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<td valign="top" width="50%"><strong>Other Names</strong>
 
 
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*).</td>
 
<td valign="top" width="53%"><strong>Dosage and Application</strong>
 
 
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 ataxia 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).
 
 
<strong>Commercial Forms and Regulations</strong>
 
 
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*).
 
 
<strong>Literature</strong>
 
 
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 serotonin transporters and
 
 
elevates serotonin. 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.</td>
 
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[[Category:Drugs]]
 
[[Category:Drugs]]
 
[[Category:Psychedelic]]
 
[[Category:Psychedelic]]

Latest revision as of 15:39, 14 July 2014

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