Other Names

Endabuse, ibogain, ibogaina, ibogaIne, NIH 10567,

12-methoxy-ibogamin, 12-methoxy-ibogamine

Substance type: indole alkaloid, indole alkylamine,

ibogane type

Chemically, ibogaine is closely related to the ~carbolines,

and particularly to harmaline and

harmine. It belongs to the group of cyclic tryptamine

derivatives.

Ibogaine was first isolated from the root cortex

of Tabernanthe iboga in France in 1901 (Dybowsky

and Landgren 1901). Ibogaine and analogous

alkaloids (ibogane type) also occur in Pandaca

retusa (Lam.) Mgf. [sYll. Tabernaemontana retusa

(Lam.) Pichon] (cf. Tabernaemontana spp.), a dogbane species native to Madagscar (Le MenOlivier

et al. 1974). Many genera in the Family ApocYllaceae,

including Tabernaemontana, Voacanga

spp., Stemmadenia, Ervatamia, and Gabunea, contain

ibogaine-type indole alkaloids (ibogamine, tabernanthine,

voacangine, ibogaline) (Prins 1988, 5).

Between 1940 and 1950, most research into

ibogaine was conducted in France. Because it

exhibited potent stimulating properties, the initial

pharmacological research focused on ibogaine's

neuropharmacological effects. Only later were the

hallucinogenic effects more precisely studied

(Sanchez-Ramos and Mash 1996,357).

In the 1960s, the Chilean psychiatrist Claudio

Naranjo introduced ibogaine into psychotherapy

as a "fantasy-enhancing drug" (Naranjo 1969*).

One subject provided the following account of a

shamanic experience during a psychotherapeutic

session with the "stomach drug" ibogaine:

I am a panther! A black panther! I defend

myself, I stand up. I snort powerfully, with the

breath of a panther, predator breath! I move

like a panther, my eyes are those of a panther, I

see my whiskers. I roar) and I bite. I react like a

panther, offense is the best defense.

Now I hear drums. I dance. My joints are

gears, hinges, hubs. I can be a knee, a bolt,

could do something, indeed almost anything.

And I can loose [sic] myself again in this chaos

of nonexistence and the perception of vague,

abstract ideas of changing forms, where there

exists a sense of the truth of all things and an

order that one should set out to discover.

(Naranjo 1979, 188*)

In Europe, the Swiss psychiatrist Peter

Baumann provided the main impetus for the use

of ibogaine in psychotherapy:

Baumann reported about experiments with

completely synthetic ibogaine, which he used

on only a few patients with whom a long and

positive therapeutic relationship existed. The

dosage was usually 5 mg/kg of body weight. At

this dosage level, the effects lasted for approximately

5 to 8 hours and diminished only very

slowly. In his experiments with ibogaine, the

author found that it was not the substance as

such that triggered a specific effect but that it

induced an unspecific psychological and

physical stimulus that was then responded to

in the language that patient was accustomed

to using with this therapist. (Leuner and

Schlichting 1986, 162)

Unfortunately, an accident led to this initially

promising research being halted. Marina Prins

(1988) subsequently compared Baumann's results

with those reported by Naranjo.

Today, ibogaine is in the spotlight of

neuropharmacological research because it has

been shown that this alkaloid can be used to

reduce and cure the addictive behavior of people

dependent on other drugs (heroine, cocaine)

(Sanchez-Ramos and Mash 1996; cf. Maps 6 [2;

1996]: 4-6). For example, ibogaine has been found

to suppress the motor activity that occurs during

opiate withdrawal. It has been proposed that

ibogaine, when

ingested by opiate addicts in a single high

dosage, dramatically reduces withdrawal

symptoms while simultaneously causing a trip

that provides the patient with such deep

insights into the personal causes of the

addiction that a majority of the individuals

who receive such therapy can live for months

without relapse. However, it should be noted

that several additional sessions may be necessary before a persistent stabilization

occurs. (Naeher 1996, 12)

Experiments with primates have shown that

ibogaine reduces opiate addiction and partially

blocks withdrawal symptoms. Although the

neuropharmacological mechanism behind these

effects has not yet been discovered, Deborah Mash

and her team in Miami (Mash 1993; Mash et al.

1995) are researching this question. Ibogaine has

been demonstrated to interact with numerous

different receptors, and it has been concluded

that this breadth of interaction is the reason for

ibogaine's effectiveness in addiction therapy

(Sweetman et al. 1995).

In the United States, the use of ibogaine to treat

addiction has been patented as the clinical Lotsof

procedure (Lotsof 1995). Whether this procedure

will receive endorsement from the medical community

remains to be seen (Touchette 1995). A

novel about this facet of ibogaine (which incorporates

such actual people as Howard Lotso£) was

published in Slovenia (Knut 1994).

Ibogaine enjoys a reputation for being an

exceptionally potent and stimulating aphrodisiac

(Naranjo 1969*).500 The research to date has

entirely neglected this aspect.

Another substance of pharmacological and

therapeutic interest is noribogaine, which is

chemically and pharmacologically very similar to

Prozac (fluoxetine). In the United States, Prozac is

one of the most frequently prescribed psychopharmaca

for depression, and it is celebrated as

the "happy drug" in the popular press (Kramer

1995; Rufer 1995*).
Dosage and Application

Two to four tablets containing up to 8 mg ibogaine

per tablet may be given daily as a stimulant for

states of exhaustion, debility, et cetera. Nausea,

vomiting, and ataxiaLoss of motor coordination are possible side effects. When

used for psychotherapeutic purposes (Baumann),

dosages of 3 to 6 mg of ibogaine hydrochloride per

kg of body weight were administered. For psychoactive

purposes, dosages of around 200 mg are

recommended (Prins 1988, 47).

Commercial Forms and Regulations

Ibogaine was formerly available as a medicine

under the trade name Bogadin (Schneider and

McArthur 1956). In the United States, ibogaine is

considered a Schedule I drug and has been

prohibited since 1970. However, ibogaine

hydrochloride is marketed under the trade name

Endabuse and can be used with the appropriate

special permit. In Germany, ibogaine is not

considered a narcotic under the guidelines of the

narcotic laws and is therefore legal (Korner 1994,

1573*).

Literature

See also the entries for Tabernaemontana spp.,

Tabernanthe iboga, Voacanga spp., and indole

alkaloids.

Baumann, Peter. 1986. "Halluzinogen"-unterstiitzte

Psychotherapie heute. Schweizerische Arztezeitung

67 (47): 2202-5.

Dybowski, J., and E. Landrin. 1901. Sur l'iboga, sur

ses proprietes excitantes, sa composition et sur

l'alcaloide nouveau qu'il renferme. Comptes

Rendues 133:748.

Fromberg, Eric. 1996. Ibogaine. Pan 3:2-8. (Includes

a very good bibliography.)

Knut, Amon Jr. 1994. Iboga. Maribor: Skupina

Zrcalo. (Cf. Curare 18 (1; 1995): 245-46.)

Kramer, Peter D. 1995. GlUck aufRezept: Der

unheimliche Erfolg der GlUckspille Fluctin.

Munich: Kosel.

Le Men-Olivier, 1., B. Richards, and Jean Le Men.

1974. Alcaloides des graines du Pandaca retusa.

Phytochemistry 13:280-81.

Lotsof, Howard S. 1995. Ibogaine in the treatment of

chemical dependence disorders: Clinical

perspectives. Maps 5 (3): 15-27.

Mash, Deborah C. 1995. Development of ibogaine as

an anti-addictive drug: A progress report from

the University of Miami School of Medicine.

Maps 6 (1): 29-30.

Mash, Deborah C., Julie K. Staley, M. H. Baumann,

R. B. Rothman, and W. 1. Hearn. 1995.

Identification of a primary metabolite of

ibogaine that targets serotoninA monoamine neurotransmitter, biochemically derived from tryptophan, that is primarily found in the gastrointestinal (GI) tract, platelets, and central nervous system (CNS) of humans and animals. It is a well-known contributor to feelings of well-being. transporters and

elevates serotoninA monoamine neurotransmitter, biochemically derived from tryptophan, that is primarily found in the gastrointestinal (GI) tract, platelets, and central nervous system (CNS) of humans and animals. It is a well-known contributor to feelings of well-being.. Life Sciences 57 (3): 45-50.

Naeher, Karl. 1996. Ibogain: Eine Droge gegen

Drogenahhangigkeit? Hanjblatt 3 (21): 12-15

(interview).

Prins, Marina. 1988. "Von Iboga zu Ibogain: Dber

eine vielseitige Droge Westafrikas und ihre

Anwendung in der Psychotherapie." Unpublished

licentiate thesis, Zurich. (Very rich bibliography.)

Sanchez-Ramos, Juan R., and Deborah Mash. 1996.

Pharmacotherapy of drug-dependence with

ibogain. Jahrbuch fur Transkulturelle Medizin und

Psychotherapie 6 (1995): 353-67.

Schneider, J., and M. McArthur. 1956. Potentiation

action of ibogain (BogadinTM) on morphin

analgesia. Experimenta 8:323-24.

Sweetman, P. M., J. Lancaster, Adele Snowman, J. 1.

Collins, S. Perschke, C. Bauer, and J. Ferkany.

1995. Receptor binding profile suggests multiple

mechanisms of action are responsible for

ibogaine's putative anti-addiction activity.

Psychopharmacology 118:369-76.

Touchette, Nancy. 1995. Anti-addiction drug ibogain

on trial. Nature Medicine 1 (4): 288-89.

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