attached to drug addiction that the people with the money and power are reluctant to listen to others with real, front-line experience — the addicts.

There should be a variety of treatment options available to addicts who decide to kick their habits. There may be a place for ibogaine in treatment methodology, but I doubt it’s the magic bullet to end all addictions. When I broke my own heroin habit back in 1991, I went through what treatment experts called "spontaneous recovery." Everybody else called it going cold turkey. I know other former users who are joined at the hip to doctors and clinics because they’ve succeeded in getting onto a methadone program.

Earlier this year I met Bob Sisko, an activist from New York involved in ICASH. He spoke about ibogaine like a TV evangelist talks about Jee-Zus. He told me that ibogaine doesn’t cure addiction, but puts it in remission. He went on to say that detoxification is the first step in any drug treatment program, and ibogaine allows the addict to detoxify with dignity.

In Toronto it is virtually impossible to kick a drug habit with any dignity. This city, with its thousands of heroin addicts, only has room for about 200 people in its handful of methadone programs. Alcohol detox centres are overcrowded. Barring bad-tasting chewing gum or odd little patches, there’s nothing available to help those who want to quit smoking. People addicted to crack, this decade’s big evil, pretty well have to go it alone when they want to stop using. This is a disgrace.

Sure, there have been problems with ibogaine — it’s probably not the wonder cure. But isn’t it worse to ignore the possibility that a non- narcotic, non-addictive drug like ibogaine could help to eliminate the belief that it’s really a waste of time trying to help an addict? The drug could prove to be an important part of a rational, humane approach to treating the problem of drug abuse. It’s certainly worth trying to find out.

Created 9/12/2000 22:48:57

Extracting Ibogaine from Tabernanthe iboga and Trachelospermum jasminoides

A guide to extracting Ibogaine from J Amer. Chem. soc #80: 123, 1958


Isolation of Ibogaine from Tabernanthe iboga

from J Amer. Chem. soc #80: 123, 1958.

In this case it was for the root/root bark of tabernanthe iboga used as the plant material, which may contain up to 2.5 % or 6 % alkaloids respectively. The plant material was extracted with methanol four times, filtered and the methanol reduced to a small volume. An equal amount of water and acetic acid solution is added and shaken with petroleum naphtha, which is then separated and backwashed with acetic acid solution.

All the aqueous phases are combined. The aqueous phases are reduced in volume, then basified with ammonia hydroxide. This is then extracted four times with ethylene dichloride (possibly chloroform too). The solvent is washed with water, dried and concentrated. An equal amount of ethanol is added and the whole reduced to the original volume, then about twice the amount of ethanol is added. After chilling in the fridge for two days or so, ibogaine crystallises out, and can be collected by filtration. The remaining liquid was again reduced in volume and re-chilled for a second crop of ibogaine.

Evaporation to dryness of the liquid yielded other alkaloids and residual ibogaine, which can be separated by chromatography, though can be laborious. To purify the ibogaine 100 mg of the crude ibogaine, as obtained above, was dissolved in 1 l of acetone, then 53.1 ml of 1:1 HCl was added, with ibogaine HCl precipitating (108 mg in this case) out straight away, this compound being relatively insoluble in acetone, compared to the base. Isolated by filtration.

ibogaine mp 151-153* C sol – ethanol, ether, chloroform, acetone

ibogaine HCl mp 299-300* C.

In tabernanthe iboga, ibogaine seems to be the most active and prominent alkaloid. In other species that are recorded as containing ibogaine, other alkaloids sometimes make up the majority of the alkaloids, with ibogaine being a minor component. Many related alkaloids however have a similar but not such strong action as ibogaine. The isolation of ibogaine from more complex mixtures of alkaloids may be a bit more tricky, especially if ibogaine is not a major component of the alkaloids.
Ibogaine from Trachelospermum jasminoides
(Star Jasmine)

"Leaves and stems (50 kg) were dried in the shade and extracted with ethanol. The crude alcoholic extracts were concentrated and partitioned between 10% hydrochloric acid and chloroform (pH 1). The chloroform layer was dried with anhydrous sodium sulfate and concentrated to a gum (25 g, F1). The aqueous acidic layer was basified with aqueous ammonia and extracted into chloroform at various pH values (5, 7, 9, and 11). The fraction obtained at pH-5 (20 g, F2) was found to contain major alkaloids. We have recently reported five indole alkaloids from this plant (2)."

"The crude alkaloidal fraction (F1, 25 g) was subjected to flash chromatography. […] The alkaloid isolated was identified as voacangine-7-hydroxyindolenine by comparison of its spectral data with those reported in the literature (3). […] Voacangine-7-hydroxyindolenine may have been formed by air oxidation during the extraction and isolation process."

"Fraction F2 (20 g) was also loaded on a silica column (750 g) and was eluted with increasing polarities of mixtures of petroleum ether, chloroform, ethyl acetate, and methanol." "The fraction obtained on elution with chloroform:ethyl acetate (3:1) consisted of a mixture of four alkaloids. This fraction was subjected to a flash chromatography which was eluted with increasing polarities of mixtures of petroleum ether in acetone. The fraction obtained on elution with 70% petroleum ether in acetone was found to contain two major alkaloids. These alkaloids were separated by preparative TLC on silica gel (petroleum ether:acetone:ammonia, 6:3.95:0.05). The faster moving alkaloid was identified as ibogaine by comparison of its spectral data with those reported in the literature (7) while the slower moving alkaloid was identified as tabernaemontanine (8)."

"Further elution of the same column with 60% petroleum ether in acetone afforded another alkaloid which was further purified by preparative TLC on silica gel (petroleum ether:acetone:ammonia, 1:1:0

Created 7/31/2001 4:08:23
Modified 7/31/2001 4:11:12
Leda version 1.4.3

Modified 9/12/2000 22:48:57

Leda version 1.4.3

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