Kenneth R. Alper,
M.D.; Marina Stajic
Ph.D.; and James R. Gill,
Fatalities Temporally Associated with the
Ingestion of Ibogaine
ABSTRACT: Ibogaine is a naturally occurring psychoactive plant alkaloid that is used globally in medical and nonmedical settings for opioid
detoxification and other substance use indications. All available autopsy, toxicological, and investigative reports were systematically reviewed for the
consecutive series of all known fatalities outside of West Central Africa temporally related to the use of ibogaine from 1990 through 2008. Nineteen
individuals (15 men, four women between 24 and 54 years old) are known to have died within 1.5–76 h of taking ibogaine. The clinical and post-
mortem evidence did not suggest a characteristic syndrome of neurotoxicity. Advanced preexisting medical comorbidities, which were mainly cardio-
vascular, and ⁄or one or more commonly abused substances explained or contributed to the death in 12 of the 14 cases for which adequate
postmortem data were available. Other apparent risk factors include seizures associated with withdrawal from alcohol and benzodiazepines and the
uninformed use of ethnopharmacological forms of ibogaine.
KEYWORDS: forensic science, toxicology, ibogaine, iboga alkaloid, substance abuse, human, fatality, opioid, opioid detoxification,
The iboga alkaloids are a group of monoterpene indole alkaloids,
some of which reportedly reduce the self-administration of drugs of
abuse and opiate withdrawal symptoms in animal models and
humans (1,2). Ibogaine (Fig. 1), the most extensively studied iboga
alkaloid, occurs in the root bark of the West African Apocynaceous
shrub Tabernanthe iboga Baill. In Gabon, eboga, the scrapings of
the root bark, has been used as a psychopharmacological sacrament
in the Bwiti religion for several centuries (3,4). Elsewhere, includ-
ing North America, Europe, and South Africa, ibogaine is used for
the purpose of acute opioid detoxification, and to reduce craving
and maintain abstinence from opioids and other abused substances
including stimulants and alcohol, as well as for psychological or
spiritual purposes (5).
Ibogaine is used most frequently as a single oral dose in the
range of 10–25 mg ⁄kg of body weight for the specific indication
of detoxification from opioids (5,6). It is most commonly used in
the form of the hydrochloride (HCl), which certificates of analysis
typically indicate is 95–98% pure, with present retail prices in the
range of c. $125–$250 USD per gram. Ibogaine is also used in the
form of alkaloid extracts or dried root bark (Fig. 2).
Ibogaine is a schedule I substance in the United States, and simi-
larly is illegal in France, Denmark, Sweden, Belgium, Switzerland,
and Australia. However, it is unregulated in most countries, where
it is neither illegal nor officially approved. Lay providers administer
ibogaine in nonmedical settings and have accounted for the
majority of treatments (5). Ibogaine is administered in medical set-
tings in countries such as Mexico and South Africa, where physi-
cians have the legal prerogative to prescribe unapproved
Published case series and individual accounts regarding ibogaine
remission of acute withdrawal symptoms following a single admin-
istration that is subsequently sustained without further ibogaine
treatment or the use of opioids (1,6,7). This effect of ibogaine
appears to be pharmacologically mediated and not accounted for
by placebo, which has clinically negligible effects in opioid detoxi-
fication (8–10). In the naloxone-precipitated withdrawal model of
opioid detoxification, iboga alkaloids have attenuated opioid with-
drawal signs in 13 of 14 independent replications in two rodent
and two primate species (11–24). Ibogaine administered to rats or
mice as a single dose reduces the self-administration of morphine
(25–28), cocaine (26,29,30), and alcohol (31,32), with sustained
treatment effects for 48–72 h averaged for an entire sample, and an
even longer duration in individual animals (25,26,28,30). The
serum half-life of ibogaine in the rat is c. 1–2 h (33,34), indicating
that the prolonged effect on self-administration outlasts the presence
of ibogaine itself, without compelling evidence that it is mediated
by a long-lived metabolite (35).
Ibogaine does not appear to be an abused substance. The
National Institute on Drug Abuse (NIDA) did not identify potential
abuse as an issue in the context of its research program on iboga-
ine, which included preclinical testing and the development of a
clinical trial protocol (1). Animals do not self-administer 18-meth-
oxycoronaridine (18-MC), a closely structurally related ibogaine
congener with the same effects as ibogaine on self-administration
and withdrawal in preclinical models (36). Aversive side effects
such as nausea and ataxia limit ibogaine’s potential for abuse.
Ibogaine potentiates the lethality of opioids (33,37–39). This is
apparently because of an enhancement of opioid signaling (1,40),
and not because of binding at opioid receptors as an agonist (such
Departments of Psychiatry and Neurology, New York University School
of Medicine, 550 First Avenue, New York, NY 10016.
Department of Forensic Toxicology, New York City Office of Chief
Medical Examiner and Department of Forensic Medicine, New York Uni-
versity School of Medicine, 520 First Avenue, New York, NY 10016.
New York City Office of Chief Medical Examiner and Department of
Forensic Medicine, New York University School of Medicine, 520 First
Avenue, New York, NY 10016.
Received 28 July 2010; and in revised form 17 Nov. 2010; accepted 20
J Forensic Sci, March 2012, Vol. 57, No. 2
Available online at: onlinelibrary.wiley.com
398 2012 American Academy of Forensic Sciences
as methadone) or antagonist. Doses of ibogaine used in opioid
detoxification do not produce signs of overdose in individuals who
lack tolerance to opioids, such as African Bwiti adepts, or individu-
als in non-African contexts who take ibogaine for psychological or
spiritual purposes or the treatment of addiction to substances other
than opioids. If ibogaine was acting as an opioid agonist, it would
not be tolerated by opioid-nave individuals because the methadone
dosage of 60–100 m g ⁄day that is used to stabilize withdrawal
symptoms in the maintenance treatment of opioid-dependent
patients (41) substantially exceeds the estimated LD
of 40–50 mg
in humans who are not pharmacologically tolerant to opioids (42).
Other evidence that ibogaine alters signaling through opioid recep-
tors but is not itself an orthosteric agonist includes its potentiation
of morphine analgesia in the absence of a direct analgesic effect
(22,38,39,43–47). Ciba Pharmaceutical patented the use of ibogaine
to reduce tolerance to opioid analgesics in 1957 (47).
Although ibogaine contains an indole ring and is designated as a
‘‘hallucinogen,’’ it is pharmacologically distinct from the ‘‘classi-
cal’’ hallucinogens such as LSD, mescaline, or psilocybin, which
are thought to act by binding as agonists to the serotonin type 2A
) receptor (48). Serotonin agonist or releasing activity does
not appear to explain ibogaine’s effects in opioid withdrawal
(2,49). There is no anecdotal or preclinical evidence for a signifi-
cant effect of classical hallucinogens in acute opioid withdrawal,
and in the animal model ablation of 90% of the raphe, the major
serotonergic nucleus of the brain does not significantly affect the
expression of opioid withdrawal (50). Descriptions of subjective
experiences associated with ibogaine differ from those associated
with the classical hallucinogens (5,48,51). The visual effects of
classical hallucinogens are typically most strongly experienced with
the eyes open and limited to alterations of colors, textures, and pat-
terns. In contrast, the psychoactive state associated with ibogaine is
experienced most intensely with the eyes closed and has been
described as ‘‘oneiric’’ and likened to a ‘‘waking dream,’’ with
Iboga alkaloid R1R2R3
Noribogaine OH H H
Ibogamine H H H
Tabernanthine H OCH3H
FIG. 1—Chemical structures of ibogaine and its major metabolite norib-
ogaine, and the alkaloids ibogamine, ibogaline, tabernanthine, and voacan-
gine that co-occur with ibogaine in T. iboga. In the Chemical Abstracts
system the positions of R
, and R
on the ibogamine parent structural
skeleton are respectively numbered 12, 13 and 18, whereas in the Le Men
and Taylor system these same positions are numbered 10, 11 and 16.
FIG. 2—Forms of availability of ibogaine: Ibogaine is available in form of the hydrochloride (HCl) dried root bark, or alkaloid extract. The upper left
photo shows 96% pure ibogaine HCl in the form of powder in the upper left quadrant of the photo. In the lower left quadrant of the photo are five capsules.
The four lighter colored capsules contain 96% pure ibogaine HCl; the smaller two contain 120 mg and the larger two contain 250 mg respectively. The larg-
est capsule is darker and contains 330 mg of 85% ibogaine HCl. In the lower right quadrant of the photo is ground dried root bark. The upper right photo
shows alkaloid extract with an estimated total iboga alkaloid content of about 40–50%. The lower photo shows a partially scraped dried Tabernanthe iboga
root, with external bark layer, an inner bark layer, and wood. The alkaloid content is mainly concentrated in the inner root bark layer, which is exposed
along the lower border of the bare wood in left middle portion of the photo (photos courtesy of Robert Bovenga Payne and Rocky Caravelli).
ALPER ET AL. •FATALITIES TEMPORALLY ASSOCIATED WITH THE INGESTION OF IBOGAINE 399
interrogatory verbal exchanges involving ancestral and archetypal
beings, and movement and navigation within visual landscapes.
Another frequently described experience is panoramic memory, the
recall of a rapid, dense succession of vivid autobiographical visual
memories. Mechanistically, these subjective experiences associated
with ibogaine might possibly suggest functional muscarinic cholin-
ergic effects, which are prominent in the mechanisms of dreaming
and memory (52). In animals, ibogaine is reported to enhance spa-
tial memory retrieval (53,54), and to produce an atropine-sensitive
EEG rhythm (55,56), commonly regarded as a model of REM
Ibogaine’s highest affinity receptor interactions are as an agonist
at the r
receptor, and an antagonist at the N-methyl-d-aspartate-
type (NMDA) glutamate and a3b4 nicotinic acetylcholine recep-
tors (1,2,58). Initially, ibogaine’s mechanism of action in drug
self-administration and withdrawal was hypothesized to involve
NMDA receptor antagonism (59); however, this hypothesis is now
viewed as unlikely because the synthetic ibogaine congener 18-
MC has negligible NMDA receptor affinity but is equally effec-
tive as ibogaine in reducing withdrawal and self-administration in
the animal model (2). Studies of iboga alkaloids and nicotinic
agents (60–64) provide some support for antagonism of the a3b4
nicotinic receptor as a possible mechanism of action with regard
to drug craving and self-administration but do not appear to
explain detoxification in the setting of extensive physical depen-
dence on opioids. Likewise, the increased expression of glial cell-
derived neurotrophic factor may mediate reduction in drug craving
and self-administration (32) but does not explain ibogaine’seffect
in opioid detoxification.
Ibogaine was administered to human subjects in a clinical Phase
I dose escalation study under a physician-initiated Investigational
New Drug Application approved by the FDA in 1993 (65). The
study was eventually discontinued because of disputes related to
contractual and intellectual property issues (66); however, the avail-
able safety data indicated no adverse events (65). Most of the
available preclinical pharmacological, toxicological, and pharmaco-
kinetic data on ibogaine are derived from research supported by
NIDA between 1991 and 1995. NIDA eventually ended its iboga-
ine project without having initiated a clinical trial apparently
because of its high cost and complexity relative to NIDA’sexisting
resources (1). Ibogaine’s underlying structure cannot be patented
because it is naturally occurring, which limits the financial incen-
tive for its development. Ibogaine continues to be used in unregu-
lated contexts with associated risks because of a lack of clinical
and pharmaceutical standards (5).
Deaths have occurred temporally related to the use of ibogaine.
This article presents a systematic review of all available autopsy,
toxicological, and investigative reports on the consecutive series
consisting of all known fatalities temporally related to the use of ib-
ogaine that have occurred outside of West Central Africa from
1990 through 2008.
Materials and Methods
The Institutional Review Board of the New York University
School of Medicine and the General Counsel of the New York City
Office of Chief Medical Examiner (OCME) approved this research.
Identification of Cases
This series spans the time interval beginning with the first
reported fatality in 1990 (1) until December 2008. Eighteen of the
19 fatalities in this series were found through contact with ibogaine
treatment providers since the mid-1990s (5,6,67,68). One of these
fatalities was also investigated by the OCME (69) as are all unex-
pected, violent, and suspicious deaths in New York City. One fatal-
ity was found by literature search (70). The ethnographic
methodology and access to the network of the providers of iboga-
ine treatment and other participants in the ibogaine subculture are
described in detail elsewhere (5,67).
All fatalities were followed up by contact with appropriate
medico-legal death investigation agencies to obtain all available
autopsy and toxicology reports, inquest testimony, and other inves-
tigative reports. In addition to documentary evidence, in most
instances, treatment providers and other first-hand observers of the
death scene were interviewed. Systematic evaluation of the litera-
ture included Medline searches from 1966 to June 2010 utilizing
PubMed and ISI Web of Knowledge with the search terms ‘‘iboga-
ine’’ combined with ‘‘death’’ or ‘‘fatality’’ in addition to searches of
periodical and nonindexed ‘‘grey’’ literature as described elsewhere
Various methodologies for toxicological analysis of ibogaine
(molecular weight 310.44) have been previously described, includ-
ing liquid chromatography with flourimetric detection (71), gas
chromatography ⁄mass spectrometry (GC ⁄MS) (72–76) liquid chro-
matography ⁄mass spectrometry (LC-MS) (70,75,77–80), and liquid
chromatography-tandem mass spect rometry (LC-MS ⁄MS) (81–83).
There is a potential for confusion because of the use of two differ-
ent schemes for numbering the iboga alkaloid parent ibogamine
skeleton (84), the Chemical Abstracts system, which is common in
the biological and medical literature, and the Le Men and Taylor
system, which tends to be favored by natural products and synthetic
chemists and is also frequently encountered in the biological
literature (see Fig. 1).
Ibogaine screening usually is not included in most routine foren-
sic toxicological laboratories and a suspicion of use is required for
analysis, which is typically performed by a referral laboratory. For
two fatalities in this series (cases #3 and #10 in Table 1), the
Forensic Toxicology Laboratory at the OCME performed the analy-
sis. The presence of ibogaine was confirmed by GC ⁄MS and the
concentration determined using GC with a nitrogen phosphorus
Cause of Death
The certified cause of death is included in Table 1, entitled
‘‘Official cause of death.’’ The certified cause of death is that which
is indicated by the official documentation, that is, autopsy report or
death certificate, by the local authority that investigated and
recorded the death. The available documentation varied greatly with
regard to investigative rigor, level of detail, and geographic location
of the official entity that issued the report. As an approach to con-
trolling for this variance, a coauthor (JRG, a board-certified foren-
sic pathologist) made a determination regarding the cause of each
official documentation, included any information that was provided
by treatment providers and other first-hand observers of the death
scene, or friends and acquaintances of the decedent. Table 1 pro-
vides the conclusions of this systematic, critical evaluation of all
available evidence in the far right-hand column entitled ‘‘Proximate
cause of death.’’
The cause of death is defined as the original, etiologically spe-
cific, underlying medical condition that initiates the lethal sequence
400 JOURNAL OF FORENSIC SCIENCES
TABLE 1—Worldwide known fatalities outside of West Central Africa temporally associated with the ingestion of ibogaine, 1990–2008.
Ibogaine Use Country Year Circumstance
(Blood, mg ⁄L
or mg ⁄kg)
France 1990 Witnessed
4 h Ibogaine
300 mg (c.
4.5 mg ⁄kg)
inverted T waves
noted on EKG
3 months prior to
Netherlands 1993 Died during
19 h Ibogaine HCl
29 mg ⁄kg
Charred tin foil
found in room
role of ibogaine
unknown due to
lack of information
relating levels to
due to the
USA 1999 Found dead
8–9 h Ibogaine HCl;
believed to be
16–20 mg ⁄kg
events prior to
aware of dangers
of use of cocaine
due to the
of opiates, cocaine,
due to the
2000 Died in
prior to death
40 h Tabernanthe
extract 6 g
0.36 Other toxicology:
Hepatitis C with
Fatal reaction to
5. 35 F
Germany 2002 Found dead
of not feeling
1.5 h Ibogaine HCl
Unknown Unknown Childhood
ALPER ET AL. •FATALITIES TEMPORALLY ASSOCIATED WITH THE INGESTION OF IBOGAINE 401
Ibogaine Use Country Year Circumstance
(Blood, mg ⁄L
or mg ⁄kg)
6. 32 M
by opiate abuser)
USA 2003 Found dead
in bed at his
Unknown Bag of brown
powder at scene
History of opiate
abuse, and had
Mexico 2003 Died at
60 h Ibogaine HCl
13 mg ⁄kg
Unknown Unknown Obesity, chronic
Mexico 2004 Died at
20 h Ibogaine HCl
15 mg ⁄kg
Unknown Unknown Chronic
in the US)
2005 Died at
2 days Ibogaine HCl
14 mg ⁄kg
with 135 lb
weight loss in
death due to
infarct due to
infarct due to
402 JOURNAL OF FORENSIC SCIENCES
Ibogaine Use Country Year Circumstance
(Blood, mg ⁄L
or mg ⁄kg)
10 43 M
USA 2005 Witnessed
seizure 17 h after
27 h Ibogaine HCl,
2.8 Diazepam: 0.03
11 51 M
Mexico 2005 Died at ibogaine
24 h Ibogaine HCl
12 mg ⁄kg
Unknown Unknown Autopsy not
arrest due to
12 38 M
Mexico 2006 Died at ibogaine
Found dead within
1 h of having last
been seen alive
12 h Ibogaine HCl
13 mg ⁄kg
Unknown Cocaine and
cause of death
13 48 M
France 2006 Ingested root bark
iboga followed by
53 h 18 ‘‘soup-spoons’’ of
a mixture of
root bark and
milk over 10 h
Vena cava: 6.6
Femoral vein: 5.4
Vena cava: 15.5
Femoral vein: 5.6
parts of plants
found at the
that some sort of
may have taken
ALPER ET AL. •FATALITIES TEMPORALLY ASSOCIATED WITH THE INGESTION OF IBOGAINE 403
Ibogaine Use Country Year Circumstance
(Blood, mg ⁄L
or mg ⁄kg)
14 28 M
The Netherlands 2006 Fluctuating
immersion in a
for a 4-h period
prior to death.
observed and at no
time was his head
76 h Tabernanthe
cause of death.
of third ventricle,
and ⁄or partial
from the temporal
cause not likely’’
15 30 M
South Africa 2006 ‘‘Gurgling sounds’’
Died en route to
8 h Ibogaine HCl
17 mg ⁄kg
Not tested Not tested Autopsy not
secondary to drug
16 27 M
France 2006 Discovered dead
room at a center
£20 h Powdered root
bark (7.2% ibogaine,
was not provided
in the report.
13 teaspoons at
been required to
Peripheral blood at
autopsy 8 days
due to ibogaine,
due to the
404 JOURNAL OF FORENSIC SCIENCES
Ibogaine Use Country Year Circumstance
(Blood, mg ⁄L
or mg ⁄kg)
17 45 M
USA 2006 Found dead in
at a private
8–12 h Ibogaine HCl
22 mg ⁄kg
77 ng ⁄ml
1.2 ng ⁄ml
1.5 ng ⁄ml
Hepatic steatosis Mixed drug
due to the
18 33 M
Mexico 2007 Died at ibogaine
6.5 h Ibogaine HCl
11 mg ⁄kg
Not tested Not tested.
crack cocaine in
during a prior
admission to the
in patient’s father.
cause of death
at time of death)
19 41 M
in the US)
2007 Died at
6 h Ibogaine HCl
13 mg ⁄kg
Not tested Not tested Cardiac
397 mg ⁄dL
ALPER ET AL. •FATALITIES TEMPORALLY ASSOCIATED WITH THE INGESTION OF IBOGAINE 405
of events (85). A competent cause of death includes the proximate
(underlying) cause, defined as that which in a natural and continu-
ous sequence, unbroken by any efficient intervening cause,
produces the fatality and without which the end result would not
have occurred. Contributing conditions were additional disorders
contributory to death but unrelated to the underlying cause of
The conclusion that death was caused by an acute intoxication
requires that three conditions be met: the toxicological results are
within the range typically encountered in such fatalities, the history
and circumstances are consistent with a fatal intoxication, and the
autopsy fails to disclose a disease or physical injury that has an
extent or severity inconsistent with continued life (86). In deaths
caused by drug intoxication with more than one drug in concentra-
tions greater than trace amounts, it is customary to include all of
the identified drugs in the cause of death.
We report a summary of 19 ibogaine-associated deaths that have
occurred worldwide between 1990 and 2008 including the probable
causes of death based on the available clinical and pathologic infor-
mation (see Table 1). There were 15 men and four women with a
mean age of 39.1 € 8.6 years ranging from 24 to 54 years. In 18
decedents, the estimated time intervals were available from the
most recent ingestion of ibogaine in any form until death, and the
mean interval was 24.6 € 21.8 h and ranged from 1.5 to 76 h. In
one other fatality (case #6) the time interval between death and the
time when the decedent was last noted to be alive was 20 h, the
decedent had been dead for at least several hours at the time the
body was found. The time interval from the most recent ingestion
of ibogaine until death in this instance was likely less than 76 h,
but it was not included in the calculation of the mean interval.
Fifteen individuals took ibogaine for the indication of opioid
detoxification, four of who were also dependent on alcohol, three
on cocaine, and one on methamphetamine. Two individuals used it
for a spiritual ⁄psychological purpose and had no known substance
abuse history, and two took it for unknown reasons but had a his-
tory of substance abuse. Ibogaine was given as the HCl form in 14
instances, as an alkaloid extract in two (cases #4 and #14), dried
root bark in two (cases #13 and #16), and a brown powder that
was probably either root bark or alkaloid extract in another (case
#6). In the 12 fatalities where ibogaine was given as the HCl and a
dose was reported, the mean dose was 14.3 € 6.1 mg ⁄kg (range
4.5–29 mg ⁄kg). In the 10 fatalities in which ibogaine blood con-
centrations were determined, the mean was 2.38 € 3.08 mg ⁄L
(range 0.24–9.3 mg ⁄L), obtained at a mean of 25.5 € 17.8 h fol-
lowing the ingestion of ibogaine (range 4–53 h). In addition, com-
monly abused drugs (including benzodiazepines, cocaine, opiates,
and methadone) were detected in eight of 11 decedents on whom
toxicological analysis for abused substances was performed.
Twelve of the decedents had medical comorbidities including
liver disease, peptic ulcer disease, brain neoplasm, hypertensive and
atherosclerotic cardiovascular disease, and obesity. Among the three
decedents in which no other drugs of abuse were detected in post-
mortem toxicology analysis, one had advanced heart disease and
another had liver fibrosis. Full toxicology and autopsy results were
not available in eight and five decedents, respectively.
In this series, 19 deaths occurred between 1990 and 2008, with
an interval of 76 h or fewer between the most recent ingestion of
ibogaine and death. In 14 instances, an autopsy was performed that
allowed the determination of the proximate cause of death. The
lack of clinical and pharmaceutical controls in settings in which ib-
ogaine has been given, and the limited data regarding toxic concen-
trations of ibogaine in humans make the determination of the
causes of these deaths difficult. Nonetheless, advanced comorbidi-
ties and contributing conditions appear to include preexisting medi-
cal, particularly cardiovascular disease, and drug use around the
time of treatment.
This series of fatalities is consecutive in the sense that it repre-
sents a systematic application of an intensive methodology for iden-
tifying cases over the time interval spanned by this study. It is
possible that additional fatalities may have occurred which were
missed by death investigation agencies and this study. In the United
States, this could relate to the surreptitiousness regarding the use of
ibogaine because of its status as a schedule I substance, and indi-
viduals aware that ibogaine was used in temporal association with
a fatal outcome might be reluctant to disclose that history. Without
investigative information about the recent use of ibogaine, special-
ized analysis for ibogaine may not be performed. Under these cir-
cumstances, the cause of death of an individual treated with
ibogaine for a substance use indication could be certified as a typi-
cal multidrug intoxication, particularly in view of the likelihood of
detecting other drugs of abuse in these deaths. In most of the
world, however, ibogaine is not illegal. In this series, outside of the
United States, ibogaine was not illegal at the time of occurrence of
the fatality in any country in which the fatality occurred.
In at least five instances, providers contacted the first author
immediately regarding the death, and in a number of others,
another individual close to the provider relayed the information,
usually with the provider’s consent. Their motivation to disclose
this information included the wish to understand the causality of
the death and prevent a future occurrence, abreaction regarding a
traumatic event, and anxiety regarding legal liability. In a country
in which ibogaine is not illegal, however, concealing its use is not
necessarily perceived to be, or actually safer than disclosing it.
Regardless of their distress regarding a death, experienced treatment
providers such as those in Mexico or the Netherlands were aware
that they did not face significant legal consequences. In a prior
study by the first author of this article that surveyed the settings
and extent of ibogaine use (5), it was estimated that 20–30% of the
actual total number of ibogaine treatments had been missed by that
study. Six of the series of 19 fatalities in this article occurred in
settings and circumstances that are likely to have otherwise been
hidden from the medical ethnographic study mentioned previously
(5). While it is likely that some deaths temporally related to the
use of ibogaine escaped inclusion in this series, it is also possible
that treatments that are associated with a fatal outcome may come
to attention relatively more frequently than those that are not.
For the purpose of this discussion, the terms ‘‘proximate cause’’
and ‘‘contributing condition’’ are used as they are defined previ-
ously in the methods section and appear in the extreme right-hand
column of Table 1. A striking factor in this series of deaths is the
identification of a comorbidity or intoxication (in addition to iboga-
ine) that could adequately explain or contribute to the death in 12
of 14 decedents that have adequate postmortem data. There are
multiple possible pathways by which ibogaine may cause or con-
tribute to death in these instances and include toxicological interac-
tions with substances of abuse and direct cardiac effects.
Cardiac disease was a contributing condition or proximate cause
in six deaths, suggesting cardiac mechanisms are an important
mediator of fatal outcomes. Although preclinical toxicological test-
ing by NIDA did not indicate prolongation of the QT interval (87),
406 JOURNAL OF FORENSIC SCIENCES
it has been observed during ibogaine treatments with continuous
EKG monitoring (88). Blockade of the potassium voltage-gated ion
channel encoded by the human ether-a-go-go-related gene (hERG)
is regarded as the most common cause of drug-related QT prolon-
gation (89,90), which is associated with torsades de pointes (TdP),
a morphologically distinctive polymorphic ventricular tachycardia.
The effect of ibogaine differs from that of the hERG channel
antagonist WAY-123.398 in studies of chromaffin cells (91–93);
however, ibogaine is an hERG channel antagonist in the low
micromolar range in human embryonic kidney tsA-201 cells (94).
Ibogaine has low micromolar affinity for sodium channels
(2,95,96), which might also possibly relate to cardiac risk in view
of the possible association of sodium channel blockade with slow-
ing of intraventricular conduction and the subsequent development
of a re-entrant circuit resulting in ventricular tachyarrhythmia
(89,97), and there is evidence for altered sodium channel function-
ing in some drug-induced forms of long QT syndrome (98–101).
QT prolongation is also regarded as a general correlate of car-
diac instability that is associated with arrhythmias other than TdP
(89,102,103), and with multiple risk factors relevant to the present
study including bradycardia, coronary artery disease, dilated cardio-
myopathy, recent myocardial infarction, ventricular hypertrophy,
and liver disease (89,104). Bradycardia has been reported in
humans in association with the ingestion of ibogaine in medical
(88,105) and nonmedical (106) settings, and in some preclinical
studies (33,36,107,108). The frequently altered nutritional status of
substance abusers puts them at risk of hypomagnesemia and hypo-
kalemia (90), which are associated with QT prolongation, as are
bulimia and anorexia (109). Methadone is associated with QT pro-
longation, particularly in the presence of other drugs (110). Alcohol
or cocaine use is associated with prolongation of the QT interval
both acutely (111,112) and during withdrawal (113–115). In
patients with alcohol dependence, QT prolongation has been
observed to persist for 7 days after the last intake of alcohol (116),
and withdrawal seizures contribute further independent and additive
risk (114). Epileptic seizures, even in the absence of substance use
or withdrawal, are an independent risk factor for QT prolongation
A case report of QT prolongation and ventricular arrhythmia in
association with the ingestion of T. iboga alkaloid extract (118)
illustrates the variety of potential arrhythmogenic factors in the
clinically uncontrolled settings in which ibogaine has been used.
The patient survived in that case, which is not included in this pres-
ent series. The patient had taken ‘‘Indra,’’ an apocryphal brand of
alkaloid extract that subsumes multiple sources of diverse origin,
composition, and conditions of storage (67). Multiple confounding
risk factors for QT prolongation and ventricular arrhythmia were
present. The patient had presented with a witnessed generalized
tonic-clonic seizure (GTCS) in the setting of acute alcohol with-
drawal with hypomagnesemia and hypokalemia. Although the
report made no mention of toxicological testing for illicit drugs, the
patient had a prior history of cocaine abuse and a history of buli-
mia and had been purging prior to admission.
Bradycardia is a functional effect of potential medical signifi-
cance that could possibly involve muscarinic cholinergic transmis-
sion. Ibogaine binds with reported affinities in the 10–30 lM range
to M1 and M2 muscarinic cholinergic receptors and is generally
assumed to act as an agonist (1,2); however, functional studies have
not been performed. Although ibogaine is concentrated in brain tis-
sue relative to serum in the animal model (119) and in the two
cases reported here that reported on brain levels (cases #3 and
#13), an older literature (120,121), as well as more recent data
(122), indicates that the inhibition of acetylcholinesterase by
ibogaine in vitro is negligible over the range of ibogaine concentra-
tionsobservedinbothbloodandbrain in this series. It is unclear
whether the apparent association of ibogaine with bradycardia could
possibly be related to orthosteric agonist actions at muscarinic cho-
linergic receptors, or to effects involving sodium channels (123) or
other signal transduction pathways.
Pulmonary thromboembolism (PE) was the reported cause of
death in three deaths (cases #7, #12, and #18) all of which
occurred in Mexico. Two were not under direct observation at the
time of the death. In all three of these cases, autopsy reports were
inadequate as a basis for the determination of a proximate cause of
death due the lack of evidence of systematic examination of the
lungs and pulmonary vasculature. In Mexico, the death certificate
provides the clinical conclusion reached by the physician who pro-
nounced the death. In case #18, the attending physician patient
observed the patient directly and based the clinical diagnostic
impression of PE on acute dyspnea, tachypnea, and desaturation
indicated by pulse oximetry. Although an adequate autopsy is lack-
ing, the clinical picture mentioned previously is frequently seen
with PE (124), and in instances where there is verification by a
subsequent autopsy, the prospective clinical diagnosis of PE is less
commonly falsely positive than falsely negative (125). The dece-
dent had a family history of PE, and if he did indeed die from
venous thrombotic disease, the family history suggests a possible
etiological contribution because of genetic risk (126). Other possi-
ble risk factors for PE include travel to the treatment location (127)
and ⁄or inactivity and immobility during the treatment (128). Intra-
venous drug use is a risk factor for deep venous thrombosis
(129–131), and hence for PE, and appears to be associated with
injection per se, independent of the use of opioids versus other
In this series, there appeared to be no clinical or postmortem evi-
dence suggestive of a characteristic syndrome of neurotoxicity. Ib-
agonist activity potentiates excitatory transmission in
the olivocerebellar projection, where the redundancy of inputs to
cerebellar Purkinje cells renders them vulnerable to excitotoxic
injury (133,134). This is believed to be the mechanism of degener-
ation of cerebellar Purkinje cells observed in rats given substan-
tially larger dosages of ibogaine than those used to study drug self-
administration and withdrawal (135). Subsequent research found no
evidence of neurotoxicity in the primate (65) or mouse (136) at
dosages that produced cerebellar degeneration in the rat, or in the
rat at dosages used in studies of drug self-administration and with-
drawal (137). Neuropathological examination revealed no evidence
of degenerative changes in a woman who had received four sepa-
rate doses of ibogaine ranging between 10 and 30 mg ⁄kg over a
15-month interval prior to her death due to a mesenteric artery
thrombosis with small bowel infarction 25 days after her last inges-
tion of ibogaine (65).
In one fatality in this series, a GTCS occurred (case #10), which
might have been due to alcohol or benzodiazepine withdrawal. In
another death (case #14), a brain neoplasm might have explained
the possibility of complex partial seizures mentioned in the autopsy
report. The neurodegeneration observed in the rat following high
dosages of ibogaine has mainly involved the cerebellum (134,135),
which is an unlikely location for a seizure focus in humans. Sei-
zures originating from the cerebellum in humans appear to be lim-
ited to rare instances in which a focus is located in a tumor mass
distinct from normal cerebellar tissue, most commonly a gangliogli-
oma (138). Furthermore, cerebellar stimulation is viewed as a pos-
sible antiepileptic treatment (139), and ibogaine has been observed
to protect against convulsions in animal models (140–142), which
has been attributed to NMDA antagonist activity. Ibogaine causes
ALPER ET AL. •FATALITIES TEMPORALLY ASSOCIATED WITH THE INGESTION OF IBOGAINE 407
serotonin release in selected brain regions in the animal model
(49), and seizures are sometimes seen in serotonin syndrome (143),
but characteristic features of serotonin syndrome such as hyperther-
mia or rigidity were not present and a clinical picture suggestive of
serotonin syndrome does not appear to have been evident in this
The apparent potentiation of both the analgesic (22,38,39,43–47)
and toxic (33,37–39) effects of opioids by ibogaine may be medi-
ated by enhanced transduction of signaling via opioid receptors
(40), which might have been a factor in deaths involving the use
of opioids in temporal proximity to the ingestion of ibogaine. In
one fatality (case #2), it appeared that the decedent smoked heroin
following ibogaine treatment and shortly before death (6). Toxico-
logical analysis detected a low morphine concentration that none-
theless was in the range measured in human subjects within
30 min after inhalation of volatilized heroin (144), similar to the
the dragon’’ (145), and suggests possible potentiation of opioid tox-
icity by ibogaine in this death. Ibogaine increases cocaine-induced
stereotypic motor behavior in the animal model (146), suggesting
that ibogaine might also potentiate the toxicity of stimulants as
well as opioids.
Postmortem toxicological analysis detected commonly abused
drugs in eight of the 11 cases in which toxicological analysis was
performed in this series. When considering a drug intoxication
death because of multiple substances, it usually is not possible to
differentiate the individual roles and complex interactions of these
substances in causing the death. These deaths typically are certified
as intoxications because of the combined effects of all substances
detected. Therefore, it is not possible to determine whether the
deaths in which drugs of abuse were detected were because of ib-
ogaine alone, to one or more of the drugs of abuse, or a combina-
tion. There is also a general effect of the number of abused
substances, with a larger number associated with a greater risk of
death independent of the identity of specific substances involved
(147). The unexplained variance of lethal outcome as a function of
dose further adds to the difficulty of the determination of causality
for ibogaine and drugs of abuse. For example, morphine concentra-
tions associated with heroin overdose overlap substantially with
concentrations obtained from living current heroin users (148),
which may relate to the wide ranges of tolerance among opioid-
dependent individuals, and within the same individual at different
Systemic disease is a confounding factor that contributes to the
mortality associated with substance use and further complicates the
identification of the cause of death.Theriskofdeathmayrepresent
a complex interaction involving a substance of abuse against a
backdrop of systemic medical illness related to addiction. For
example, the risk of death from opioid overdose is associated with
cardiac hypertrophy and atherosclerotic disease (149), which were
contributing conditions in this case series and which in turn are
associated with a history of methamphetamine and cocaine use
(150,151). The role of advanced preexisting medical comorbidities
in this series of fatalities appears to be an instance of a more gen-
eral association between systemic disease and risk of fatal overdose
The reported elimination half-life of ibogaine in humans is on
the order of 4–7 h (7,70), and that of noribogaine is apparently
longer (7,35). Ibogaine is relatively lipophilic and accumulates pref-
erentially in tissues containing a high density of lipids, such as
brain or fat (119). Ibogaine undergoes demethylation to noribogaine
via cytochrome P450 2D6 (CYP2D6) (152), which is expressed in
the brain (153), where noribogaine may be ‘‘trapped’’ because it is
more polar than ibogaine and may cross the blood–brain barrier
more slowly. Postmortem redistributionofdrugsanddrugmetabo-
lites may occur due to passive drug release from drug reservoirs,
cell autolysis, and putrefaction (154,155). In the three instances in
which peripheral and cardiac concentrations of ibogaine were
reported (cases #2, #6, and #13), the concentrations from the femo-
ral and cardiac or vena cava sites were similar. However, the two
that reported noribogaine concentrations (cases #2 and #13) demon-
strated evidence for postmortem redistribution of noribogaine with
ratios of c. 3:1 between cardiac and peripheral blood. The one
instance that reported ibogaine concentrations at two time points
(case #16) indicated 0.65 mg ⁄L in blood at autopsy and 1.27 mg ⁄L
days following death.
The available data do not provide a basis for a reliable estimate
of toxic concentrations of ibogaine. In humans administered fixed
oral doses of ibogaine of 10 mg⁄kg, mean peak blood levels were
0.74 € 0.08 and 0.90 € 0.17 mg ⁄L in extensive and poor CYP2D6
metabolizers, respectively (7). In series of cases reported here, the
mean dosage was 14.3 € 6.1 mg ⁄kg (range 4.5–29 mg ⁄kg), and
the mean blood level was 2.38 € 3.08 mg⁄L. The presence of coin-
toxicants and comorbidities, difference in dosages used, and the
higher variance in dosages and blood levels in the present series
does not provide for a meaningful comparison regarding a lethal
dosage or level in humans.
In the rat, the animal model that is predominantly used in
research on ibogaine, the dose that is usually used in models of
drug self-administration and opioid withdrawal is 40 mg⁄kg admin-
istered intraperitoneally (i.p.) (1,2). This dose is approximately one-
third of the LD
of ibogaine administered i.p. (33), which in turn
is approximately one-half to one-third of the LD
by the intraga-
stric route of administration (33,156). The animal data indicate a
significant effect of abused substances on toxicity associated with
ibogaine (33,37–39), and taken together with the clinical evidence
for the effect systemic disease on fatal overdose (149) suggests that
interactions involving cointoxicants and medical comorbidities pre-
clude a reasonable estimate regarding a lethal dosage or level of ib-
ogaine in humans.
Cointoxicants or contributing medical comorbidities were not
reported in only two fatalities for which there were an adequate
postmortem examination and toxicological analysis (cases #4 and
#13). These two deaths involved the ingestion of crude alkaloid
extract in one case, and root bark in the other. The overall compo-
sition, age, and origin of these sources of ibogaine are unknown.
The iboga alkaloid content of T. iboga root bark extracts depends,
among other factors, on the extraction method. The total alkaloid
content of the root bark is c. 2–8% of the dry weight of the root
bark, about half of which is iboga alkaloids, 80% of which is ib-
ogaine (157,158). Utilization of water-soluble extractants yields an
extract with an alkaloid fraction composed of c. 40% ibogaine,
10% related iboga alkaloids, and 50% other alkaloids, whereas uti-
lization of an organic solvent such as acetone or methanol yields
a total alkaloid fraction with relatively less non-iboga alkaloid con-
tent (157). Other iboga alkaloids that co-occur with ibogaine in
T. iboga root bark include ibogamine, ibogaine, tabernanthine, and
voacangine (157–159) (see Fig. 1). The overall iboga alkaloid
composition of T. iboga alkaloid extracts may range from c. 15%
to 50% (157) (C. Jenks, personal communication). Sources of ib-
ogaine HCl are restricted and tend to be known to providers,
and certificates of analysis have generally been available and
corroborated when verified by independent laboratories, which up
to the present time has distinguished ibogaine from the counterfeit-
ing and adulteration seen with commonly abused ‘‘street’’ drugs
408 JOURNAL OF FORENSIC SCIENCES
Inexperience and lack of information regarding the use of ethno-
pharmacological forms of ibogaine may itself constitute a salient
domain of risk, independent of the uncertain composition of alka-
loid extracts and the undefined potential toxicity of the alkaloids
that co-occur with ibogaine in T. iboga root bark. For example,
one decedent (case #13) (70) may have ingested an amount of
dried T. iboga root bark in excess of that which would typically be
given in a full Bwiti initiation ceremony (5). The blood ibogaine
concentration in this case was the second highest in the series, even
though it was measured an estimated 53 h after ingestion, and does
not take into account the likely presence of other alkaloids. This
case additionally suggests that the bioavailability of the alkaloid
content of dried root bark may be high.
The incidence of fatalities may have decreased in the recent past.
As indicated in Table 1, in 2008, there were no known fatalities,
and in 2007, there were 2. In contrast, there were a total of nine
fatalities that occurred in 2005 and 2006. It is unlikely that this
reflects a decline in the number of individuals treated, which
appears to be continuing the trend of growth evident over the last
decade (5). Greater recognition of medical risk on the part of treat-
ment providers may have been a factor in the apparent reduction in
the incidence of fatalities. Pretreatment screening including basic
blood chemistries and EKG, the exclusion of patients with signifi-
cant medical, particularly cardiac illness, and the recognition of the
need to stabilize physical dependence on alcohol and benzodiaze-
pines prior to ibogaine treatment has gradually become more
widely accepted norms in the settings of ibogaine use (161). This
might to a significant extent reflect the collective, cumulative expe-
rience of the fatal outcomes presented here.
In conclusion, in this series of 19 cases, advanced preexisting
medical comorbidities, which were mainly cardiovascular, and ⁄or
one or more commonly abused substances explained or contributed
to the death in 12 of the 14 cases for which adequate postmortem
data were available. Significant factors in this series appear to
include preexisting medical, particularly cardiovascular disease,
possible PE, drug use during treatment, seizures associated with
withdrawal from alcohol and benzodiazepines, and the uninformed
use of ethnopharmacological forms of ibogaine.
We gratefully acknowledge the valuable assistance of How-
ard Lotsof in identifying cases and providing documents.
1. Alper KR. Ibogaine: a review. Alkaloids Chem Biol 2001;56:1–38.
2. Glick SD, Maisonneuve IM, Szumlinski KK. Mechanisms of action of
ibogaine: relevance to putative therapeutic effects and development of
a safer iboga alkaloid congener. Alkaloids Chem Biol 2001;56:39–53.
3. Fernandez JW. Bwiti: an ethnography of religious imagination in
Africa. Princeton, NJ: Princeton University Press, 1982.
4. Fernandez JW, Fernandez RL. ‘‘Returning to the path’’: the use of ib-
oga[ine] in an equatorial African ritual context and the binding of time,
space, and social relationships. Alkaloids Chem Biol 2001;56:235–47.
5. Alper KR, Lotsof HS, Kaplan CD. The ibogaine medical subculture. J
6. Alper KR, Lotsof HS, Frenken GM, Luciano DJ, Bastiaans J. Treatment of
acute opioid withdrawal with ibogaine. Am J Addict 1999;8(3):234–42.
7. Mash DC, Kovera CA, Pablo J, Tyndale R, Ervin FR, Kamlet JD,
et al. Ibogaine in the treatment of heroin withdrawal. Alkaloids Chem
8. Gowing L, Ali R, White JM. Buprenorphine for the management of
opioid withdrawal. Cochrane Database Syst Rev 2009 (3):Art. No.
9. Gowing L, Farrel M, Ali R, White JM. Alpha
-adrenergic agonists for
the management of opioid withdrawal. Cochrane Database Syst Rev
2009 (2):Art. No. CD002024.
10. Amato L, Davoli M, Minozzi S, Ali R, Ferri M. Methadone at tapered
doses for the management of opioid withdrawal. Cochrane Database
Syst Rev 2009 (3):Art. No. CD003409.
11. Panchal V, Taraschenko OD, Maisonneuve IM, Glick SD. Attenuation
of morphine withdrawal signs by intracerebral administration of 18-
methoxycoronaridine. Eur J Pharmacol 2005;525(1–3):98–104.
12. Rho B, Glick SD. Effects of 18-methoxycoronaridine on acute signs of
morphine withdrawal in rats. Neuroreport 1998;9(7):1283–5.
13. Maisonneuve IM, Keller RW Jr, Glick SD. Interactions between iboga-
ine, a potential anti-addictive agent, and morphine: an in vivo microdi-
alysis study. Eur J Pharmacol 1991;199(1):35–42.
14. Parker LA, Burton P, McDonald RV, Kim JA, Siegel S. Ibogaine inter-
feres with motivational and somatic effects of naloxone-precipitated
withdrawal from acutely administered morphine. Prog Neuropsycho-
pharmacol Biol Psychiatry 2002;26(2):293–7.
15. Dzoljic ED, Kaplan CD, Dzoljic MR. Effect of ibogaine on naloxone-
precipitated withdrawal syndrome in chronic morphine-dependent rats.
Arch Int Pharmacodyn Ther 1988;294:64–70.
16. Glick SD, Rossman K, Rao NC, Maisonneuve IM, Carlson JN. Effects
of ibogaine on acute signs of morphine withdrawal in rats: indepen-
dence from tremor. Neuropharmacology 1992;31(5):497–500.
17. Sharpe LG, Jaffe JH. Ibogaine fails to reduce naloxone-precipitated with-
drawal in the morphine-dependent rat. Neuroreport 1990;1(1):17–9.
18. Cappendijk SL, Fekkes D, Dzoljic MR. The inhibitory effect of norhar-
man on morphine withdrawal syndrome in rats: comparison with iboga-
ine. Behav Brain Res 1994;65(1):117–9.
19. Popik P, Layer RT, Fossom LH, Benveniste M, Geter-Douglass B,
Witkin JM, et al. NMDA antagonist properties of the putative antiad-
dictive drug, ibogaine. J Pharmacol Exp Ther 1995;275(2):753–60.
20. Layer RT, Skolnick P, Bertha CM, Bandarage UK, Kuehne ME, Popik
P. Structurally modified ibogaine analogs exhibit differing affinities for
NMDA receptors. Eur J Pharmacol 1996;309(2):159–65.
21. Leal MB, Michelin K, Souza DO, Elisabetsky E. Ibogaine attenuation
of morphine withdrawal in mice: role of glutamate N-methyl-D-aspar-
tate receptors. Prog Neuropsychopharmacol Biol Psychiatry
22. Frances B, Gout R, Cros J, Zajac JM. Effects of ibogaine on naloxone-
precipitated withdrawal in morphine-dependent mice. Fundam Clin
23. Aceto MD, Bowman ER, Harris LS, May EL. Dependence studies of
new compounds in the rhesus monkey and mouse (1991). NIDA Res
24. Koja T, Fukuzaki K, Kamenosono T, Nishimura A, Nagata R, Lukas
SE. Inhibition of opioid abstinent phenomena by Ibogaine. 69th Annual
Meeting of the Japanese Pharmacological Society, March 20–23, 1996.
Jpn J Pharmacol 1996;71(Suppl. 1):89.
25. Glick SD, Rossman K, Steindorf S, Maisonneuve IM, Carlson JN.
Effects and aftereffects of ibogaine on morphine self-administration in
rats. Eur J Pharmacol 1991;195(3):341–5.
26. Glick SD, Kuehne ME, Raucci J, Wilson TE, Larson D, Keller RW Jr,
et al. Effects of iboga alkaloids on morphine and cocaine self-adminis-
tration in rats: relationship to tremorigenic effects and to effects on
dopamine release in nucleus accumbens and striatum. Brain Res
27. Glick SD, Pearl SM, Cai J, Maisonneuve IM. Ibogaine-like effects of
noribogaine in rats. Brain Res 1996;713(1–2):294–7.
28. Glick SD, Maisonneuve IM, Pearl SM. Evidence for roles of kappa-
opioid and NMDA receptors in the mechanism of action of ibogaine.
Brain Res 1997;749(2):340–3.
29. Sershen H, Hashim A, Lajtha A. Ibogaine reduces preference for
cocaine consumption in C57BL ⁄6By mice. Pharmacol Biochem Behav
30. Cappendijk SL, Dzoljic MR. Inhibitory effects of ibogaine on cocaine
self-administration in rats. Eur J Pharmacol 1993;241(2–3):261–5.
31. Rezvani AH, Overstreet DH, Lee YW. Attenuation of alcohol intake
by ibogaine in three strains of alcohol-preferring rats. Pharmacol Bio-
chem Behav 1995;52(3):615–20.
32. He DY, McGough NN, Ravindranathan A, Jeanblanc J, Logrip ML,
Phamluong K, et al. Glial cell line-derived neurotrophic factor medi-
ates the desirable actions of the anti-addiction drug ibogaine against
alcohol consumption. J Neurosci 2005;25(3):619–28.
33. Dhahir HI. A comparative study on the toxicity of ibogaine and seroto-
nin [Doctoral Thesis]. Indianapolis (IN): Indiana University, 1971.
ALPER ET AL. •FATALITIES TEMPORALLY ASSOCIATED WITH THE INGESTION OF IBOGAINE 409
34. Baumann MH, Rothman RB, Pablo JP, Mash DC. In vivo neurobiolog-
ical effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyi-
bogamine (noribogaine), in rats. J Pharmacol Exp Ther
35. Pearl SM, Hough LB, Boyd DL, Glick SD. Sex differences in ibogaine
antagonism of morphine-induced locomotor activity and in ibogaine
brain levels and metabolism. Pharmacol Biochem Behav
36. Glick SD, Maisonneuve IM, Hough LB, Kuehne ME, Bandarage UK.
(€)-18-Methoxycoronaridine: a novel iboga alkaloid congener having
potential anti-addictive efficacy. CNS Drug Rev 1999;5(1):27–42.
37. MPI Research. Determination of the acute interaction of combined ib-
ogaine and morphine in rats. MPI Research Identification: 693-082. Ib-
ogaine Drug Master File Volume 8. Bethesda, MD: National Institute
on Drug Abuse (NIDA), 1996;1–377.
38. Schneider JA, McArthur M. Potentiation action of ibogaine (bogadin
TM) on morphine analgesia. Experientia 1956;12(8):323–4.
39. Bhargava HN, Cao YJ. Effects of noribogaine on the development of
tolerance to antinociceptive action of morphine in mice. Brain Res
40. Rabin RA, Winter JC. Ibogaine and noribogaine potentiate the inhibi-
tion of adenylyl cyclase activity by opioid and 5-HT receptors. Eur J
41. Fareed A, Casarella J, Amar R, Vayalapalli S, Drexler K. Methadone
maintenance dosing guideline for opioid dependence, a literature
review. J Addict Dis 2010;29(1):1–14.
42. Corkery JM, Schifano F, Ghodse AH, Oyefeso A. The effects of metha-
done and its role in fatalities. Hum Psychopharmacol 2004;19(8):565–76.
43. Bagal AA, Hough LB, Nalwalk JW, Glick SD. Modulation of mor-
phine-induced antinociception by ibogaine and noribogaine. Brain Res
44. Cao YJ, Bhargava HN. Effects of ibogaine on the development of tol-
erance to antinociceptive action of mu-, delta- and kappa-opioid recep-
tor agonists in mice. Brain Res 1997;752(1–2):250–4.
45. Bhargava HN, Cao YJ, Zhao GM. Effects of ibogaine and noribogaine
on the antinociceptive action of mu-, delta- and kappa-opioid receptor
agonists in mice. Brain Res 1997;752(1–2):234–8.
46. Sunder Sharma S, Bhargava HN. Enhancement of morphine antinoci-
ception by ibogaine and noribogaine in morphine-tolerant mice. Phar-
47. Schneider JA, inventor Ciba Pharmaceutical Products Inc., Summit,
N.J., assignee. Tabernanthine, Ibogaine Containing Analgesic Composi-
tions. US patent 2,817,623. 1957.
48. Nichols DE. Hallucinogens. Pharmacol Ther 2004;101(2):131–81.
49. Wei D, Maisonneuve IM, Kuehne ME, Glick SD. Acute iboga alkaloid
effects on extracellular serotonin (5-HT) levels in nucleus accumbens
and striatum in rats. Brain Res 1998;800(2):260–8.
50. Caille S, Espejo EF, Koob GF, Stinus L. Dorsal and median raphe
serotonergic system lesion does not alter the opiate withdrawal syn-
drome. Pharmacol Biochem Behav 2002;72(4):979–86.
51. Alper KR, Lotsof HS. The use of ibogaine in the treatment of addic-
tions. In: Winkelman M, Roberts T, editors. Psychedelic medicine.
Westport, CT: Praeger ⁄Greenwood Publishing Group, 2007;43–66.
52. Cantero JL, Atienza M, Stickgold R, Kahana MJ, Madsen JR, Kocsis
B. Sleep-dependent theta oscillations in the human hippocampus and
neocortex. J Neurosci 2003;23(34):10897–903.
53. Popik P. Facilitation of memory retrieval by the ‘‘anti-addictive’’ alka-
loid, ibogaine. Life Sci 1996;59(24):PL379–85.
54. Helsley S, Fiorella D, Rabin RA, Winter JC. Effects of ibogaine on
performance in the 8-arm radial maze. Pharmacol Biochem Behav
55. Depoortere H. Neocortical rhythmic slow activity during wakefulness
and paradoxical sleep in rats. Neuropsychobiology 1987;18(3):160–8.
56. Schneider JA, Sigg EB. Neuropharmacological studies on ibogaine, an
indole alkaloid with central-stimulant properties. Ann N Y Acad Sci
57. Leung LS. Generation of theta and gamma rhythms in the hippocam-
pus. Neurosci Biobehav Rev 1998;22(2):275–90.
58. Popik P, Skolnick P. Pharmacology of ibogaine and ibogaine-related
alkaloids. Alkaloids Chem Biol 1998;52:197–231.
59. Skolnick P. Ibogaine as a glutamate antagonist: relevance to its puta-
tive antiaddictive properties. Alkaloids Chem Biol 2001;56:55–62.
60. Pace CJ, Glick SD, Maisonneuve IM, He LW, Jokiel PA, Kuehne ME,
et al. Novel iboga alkaloid congeners block nicotinic receptors and
reduce drug self-administration. Eur J Pharmacol 2004;492(2–3):
61. Taraschenko OD, Panchal V, Maisonneuve IM, Glick SD. Is antago-
nism of a3b4 nicotinic receptors a strategy to reduce morphine depen-
dence? Eur J Pharmacol 2005;513(3):207–18.
62. Glick SD, Maisonneuve IM, Kitchen BA, Fleck MW. Antagonism of
a3b4 nicotinic receptors as a strategy to reduce opioid and stimulant
self-administration. Eur J Pharmacol 2002;438(1–2):99–105.
63. Fryer JD, Lukas RJ. Noncompetitive functional inhibition at diverse,
human nicotinic acetylcholine receptor subtypes by bupropion, phen-
cyclidine, and ibogaine. J Pharmacol Exp Ther 1999;288(1):88–92.
64. Glick SD, Maisonneuve IM, Kitchen BA. Modulation of nicotine self-
administration in rats by combination therapy with agents blocking
alpha 3 beta 4 nicotinic receptors. Eur J Pharmacol 2002;448(2–
65. Mash DC, Kovera CA, Buck BE, Norenberg MD, Shapshak P, Hearn
WL, et al. Medication development of ibogaine as a pharmacotherapy
for drug dependence. Ann N Y Acad Sci 1998;844:274–92.
66. Deborah Mash v. NDA International, Inc., Case Number: 96-3712,
CIV Moreno. United States District Court, District of Southern Florida,
Miami Division; 1997; Ammended Complaint.
67. Alper KR, Beal D, Kaplan CD. A contemporary history of ibogaine in
the United States and Europe. Alkaloids Chem Biol 2001;56:249–81.
68. Alper KR, Glick SD, Cordell GA, editors. Ibogaine: Proceedings of the
First International Conference (also published as The Alkaloids Chem-
istry and Biology Vol. 56). San Diego, CA: Academic Press, 2001.
69. Marker EK, Stajic M. Ibogaine related fatality. 40th meeting of The
International Association of Forensic Toxicologists (TIAFT), 2002 Oral
presentation No. 59, August 30; Paris, France. 2002.
e V, Mathieu O, Mathieu-Daud JC, Vainauskas P, Cas-
per T, Baccino E, et al. Distribution of ibogaine and noribogaine in a
man following a poisoning involving root bark of the Tabernanthe ib-
oga shrub. J Anal Toxicol 2006;30(7):434–40.
e V, Larroque M, Briedis V, Margout D, Bressolle F.
Quantitation of ibogaine and 12-hydroxyibogamine in human plasma
by liquid chromatography with fluorimetric detection. J Chromatogr B
Analyt Technol Biomed Life Sci 2005;822(1–2):285–93.
72. Gallagher CA, Hough LB, Keefner SM, Seyed-Mozaffari A, Archer S,
Glick SD. Identification and quantification of the indole alkaloid ibog-
aine in biological samples by gas chromatography-mass spectrometry.
Biochem Pharmacol 1995;49(1):73–9.
73. Alburges ME, Foltz RL, Moody DE. Determination of ibogaine and
12-hydroxy-ibogamine in plasma by gas chromatography-positive ion
chemical ionization-mass spectrometry. J Anal Toxicol 1995;19(6):
74. Hearn WL, Pablo J, Hime GW, Mash DC. Identification and quantita-
tion of ibogaine and an o-demethylated metabolite in brain and biologi-
cal fluids using gas chromatography-mass spectrometry. J Anal
75. Beyer J, Drummer OH, Maurer HH. Analysis of toxic alkaloids in
body samples. Forensic Sci Int 2009;185(1–3):1–9.
76. Ley FR, Jeffcoat AR, Thomas BF. Determination of ibogaine in
plasma by gas chromatography—chemical ionization mass spectrome-
try. J Chromatogr A 1996;723(1):101–9.
e V, Breton H, Barnay F, Mathieu-Daud JC, Bressolle
FMM. Liquid chromatography-electrospray mass spectrometry determi-
nation of ibogaine and 12-hydroxy-ibogamine in human urine. Chroma-
e V, Breton H, Mathieu O, Mathieu-Daud JC, Bressolle
FM. Liquid chromatography-electrospray mass spectrometry determina-
tion of ibogaine and noribogaine in human plasma and whole blood.
Application to a poisoning involving Tabernanthe iboga root. J Chro-
matogr B Analyt Technol Biomed Life Sci 2006;843(2):131–41.
79. Lepine F, Milot S, Zamir L, Morel R. Liquid chromatographic ⁄mass
spectrometric determination of biologically active alkaloids in extracts
of Peschiera fuschiaefolia. J Mass Spectrom 2002;37(2):216–22.
80. Bogusz MJ, Maier RD, Kruger KD, Kohls U. Determination of com-
mon drugs of abuse in body fluids using one isolation procedure and
liquid chromatography—atmospheric-pressure chemical-ionization mass
spectromery. J Anal Toxicol 1998;22(7):549–58.
81. Bjçrnstad K, Beck O, Helander A. A multi-component LC-MS⁄MS
method for detection of ten plant-derived psychoactive substances in
urine. J Chromatogr B Analyt Technol Biomed Life Sci 2009;877(11–
82. Chze M, Lenoan A, Deveaux M, Ppin G. Determination of ibogaine
and noribogaine in biological fluids and hair by LC-MS ⁄MS after Tab-
ernanthe iboga abuse Iboga alkaloids distribution in a drowning death
case. Forensic Sci Int 2008;176(1):58–66.
410 JOURNAL OF FORENSIC SCIENCES
83. Bjçrnstad K, Hultn P, Beck O, Helander A. Bioanalytical and clinical
evaluation of 103 suspected cases of intoxications with psychoactive
plant materials. Clin Toxicol (Phila) 2009;47(6):566–72.
84. Alper KR, Cordell GA. A note concerning the numbering of the iboga
alkaloids. In: Alper KR, Glick SD, Cordell GA, editors. Ibogaine: Pro-
ceedings of the First International Conference (also published as The
Alkaloids Chemistry and Biology Vol. 56). San Diego: Academic
85. Adams VI, Flomenbaum MA, Hirsch CS. Trauma and disease. In:
Spitz WU, editor. Spitz and Fisher’s medicolegal investigation of
death. Springfield, IL: Charles C Thomas, 2006;436–59.
86. Adelson L. The pathology of homicide. Springfield, IL: Charles C
87. MPI Research. Re-evaluation of repeat dose oral toxicity study of ibog-
aine HCl in dogs: Pathology peer review of Southern Research Study
B06-TXD-5. MPI Research Identification: 693-085. NIDA Ibogaine
Drug Master File Volume 13. Bethesda, MD: National Institute on
Drug Abuse (NIDA), 1996;686–707.
88. Kamlet J. Safety issues and cardiac side-effects in the administration
of ibogaine HCl. International Drug Policy Reform Conference, Albu-
querque, New Mexico, November 14, 2009, [Video] http://vimeo.com/
7843758 (accessed November 25, 2011).
89. van Noord C, Eijgelsheim M, Stricker BHC. Drug- and non-drug-asso-
ciated QT interval prolongation. Br J Clin Pharmacol 2010;70(1):16–
90. Kannankeril P, Roden DM, Darbar D. Drug-induced long QT syn-
drome. Pharmacol Rev 2010;62(4):760–81.
91. Mah SJ, Tang Y, Liauw PE, Nagel JE, Schneider AS. Ibogaine acts at
the nicotinic acetylcholine receptor to inhibit catecholamine release.
Brain Res 1998;797(1):173–80.
92. Schneider AS, Nagel JE, Mah SJ. Ibogaine selectively inhibits nicotinic
receptor-mediated catecholamine release. Eur J Pharmacol 1996;317(2–
93. Gullo F, Ales E, Rosati B, Lecchi M, Masi A, Guasti L, et al. ERG
K+ channel blockade enhances firing and epinephrine secretion in rat
chromaffin cells: the missing link to LQT2-related sudden death?
FASEB J 2003;17(2):330–2.
94. Kovar M, Koenig X, Mike , Cervenka R, Lukcs P, Todt H, et al.
The anti-addictive drug ibogaine modulates voltage-gated ion channels
and may trigger cardiac arrhythmias. BMC Pharmacol 2011;11(Suppl.
95. Deecher DC, Teitler M, Soderlund DM, Bornmann WG, Kuehne ME,
Glick SD. Mechanisms of action of ibogaine and harmaline congeners
based on radioligand binding studies. Brain Res 1992;571(2):242–7.
96. Sweetnam PM, Lancaster J, Snowman A, Collins JL, Perschke S, Bau-
er C, et al. Receptor binding profile suggests multiple mechanisms of
action are responsible for ibogaine’s putative anti-addictive activity.
Psychopharmacology (Berl) 1995;118(4):369–76.
97. Lu HR, Rohrbacher J, Vlaminckx E, Van Ammel K, Yan GX, Gallach-
er DJ. Predicting drug-induced slowing of conduction and pro-arrhyth-
mia: identifying the ‘bad’sodium current blockers. Br J Pharmacol
98. Lim KS, Jang IJ, Kim BH, Kim J, Jeon JY, Tae YM, et al. Changes in
the QTc interval after administration of flecainide acetate, with and
without coadministered paroxetine, in relation to cytochrome P450
2D6 genotype: data from an open-label, two-period, single-sequence
crossover study in healthy Korean male subjects. Clin Ther
99. Antzelevitch C. Ionic, molecular, and cellular bases of QT-interval pro-
longation and torsade de pointes. Europace 2007;9(Suppl. 4):4–15.
100. Kuhlkamp V, Mewis C, Bosch R, Seipel L. Delayed sodium channel
inactivation mimics long QT syndrome 3. J Cardiovasc Pharmacol
101. Wu L, Guo DL, Li H, Hackett J, Yan GX, Jiao Z, et al. Role of late
sodium current in modulating the proarrhythmic and antiarrhythmic
effects of quinidine. Heart Rhythm 2008;5(12):1726–34.
102. Roden DM. Keep the QT interval: it is a reliable predictor of ventricu-
lar arrhythmias. Heart Rhythm 2008;5(8):1213–5.
103. Hondeghem LM. QT prolongation is an unreliable predictor of ventric-
ular arrhythmia. Heart Rhythm 2008;5(8):1210–2.
104. Farkas AS, Nattel S. Minimizing repolarization-related proarrhythmic risk
in drug development and clinical practice. Drugs 2010;70(5):573–603.
105. Mash DC, Allen-Ferdinand K, Mayor M, Kovera CA, Ayafor JF, Wil-
liams IC, et al. Ibogaine: clinical observations of safety after single
oral dose administrations. In: Harris LS, editor. Problems of Drug
Dependence, 1998: Proceedings of the 60th Annual Scientific Meeting,
The College on Problems of Drug Dependence Inc.; 1998 June 12–17;
Scottsdale, AZ. NIDA Research Monograph 179. Bethesda, MD:
National Institute on Drug Abuse, 1998;294.
106. Samorini G. The initiation rite in the Bwiti religion (Ndea Narizanga
Sect, Gabon). Jahrbuch fr Ethnomedizin und Bewusstseinsforschung
107. Binienda ZK, Pereira F, Alper K, Slikker W Jr, Ali SF. Adaptation to
repeated cocaine administration in rats. Ann N Y Acad Sci
108. Schneider JA, Rinehart RK. Analysis of the cardiovascular action of
ibogaine hydrochloride. Arch Int Pharmacodyn Ther 1957;110(1):92–
109. Takimoto Y, Yoshiuchi K, Kumano H, Yamanaka G, Sasaki T, Suema-
tsu H, et al. QT interval and QT dispersion in eating disorders. Psycho-
ther Psychosom 2004;73(5):324–8.
110. Pacini M, Maremmani AGJ, Dell’Osso L, Maremmani I. Opioid treat-
ment and ‘‘long-QT syndrome (LQTS)’’: a critical review of the litera-
ture. Heroin Addict Relat Clin Probl 2009;11(4):21–8.
111. Aasebø W, Erikssen J, Jonsbu J, Stavem K. ECG changes in patients
with acute ethanol intoxication. Scand Cardiovasc J 2007;41(2):79–84.
112. Hoffman RS. Treatment of patients with cocaine-induced arrhythmias:
bringing the bench to the bedside. Br J Clin Pharmacol
113. Otero-Anton E, Gonzalez-Quintela A, Saborido J, Torre JA, Virgos A,
Barrio E. Prolongation of the QTc interval during alcohol withdrawal
syndrome. Acta Cardiol 1997;52(3):285–94.
114. Cuculi F, Kobza R, Ehmann T, Erne P. ECG changes amongst patients
with alcohol withdrawal seizures and delirium tremens. Swiss Med
115. Levin KH, Copersino ML, Epstein D, Boyd SJ, Gorelick DA. Longitu-
dinal ECG changes in cocaine users during extended abstinence. Drug
Alcohol Depend 2008;95(1–2):160–3.
116. Kino M, Imamitchi H, Morigutchi M, Kawamura K, Takatsu T. Car-
diovascular status in asymptomatic alcoholics, with reference to the
level of ethanol-consumption. Br Heart J 1981;46(5):545–51.
117. Brotherstone R, Blackhall B, McLellan A. Lengthening of corrected
QT during epileptic seizures. Epilepsia 2010;51(2):221–32.
118. Hoelen DW, Spiering W, Valk GD. Long-QT syndrome induced by
the antiaddiction drug ibogaine. N Engl J Med 2009;360(3):308–9.
119. Hough LB, Pearl SM, Glick SD. Tissue distribution of ibogaine after
intraperitoneal and subcutaneous administration. Life Sci
120. Vincent D, Lagreu R. Sur la cholinestrase du pancras. tude de son
comportement en prsence d’inhibiteurs (ibogane, cafine, srine)
comparativement avec les cholinesterases du srum et du cerveau. [On
pancreatic cholinesterase. Comparative study of its behavior in the
presence of inhibitors (ibogaine, caffeine and physostigmine) with
brain and serum cholinesterases]. Bulletin De La Societe De Chimie
121. Vincent D, Sero I. Action inhibitrice de Tabernanthe iboga sur la chol-
inestrase du srum (Inhibitory effect of Tabernanthe iboga on serum
cholinesterase). C R Seances Soc Biol Fil 1942;136:612–4.
122. Alper K, Reith MEA, Sershen H. Ibogaine and the inhibition of acetyl-
cholinesterase. J Ethnopharmacol 2012; in press. doi: 10.1016/j.jep.
123. Kolecki PF, Curry SC. Poisoning by sodium channel blocking agents.
Crit Care Clin 1997;13(4):829–48.
124. Torbicki A, van Beek EJR, Charbonnier B, Meyer G, Morpurgo M,
Palla A, et al. Guidelines on diagnosis and management of acute pul-
monary embolism. Eur Heart J 2000;21(16):1301–36.
125. Mandelli V, Schmid C, Zogno C, Morpurgo M. ‘‘False negatives’’ and
‘‘false positives’’ in acute pulmonary embolism: a clinical-postmortem
comparison. Cardiologia 1997;42(2):205–10.
126. Ely SE, Gill JR. Fatal pulmonary thromboembolism and hereditary
thrombophilias. J Forensic Sci 2005;50(2):411–8.
127. Chandra D, Parisini E, Mozaffarian D. Meta-analysis: travel and
risk for venous thromboembolism. Ann Intern Med 2009;151(3):
128. Pottier P, Hardouin JB, Lejeune S, Jolliet P, Gillet B, Planchon B.
Immobilization and the risk of venous thromboembolism. A meta-anal-
ysis on epidemiological studies. Thromb Res 2009;124(4):468–76.
129. McColl MD, Tait RC, Greer IA, Walker ID. Injecting drug use is a
risk factor for deep vein thrombosis in women in Glasgow. Br J Hae-
130. Cooke VA, Fletcher AK. Deep vein thrombosis among injecting drug
users in Sheffield. Emerg Med J 2006;23(10):777–9.
ALPER ET AL. •FATALITIES TEMPORALLY ASSOCIATED WITH THE INGESTION OF IBOGAINE 411
131. Syed FF, Beeching NJ. Lower-limb deep-vein thrombosis in a general
hospital: risk factors, outcomes and the contribution of intravenous
drug use. QJM 2005;98(2):139–45.
132. Masoomi M, Ramezani MA, Shahriari S, Shahesmaeeli A, Mirzaeepour
F. Is opium addiction a risk factor for deep vein thrombosis? A case-
control study. Blood Coagul Fibrinolysis 2010;21(2):109–12.
133. Bowen WD. Sigma receptors and iboga alkaloids. Alkaloids Chem
134. O’Hearn E, Molliver ME. The olivocerebellar projection mediates ib-
ogaine-induced degeneration of Purkinje cells: a model of indirect,
trans-synaptic excitotoxicity. J Neurosci 1997;17(22):8828–41.
135. O’Hearn E, Molliver ME. Degeneration of Purkinje cells in parasagittal
zones of the cerebellar vermis after treatment with ibogaine or harma-
line. Neuroscience 1993;55(2):303–10.
136. Scallet AC, Ye X, Rountree R, Nony P, Ali SF. Ibogaine produces
neurodegeneration in rat, but not mouse, cerebellum. Neurohistological
biomarkers of Purkinje cell loss. Ann N Y Acad Sci 1996;801:217–26.
137. Molinari HH, Maisonneuve IM, Glick SD. Ibogaine neurotoxicity: a
re-evaluation. Brain Res 1996;737(1–2):255–62.
138. Harvey AS, Jayakar P, Duchowny M, Resnick T, Prats A, Altman N,
et al. Hemifacial seizures and cerebellar ganglioglioma: an epilepsy
syndrome of infancy with seizures of cerebellar origin. Ann Neurol
139. Vanburen JM, Wood JH, Oakley J, Hambrecht F. Preliminary evalu-
ation of cerebellar stimulation by double-blind stimulation and bio-
logical criteria in treatment of epilepsy. J Neurosurg 1978;48(3):
140. Geter-Douglass B, Witkin JM. Behavioral effects and anticonvulsant
efficacies of low-affinity, uncompetitive NMDA antagonists in mice.
Psychopharmacology (Berl) 1999;146(3):280–9.
141. Chen K, Kokate TG, Donevan SD, Carroll FI, Rogawski MA. Ibogaine
block of the NMDA receptor: in vitro and in vivo studies. Neurophar-
142. Leal MB, de Souza DO, Elisabetsky E. Long-lasting ibogaine protec-
tion against NMDA-induced convulsions in mice. Neurochem Res
143. Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med
144. Jenkins AJ, Keenan RM, Henningfield JE, Cone EJ. Pharmacokinetics
and pharmacodynamics of smoked heroin. J Anal Toxicol
145. Strang J, Griffiths P, Gossop M. Heroin smoking by ‘chasing the dra-
gon’: origins and history. Addiction 1997;92(6):673–83.
146. Szumlinski KK, Maisonneuve IM, Glick SD. Differential effects of ib-
ogaine on behavioural and dopamine sensitization to cocaine. Eur J
147. Brdvik L, Berglund M, Frank A, Lindgren A, Lçwenhielm P. Number
of addictive substances used related to increased risk of unnatural
death: a combined medico-legal and case-record study. BMC Psychia-
148. Darke S, Sunjic S, Zador D, Prolov T. A comparison of blood toxicol-
ogy of heroin-related deaths and current heroin users in Sydney, Aus-
tralia. Drug Alcohol Depend 1997;47(1):45–53.
149. Darke S, Kaye S, Duflou J. Systemic disease among cases of fatal opi-
oid toxicity. Addiction 2006;101(9):1299–305.
150. Knuepfer MM. Cardiovascular disorders associated with cocaine use:
myths and truths. Pharmacol Ther 2003;97(3):181–222.
151. Kaye S, McKetin R, Duflou J, Darke S. Methamphetamine and cardio-
vascular pathology: a review of the evidence. Addiction
152. Obach RS, Pablo J, Mash DC. Cytochrome P4502D6 catalyzes the O-
demethylation of the psychoactive alkaloid ibogaine to 12-hydroxyi-
bogamine. Drug Metab Dispos 1998;26(8):764–8.
153. Miksys S, Rao Y, Hoffmann E, Mash DC, Tyndale RF. Regional and
cellular expression of CYP2D6 in human brain: higher levels in alco-
holics. J Neurochem 2002;82(6):1376–87.
154. Pelissier-Alicot AL, Gaulier JM, Champsaur P, Marquet P. Mecha-
nisms underlying postmortem redistribution of drugs: a review. J Anal
155. Moriya F, Hashimoto Y. Redistribution of basic drugs into cardiac
blood from surrounding tissues during early-stages postmortem. J
Forensic Sci 1999;44(1):10–6.
156. Southern Research Institute. Acute oral toxicity study of ibogaine HCI
in rats. Southern Research Study B06-TXR-6. Ibogaine Drug Master
File Volume 4. Bethesda, MD: National Institute on Drug Abuse
157. Jenks CW. Extraction studies of Tabernanthe iboga and Voacanga
africana. Nat Prod Lett 2002;16(1):71–6.
e V, Mathieu O, Balas L, Escale R, Blayac JP, Bressolle
FMM. Ibogaine and noribogaine: structural analysis and stability stud-
ies. Use of LC-MS to determine alkaloid contents of the root bark of
Tabernanthe iboga. J Liq Chromatogr Relat Technol 2007;30:1077–92.
159. Dickel DF, Holden CL, Maxfield RC, Paszek LE, Taylor WI. The
alkaloids of Tabernanthe iboga. Part III. Isolation studies. J Am Chem
160. Gill JR, Hayes JA, DeSouza IS, Marker E, Stajic M. Ecstasy (MDMA)
deaths in New York City: a case series and review of the literature. J
Forensic Sci 2002;47(1):121–6.
161. Lotsof HS, Wachtel B. Manual for ibogaine therapy screening, safety,
monitoring and aftercare, Second Revision, 2003, [Downloadable PDF]
http://www.ibogaine.desk.nl/manual.html (accessed November 25,
Additional information and reprint requests:
Kenneth R. Alper, M.D.
Associate Professor of Psychiatry and Neurology
New York University School of Medicine
Brain Research Laboratories
8th Floor Old Bellevue Administration Building
462 First Avenue
New York, NY 10016
412 JOURNAL OF FORENSIC SCIENCES