The Ibogaine Dossier
NYU Conference on Ibogaine Nov 5-6, 1999
variety iboga fruit
T. iboga roots
Photo by Gollnhofer
Art Buro, Amsterdam
Prepared for ICASH
for Addict Self-Help
The ibogaine medical subculture
Journal of Ethnopharmacology 115 (2008) 9-24
Kenneth R. Alper a,b, Howard S. Lotsof c, Charles D. Kaplan d
a Department of Psychiatry, New York University School of Medicine, New York, NY 10016, USA
b Department of Neurology, New York University School of Medicine, New York, NY 10016, USA
c Dora Weiner Foundation, 46 Oxford Place, Staten Island, NY 10301, USA
d Department of Psychiatry and Neuropsychology, Maastricht University, 6200 MD Maastricht, The Netherlands
Elsevier © 2008
Aim of the study: Ibogaine is a naturally occurring psychoactive indole alkaloid that is used to treat substance-related disorders in a
global medical subculture, and is of interest as an ethnopharmacological prototype for experimental investigation and possible rational pharmaceutical
development. The subculture is also significant for risks due to the lack of clinical and pharmaceutical standards. This study
describes the ibogaine medical subculture and presents quantitative data regarding treatment and the purpose for which individuals have taken
Materials and methods: All identified ibogaine "scenes" (defined as a provider in an associated setting) apart from the Bwiti religion in Africa
were studied with intensive interviewing, review of the grey literature including the Internet, and the systematic collection of quantitative data.
Results: Analysis of ethnographic data yielded a typology of ibogaine scenes, "medical model", "lay provider/treatment guide", "activist/selfhelp",
and "religious/spiritual". An estimated 3414 individuals had taken ibogaine as of February 2006, a fourfold increase relative to
5 years earlier, with 68% of the total having taken it for the treatment of a substance-related disorder, and 53% specifically for opioid
Conclusions: Opioid withdrawal is the most common reason for which individuals took ibogaine. The focus on opioid withdrawal in the ibogaine
subculture distinguishes ibogaine from other agents commonly termed "psychedelics", and is consistent with experimental research and case series
evidence indicating a significant pharmacologically mediated effect of ibogaine in opioid withdrawal.
© 2007 Elsevier Ireland Ltd. All rights reserved.
Keywords: Ibogaine; Iboga alkaloid; Substance-related
Ibogaine is the most studied of the iboga alkaloids (Bartlett et al., 1958), a group
of naturally occurring and synthetic indole alkaloids, some of which reportedly reduce opioid
withdrawal symptoms and drug self-administration in humans (Luciano, 1998; Alper et al., 1999; Mash
et al., 2001) or preclinical models (Glick et al., 2001). Presently in the setting of homes, hotel
rooms and private clinics in North America and Europe, individuals in increasing numbers are taking
ibogaine in what has been termed, "a vast uncontrolled experiment" (Vastag, 2005).
The ritual eating of iboga has been a psychopharmacological sacrament in the Bwiti
religion for several centuries, and was likely practiced among Pygmies in much earlier times
(Fernandez, 1982). In Gabon and elsewhere in West Central Africa, ibogaine is ingested in the form
of scrapings of Tabernanthe iboga root bark. The ritual aim of eating iboga has been conceptualized
as "binding"; the binding across time through ancestral contact, or binding participants socially on
the basis of a common shared experience of a distinctive consciousness and system of belief
(Fernandez, 1982; Fernandez and Fernandez, 2001). In the colonial era Bwiti became a context of
collective psychological resistance to the anomie and demoralization related to the strain on
indigenous community and family institutions. Bwiti offered a dignified realm of spiritual endeavor,
"the work of the ancestors" and social cohesion. Following Gabonese independence in 1960, Bwiti has
remained constellated with national identity and contemporarily retains significant social and
political importance (Swiderski, 1988; Samorini, 1995).
Iboga has not commonly been used to treat addiction in the traditional African Bwiti
context. Iboga has been sought as a treatment for some somatic conditions, in particular for
infertility (Fernandez, 1982). In the colonial era the indigenous community experienced a crisis due
to a sharp decline in fertility caused by venereal disease stemming from prostitution and the
separation of men from their families by the large-scale physical relocation of indigenous workers.
The possibility of an objective basis for the use of iboga in this setting is suggested by evidence
associating iboga alkaloids with antimicrobial activity or effects on cell-mediated immunity. Iboga
alkaloids are reportedly active against Candida albicans in the intact animal (Yordanov et al.,
2005). In vitro studies indicate reversal of multidrug resistance in human cancer cells (Kam et al.,
2004) and activity against Mycobacterium tuberculosis (Rastogi et al., 1998), human immunodeficiency
type 1 virus (Silva et al., 2004), and the tropical parasite Leishmania amazonensis (Delorenzi et
The first observation of ibogaine as treatment for substance related disorders in
1962 involved a network of lay drug experimenters who ingested a variety of hallucinogens and
systematically recorded their experiences (Lotsof and Alexander, 2001). Withdrawal symptoms were
unexpectedly absent in heroin-dependent individuals who had taken ibogaine. Common to various
sociological definitions of the term "subculture" is a system of beliefs, norms and values apart
from a superordinate culture (Clarke, 1974; Dowd and Dowd, 2003). The ibogaine subculture has
elicited wariness from the "superordinate culture" of conventional clinical medicine (Kleber, 2001),
and has been invoked regarding the null hypothesis that ibogaine's reported effect in opioid
withdrawal is not pharmacologically mediated, but is instead accounted for by suggestion and ritual
(Sharpe and Jaffe, 1990). The ibogaine subculture is also significant as the setting of case report
evidence that influenced the decision of the National Institute on Drug Abuse (NIDA) to pursue its
ibogaine project (Alper, 2001), and the Food and Drug Administration (FDA) to approve a clinical
trial (Mash et al., 1998).
Ibogaine is unscheduled in most of the world, with the exception of the US, Belgium,
Denmark, France, Sweden, Switzerland, and Australia where it is illegal. Ibogaine has not been
popular as a recreational drug regardless of its legal status (Kleber, 2001), and apparently only
two arrests involving ibogaine are known to have occurred in the US (Ranzal, 1967; Lane, 2005).
Iboga alkaloids reportedly are not self-administered, and do not produce withdrawal signs following
chronic administration in animals (Aceto et al., 1992). As of late 2006, ibogaine hydrochloride
(HCl)was available for $400-$500USDper gram (ethnogarden.com, 2006), and the dosage typically used
for opioid withdrawal is in the range of 1-2 g. Purity on the order of 97-98% has been reported on
certificates of analysis for supplies of ibogaine HCl used in the subculture. Ibogaine is also
available as Tabernanthe iboga extract or dried root bark.
1.2. Clinical use
Ibogaine, either as Tabernanthe iboga root bark or ibogaine HCl is the only iboga
alkaloid that has reportedly been administered to humans, with apparently only one exception, a
study in which 12 normal volunteers were evaluated with some brief neuropsychological tests after
receiving the naturally occurring iboga alkaloid ibogaline (Schmid, 1967). Ibogaine HCl has been
typically administered as a single oral dose in the range of 10-25 mg/kg of body weight. Patients
physically dependent on opioids have described significant attenuation of withdrawal symptoms within
several hours of ingesting ibogaine, with subsequently sustained resolution of the opioid withdrawal
syndrome (Alper et al., 1999; Mash et al., 2001). The advantages attributed to ibogaine are higher
tolerability relative to other standard treatments for acute opioid withdrawal, and an interval of
diminished drug craving that may last days to months following a treatment. Individuals also take
ibogaine in search of psychological or religious insight, typically at dosages lower than those used
in the treatment of opioid withdrawal.
There are no randomized controlled clinical trials of ibogaine, and the available
clinical data is limited mainly to two open label case series. One series from the US and the
Netherlands included self-reported outcomes of a consecutive series of 52 treatments involving 41
different individuals, some of who were treated on multiple occasions mainly for the indication of
dependence on opioids or stimulants (Alper, 2001). Thirty-six percent of the treatments were
associated with self-reported intervals of 6 months or longer of abstinence from the primary drugs
of dependence for which treatment had been sought.Asubset of 33 individuals were treated for the
indication of opioid withdrawal with a single dose of ibogaine averaging 19.3 mg/kg (Alper et al.,
1999). Twenty-five of these patients had full resolution of opioid withdrawal without drug seeking
behavior that was sustained throughout a 72-h period of post-treatment observation, and another four
individuals denied withdrawal symptoms but expressed their preference to continue to use heroin. The
other series, from a clinic in St. Kitts consists of 32 patients treated with a fixed dose of 800 mg
of ibogaine HCl for the indication of withdrawal from heroin (Mash et al., 2001). Physician-rated
structured instruments indicated resolution of withdrawal signs and symptoms at 24 h after the last
use of opioids (an interval of abstinence commonly associated with significant withdrawal symptoms)
thatwas sustained during subsequent observation for 1 week following ibogaine administration.
An unpublished Dutch doctorandus thesis (Bastiaans, 2004) presents data obtained
from 21 subjects who responded to a Web-based questionnaire adapted from the European Addiction
Severity Index a mean of 21.8 months after they had taken ibogaine for treatment of a
substance-related disorder. Seventeen of the 21 patients (81%) identified opioids as the primary
drug of dependence for which they had sought treatment. Five individuals reported stopping the use
of all substances following treatment with ibogaine, and another nine reported stopping the use of
their primary drug while continuing to use alcohol or cannabis. Nineteen patients reported stopping
their use of their primary drug for at least a week following treatment, suggesting frequent
resolution of acute opioid withdrawal.
1.3. Preclinical research
Research utilizing animal models has involved the iboga alkaloids ibogaine (Alper,
2001) and its desmethylated metabolite noribogaine (Baumann et al., 2001), and a synthetic congener,
18-methoxycoronaridine (18-MC) (Maisonneuve and Glick, 2003). Eleven of the 13 published preclinical
studies of iboga alkaloids in opioid withdrawal indicate a significant attenuation of opioid
withdrawal signs in the rat (Dzoljic et al., 1988; Sharpe and Jaffe, 1990; Maisonneuve et al., 1991;
Glick et al., 1992; Cappendijk et al., 1994; Rho and Glick, 1998; Parker et al., 2002; Panchal et
al., 2005), mouse (Frances et al., 1992; Popik et al., 1995; Layer et al., 1996; Leal et al., 2003),
and primate (Aceto et al., 1992). Iboga alkaloids are also reported to reduce the
self-administration of morphine (Glick et al., 1991; Glick et al., 1994; Glick et al., 1996;
Maisonneuve and Glick, 1999; Pace et al., 2004), cocaine (Cappendijk and Dzoljic, 1993; Glick et
al., 1994), amphetamine (Maisonneuve et al., 1992), methamphetamine (Glick et al., 2000; Pace et
al., 2004), alcohol (Rezvani et al., 1995; Rezvani et al., 1997; He et al., 2005) and nicotine
(Glick et al., 1998; Glick et al., 2000), and to diminish dopamine efflux in the nucleus accumbens
(NAc), which is regarded as a correlate of drug salience (Berridge, 2007), in response to opioids
(Maisonneuve et al., 1991; Glick et al., 1994; Glick et al., 2000; Taraschenko et al., 2007b) or
nicotine (Benwell et al., 1996; Maisonneuve et al., 1997; Glick et al., 1998).
1.4. Mechanisms of action
Initially, ibogaine's mechanism of action was hypothesized to involve antagonism at
the N-methyl-d-aspartate-type glutamate (NMDA) receptor (Skolnick, 2001). However, 18-MC, which has
negligible NMDA receptor affinity, also reduces opiate withdrawal and drug self-administration in the
animal model (Glick et al., 2001). Antagonism of the α3β4 nicotinic acetylcholine receptor (nAChR)
is a possible mechanism of action, as indicated by a series of studies of iboga alkaloids and
nicotinic agents (Fryer and Lukas, 1999; Glick et al., 2002a,b; Pace et al., 2004; Taraschenko et
al., 2005). The α3β4 nAChR is relatively concentrated in the medial habenula and interpeduncular
nucleus, where 18-MC's antagonism of α3β4 nAChRs diminishes sensitized dopamine efflux in the NAc
(Taraschenko et al., 2007a,b).
Ibogaine's mechanism of action has frequently been suggested to involve the
modification of neuroadaptations related to prior drug exposure (Rabin and Winter, 1996b; Popik and
Skolnick, 1998; Alper, 2001; Glick et al., 2001; Sershen et al., 2001; Levant and Pazdernik, 2004).
Ibogaine may modulate intracellular signaling linked to opioid receptors, and potentiates the
morphine-induced inhibition of adenylyl cyclase (AC) (Rabin and Winter, 1996b), an effect that is
opposite to the activation of AC that is classically associated with opioid withdrawal (Sharma et
al., 1975). In animals, ibogaine enhances the antinociceptive effect of morphine or other opioids
without by itself having an effect on nociception (Schneider and McArthur, 1956; Schneider, 1957;
Frances et al., 1992; Bagal et al., 1996), and inhibits the development of tolerance to morphine
antinociception (Cao and Bhargava, 1997). Prior exposure to morphine potentiates ibogaine’s
diminution of sensitized dopamine efflux in the NAc in response to morphine (Pearl et al., 1996) or
ibogaine's enhancement of morphine antinociception (Sunder Sharma and Bhargava, 1998), suggesting an
effect on neuroadaptations related to opioid tolerance or dependence.
Increased glial cell line-derived neurotrophic factor (GDNF) in the ventral
tegmental area has been suggested to mediate decreased ethanol consumption following the
administration of ibogaine to rats (He et al., 2005; He and Ron, 2006). GDNF enhances the
regeneration of dopaminergic function (Ron and Janak, 2005) and is increased by antidepressant
treatment (Hisaoka et al., 2007). The hypothesis that GDNF may mediate improvement in hedonic
functioning and mood in chronic withdrawal from addictive substances is appealing, but does not
appear likely to explain efficacy in acute opioid withdrawal.
Although designated as a hallucinogen, ibogaine's use in opioid withdrawal
distinguishes it from other compounds that are commonly termed "psychedelics", namely the serotonin
type 2A receptor agonist classical hallucinogens such as lysergic acid diethylamide (LSD),
psilocybin and mescaline, or the serotonin releasing substituted amphetamine
3,4-methylenedioxymethamphetamine (MDMA). In contrast with ibogaine, there is no preclinical or case
report evidence that suggests a significant therapeutic effect of classical hallucinogens or MDMA in
acute opioid withdrawal. Ibogaine's effects in opioid withdrawal do not appear to involve serotonin
agonist or releasing activity (Wei et al., 1998; Glick et al., 2001). Serotonergic neurotransmission
does not appear to play a significant role in mediating the expression of the opioid withdrawal
syndrome, which remains unchanged even after extensive lesioning of the raphe (Caille et al., 2002).
The phenomenology of the subjective state produced by ibogaine has been attributed
with the quality of a "waking dream" and distinguished from the state associated with classical
hallucinogens (Goutarel et al., 1993; Lotsof and Alexander, 2001). The visual phenomena associated
with ibogaine tend to occur with greatest intensity with the eyes closed, and to be suppressed with
the eyes open, and often involve a sense of location within an internally represented visual or
dream landscape, in contrast to an alteration of the visual environment experienced with the eyes
open while awake which is often reported with classical hallucinogens. The occurrence of an
atropine-sensitive electroencephalogram (EEG) rhythm in animals treated with ibogaine (Schneider and
Sigg, 1957; Depoortere, 1987) suggests a waking neurophysiological state with an analogy to rapid
eye movement sleep (Goutarel et al., 1993; Alper, 2001).
1.5. Research objectives of this study
A previous publication provides a history and description of the ibogaine subculture
in the U.S. and Europe from its origin in 1962 until early 2001 (Alper et al., 2001). The major
objectives of this study are the qualitative analysis of observational and textual data (Bailey,
1994; Malterud, 2001) to provide an updated description as well as a typology of the ibogaine
medical subculture, and the systematic collection of quantitative data regarding treatment and the
purpose for which individuals took ibogaine.
The Institutional Review Board of the New York University School of Medicine
approved this research.
2.1. Observational methods
The providers of ibogaine treatment were conceptualized as participants in a global
medical subculture and studied from an "observing participant" research perspective (Gold, 1958).
The qualitative and quantitative information was obtained from face to face discussions, phone
conversations and e-mail correspondence with treatment providers and other participants.
2.2. Study sample
The study included only treatment providers who had already publicly identified
their activities by maintaining Web sites, publishing in the lay or scientific press, presenting at
public meetings, or posting to ibogaine list servers. Because ibogaine is not regulated in most of
the world, providers are very often open about their activity.
A "scene" is defined in this study as a provider of ibogaine in an associated
setting. The term "ibogaine subculture" refers to all ibogaine scenes collectively outside of
Africa. The sample in this study that represented the ibogaine subculture consisted of all known
presently or previously existing ibogaine scenes outside of Africa involving publicly identified
providers, with the exception of a scene in Gabon which was included that involved European and US
participants and African Bwiti adept providers. Otherwise no systematic attempt was made to study
the Bwiti religious context in Africa. No data was encountered regarding the use of Lambarene, a
tablet that was marketed in France between 1939 and 1970 that contained an estimated 8mg of ibogaine
(Goutarel et al., 1993).
2.3. Excluded scenes
A large ibogaine scene was alleged to have existed in the Christiana squatter
community in Copenhagen but was concluded to lack corroborative evidence on the basis of
communication with the Danish Drug Users Union and former Christiana residents (Alper et al., 2001).
Reported ibogaine scenes in Pakistan and Thailand were not included due to lack of independent
verification. Due to the inability to obtain quantitative data, the study did not include a sample
of probably about 20 individuals who were provided ibogaine by Dan Lieberman, a South African
ethnobotanist who died in a motor vehicle accident in August 2000. Psychologist Leo Zeff and others
administered ibogaine (typically as a single doses in the range of 150-300 mg) and other
hallucinogens as an adjunct to psychotherapy beginning in the 1950s in a scene that existed on the
West Coast of the US (Stolaroff, 2004) that was excluded due to a lack of quantitative data.
2.4. Data collection
The data collection for this study began with a previously published description and
history of the ibogaine subculture as of early 2001 (Alper et al., 2001). The authors subsequently
continued their contact with the ibogaine subculture by email, phone, and in person. Quantitative
information thatwas assessed systematically from the providers included cumulative numbers of people
treated, percentage seeking treatment for addiction and specifically acute opioid withdrawal, as
well as ibogaine form and dosage and the cost of treatment. The approach to pretreatment medical
screening and laboratory evaluation, and monitoring during the treatment was also discussed. The
estimates of cumulative numbers of subjects treated obtained from providers are current as of
February 2006 except for the figure for the St. Kitts Clinic, which is taken from an abstract
published in June 2005 (Mash et al., 2005).
To determine if any further scenes existed in addition to those
of which the authors were aware, in May of 2005 a series of messages was posted to
Mindvox (Kroupa, 2006), the most frequently used ibogaine list server. The Internet, which is an
important aspect of the ibogaine subculture and comprises an extensive unpublished "grey literature"
(Boukacem-Zeghmouri and Schöpfel, 2006) was searched monthly from May 2005 to February 2006 using
the terms "ibogaine" or "iboga" alone, and combined with the term "treatment". The list server
postings and Internet searches yielded no usable information regarding new scenes that had not
already been previously obtained by longstanding, ongoing contact with subculture participants. In
May of 2005, and again near the conclusion of data gathering in February 2006, all known treatment
providers were systematically contacted to update the quantitative information. The typology of
scenes was created between the first and second data collections.
The study also reviewed the academic literature, and the "white literature"
(Boukacem-Zeghmouri and Schöpfel, 2006) including public media and officially published government
or industrial documents. Databases with white literature content including ProQuest, LexisNexis, and
the New York Times, and academic literature databases including PubMed, PsycInfo, JSTOR, UMI
Dissertation Abstracts, WorldCat, and the SAGE Sociology Full-Text Collection were searched
utilizing the terms "ibogaine" and "iboga". The references cited by the articles retrieved utilizing
the above searches were reviewed until they no longer yielded new references containing the search
terms. The above searches yielded relatively little material that was new to the authors because of
their extensive prior use of the iboga alkaloid conventional and nonconventional literature, as well
as substantial access to ibogaine-related material that is not indexed in any searchable database
(Lotsof, 1985; Alper, 2001; Alper et al., 2001; Lotsof and Wachtel, 2003; Lotsof, 2007).
2.5. Data validation
Triangulation of the data, i.e., viewing the data from multiple observational
perspectives (Malterud, 2001; Denzin and Lincoln, 2005), was possible for all of the currently
operating scenes listed in Table 1 on the basis of independent corroboration from provider and
patient participants in the same scenes, providers regarding other providers, and other informants.
Most treatment providers interviewed in the present study had previously supplied data that was
published 5 years earlier (Alper et al., 2001) and were known to at least two of the authors. For
three medical model scenes that no longer exist (Lexington 1955-1956, Santiago 1966-1967, and
Zürich 1980-1989) textual evidence was used for validation. This study omitted providers who had
not publicly disclosed their activity, which would tend to lead toward underestimation of the total
numbers of individuals who have taken ibogaine. This is particularly likely for scenes involving
small numbers of patient participants, such as individuals obtaining ibogaine from the Internet. In
order to account for this effect, estimates of hidden populations were obtained from individuals
with extensive contact with the subculture as described below in Section 3.2.
2.6. Data analysis
A typology of scenes was constructed (Bailey, 1994), based on the classificatory
dimensions of setting and the provider's set and credentials. The setting is the physical and
ecological location in which the treatment takes place: a clinic or hospital, a private residence or
hotel, or a religious shrine. A provider is an individual or group that administers ibogaine to the
patient participant, and specifies the form and dose to be given. The provider determines the
parameters of the treatment such as setting, inclusion and exclusion criteria, and medical
monitoring. Providers may or may not have a credential as a licensed physician. The provider's set
consists of the beliefs, expectations, attitudes and motivation that determine the intention to
provide ibogaine. Provider set subsumes beliefs and expectations regarding ibogaine as a treatment
for substance-related disorders, a psychotherapeutic adjunct, or religious sacrament. Motivational
aspects of set may include the giving of care, activism, or ritual.
Quantitative data included the number of individuals who took ibogaine, and the
number who took it for the treatment of a substance-related disorder, and specifically for acute
opioid withdrawal. This data for each scene was included in Table 1, and the totals for each of the
four types of scenes are indicated in Table 2.
As indicated in Table 1, four types of scenes were identified and classified on the
basis of the features of treatment setting, provider credentials and provider set; "medical model",
"lay provider/guide", "activist/self-help" and "religious/ceremonial".
3.1.1. Medical model
In this type of scene the provider is a licensed physician. In the variation of the
medical model type involving clinical research, some roles of the provider are distributed among
authors of the study protocol and the physician investigator who prescribes ibogaine. Settings of
the medical model are medical hospitals or clinics, or clinical research facilities, which are
officially credentialed according to national and local requirements in a given country, as well as
offices or residential settings in the case of treatment intended as psychotherapy. The set of the
treatment provider includes the aim of emulating existing conventional medical standards in the
treatment of addiction, clinical research, and/or psychotherapy.
Historically, the use of ibogaine in the medical model began in the 1950s, when
clinicians and researchers viewed ibogaine much as they did other compounds classified as
hallucinogens. Some, such as Jan Bastiaans, M.D. (Snelders and Kaplan, 2002), Leo Zeff, Ph.D.
(Stolaroff, 2004), and Claudio Naranjo, M.D. (Naranjo, 1973), were interested in ibogaine as an
adjunct to psychotherapy. Ibogaine, like other hallucinogens,was of interest as an experimental
model of psychosis (Turner et al., 1955; Fabing, 1956; Salmoiraghi and Page, 1957; Schneider and
Sigg, 1957). As with other hallucinogens, ibogaine may have also been investigated for military or
intelligence purposes as a "truth serum", or a means of "brainwashing" or incapacitating an
adversary which was the focus of MKULTRA (1977), a US Central Intelligence Agency project
acknowledged to have existed from 1953 until 1964. Harris Isbell, M.D., an apparent participant in
the MKULTRA project, directed the Addiction Research Center in Lexington, Kentucky where he reported
administering ibogaine to human subjects in a letter to the Ciba Pharmaceutical, the manufacturer at
that time (Isbell, 1955).
The medical treatment model presently exists mainly in countries adjacent to the US,
such as Mexico, where ibogaine is subsumed within a physician's legal prerogative to prescribe
experimental treatment, or Saint Kitts, where the government includes ibogaine in its national
formulary and provides specific approval to the clinic there to administer it. The most common
setting is a private clinic with less frequent use of hospitals. The clinics' Web sites tend to
emphasize images that suggest comfort, safety, and the experience and expertise of the clinical team.
The standard of care varies among scenes in the medical model, but typically at a
minimum involves pretreatment laboratory and electrocardiogram (EKG), vital signs and evaluation of
the medical and psychiatric history, and some participation of nurses and physicians. The most
intensive approach appears to have been that developed at the St. Kitts clinic (see Table 1). A
recently started clinic in Mexico reported a similar clinical standard (villaserena.org, 2006).
Prior to treatment with ibogaine, opioid dependent patients are converted to equivalent doses of
orally administered short acting opioids. All centrally acting medications are tapered and
discontinued for at least three serum half lives, although no specific drug interactions with
ibogaine have yet been identified. Evaluation includes pretreatment Holter monitor and 12 lead EKG,
and the following continuously during the treatment: EKG, vital sign and pulse oximetry monitoring,
intravenous access, and the presence on site of an emergency physician with advanced cardiac life
support certification and a registered nurse in the room with the patient continuously throughout
the treatment (Mash et al., 2000, 2001).
Ibogaine scenes: quantitative and descriptive features, grouped by scene type
|Scene, year began- (year ended, if applicable)
||Reason for taking ibogaine: na, n(%)b [n (%)]c
||Other non-substance-related reason for taking ibogaine
||Setting/provider, medical evaluation and monitoring
|Medical model type
|US, 1955 Lexington, KY (Isbell, 1955)
||8 (research, subjects not seeking treatment)
||Research, determination of psychoactive threshold
||50-300 mg ibogaine HCl
||Clinical research, US Public Health Service Hospital, Lexington, KY;
Harris Isbell, M.D. Subjects were prisoners with prior histories of
opioid dependence who had been abstinent for periods of months
||Volunteers / prisoners
|Chile, 1966-1967 Santiago (Naranjo, 1973)
||Adjunct to psychotherapy
||3-5 mg/kg ibogaine HCl
||Claudio Naranjo, M.D., psychiatrist. Ibogaine administered in office setting in context of ongoing psychotherapy
|Switzerland, 1980-1989 Zurich (Prins, 1988)
||Adjunct to psychotherapy
||4-10 mg/kg ibogaine HCl
||Peter Baumann M.D., psychiatrist. Ibogaine administered in office or residential setting, given in context of ongoing psychotherapy
|US, 1994-1995 Miami FL (Mash et al., 1998)
||15 (Phase I clinical trial subjects not seeking treatment)
||FDA approved clinical research
||1-4 mg/kg ibogaine HCl
||Phase I/II dose-ranging study. Juan Sanchez-Ramos, Ph.D., M.D., Principal Investigator, Deborah Mash, Ph.D., Co-Investigator. Jackson Memorial Hospital in Miami
|Panama, 1994-1995 Panama City (Luciano, 1998)
||11, 11 (100%)
|Substance dependence only
||10-25 mg/kg ibogaine HCl
||Hospital Centro Medico Paitilla, full medical staff. Pretreatment evaluation included EKG, blood chemistry, medical and psychiatric history
||No cost to $35,000 USD
|Brazil, 1994-Sao Paulo (Sandberg,2006)
||9, 9 (100%)
|Substance dependence only
||10-20 mg/kg ibogaine HCl
||Hospital Maternidade Maria Perpetua Piedade Goncalves, full medical staff. Pretreatment evaluation includes EKG, blood chemistry, medical and psychiatric history
|St. Kitts, 1996- (Mash et al., 2001)
||400, 400 (100%)
|Substance dependence only
||600-1200 mg ibogaine HCl
||See text for description of the approach to medical evaluation and< monitoring developed by Jeffrey Kamlet, M.D
||$10,000 - $12,500 USD
|Mexico, 2001- Playas de Tijuana, Baja California (Ibogaine Association, 2006)
||283, 252 (89%)
||12-18 mg/kg ibogaine HCl
||Clinic or hospital. Pretreatment evaluation includes EKG, blood chemistry, medical and psychiatric history. Continuous EKG monitoring and presence of a nurse in the room with the patient during the treatment
|Mexico, 2005- Cancun (villaserena.org, 2006)
||34, 34 (100%)
|Substance dependence only
||8-18 mg/kg ibogaine HCl
||Clinic, private rooms. See text regarding medical evaluation and monitoring
Lay provider/guide type
|US, 1962-1963 New York City (Lotsof and Alexander, 2001)
||20; none sought treatment, 7 were opioid dependent
||Lay experimentation and research, Psychotherapeutic
||0.14-19.0 mg/kg ibogaine HCl
||Apartments, private homes. No medical support. Self-administration and systematic self-observation
||$15 USD for 500 mg
|Central America, Caribbean, 1993- (Taub, 2006)
||607, 455 (75%)
||9-36 mg/kg ibogaine HCl
||Rented cottages in resort settings, private residences. Pretreatment medical and psychiatric history, EKG and blood chemistry
||No cost to $4000 USD
|Italy/France, 1994- (Naeher, 2006)
||101, 44 (44%)
||10-23 mg/kg ibogaine HCl
||Apartment. Physician available. Pretreatment medical and psychiatric history, EKG and blood chemistry
|Netherlands, 1999- Breukelen (Glatt, 2006)
||200, 160 (80%)
||2-6 g Tabernanthe iboga extract (estimated 15% ibogaine)
||Private home. Use of other "plant medicine or fungi" in combination with ibogaine. Pretreatment medical and psychiatric history, no medical testing
||No cost to $2000 USD
|Czech Republic, 2000- (Mariano, 2006)
||102, 94 (92%)
||900-1600 mg ibogaine HCl
||Apartments and private homes. Medical assessment by local consulting clinic, including medical and psychiatric history, EKG and blood chemistry
|UK, 2000- London, West Sussex (Conn, 2006; Wells, 2006)
||83, 54 (65%)
||14-20 mg/kg, or 250-2000 mg ibogaine HCl
||Multiple Providers; apartment or private home. Pretreatment medical and psychiatric history, EKG and blood chemistry
||£400 - £850 GBP
|Canada, 2002-Vancouver, Toronto (ibogatherapyhouse.net, 2007)
||64, 52 (81%)
||16-23 mg/kg ibogaine HCl
||Multiple Providers; dedicated clinic, private residences. Pretreatment medical and psychiatric history, EKG and blood chemistry. Emergency medical technician on premises during treatment at clinic
||$1000 - $3500 CAD
|South Africa, 2004- Eldoraigne (Rossouw, 2006)
||36, 36 (100%)
|Substance dependence only
||15-19 mg/kg ibogaine HCl
||Treatments conducted in private residences. Pretreatment medical and psychiatric history, EKG and blood chemistry. Arrangement for very rapid response emergency medical support
|Netherlands, 1989-1993 Rotterdam, other Dutch cities (Alper et al., 2001)
||40, 40 (100%)
|Substance dependence only
||10-29 mg/kg ibogaine HCl
||Multiple treatment providers; private residences and hotels. Pre and post-treatment medical evaluation. Strong involvement of activist drug user network
||No cost to $18,000 USD
|US, 2003- New York, San Francisco, other U.S. cities (Freedomroot.com, 2007)
||160, 160 (100%)
|Substance dependence only
||21-24 mg/kg ibogaine HCl
||The "ibogaine underground"; multiple treatment providers. Private residences and hotels. Pretreatment medical and psychiatric history, EKG and blood chemistry
||No cost to $1500 USD
|Slovenia/Croatia, 1995- Ljubljana (Sacrament of Transition, 2006)
||433, 424 98%
||20 mg/kg ibogaine HCl
||Religious Ritual, treatment guide/priest. The Republic of Slovenia officially recognizes the Church of the Sacrament of Transition as a religion. Private homes. Initiates are interviewed and sign a statement attesting to their good health without clinical evaluation
||D 750 EUR
|France, 2000- (Meyaya, 2006)
||378 45 (12%)
|Bwiti initiation, psychotherapeutic, spiritual, general health issues
||Dried root bark, 6-10 teaspoonse
||Bwiti Religious ritual. Chateau, private residences. Nganga (ritual leader or priest) with African and European assistants. Requires only a doctor's or the prospective patient's statement assuring good health without clinical evaluation.
||D 650 EUR
|France/UK, 2003- (myeboga.com, 2006)
||316, 32 (10%)
|Bwiti initiation, psychotherapeutic, spiritual, general health issues
||Dried root bark 3-4 teaspoonse
||Bwiti religious ritual, retreat. Resort settings, private residences. European initiates of the African Bwiti tradition with African and European assistants. Pretreatment medical and psychiatric history, blood chemistry and EKG. Medical doctor in attendance throughout the treatment
||D 500 EUR
|Gabon, 1999- (Ebando, 2006)
||50, 8 (16%)
|Bwiti initiation, psychotherapeutic, spiritual, general health issues, fertility
||Infusion, 20-25 teaspoons of fresh root bark scrapings
||Bwiti religious ritual. Bwiti chapels in which Europeans and non-Africans are accepted. Prospective interview by a Nganga, without clinical evaluation
||$4000 USD (for 1 month stay)
a n = number of individuals within each scene who took ibogaine.
b n (%) = subset of n who took ibogaine for the treatment of any substance-related disorder, expressed as absolute number, and as (%) of n.
c [n (%)] = subset of n who took ibogaine for the treatment of opioid withdrawal expressed as absolute number, and as (%) of the number of individuals who took
ibogaine for the treatment of any substance-related disorder.
d Data regarding the number of individuals taking ibogaine for opioid withdrawal among all those who took ibogaine for the treatment of any substance-related disorder were missing for the St. Kitts and France 2000 scenes. For these scenes, the proportion seeking treatment specifically for
opioid withdrawal relative to all those seeking treatment for any substance-related disorder was assumed to be the same as the rest of the sample. This yielded estimates of (0.79 × 400 = 316) for St. Kitts, and (0.79 × 45 = 36) for France 2000.
e One teaspoon of dried Tabernanthe iboga root bark weighs approximately 2-3 g. Also often referenced as a "coffee spoon" by French speaking providers.
Numbers of individuals and reason for having taken ibogaine in each the four types of scenes
|Type of scene
||%Opioidd of substance-related (%)
Summary data regarding numbers of individuals who took ibogaine and their reason for taking it, from the second column of Table 1 entitled "Reason for taking ibogaine...". The rows in this table summarize the data from the individual scenes for each type.
a n = total number of individuals who took ibogaine within each of the four types of scenes indicated in the left hand column.
b Percentage of n.
c Opioid = number of individuals who took ibogaine for the treatment of opioid withdrawal in the given type of scene.
d % Opioid of substance-related = percentage of individuals who took ibogaine for the treatment of opioid withdrawal relative to the number of individuals who took ibogaine for the treatment of any substance-related disorder.
e N = the total number of individuals who took ibogaine across all scenes.
f Percentage of N.
3.1.2. Lay provider/guide
The term lay provider designates a provider without an official medical credential.
The set and purpose of the treatment may be the medical treatment of addiction, psychotherapy,
and/or spiritual growth. The dosage utilized for "psychospiritual" goals is typically on the order
of half that required for opioid withdrawal. The treatment setting is a private residence or hotel,
and the provider typically functions in the role of a "guide", or in the UK, a "sitter", and manages
the treatment setting and the interaction with the patient with the goal of facilitating the
therapeutic process. The treatment is conducted in a quiet, darkened room over a time interval of
12-18 h. Interaction with the patient is typically minimized during the treatment unless the patient
initiates verbal communication because of the importance attributed to the patient's focus on the
content of the experience. Some guides view ibogaine as unlinking mental representations from the
pathological salience and obsessive motivational states with which they have become associated,
allowing an opportunity for insight and positive change (Stolaroff, 2004). Goutarel et al. (1993)
described the use of ibogaine in dosages of 10-50 mg as an antidepressant, and some contemporary lay
providers presently use similar dosages given daily over periods of several days or weeks, to which
they attribute an antidepressant effect or the diminution of craving (Kroupa and Wells, 2005).
Interestingly, the low dose regimen is also reportedly used to limit or reduce opioid tolerance,
which is an effect attributed to ibogaine in a patent obtained by Ciba Pharmaceutical 50 years ago
(Schneider, 1957), and has been observed in subsequent preclinical research (Cao and Bhargava,
Regardless of their beliefs concerning ibogaine's psychotherapeutic benefits, lay
treatment providers are aware of medical risk, which they make some attempt to minimize. A
downloadable manual for ibogaine treatment (Lotsof and Wachtel, 2003) reflects collective views
among lay providers regarding clinical issues such as the use of exclusion criteria and pretreatment
laboratory tests, assuring adequate hydration during a treatment, or contingencies for accessing
emergency medical intervention. A significant consensus exists among lay providers regarding the use
of EKG and liver function tests in pretreatment screening, and with respect to a set of medical and
psychiatric conditions are commonly designated as exclusionary such as cardiac disease, acute
hepatitis and psychotic disorders.
This type of scene involves a lay provider with an activist or evangelical set that
prominently includes the explicit objective of gaining acceptance of the use of ibogaine. Activist
self-help providers often view their activities as a form of civil disobedience affirming the right
to better treatment for a stigmatized group. A nexus exists involving the harm reduction movement
and the ibogaine subculture. The ibogaine scene that existed in the Netherlands from 1989 to 1993
featured strong participation of European and U.S. addict self-help including the Dutch Junkiebond,
which was a model for subsequent European drug user unions and a vanguard of the harm reduction
movement (Grund, 1995; De Rienzo and Beal, 1997; Alper et al., 2001; Frenken, 2001; Lotsof and
Alexander, 2001). The "ibogaine underground", or "Freedomroot" (Freedomroot.com, 2007) is a scene
that recently emerged in the U.S. that recalls the earlier aggressive advocacy in the Netherlands.
It is a network of individual providers, many of whom themselves are former patient participants in
the subculture, who actively reach out to heroin users in New York and some other US cities.
The following quote from a post to an ibogaine list server
captures some important attitudes and beliefs of the subculture
associated with the activist/self-help type. These include the
identification of individuals with severe opioid dependence as
a marginalized population abandoned by the institution of conventional
medicine, the theme of self-help, and the attribution of
aspects of the medical model to "underground providers", who
are referenced sympathetically as doing "most of the research".
". . .No one with the money and clout to do so wants to touch ibogaine.
. . The reasons are numerous, from its illegal status in some places, to the stigma attached to drug
addiction to begin with . . . with the result that most of the research is being done by underground
providers who only have lists like this and the internet to help share information with each other.
I can tell you from personal experience with an 8+ year opiate addiction . . . if it wasn't for
ibogaine I doubt I would be clean today, two and a half years later. There are many more people on
this list who can also tell you the same thing from their own personal experience. It's a risk to be
sure. The risk of death, and the risk that it might not work . . . But for me it came down to the
fact that absolutely nothing else had worked for me . . . in the end it was through ibogaine that I
finally got clean."
3.2. Quantitative data
Table 2 summarizes the quantitative data regarding numbers of individuals taking
ibogaine and their reason for taking it, totaled across each scene type from Table 1. The total
number of individuals across all scenes who have taken ibogaine is 3414. This is approximately a
fourfold increase relative to the estimate of 857 of 5 years before based on previously published
quantitative data from early 2001 (Alper et al., 2001). As indicated in table, 68% of the total
number of individuals across all scenes took ibogaine for the treatment of substance-related
disorders, and 53% specifically for opioid withdrawal.
The effect of hidden populations would lead to underestimation of the true number of
participants in the ibogaine subculture. In order to estimate this effect, the editors of the most
frequently utilized ibogaine list server (Kroupa, 2006), and a popular ibogaine Web site (Sandberg,
2006) were asked to blindly and independently estimate the “hidden proportion”, i.e. the proportion
of participants in the ibogaine subculture in scenes that would have been overlooked by the criteria
used in this study. Both estimates of the hidden proportion fell within a range of 20-30% (personal
communication, Patrick Kroupa, December 3, 2006 and Nick Sandberg, December 4, 2006), as did the
hidden proportion of an unpublished sample (Bastiaans, 2004), suggesting that most treatments
involve experienced providers who are open about their activity. These sources agreed regarding the
view that opioid withdrawal was the most common reason for taking ibogaine, and that the subculture
had expanded greatly over the prior 5 years. Taking the hidden proportion estimates into account
yields an estimated range of approximately 4300-4900 individuals who took ibogaine outside of Africa
as of February 2006.
4.1. A medical subculture, distinct from other drug
The clinical focus on the treatment of opioid withdrawal distinguishes the ibogaine
subculture from subcultures associated with psychedelic or other illegal drugs. The reason for
taking ibogaine was more frequently to alleviate the symptoms of opioid withdrawal than to pursue
spiritual or psychological goals. In the US, the expansion of the ibogaine subculture coincides
temporally with a substantial increase in the public health impact of opioid use disorders (Compton
and Volkow, 2006). The incidence of opioid-related deaths in the US doubled between 1999 and 2004
(Fingerhut, 2007), with methadone and oxycodone accounting for most of this increase. In contrast to
trends regarding opioids, there was no increase in use of hallucinogen and MDMA among young adults
in the US between 2002 and 2005 (Substance Abuse and Mental Health Services Administration, 2006),
suggesting that the recent expansion of the ibogaine subculture is not an epiphenomenon of popular
interest in psychedelic drugs and the availability of psychoactive substances on the Internet
(Schifano et al., 2006).
The ibogaine subculture is not a counterculture (Yinger, 1960) because its identity
is not defined on the basis of opposition to conventional medicine. The subculture is to a
significant extent an innovation by its participants in response to a demand for a treatment that is
unavailable in the conventional medical setting. Although it involves alternative means, the
ibogaine subculture shares with the conventional medical culture thecommon goal of providing
treatment, which it emulates in the medical model type, or the utilization by lay treatment
providers of medical tests for pretreatment evaluation. Criminality per se is not a significant
focus of the subculture, which exists because of ibogaine's lack of availability within the
institution of clinical medicine, and not its illegality. Ibogaine is not illegal and available by
Internet in most of the world. It is illegal in the US, Australia and five EU countries, but it is
available throughout Europe and the Americas including Canada and Mexico.
4.2. Study limitations and methodological concerns
The issue of observer subjectivity is an important concern regarding the
participant-observer approach. The need to establish rapport and elicit collaboration and disclosure
may conflict with the imperative of scientific objectivity (Jackson, 1983; Malterud, 2001), and
beliefs and attitudes that motivated interest in ibogaine and provided contacts and access within
the subculture are also a potential cause of bias. Qualitative methodology acknowledges that the
problem of observer subjectivity always exists, and addresses it by and attempting to account for
its effect by the use of multiple validating approaches (Malterud, 2002). Validating approaches
utilized in this study include triangulation of the data across providers, patient participants and
other informants, as well as longitudinal observation involving multiple contacts over time.
The authors' collective access and intensive observation of the ibogaine subculture
suggests that this study approaches an exhaustive, and not merely representative sampling of
publicly identified ibogaine scenes. The intensiveness of the sampling in this study indicates that
most of the use of ibogaine outside of Africa has taken place in the scenes that are included in
Table 1, even taking into account the problem of hidden populations.
4.3. Implications of the "vast uncontrolled experiment"
Frank Vocci, who oversaw NIDA's ibogaine project as the head of Medications
Development (Vastag, 2005), characterized the ibogaine subculture as a "vast uncontrolled
experiment". The term has significant literal merit. The data on iboga alkaloids collectively
subsumes significant elements of a drug development process in various stages of completion,
including substantial preclinical and open label study evidence, preclinical toxicological studies,
and some initial Phase I safety and pharmacokinetic data.
Reports of efficacy of ibogaine in opioid withdrawal may be valid irrespective of
the methodological limitations associated or craving, the clinical expression of acute opioid
withdrawal occurs within a limited time frame, is easily operationalized, tends to be robust, and
can be assessed accurately by typically experienced lay providers. It appears unlikely that
suggestion or placebo could solely mediate the effect attributed to ibogaine in acute opioid
withdrawal. Recent Cochrane reviews on the management of acute opioid withdrawal with a2-agonists
(Gowing et al., 2004), buprenorphine (Gowing et al., 2006) or methadone taper (Amato et al., 2005)
evaluated a combined total of 56 studies. Overall rates of treatment completion among studies of
a2-agonists, buprenorphine, or methadone, respectively ranged from 48 to 64%. Only 3 of the 56
studies included a placebo comparison, and all indicated a strong distinction of placebo from any
active drug treatment at a level of significance of p < .001 on the basis of more frequent failure
to complete detoxification (Benos, 1985; San et al., 1992) or higher ratings of withdrawal symptoms
(Gerra et al., 1995) in the placebo group. The relatively negligible effect of placebo in acute
opioid withdrawal is likely further reduced with the greater severity of physical dependence that is
generally characteristic of individuals who take ibogaine, such as a series of 33 patients whose
average daily heroin use was 0.64 g, mainly by the intravenous route (Alper et al., 1999; Frenken,
The authors are aware of a total of 11 individuals that are reported to have died
within 72 h of taking ibogaine from the time of the first such fatality in 1990 (Alper, 2001) until
February 2006. Collectively, the cases suggest that cardiac rhythm may be a particularly significant
domain of medical risk. Deaths were most commonly attributed to a cardiac cause in association with
significant risk factors such as a prior myocardial infarction, cardiomyopathy or valvular disease,
or to pulmonary embolus. Other deaths were regarded as mixed drug overdoses involving opioids with
or without the additional ingestion of cocaine (Alper et al., 1999; Marker and Stajic, 2002). Deaths
not involving the above factors have been associated with the use of Tabernanthe iboga alkaloid
extract (Alper, 2001) or dried root bark (Kontrimaviciute et al., 2006b). This subset of fatalities
may reflect a general hazard associated with the use of indigenous ethnopharmaceutical forms outside
of their traditional context by the uninformed or inexperienced (Callaway and Grob, 1998; Maas and
Strubelt, 2006). For example, one death (Kontrimaviciute et al., 2006b) involved ingestion of an
amount of powdered dried root bark that is at least twice the maximum upper limit used by the
providers in this study who are traditional African Bwiti adepts. Other potential hazards may be
associated with the lack of pharmaceutical standards for ibogaine, including unregulated procedures
for manufacturing and storage or the possibility of naturally co-occurring toxic alkaloids
(Singbartl et al., 1973; Jenks, 2002; Kontrimaviciute et al.,
Cerebellar Purkinje cell degeneration reported in rats administered ibogaine at high
dosages of 100 mg/kg (O'Hearn and Molliver, 1993, 1997) prompted concern regarding potential
neurotoxicity. The FDA was aware of this research at the time it approved the Phase I study; other
work indicated no evidence of neurotoxicity rats at the dosage of 40 mg/kg typically used to study
drug self-administration and withdrawal (Molinari et al., 1996). Evidence of neurotoxicity due to
ibogaine is reportedly absent in mice (Scallet et al., 1996), primates (Mash et al., 1998) and a
postmortem neuropathological examination of a woman who had taken ibogaine four times in the prior
15 months at doses up to 30 mg/kg. In the Phase I study, quantitative dynamic measures of cerebellar
motor function were unremarkable in human subjects that received low doses of ibogaine of 1 and 2
mg/kg (Mash et al., 1998). The study was never finished due to contractual disputes with eventual
litigation among the study sponsors, unrelated to clinical issues. The σ2 receptor mediates
neurotoxic injury (O'Hearn and Molliver, 1997; Bowen, 2001), and is apparently not involved in
effects of ibogaine on drug self-administration and withdrawal (Glick et al., 2001). This suggests
that the therapeutic and neurotoxic effects of iboga alkaloids can be resolved from one another by
rational drug design, as indicated by the example of 18-MC, which has lower affinity for the σ2
receptor and is not associated with evidence of neurotoxicity even at very high dosages (Maisonneuve
and Glick, 2003).
4.4. Suggestions for future research
Experimental pharmacologists are increasingly interested in the development of
approaches to addiction that extend beyond the present repertoire of agonist or antagonist actions,
and instead are targeted at effects on intracellular signaling downstream from the receptor (Bonci
and Carlezon, 2005). Ibogaine may provide a prototypic example of an agent with such novel
mechanisms of action. Future work should replicate and extend on prior research indicating that
iboga alkaloids modulate signal transduction in second messenger pathways linked to G proteincoupled
receptors (GPCRs) (Rabin and Winter, 1996a,b).
Constitutive spontaneous activity without the binding of an agonist (Costa and
Cotecchia, 2005) occurs in GPCRs such as opioid receptors (Shoblock and Maidment, 2006).
Constitutive signaling mediated by conformational states of receptorassociated proteinsmaybe
modulated relatively rapidly and span a wide signal range, consistent with a possible role in the
highly dynamic neuroadaptations associated with opioid tolerance and withdrawal. It may be
worthwhile to investigate the possibility that iboga alkaloids interact allosterically or
orthosterically with GPCRs to affect constitutive signaling.Apossible role of orphan receptors
should be also considered (Civelli et al., 2006).
Functional and clinical evidence of muscarinic cholinergic actions of iboga
alkaloids includes the occurrence of a state with some neurophysiological and behavioral features
common to REM sleep (Schneider and Sigg, 1957; Depoortere, 1987; Goutarel et al., 1993; Alper,
2001), and recent work suggesting that muscarinic acetylcholine receptors (mAChRs) as well as nAChRs
in the habenulopeduncular pathway mediate the effects of 18-MC on dopamine efflux in the NAc
(Taraschenko et al., 2007a,b). Ibogaine interacts with cholinergic neurotransmission in
multipleways; as a strong antagonist at nAChRs (Daly, 2005), binding to mAChRs with affinities on
the order of approximately 10 M with actions that are not well characterized with regard to
antagonist versus agonist effects, and according to an older literature, inhibition of
acetylcholinesterase (Vincent and Sero, 1942). The knockout mouse, which exists for each of the five
basic subtypes of mAChRs (Wess et al., 2003), provides an in vivo approach that makes it possible to
study functional correlates of activity at mAChRs such as the EEG or cardiac electrophysiology, as
well as the role of mAChRs in ibogaine’s effects on models of substance-related disorders.
Structure-function relationships mediating toxic and therapeutic effects of iboga
alkaloids have been identified and utilized to guide rational synthesis (Glick et al., 1994; Kuehne
et al., 2003; Maisonneuve and Glick, 2003). Preclinical toxicological testing, and if appropriate,
clinical research on iboga alkaloids will require the development of pharmaceutical synthetic and
chemical manufacturing technology in order to produce adequate quantities of investigational drug in
conformance with international Good Manufacturing Practice standards. The chemical, manufacturing
and control stage of pharmaceutical development generally is accomplished in the private sector, but
the pharmaceutical industry historically has shown less interest in developing drugs for
substance-related disorders relative to other indications (Gorodetzky and Grudzinskas, 2005),
indicating an important need for involvement of the public sector.
The estimated number of participants in the ibogaine subculture increased fourfold
relative to the prior estimate of 5 years earlier, an average yearly rate of growth of approximately
30%. The existence and expansion of the subculture indicates a demand for newtreatment, which is
sought regardless of medical risk, inconvenience, expense, and in some cases legal prohibition.
Across a diversity of settings, most individuals who took ibogaine did so for the treatment of a
substance-related disorder, specifically for opioid withdrawal. Ibogaine's effect in opioid
withdrawal is consistent with case series and preclinical evidence, and is unlikely to be mediated
by placebo. The mechanism of ibogaine's action in opioid withdrawal merits further investigation as
a paradigm for neurobiological research and rational pharmaceutical development.
Conflict of interest statement
We declare that we have no conflict of interest. Howard Lotsof
was awarded multiple patents on the use of ibogaine in
substance-related disorders, which he divested in 1998.
The authors gratefully acknowledge Geoffrey Cordell, Ph.D.,
James W. Fernandez, Ph.D., Renate L. Fernandez, Ph.D., Marc
Galanter, M.D., and Stephen Sifaneck, Ph.D. for their review
and helpful comments regarding this paper.
Aceto, M.D., Bowman, E.R., Harris, L.S., May, E.L., 1992. Dependence studies
of new compounds in the rhesus monkey and mouse (1991). NIDA Research
Monograph 119, 513-558.
Alper, K.R., 2001. Ibogaine: A review. The Alkaloids: Chemistry and Biology
Alper, K.R., Lotsof, H.S., Frenken, G.M., Luciano, D.J., Bastiaans, J., 1999.
Treatment of acute opioid withdrawal with ibogaine. American Journal on
Addictions 8, 234-242.
Alper, K.R., Beal, D., Kaplan, C.D., 2001. A contemporary history of ibogaine
in the United States and Europe. The Alkaloids: Chemistry and Biology 56,
Amato, L., Davoli, M., Minozzi, S., Ali, R., Ferri, M., 2005. Methadone at
tapered doses for the management of opioid withdrawal. Cochrane Database
of Systematic Reviews, CD003409.
Bagal, A.A., Hough, L.B., Nalwalk, J.W., Glick, S.D., 1996. Modulation
of morphine-induced antinociception by ibogaine and noribogaine. Brain
Research 741, 258-262.
Bailey, K.D., 1994. Typologies and taxonomies: an introduction to classification
techniques. In: Lewis-Beck, M.S. (Ed.), Quantitative Applications in the
Social Sciences. Sage Publications, Thousand Oaks, CA, pp. 7-102.
Bartlett, M.F., Dickel, D.F., Taylor, W.I., 1958. The alkaloids of Tabernanthe-
Iboga. 4. The structures of ibogamine, ibogaine, tabernanthine and
voacangine. Journal of the American Chemical Society 80, 126-136.
Bastiaans, E., 2004. Life after ibogaine: an exploratory study of the
long-term effects of ibogaine treatment on drug addicts. Doctorandus
thesis. Vrije Universiteit Amsterdam, Faculty of Medicine. URL:
http://www.ibogaine.org/ibogaine_udi_bastiaans.pdf (accessed 11.08.07).
Baumann, M.H., Rothman, R.B., Pablo, J.P., Mash, D.C., 2001. In vivo
neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-
hydroxyibogamine (noribogaine), in rats. Journal of Pharmacology and
Experimental Therapeutics 297, 531-539.
Benos, J., 1985. Clonidine in opiate withdrawal syndrome. Fortschritte der
Medizin 103, 991-994.
Benwell, M.E., Holtom, P.E., Moran, R.J., Balfour, D.J., 1996. Neurochemical
and behavioural interactions between ibogaine and nicotine in the rat. British
Journal of Pharmacology 117, 743-749.
Berridge, K.C., 2007. The debate over dopamine's role in reward: the
case for incentive salience. Psychopharmacology (Berl) 191, 391-
Bonci, A., Carlezon Jr.,W.A., 2005. Ion channels and intracellular signaling proteins
as potential targets for novel therapeutics for addictive and depressive
disorders. Pharmacology and Therapeutics 108, 65-75.
Boukacem-Zeghmouri, C., Sch¨opfel, J., 2006. Document supply and open
access: an international survey on grey literature. Interlending and Document
Supply 34, 96-104.
Bowen,W.D., 2001. Sigma receptors and iboga alkaloids. The Alkaloids: Chemistry
and Biology 56, 173-191.
Caille, S., Espejo, E.F., Koob, G.F., Stinus, L., 2002. Dorsal and median raphe
serotonergic system lesion does not alter the opiate withdrawal syndrome.
Pharmacology, Biochemistry, and Behavior 72, 979-986.
Callaway, J.C., Grob, C.S., 1998.Ayahuasca preparations and serotonin reuptake
inhibitors: a potential combination for severe adverse interactions. Journal
of Psychoactive Drugs 30, 367-369.
Cao, Y.J., Bhargava, H.N., 1997. Effects of ibogaine on the development of
tolerance to antinociceptive action of mu-, delta- and kappa-opioid receptor
agonists in mice. Brain Research 752, 250-254.
Cappendijk, S.L., Dzoljic, M.R., 1993. Inhibitory effects of ibogaine on
cocaine self-administration in rats. European Journal of Pharmacology 241,
Cappendijk, S.L., Fekkes, D., Dzoljic, M.R., 1994. The inhibitory effect of
norharman on morphine withdrawal syndrome in rats: comparison with
ibogaine. Behavioural Brain Research 65, 117-119.
Civelli, O., Saito,Y.,Wang, Z., Nothacker, H.P., Reinscheid, R.K., 2006. Orphan
GPCRs and their ligands. Pharmacology and Therapeutics 110, 525-532.
Clarke, M., 1974. On the concept of 'subculture'. British Journal of Sociology
Compton,W.M., Volkow, N.D., 2006. Major increases in opioid analgesic abuse
in the United States: concerns and strategies. Drug and Alcohol Dependence
Conn, E., 2006. Become Whole Treatment and Consultation Center. URL:
http://www.becomewhole.co.uk/ (accessed 25.11.06).
Costa, T., Cotecchia, S., 2005. Historical review: negative efficacy and the constitutive
activity of G-protein-coupled receptors. Trends in Pharmacological
Sciences 26, 618-624.
Daly, J.W., 2005. Nicotinic agonists, antagonists, and modulators from natural
sources. Cellular and Mollecular Neurobiology 25, 513-552.
De Rienzo, P., Beal, D., 1997. The Ibogaine Story. Autonomedia, New York.
Delorenzi, J.C., Freire-de-Lima, L., Gattass, C.R., de Andrade Costa, D., He,
L., Kuehne, M.E., Saraiva, E.M., 2002. In vitro activities of iboga alkaloid
congeners coronaridine and 18-methoxycoronaridine against Leishmania
amazonensis. Antimicrobial Agents and Chemotherapy 46, 2111-2115.
Denzin, N.K., Lincoln, Y.S. (Eds.), 2005. Handbook of Qualitative Research,
3rd ed. Sage Publications, Thousand Oaks, CA.
Depoortere, H., 1987. Neocortical rhythmic slow activity during wakefulness
and paradoxical sleep in rats. Neuropsychobiology 18, 160-168.
Dowd, J.D., Dowd, L.A., 2003. The center holds: from subcultures to social
worlds. Teaching Sociology 31, 20-37.
Dzoljic, E.D., Kaplan, C.D., Dzoljic, M.R., 1988. Effect of ibogaine on
naloxone-precipitated withdrawal syndrome in chronic morphine-dependent
rats. Archives Internationales de Pharmacodynamie et de Therapie 294,
Ebando, 2006. Association for Nature and Culture, Ebando. URL: http://www.fi-
a.org/ebando (accessed 25.11.06).
ethnogarden.com, 2006. Ethnogarden botanicals: ibogaine HCl and iboga pure
alkaloid extract (Tabernanthe iboga). URL: http://www.ethnogarden.com/
cart/index.pl/catid_80/proid_189 (accessed 25.11.06).
Fabing, H., 1956. Trends in biological research in schizophrenia. Journal of
Nervous and Mental Disease 124, 1-7.
Fernandez, J.W., 1982. Bwiti: An Ethnography of Religious Imagination in
Africa. Princeton University Press, Princeton, NJ.
Fernandez, J.W., Fernandez, R.L., 2001. Returning to the path”: the use of
iboga[ine] in an equatorial African ritual context and the binding of time,
space, and social relationships. The Alkaloids: Chemistry and Biology 56,
Fingerhut, L., 2007. Increases in methadone-related deaths: 1999-2004. URL:
04/methadone1999-04.htm (accessed 17.08.07).
Frances, B., Gout, R., Cros, J., Zajac, J.M., 1992. Effects of ibogaine on
naloxone-precipitated withdrawal in morphine-dependent mice. Fundamental
and Clinical Pharmacology 6, 327-332.
Freedomroot.com, 2007. Freedomroot.com Ibogaine Information. URL:
http://www.freedomroot.com/ (accessed 17.3.07).
Frenken, G., 2001. From the roots up: ibogaine and addict self-help. The Alkaloids:
Chemistry and Biology 56, 283-292.
Fryer, J.D., Lukas, R.J., 1999. Noncompetitive functional inhibition at diverse,
human nicotinic acetylcholine receptor subtypes by bupropion, phencyclidine,
and ibogaine. Journal of Pharmacology and Experimental Therapeutics
Galanter, M., 2006. Spirituality and addiction: a research and clinical perspective.
American Journal on Addictions 15, 286-292.
Gerra, G., Marcato, A., Caccavari, R., Fontanesi, B., Delsignore, R., Fertonani,
G., Avanzini, P., Rustichelli, P., Passeri, M., 1995. Clonidine and
opiate receptor antagonists in the treatment of heroin addiction. Journal of
Substance Abuse Treatment 12, 35-41.
Glatt, S., 2006. Sara Glatt (Holland)-Outlook & Experience with Iboga. URL:
http://www.myeboga.com/SaraGlatt.html (accessed 25.11.06).
Glick, S.D., Rossman, K., Steindorf, S., Maisonneuve, I.M., Carlson, J.N., 1991.
Effects and after effects of ibogaine on morphine self-administration in rats.
European Journal of Pharmacology 195, 341-345.
Glick, S.D., Rossman, K., Rao, N.C., Maisonneuve, I.M., Carlson, J.N., 1992.
Effects of ibogaine on acute signs of morphine withdrawal in rats: independence
from tremor. Neuropharmacology 31, 497-500.
Glick, S.D., Kuehne, M.E., Raucci, J.,Wilson, T.E., Larson, D., Keller Jr., R.W.,
Carlson, J.N., 1994. Effects of iboga alkaloids on morphine and cocaine selfadministration
in rats: relationship to tremorigenic effects and to effects on
dopamine release in nucleus accumbens and striatum. Brain Research 657,
Glick, S.D., Pearl, S.M., Cai, J., Maisonneuve, I.M., 1996. Ibogaine-like effects
of noribogaine in rats. Brain Research 713, 294-297.
Glick, S.D., Maisonneuve, I.M., Visker, K.E., Fritz, K.A., Bandarage, U.K.,
Kuehne, M.E., 1998. 18-Methoxycoronardine attenuates nicotine-induced
dopamine release and nicotine preferences in rats. Psychopharmacology
(Berl) 139, 274-280.
Glick, S.D., Maisonneuve, I.M., Dickinson, H.A., 2000. 18-MC reduces
methamphetamine and nicotine self-administration in rats. Neuroreport 11,
Glick, S.D., Maisonneuve, I.M., Szumlinski, K.K., 2001. Mechanisms of action
of ibogaine: relevance to putative therapeutic effects and development of a
safer iboga alkaloid congener. The Alkaloids: Chemistry and Biology 56,
Glick, S.D., Maisonneuve, I.M., Kitchen, B.A., 2002a. Modulation of nicotine
self-administration in rats by combination therapy with agents blocking
alpha 3 beta 4 nicotinic receptors. European Journal of Pharmacology 448,
Glick, S.D., Maisonneuve, I.M., Kitchen, B.A., Fleck, M.W., 2002b. Antagonism
of alpha 3 beta 4 nicotinic receptors as a strategy to reduce opioid
and stimulant self-administration. European Journal of Pharmacology 438,
Gold, R.L., 1958. Roles in sociological field observations. Social Forces 36,
Gorodetzky, C.W., Grudzinskas, C., 2005. Involving the pharmaceutical and
biotech communities in medication development for substance abuse. Pharmacology
and Therapeutics 108, 109-118.
Goutarel, R., Gollnhofer, O., Sillans, R., 1993. Pharmacodynamics and therapeutic
applications of iboga and ibogaine. Psychedelic Monographs and
Essays 66, 71-111.
Gowing, L., Farrell, M., Ali, R., White, J., 2004. Alpha2 adrenergic agonists for
the management of opioid withdrawal. Cochrane Database of Systematic
Gowing, L., Ali, R., White, J., 2006. Buprenorphine for the management of
opioid withdrawal. Cochrane Database of Systematic Reviews, CD002025.
Grund, J.P., 1995. Nico Adriaans. International Journal of Drug Policy 6,
He, D.Y., Ron, D., 2006. Autoregulation of glial cell line-derived neurotrophic
factor expression: implications for the long-lasting actions of the antiaddiction
drug, Ibogaine. FASEB (Federation of American Societies for
Experimental Biology) Journal 20, 2420-2422.
He, D.Y., McGough, N.N., Ravindranathan, A., Jeanblanc, J., Logrip, M.L.,
Phamluong, K., Janak, P.H., Ron, D., 2005. Glial cell line-derived neurotrophic
factor mediates the desirable actions of the anti-addiction drug
ibogaine against alcohol consumption. Journal of Neuroscience 25, 619-628.
Hisaoka, K.,Takebayashi, M., Tsuchioka, M., Maeda, N., Nakata,Y.,Yamawaki,
S., 2007. Antidepressants increase glial cell line-derived neurotrophic factor
production through monoamine-independent activation of protein tyrosine
kinase and extracellular signal-regulated kinase in glial cells. Journal of
Pharmacology and Experimental Therapeutics 321, 148-157.
Ibogaine Association, 2006. Ibogaine Association. URL:
http://www.ibogaine-therapy.net/ (accessed 25.11.06).
ibogatherapyhouse.net, 2007. Iboga Therapy House. URL:
http://www.ibogatherapyhouse.net/cms/ (accessed 17.03.07).
Isbell, H., 1955. Letter from Harris Isbell to Ciba-Geigy Pharmaceutical Products
dated 29.11.55, Ciba Document no. AB0491-492 410.
Jackson, P., 1983. Principles and problems of participant observation.
Geografiska Annaler Series B, Human Geography 65, 39-46.
Jenks, C.W., 2002. Extraction studies of Tabernanthe iboga and Voacanga
africana. Natural Product Letters 16, 71-76.
Kam, T.S., Sim, K.M., Pang, H.S., Koyano, T., Hayashi, M., Komiyama, K.,
2004. Cytotoxic effects and reversal of multidrug resistance by ibogan and
related indole alkaloids. Bioorganic and Medicinal Chemistry Letters 14,
Kleber, H., 2001. Foreword. In: Alper, K.R., Glick, S.D., Cordell, G.A. (Eds.),
Proceedings of the First International Conference on Ibogaine. Academic
Press, San Diego, pp. xv-xvii.
Kontrimaviciute, V., Breton, H., Mathieu, O., Mathieu-Daude, J.C., Bressolle,
F.M., 2006a. Liquid chromatography-electrospray mass spectrometry determination
of ibogaine and noribogaine in human plasma and whole blood.
Application to a poisoning involving Tabernanthe iboga root. Journal of Chromatography B, Analytical Technologies in the Biomedical and Life
Sciences 843, 131-141.
Kontrimaviciute, V., Mathieu, O., Mathieu-Daude, J.C., Vainauskas, P., Casper,
T., Baccino, E., Bressolle, F.M., 2006b. Distribution of ibogaine and noribogaine
in a man following a poisoning involving root bark of the Tabernanthe
iboga shrub. Journal of Analytical Toxicology 30, 434-440.
Kroupa, P.K., 2006. Mindvox Ibogaine List (List Server). URL:
http://ibogaine.mindvox.com/ (accessed 2.12.06).
Kroupa, P.K., Wells, H., 2005. Ibogaine in the 21st century: boosters, tuneups
and maintenance. Multidisciplinary Association for Psychedelic Studies
(MAPS) Bulletin XV, 21-24.
Kuehne, M.E., He, L., Jokiel, P.A., Pace, C.J., Fleck, M.W.,Maisonneuve, I.M.,
Glick, S.D., Bidlack, J.M., 2003. Synthesis and biological evaluation of 18-
methoxycoronaridine congeners. Potential antiaddiction agents. Journal of
Medicinal Chemistry 46, 2716-2730.
Lane, A., 2005 Dec. 9. Couple to be held in jail. Casper Star Tribune, p. B1.
Layer, R.T., Skolnick, P., Bertha, C.M., Bandarage, U.K., Kuehne, M.E., Popik,
P., 1996. Structurally modified ibogaine analogs exhibit differing affinities
for NMDA receptors. European Journal of Pharmacology 309, 159-
Leal, M.B., Michelin, K., Souza, D.O., Elisabetsky, E., 2003. Ibogaine attenuation
of morphine withdrawal in mice: role of glutamateN-methyl-d-aspartate
receptors. Progress in Neuro-Psychopharmacology and Biological Psychiatry
Levant, B., Pazdernik, T.L., 2004. Differential effects of ibogaine on local cerebral
glucose utilization in drug-naive and morphine-dependent rats. Brain
Research 1003, 159-167.
Lotsof, H.S., 1985. Rapid Method for Interrupting the Narcotic Addiction Syndrome.
US patent 4,499,096.
Lotsof, H.S., 2007. The Ibogaine Dossier. URL:
Lotsof, H.S., Alexander, N.E., 2001. Case studies of ibogaine treatment: implications
for patient management strategies. The Alkaloids: Chemistry and
Biology 56, 293-313.
Lotsof, H.S., Wachtel, B., 2003. Manual for Ibogaine Therapy Screening,
Safety, Monitoring & Aftercare, Second Revision. URL:
http://www.ibogaine.org/Ibogaine.pdf (accessed 12.3.07).
Luciano, D., 1998. Observations on treatment with ibogaine. American Journal
on Addictions 7, 89-90.
Maas, U., Strubelt, S., 2006. Fatalities after taking ibogaine in addiction
treatment could be related to sudden cardiac death caused by autonomic
dysfunction. Medical Hypotheses 67, 960-964.
Maisonneuve, I.M., Glick, S.D., 1999. Attenuation of the reinforcing efficacy of
morphine by 18-methoxycoronaridine. European Journal of Pharmacology
Maisonneuve, I.M., Glick, S.D., 2003. Anti-addictive actions of an iboga alkaloid
congener: a novel mechanism for a novel treatment. Pharmacology
Biochemistry and Behavior 75, 607-618.
Maisonneuve, I.M., Keller Jr., R.W., Glick, S.D., 1991. Interactions between
ibogaine, a potential anti-addictive agent, and morphine: an in vivo microdialysis
study. European Journal of Pharmacology 199, 35-42.
Maisonneuve, I.M., Keller Jr., R.W., Glick, S.D., 1992. Interactions of ibogaine
and d-amphetamine: in vivo microdialysis and motor behavior in rats. Brain
Research 579, 87-92.
Maisonneuve, I.M., Mann, G.L., Deibel, C.R., Glick, S.D., 1997. Ibogaine and
the dopaminergic response to nicotine. Psychopharmacology (Berl) 129,
Malterud, K., 2001. Qualitative research: standards, challenges, and guidelines.
Lancet 358, 483-488.
Malterud, K., 2002. Reflexivity and metapositions: strategies for appraisal of
clinical evidence. Journal of Evaluation in Clinical Practice 8, 121-126.
Mariano, B., 2006. Ibogainetreatment.net. URL:
http://www.ibogainetreatment.net/ (accessed 24.11.06).
Marker, E.K., Stajic, M., 2002. Ibogaine Related Fatality. Paper presented at the
40th meeting of The International Association of Forensic Toxicologists, no.
59, August 30, 2002 (TIAFT), Paris, France.
Mash, D.C., Kovera, C.A., Buck, B.E., Norenberg, M.D., Shapshak, P., Hearn,
W.L., Sanchez-Ramos, J., 1998. Medication development of ibogaine as a pharmacotherapy for drug dependence. Annals of the New York Academy
of Sciences 844, 274-292.
Mash, D.C., Kovera, C.A., Pablo, J., Tyndale, R.F., Ervin, F.D., Williams, I.C.,
Singleton, E.G., Mayor, M., 2000. Ibogaine: complex pharmacokinetics,
concerns for safety, and preliminary efficacy measures. Annals of the New
York Academy of Sciences 914, 394-401.
Mash, D.C., Kovera, C.A., Pablo, J., Tyndale, R., Ervin, F.R., Kamlet, J.D.,
Hearn, W.L., 2001. Ibogaine in the treatment of heroin withdrawal. The
Alkaloids: Chemistry and Biology 56, 155-171.
Mash, D.C., Duque, L., Kamlet, J.D., Ervin, F.D., Allen-Ferdinand, K., 2005.
Offshore Investigations of the non-addictive plant alkaloid ibogaine: 1996
to 2004. Poster presented at the College of Problems on Drug Dependence
(CPDD), Orlando, FL, p. 118.
Meyaya, 2006. Meyaya: the first French site dedicated to Eboga. URL:
http://www.iboga.org (accessed 25.11.06).
Molinari, H.H., Maisonneuve, I.M., Glick, S.D., 1996. Ibogaine neurotoxicity:
a re-evaluation. Brain Research 737, 255-262.
myeboga.com, 2006. Iboga cures in the Bwiti tradition. URL:
http://www.myeboga.com/ibogacures.html (accessed 25.11.06).
Naeher, K., 2006. Ibogaine. URL:
http://www.ibogainetreatment.com/ (accessed 24.11.06).
Naranjo, C., 1973. The Healing Journey: New Approaches to Consciousness.
Pantheon, Random House, New York.
O'Hearn, E., Molliver, M.E., 1993. Degeneration of Purkinje cells in parasagittal
zones of the cerebellar vermis after treatment with ibogaine or harmaline.
Neuroscience 55, 303-310.
O'Hearn, E., Molliver, M.E., 1997. The olivocerebellar projection mediates
ibogaine-induced degeneration of Purkinje cells: a model of indirect, transsynaptic
excitotoxicity. Journal of Neuroscience 17, 8828-8841.
Pace, C.J., Glick, S.D., Maisonneuve, I.M., He, L.W., Jokiel, P.A.,Kuehne, M.E.,
Fleck,M.W., 2004. Novel iboga alkaloid congeners block nicotinic receptors
and reduce drug self-administration. European Journal of Pharmacology
Panchal, V., Taraschenko, O.D., Maisonneuve, I.M., Glick, S.D., 2005.
Attenuation of morphine withdrawal signs by intracerebral administration
of 18-methoxycoronaridine. European Journal of Pharmacology 525,
Parker, L.A., Burton, P., McDonald, R.V., Kim, J.A., Siegel, S., 2002.
Ibogaine interferes with motivational and somatic effects of naloxoneprecipitated
withdrawal from acutely administered morphine. Progress in
Neuro-Psychopharmacology and Biological Psychiatry 26, 293-297.
Pearl, S.M., Maisonneuve, I.M., Glick, S.D., 1996. Prior morphine exposure
enhances ibogaine antagonism of morphine-induced dopamine release in
rats. Neuropharmacology 35, 1779-1784.
Popik, P., Skolnick, P., 1998. Pharmacology of ibogaine and ibogaine-related
alkaloids. The Alkaloids: Chemistry and Biology 52, 197-231.
Popik, P., Layer, R.T., Fossom, L.H., Benveniste, M., Geterdouglass, B.,Witkin,
J.M., Skolnick, P., 1995. NMDA antagonist properties of the putative
antiaddictive drug, ibogaine. Journal of Pharmacology and Experimental
Therapeutics 275, 753-760.
Prins, M., 1988.Von Tabernanthe Iboga Zu Ibogain: Uber EineVielseitige Westafrikas und Ihre Anwendung in der Psychotherapie (From Tabernanthe
Iboga to ibogaine: on a versatile drug from West Africa and its application
in psychotherapy). Doctoral thesis. Universität Zürich, Zürich.
Rabin, R.A., Winter, J.C., 1996a. Effects of ibogaine and noribogaine on phosphoinositide
hydrolysis. Brain Research 731, 226-229.
Rabin, R.A., Winter, J.C., 1996b. Ibogaine and noribogaine potentiate the inhibition
of adenylyl cyclase activity by opioid and 5-HT receptors. European
Journal of Pharmacology 316, 343-348.
Ranzal, E., 1967 Dec. 21. Drug lab raided near City Hall. New York Times, p.
Rastogi, N., Abaul, J., Goh, K.S., Devallois, A., Philogene, E., Bourgeois, P.,
1998. Antimycobacterial activity of chemically defined natural substances
from the Caribbean flora in Guadeloupe. FEMS Immunology and Medical
Microbiology 20, 267-273.
Rezvani, A.H., Overstreet, D.H., Lee, Y.W., 1995. Attenuation of alcohol intake
by ibogaine in three strains of alcohol-preferring rats. Pharmacology, Biochemistry,
and Behavior 52, 615-620.
Rezvani, A.H., Overstreet, D.H.,Yang,Y., Maisonneuve, I.M., Bandarage, U.K.,
Kuehne, M.E., Glick, S.D., 1997. Attenuation of alcohol consumption by
a novel nontoxic ibogaine analogue (18-methoxycoronaridine) in alcoholpreferring
rats. Pharmacology, Biochemistry, and Behavior 58, 615-619.
Rho, B., Glick, S.D., 1998. Effects of 18-methoxycoronaridine on acute signs
of morphine withdrawal in rats. Neuroreport 9, 1283–1285.
Ron, D., Janak, P.H., 2005. GDNF and addiction. Reviews in Neurosciences 16,
Rossouw, C., 2006. Substance addiction treatment. URL:
http://www.ibogaine.co.za/ (accessed 25.11.06).
Sacrament of Transition, 2006. Sacrament of transition. URL:
http://sacrament.kibla.si/ (accessed 25.11.06).
Salmoiraghi, G.C., Page, I.H., 1957. Effects of LSD 25, BOL 148, bufotenine,
mescaline and ibogaine on the potentiation of hexobarbital hypnosis
produced by serotonin and reserpine. Journal of Pharmacology and Experimental
Therapeutics 120, 20-25.
Samorini, G., 1995. The Bwiti Religion and the psychoactive plant Tabernanthe
iboga (Equatorial Africa). Integration 5, 105-114.
San, L., Cami, J., Fernandez, T., Olle, J.M., Peri, J.M., Torrens, M.,
1992. Assessment and management of opioid withdrawal symptoms in
buprenorphine-dependent subjects. British Journal of Addiction 87, 55-62.
Sandberg, N., 2006. URL: http://ibogaine.co.uk/ (accessed 2.12.06).
Scallet, A.C., Ye, X., Rountree, R., Nony, P., Ali, S.F., 1996. Ibogaine produces
neurodegeneration in rat, but not mouse, cerebellum. Neurohistological
biomarkers of Purkinje cell loss. Annals of the New York Academy of
Sciences 801, 217-226.
Schifano, F., Deluca, P., Baldacchino, A., Peltoniemi, T., Scherbaum, N., Torrens,
M., Farre, M., Flores, I., Rossi, M., Eastwood, D., Guionnet, C., Rawaf,
S., Agosti, L., Di Furia, L., Brigada, R., Majava, A., Siemann, H., Leoni,
M., Tomasin, A., Rovetto, F., Ghodse, A.H., 2006. Drugs on the web; the
Psychonaut 2002 EU project. Progress in Neuro-Psychopharmacology and
Biological Psychiatry 30, 640-646.
Schmid, P.B., 1967. Die psychische wirkung von ibogaline-hydrochlorid (The
psychological effect of Ibogalin hydrochloride). Arzneimittel-Forschung 17,
Schneider, J.A., 1957. Ciba Pharmaceutical Products Inc., Summit, New Jersey,
assignee Tabernanthine, Ibogaine containing analgesic compostions.
US patent 2,817,623.
Schneider, J.A., McArthur, M., 1956. Potentiation action of ibogaine (Bogadin
TM) on morphine analgesia. Experientia 12, 323-324.
Schneider, J.A., Sigg, E.B., 1957. Neuropharmacological studies on ibogaine,
an indole alkaloid with central-stimulant properties. Annals of the New York
Academy of Sciences 66, 765-776.
Sershen, H., Hashim, A., Lajtha, A., 2001. Characterization of multiple sites of
action of ibogaine. The Alkaloids: Chemistry and Biology 56, 115-133.
Sharma, S.K., Klee, W.A., Nirenberg, M., 1975. Dual regulation of adenylate
cyclase accounts for narcotic dependence and tolerance. Proceedings
of the National Academy of Sciences of the United States of America 72,
Sharpe, L.G., Jaffe, J.H., 1990. Ibogaine fails to reduce naloxone-precipitated
withdrawal in the morphine-dependent rat. Neuroreport 1, 17-19.
Shoblock, J.R., Maidment, N.T., 2006. Constitutively active mu opioid receptors
mediate the enhanced conditioned aversive effect of naloxone in morphinedependent
mice. Neuropsychopharmacology 31, 171-177.
Silva, E.M., Cirne-Santos, C.C., Frugulhetti, I.C., Galvao-Castro, B., Saraiva,
E.M., Kuehne, M.E., Bou-Habib, D.C., 2004. Anti-HIV-1 activity of
the Iboga alkaloid congener 18-methoxycoronaridine. Planta Medica 70,
Singbartl, G., Zetler, G., Schlosser, L., 1973. Structure-activity relationships of
intracerebrally injected tremorigenic indole alkaloids. Neuropharmacology
Skolnick, P., 2001. Ibogaine as a glutamate antagonist: relevance to its putative
antiaddictive properties. The Alkaloids: Chemistry and Biology 56, 55-62.
Snelders, S., Kaplan, C., 2002. LSD therapy in Dutch psychiatry: changing
socio-political settings and medical sets. Medical History 46, 221-
Stolaroff, M., 2004. The Secret Chief Revealed. Multidisciplinary Association
for Psychedelic Studies (MAPS), Sarasota, FL.
Substance Abuse and Mental Health Services Administration, 2006. Results
from the 2005 National Survey on Drug Use and Health: National Findings.
Office of Applied Studies, NSDUH Series H-30, DHHS Publication no.
SMA 06-4194. Rockville, MD.
Sunder Sharma, S., Bhargava, H.N., 1998. Enhancement of morphine
antinociception by ibogaine and noribogaine in morphine-tolerant mice.
Pharmacology 57, 229-232.
Swiderski, S., 1988. Le mouvement oecumenique dans la religion Bouiti au
Gabon (The ecumenical movement in the Bwiti religion in Gabon). Journal
of Religion in Africa 18, 125-140.
Taraschenko, O.D., Panchal, V., Maisonneuve, I.M., Glick, S.D., 2005. Is antagonism
of alpha3beta4 nicotinic receptors a strategy to reduce morphine
dependence? European Journal of Pharmacology 513, 207-218.
Taraschenko, O.D., Rubbinaccio, H.Y., Shulan, J.M., Glick, S.D., Maisonneuve,
I.M., 2007a. Morphine-induced changes in acetylcholine release in the
interpeduncular nucleus and relationship to changes in motor behavior in
rats. Neuropharmacology 53, 18-26.
Taraschenko, O.D., Shulan, J.M., Maisonneuve, I.M., Glick, S.D., 2007b. 18-
MC acts in the medial habenula and interpeduncular nucleus to attenuate
dopamine sensitization to morphine in the nucleus accumbens. Synapse 61,
Taub, E., 2006. I begin again treatment centers. URL:
http://www.ibeginagain.org (accessed 25.11.06).
Turner, W.J., Merlis, S., Carl, A., 1955. Concerning theories of indoles in
schizophrenigenesis. American Journal of Psychiatry 112, 466-467.
U.S. Senate, 1977. ProjectMKULTRA, The CIA's program of research in behavioral
modification. Joint Hearing Before the U.S. Senate Select Committee on Intelligence and the Subcommittee on Health and Scientific Research
of the Committee on Human Resources. U.S. Government Printing Office,
Vastag, B., 2005. Addiction research. Ibogaine therapy: a 'vast, uncontrolled
experiment'. Science 308, 345-346.
villaserena.org, 2006. Villa Serena Residential Drug Addiction Treatment Centers.
URL: http://www.villaserena.org/ingles.htm (accessed 25.11.06).
Vincent, D., Sero, I., 1942. Inhibitory effect of Tabernanthe iboga on the
cholinesterase of serum. Comptes Rendus Des Seances de la Societe de
Biologie et de Ses Filiales 136, 612-614.
Wei, D., Maisonneuve, I.M.,Kuehne, M.E., Glick, S.D., 1998. Acute iboga alkaloid
effects on extracellular serotonin (5-HT) levels in nucleus accumbens
and striatum in rats. Brain Research 800, 260-268.
Wells, H., 2006. Notes for ibogaine treatment providers. URL:
http://www.ibogaine.org/wells.html (accessed 25.11.06).
Wess, J., Duttaroy, A., Gomeza, J., Zhang,W.,Yamada, M., Felder, C.C., Bernardini,
N., Reeh, P.W., 2003. Muscarinic receptor subtypes mediating central
and peripheral antinociception studied with muscarinic receptor knockout
mice: a review. Life Science 72, 2047-2054.
Yinger, J.M., 1960. Contraculture and subculture. American Sociological
Review 25, 625-635.
Yordanov, M., Dimitrova, P., Patkar, S., Falcocchio, S., Xoxi, E., Saso, L.,
Ivanovska, N., 2005. Ibogaine reduces organ colonization in murine systemic
and gastrointestinal Candida albicans infections. Journal of Medical
Microbiology 54, 647-653.
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