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From: firstname.lastname@example.org (Ibog)
Subject: Ibogaine FAQ
Date: 20 Apr 1995 18:36:54 -0400
Ibogaine is not a substitute for narcotics or stimulants, is not
addicting and is given in a single administration modality (SAM). It is a
chemical dependence interrupter. Retreatment may occasionally be needed
until the person being treated with Ibogaine is able to extinguish certain
conditioned responses related to drugs they abuse. Early data suggests
that a period of approximately two years of intermittent treatments may be
required to attain the goal of long-term abstinence from narcotics and
stimulants for many patients. The majority of patients treated with
Ibogaine remain free from chemical dependence for a period of three to
six months after a single dose. Approximately ten percent of patients
treated with Ibogaine remain free of chemical dependence for two or more
years from a single treatment and an equal percentage return to drug
use within two weeks after treatment. Multiple administrations of Ibogaine
over a period of time are generally more effective in extending periods of
A BRIEF HISTORY
Ibogaine, a naturally occurring alkaloid found in Tabernanthe iboga and
other plant species of Central West Africa, was first reported to be
effective in interrupting opiate narcotic dependence disorders in U.S.
patent 4,499,096 (Lotsof, 1985); cocaine dependence disorders in U.S.
patent 4.587,243 (Lotsof, 1986) and poly-drug dependence disorders in
U.S. patent 5,152,994 (Lotsof, 1992). The initial studies demonstrating
Ibogaine's effects on cocaine and heroin dependence were accomplished in a
series of focus group experiments by H. S. Lotsof in 1962 and 1963.
Additional data on the clinical aspects of Ibogaine in the treatment of
chemical dependence were reported by Kaplan (1993), Sisko (1993),
Sanchez-Ramos & Mash (1994), and Sheppard (1994).
Prior to Ibogaine's evaluation for the interruption of various chemical
dependencies, the use of Ibogaine was reported in psychotherapy by Naranjo
(1969, 1973) and at the First International Ibogaine Conference held in
Paris (Zeff, 1987). The use of Ibogaine-containing plants has been
reported for centuries in West Africa in both religious practice and in
traditional medicine (Fernandez, 1982; Gollnhofer & Sillans 1983, 1985)
An overview of the history of Ibogaine research and use was published by
Goutarel et al. (1993).
Claims of efficacy in treating dependencies to opiates, cocaine, and
alcohol in human subjects were supported in preclinical studies by
researchers in the United States, the Netherlands and Canada. Dzoljic et
al. (1988) were the first researchers to publish Ibogaine's ability to
attenuate narcotic withdrawal. Stanley D. Glick et al. (1992) at Albany
Medical College published original research and a review of the field
concerning the attenuation of narcotic withdrawal. Maisonneuve et al.
(1991) determined the pharmacological interactions between Ibogaine and
morphine, and Glick et al. (1992) reported Ibogaine's ability to reduce
or interrupt morphine self-administration in the rat. Woods et al. (1990)
found that Ibogaine did not act as an opiate, and Aceto et al. (1991)
established that Ibogaine did not precipitate withdrawal signs or cause
Cappendijk and Dzoljic (1993) published Ibogaine's effect in reducing
cocaine self-administration in the rat. Broderick et al. (1992) first
published Ibogaine's ability to reverse cocaine-induced dopamine
increases and later, on Ibogaine's reduction of cocaine-induced motor
activity and other effects (1994). Broderick et al.'s research supported
the findings of Sershen et al. (1992), that Ibogaine reduced
cocaine-induced motor stimulation in the mouse. Sershen (1993) also
demonstrated that Ibogaine reduced the consumption of cocaine in mice.
Glick (1992) and Cappendijk (1993) discovered in the animal model that
multiple administrations of Ibogaine over time were more effective than a
single dose in interrupting or attenuating the self-administration of
morphine and cocaine, supporting Lotsof's findings in human subjects
Popik et al. (1994) determined Ibogaine to be a competitive inhibitor of
MK-801 binding to the NMDA receptor complex. MK-801 has been shown to
attenuate tolerance to opiates (Trujillo & Akil 1991) and alcohol (Khanna
et al. 1993). MK-801 has also shown a blockade of "reverse tolerance" of
stimulants (Karler et al. 1989). Ibogaine's effects on dopamine, a
substance hypothesized to be responsible for reinforcing pleasurable
effects of drugs of abuse, and the dopamine system were found by
Maisonneuve et al. (1991), Broderick et al. (1992) and Sershen et al.
(1992). Ibogaine binding to the kappa opiate receptor was reported by
Deecher et al. (1992). Thus we begin to see a broad spectrum of
mechanisms by which Ibogaine may moderate use of substances so diverse as
opiate narcotics, stimulants and alcohol.
Ibogaine is currently under review by the National Institute on Drug
Abuse. On March 8, 1995 an Ibogaine Review meeting was held to determine
if the Medications Development Division of NIDA would proceed to
multi-site clinical studies. That decision is now being awaited.
The FDA has already approved one human Ibogaine research project and is
considering changes that may allow the research to move more quickly.
Additionally the National Institute on Drug Abuse may proceed to
multi-site human studies to determine if Ibogaine is effective in treating
cocaine dependency. The ministry of Health in the Republic of Panama has
approved experimental Ibogaine treatments at therapeuic doses which puts
it about two years head of the United States. Researchers in Israel and
Turkey are also considering human trials for opiates and alcoholism.
Ibogaine is not an LSD-like drug and appears according to early reports
to be effective in the treatment of various forms of chemical dependence
including opiates, stimulants, alcohol, nicotine or combinations of the
above. The real surprise seemed to come when prelimiary treatment of
methadone dependent persons also appeared to be effective in the same two
to four day Lotsof procedure for the treatment of addiction. The
substance has a psycho/pharmacological effects including both Freudian and
Jungian perceptions in addition to its ability to diminish narcotic
Ibogaine's actions breaks down into three component parts. The first
is a four to six hour period emulating dreaming in which either visual
presentations or thoughts dealing with past events are experienced. The
second is a cognitive or intellectual period in which those experiences
are evaluated and the third is a period of residual stimulation eventually
resulting in sleep. It is after the patient awakes that the effects are
principally noticed in a lack of a desire in the majority of patients to
seek or use the drugs they were abusing. However, it should be noted that
the responses to the drug are very individual just as the patient has
AND THE TREATMENT OF SUBSTANCE-RELATED DISORDERS
Barbara E. Judd, CSW
The Eighth International Conference on Drug Related Harm
November 19, 1994
I have been working with chemically dependent patients, some having dual
diagnoses, for twelve years in outpatient settings. My observations have
been that the earliest phase of recovery, the first ninety days, is the
most difficult for the therapist and the patient. I would like to compare
and contrast certain issues seen as obstacles by patients, some of whom
were treated with the Lotsof method and some treated in traditional
My observations are based on a small sample of patients seen in the U.S.
and overseas. These observations are inconclusive and my work is ongoing.
My involvement with Ibogaine began in June 1993, when I was approached by
the International Coalition for Addict Self-Help (ICASH) and requested to
provide aftercare for five patients who were treated with Ibogaine and
were eager to share their experience and struggles. Four of the group
were white males ranging in age from early thirties to mid forties. One
was a female in her thirties. Their dependencies were to heroin,
Methadone and/or cocaine. Additional substance use included marijuana,
alcohol and psychedelics. This group met once a week for the duration of
Concurrent treatment was provided to one member of this group on an
individual basis. This patient, who we will refer to as "M" is still
presently under my care. "M" is thirty-three years old and formally
heroin/methadone/cocaine dependent. He has been using drugs since the age
My most recent involvement with Ibogaine has been with NDA International,
Inc. when I participated in the treatment of three patients using the
Lotsof method in Panama. All three patients were white males in the
thirty to forty age range. Two of the patient's major drug of choice was
cocaine which was taken, orally, nasally or by IV injection by one
patient; the other by oral or nasal administration only. The third
patient was heroin/cocaine dependent and occasionally used methadone in
attempts to curb his habit. All patients had used drugs from six to
One of the most difficult aspects of treatment is getting the patient to
enter treatment. The three major obstacles are the fear of
detoxification, lack of insight, and the inability of patients to control
their urges to use drugs. These are the areas where I have observed the
benefits of Ibogaine treatment versus traditional methods.
Fear of Detoxification
Across the board, addicts who enter outpatient treatment programs report
that their fear of detoxing from drugs has prevented them from attending
treatment. Although withdrawal from cocaine is not as severe or obvious
as that from opiate narcotics, there is a fear of the psychological pain
of never being able to use again. There is also a dread that once drug
free, feelings that have been blocked by self-medicating will surface and
be too overwhelming for the patient to handle.
Most heroin addicts are petrified of withdrawal symptoms and are afraid
of hospital detoxification. Outpatient clients have stated to me that
they have delayed treatment to avoid this anticipated discomfort.
My observations with Ibogaine treated patients have been that patients
are eager to be treated when they know that Ibogaine promises to eliminate
painful withdrawal, takes one administration with up to seventy-two hours
of supervised care, and promises to interrupt their urges to use drugs.
Three patients: Panama
Patient "1" had used approximately $100 each per day of heroin and
cocaine by IV administration for twenty of the thirty days prior to
Patient "2", prior to treatment was using $80 per day of cocaine and
Patient "3" was using $50 of cocaine on a daily basis via IV injection
and smoking. He had previously been heroin dependent.
I observed during treatment with the Lotsof method, all of the three
patients treated appeared calm and comfortable and exhibited no signs of
withdrawal. This is significant considering the extent of the level of
their drug use prior to treatment with Ibogaine.
For these patients to have had little discomfort during withdrawal,
speaks to the importance of the use of Ibogaine in the beginning of the
recovery process. As patient "M" had stated, "Ibogaine is a much more
humane and dignified approach to detox".
Obstacles Within Traditional Treatment
Returning to the obstacles of treatment, the second being the patients'
insight. Insight is necessary for patients to be able to focus and
develop goals while in recovery.
Patients in traditional outpatient groups who have less than ninety days
clean, spend more time struggling with their urges to use and dealing with
their defenses, specifically denial. They do develop insight into their
problems, however, it takes at least one year of group treatment meetings
one or two times a week on a regular basis.
In contrast, my involvement with providing aftercare for the Ibogaine
treated group showed these patients as having tremendous insight into
their own issues, their feelings, and what might have caused them to use
in the first place.
After their Ibogaine treatment, patients began to see their drug use as
destructive. This realization, coupled with psychotherapy, has allowed
these patients to work on how to stay clean and to focus on what they must
do to maintain a less destructive lifestyle.
The reason for this insight developed by these patients appears to be the
release of repressed material during the visualization stage of Ibogaine
treatment. This material includes both images and racing thoughts, which
somehow get processed to allow patients to have a better understanding of
their emotional histories.
The urge to use drugs again, is the highest cause for people to drop out
of traditional treatment. Relapse, I think, is clearly inherent in the
definition of substance-related disorders. In working with people treated
with or without Ibogaine, my observations have been that relapse at some
point is certain.
However, according to members in the Ibogaine group, Ibogaine had reduced
their urges to use, anywhere from two months to more than one year. This
advantage allowed these patients to get a head start in their recovery,
whereas clients in traditional outpatient treatment have a great deal of
confusion around how to control their urges. Consequently, those patients
have to learn very basic and concrete ways to stay clean as taught by
self-help meetings, and emphasized in psychotherapy. The Ibogaine
aftercare group did not appear to need self-help type assistance to reduce
their urges, but seemed to benefit well from psychotherapy.
In conclusion, there is difficulty treating the drug addicted patient,
particularly in the early stages of recovery, because of their fear of
detox, their lack of insight, and their urges to relapse.
Thus far, there is no opportunity for Ibogaine treatment within the
United States. It is my recommendation that there be future research done
with Ibogaine, so that
some of the above mentioned observations are supported by more conclusive
The prospects for a painless withdrawal method makes Ibogaine an
attractive alternative to traditional treatment methods. Because Ibogaine
interrupts substance related disorders, it gives patients a head start
in their recovery. It also increases the patients' receptiveness to
psychotherapy, which is a necessary component to the recovery process.
Brief Ibogaine Bibliography
1. Aceto MD, Bowman E, Harris LS, Dependence studies of new compounds in
the rhesus monkey, rat and mouse, NIDA Research Monograph, 95:578,607,
2. Broderick PA, Phelan FT, Berger SP, Ibogaine alters cocaine induced
biogenic amine and psychostimulant dysfunction but not [3H] GBR-12935
binding to the dopamine transporter protein, NIDA Research Monograph,
3. Broderick PA, Phelan FT, Eng F, Wechsler RT, Ibogaine Modulates Cocaine
Responses Which Are Altered Due to Environmental Habituation: In Vivo
Microvoltammetric and Behavioral Studies, Pharmacology Biochemistry and
Behavior, 49(3):711-728, 1994.
4. Cappendijk SLT, Dzoljic MR, Inhibitory effects of ibogaine on cocaine
self-administration in rats, European Journal of Pharmacology,
5. Cappendijk, SLT, Fekkes D, Dzoljic MR, The inhibitory effects of
norharman on morphine withdrawal syndrome in rats: comparison with
ibogaine, Behavioural Brain Research, 65:117-119, 1994.
6. Deecher DC, Teitler M, Soderland DM, Bornmann WG, Kuehne MR, Glick SD,
Mechanisms of action of ibogaine and harmaline congeners based on
radioligand binding studies, Brain Research, 571:242-247, 1992.
7. Depoortere H, Neocortical Rhythmic Slow Activity during Wakefulness and
Paradoxical Sleep in Rats, Neuropsychobiology, 18:160-168, 1987.
8. Dhahir HI, A Comparative Study of the Toxicity of Ibogaine and
Serotonin (Doctoral Dissertation, Indiana University) University
Microfilms International, 71-25-341, 1971.
9. Dzoljic ED, Kaplan CD, Dzoljic MR, Effects of Ibogaine on
Naloxone-Precepitated Withdrawal Syndrome in Chronic Morphine-Dependent
Rats, Archive of International Pharmacodynamics, 294:64-70, 1988.
10. Glick SD, Rossman K, Steindorf S, Maisonneuve IM, Carlson JN, Effects
and aftereffects of ibogaine on morphine self-administration in rats,
European Journal of Pharmacology, 195:341-345, 1991.
11. Glick SD, Rossman K, Rao NC, Maisonneuve IM, Carlson JN, Effects of
Ibogaine on Acute Signs of Morphine Withdrawal in Rats: Independence
from Tremor, Neuropharmacology, 31(5):497-500, 1992.
12. Glick SD, Gallagher CA, Hough LB, Rossman KL, Maisonneuve IM,
Differential effects of ibogaine pretreatment on brain levels of
morphine and (+) - amphetamine, Brain Research, 588:173-176, 1992.
13. Glick SD, Kuehne ME, Raucci J, Wilson TE, Larson E, Keller, Jr. RW,
Carlson JN, Effects of iboga alkaloids on morphine and cocaine
self-administration in rats: relationship to tremorgenic effects and
to effects on dopamine release in nucleus accumbens and striatum, Brain
Research, 657:14-22, 1994.
14a. Goutarel R, Gollnhofer O, Sillans R, Pharmacodynamics and Therapeutic
Applications of Iboga and Ibogaine, Psychedelic Monographs and Essays,
vol. 6, 1993.
14b. Goutarel R, Gollnhofer O, Sillans R, L'IBOGA CONTRE LA DEPENDENCE AUX
STUPEFIANTS. PHARMACODYNAMIE ET APPLICATIONS
PSYCHOTHERAPEAUTIQUES, Psychotropes, 3(3):63-86, 1993.
15. Harsing LG, Sershen H, Lajtha A, Evidence that ibogaine releases
dopamine from the cytoplasmic pool in isolated mouse striatum, Journal
of Neural Transmission, 96:215-225, 1994.
16. Jacobson AE, Biological Evaluation of Compounds for Their Physical
Dependence Potential and Abuse Liability. XIII. Drug Tersting Program
of the Committee on Problems of Drug Dependence, Inc., NIDA Research
Monograph, 95:563, 1990.
17. Kaplan CD, Ketzer E, de Jong J, de Vries M, Reaching a State of
Wellness: Multistage Explorations in Social Neuroscience, Social
Neuroscience Bulletin, 6(1):6-7, 1993.
18. Keefner SM, Glick SD, Ibogaine Antagonism of Morphine-Induced
Hyperactivity: Enhancement by Prior Morphine Exposure and Role of
Kappa Opioid Receptors, Society of Neuroscience Abstracts, 20:502.5,
19. Lotsof HS, U.S. patent 4,499,096; Rapid Method for Interrupting the
Narcotic Addiction Syndrome, 1985.
20. Lotsof HS, U.S. patent 4,587,243; Rapid Method for Interrupting the
Cocaine and Amphetamine Abuse Syndrome, 1986.
21. Lotsof HS, U.S. patent 4,857,523; Rapid Method for Attenuating The
Alcohol Dependency Syndrome, 1989.
22. Lotsof HS, U.S. Patent 5,026,697, Rapid Method for Interrupting or
Attenuating The Nicotine/Tobacco Dependency Syndrome., 1991.
23. Lotsof HS, U.S. patent 5,124,994; Rapid Method for Interrupting or
Attenuating Poly- drug Dependency Syndromes, 1992.
24. Lotsof HS, Ibogaine in the Treatment of Chemical Dependence
Disorders: Clinical Perspectives (A Preliminary Review), Bull. MAPS,
25. Mash DC, Douyon R, Hearn WL, Sambol NC & Sanchez-Ramos J, A
Preliminary Report on the Safety and Pharmacokinetics of Ibogaine,
Biological Psychiatry, 1995 In Press.
26. Maisonneuve IM, Keller RW, Glick SD, Interactions between ibogaine, a
potential anti- addictive agent and morphine: an in vivo microdialysis
study, European Journal of Pharmacology, 199:35-42, 1991.
27. Maisonneuve IM, Glick SD, Interactions between ibogaine and cocaine in
rats: in vivo microdialysis and motor behavior, European Journal of
Pharmacology, 212:263- 266, 1992.
28. Maisonneuve IM, Rossman KL, Keller Jr. RW, Glick SD, Acute and
prolonged effects of ibogaine on brain dopamine metabolism and
morphine-induced locomotor activity in rats, Brain Research, 574:69-73,
29. Maisonneuve IM, Keller Jr. RW, lick, SD, Interactions of ibogaine and
D-amphetamine: in vivo microdialysis and motor behavior in rats, Brain
Research, 579:87-92, 1992.
30. Molinan HH, Maisonneuve IM, Glick SD, Dose Dependence of Ibogaine
Neurotoxicity, Society for Neuroscience Abstracts, 20:504.4, 1994.
31. Naranjo C, Psychotherapeutic Possibilities New Fantasy Enhancing
Drugs, Clinical Toxicology, 2(2):209-224, 1969.
32. Naranjo C, The Healing Journey, Pantheon Books, Div. Random House, NY,
33. O'Hearn E, Long DB, Molliver MR, Ibogaine induces glial activation in
parasagittal zones of the cerebellum, Neuropharmacology and
Neurotoxicology, NeuroReport 4:299- 302, 1993.
34. O'Hearn E, Molliver ME, Degeneration of Purkinje Cells in Parasagittal
Zones of the
Cerebellar Vermis After Treatment with Ibogaine or Harmaline,
Neuroscience, 55(2):303-310, 1993.
35. Popik P, Layer RT, Skolnick P, The Putative anti-addictive drug
ibogaine is a competitive inhibitor of [3H]MK-801 binding to the NMDA
receptor complex, Psychopharmacology, 114:672-674, 1994.
36. Sanchez-Ramos J, Mash DC, Ibogaine Research Update: Phase I Human
Study, MAPS, IV(4):11, 1994.
37. Schechter MD, Gordon TL, Comparison of the behavioral effects of
ibogaine from three sources: mediation of discrimintive activity,
European Journal of Pharmacology 249:70-84, 1993.
38. Schneider JA, McArthur M, Potentiation Action of Ibogaine (Bogadin TM)
on Morphine Analgesia, Experientia, XII(8):323-324, 1956.
39. Schneider JA, Sigg EB, Neuropharmacological Studies of Ibogaine, An
Indole Alkaloid with Central Stimulant Properties, Annals New York
Academy of Sciences, 66:765-776, 1957.
40. Schneider, JA, Rinehart RK, Analysis of the Cardiovascular Action of
Ibogaine Hydrochloride, Archive of International Pharmacodynamics,
41. Sershen H, Hashim A, Harsing L, Lajtha A, Ibogaine Antagonizes Cocaine
Induced Locomotor Stimulation in Mice, Life Sciences, 50:1079-1086,
42. Sershen H, Harsing LG, Hashim A, Lajtha A, Ibogaine Reduces
Amphetamine-Induced Locomotor Stimulation C57L/6By Mice, but Stimulates
Locomotor Activity in Rats, Life Sciences, 51:10003-1011, 1992.
43. Sershen H, Hashim A, Lajtha A, Ibogaine Reduces Preference for Cocaine
Consumption in C57BL/6By Mice, Pharmacology Biochemistry and Behavior.
44. Sershen H, Hashim A, Lajtha A, Effects of Ibogaine on Serotonergic and
Dopaminergic Interactions in Striatum of Mice and Rats, Neurochemical
Research, 19(11):1463- 1465, 1994 In Press .
45. Sershen H, Hashim A, Lajtha A, The Effects of Kappa-Opioid and
5-HT3-Induced Changes in Stimulation-Evoked Dopamine Release in Vitro
from Striatum of C57BL/By Mice, Brain Research , 1994, In Press.
46. Sharpe LG, Jaffe JH, Ibogaine Fails to Reduce Naloxone-Precipitated
Withdrawal in the Morphine-Dependent Rat, Neuropharmacology and
Neurotoxicology (NeuroReport), 1:17-19, 1990.
47. Sheppard SG, A Preliminary Investigation of Ibogaine: Case Reports and
Recommendations for Further Study, Journal of Substance Abuse
Treatment, 11(4):379-385, 1994.
48. Sisko B, Interrupting Drug Dependency: A Summary of 4 Case Histories,
MAPS 4(2):15- 23, 1994.
49. Woods JH, Medzihdsky F, Smith CB, Winger GD, France CP, 1989 Annual
Report, Evaluation of New Compounds for Opioid Activity, NIDA Research
Monographs, 95:655-656, 1990.