Important information for those thinking of taking Ibogaine

March 22, 2012

With Ibogaine treatment now more available than ever before, in an ever-widening range of settings, more and more knowledge about the drug is gathering. At the time of writing, March 2007, one thing that is becoming increasingly clear is that there is a reasonable degree of risk associated with taking the drug. At least 12 people are recorded as having died in connection with taking ibogaine or other iboga substances over the last decade or so, and there is reason to believe that the number may be higher, with other deaths having occurred in non-clinical settings and without being recorded.

Here is some safety-related information about the drug:

– There is an inherent level of risk with ibogaine treatment. Twelve people are known to have died in connection with taking ibogaine or other iboga alkaloids. In actuality, the figure is likely higher, given that ibogaine is frequently administered in surroundings where people may be reluctant to contact the authorities in the event of something going wrong. Statistically, a ballpark figure for deaths during treatment is probably of the order of 1 in 300. (This is based on 12 recorded deaths having occurred within 3611 recorded treatments, outside of Africa, as of March 2007). The following factors have been identified as having caused death:

  • having a pre-existing heart condition, sometimes one not detectable by EKG
  • using opiates when on ibogaine, or shortly afterwards
  • using the rootbark or iboga extract. Ibogaine HCl is statistically much safer
  • taking ibogaine outside of a clinical facility. Persons taking ibogaine need constant supervision and, ideally, online heart monitoring

– Ibogaine is principally recognised for its ability to vastly reduce the symptoms of drug withdrawal, thus allowing addicts to detox relatively painlessly. Any other claims made for the drug, such as that it creates long-term drug-abstinence, or removes the effects of trauma or conditioning in either addicts or non-addicts, may have a degree of truth but are a great deal less substantiated.

– You must be medically tested before you take ibogaine. Proper clinical testing of heart and liver function are the absolute minimum. The site author is not aware of any reputable treatment provider who would allow you to take ibogaine without prior medical testing. Do not go with someone who does not insist on it. Ideally, you should have constant monitoring of heart function whilst on the drug, and medically-trained staff present.

– Beware of listening excessively to the advice of just one individual when deciding whether or not to take ibogaine. Ibogaine’s effects can be life-changing, and it is common for someone who has had a very positive experience to do their utmost to “spread the message,” possibly allowing their enthusiasm to override the very real concerns about safety.

– If you are thinking of taking ibogaine for personal development and haven’t yet been involved in proper therapy (therapy where there’s an open admission by the individual of the presence of emotional issues), be aware that you may be being attracted to a “quick fix” strategy that avoids really dealing with deeper issues. If this is the case, ibogaine could possibly make things worse. For some, using psychoactive substances can invoke disturbing reactions as the mind’s defences struggle to keep down rising repressed material. Drugs like ibogaine, ketamine, LSD and MDMA (Ecstasy), have been used in the past by therapists, but only as one component of an overall therapeutic strategy. Using the drug out of this context could cause more harm than good.

All the above said, ibogaine still potentially represents a major medical breaththrough, especially in the field of treating drug dependency.

Ibogaine: Complex Pharmacokinetics, Concerns for Safety, and Preliminary Efficacy Measures

March 21, 2012

(Reprinted from Neurobiological Mechanisms of Drugs of Abuse, Volume 914 of the Annals of the New York Academy of Sciences, September 2000 – Ann N Y Acad Sci 2000;914:394-401)



Departments of aNeurology, bPharmacology, and gMedicine, University of Miami School of Medicine, Miami, Florida, USA
cCentre for Addiction and Mental Health, University of Toronto, Toronto, Canada
dDepartment of Psychiatry and Human Genetics, McGill University, Montreal, Canada
eHealing Visions Institute for Addiction Recovery, Ltd., St. Kitts, West Indies
fBehavior Therapy Treatment Research Center, Johns Hopkins Medical School, Baltimore, Maryland, USA


ABSTRACT: Ibogaine is an indole alkaloid found in the roots of Tabernanthe Iboga (Apocynaceae family), a rain forest shrub that is native to western Africa. Ibogaine is used by indigenous peoples in low doses to combat fatigue, hunger and thirst, and in higher doses as a sacrament in religious rituals. Members of American and European addict self-help groups have claimed that ibogaine promotes long-term drug abstinence from addictive substances, including psychostimulants and opiates. Anecdotal reports attest that a single dose of ibogaine eliminates opiate withdrawal symptoms and reduces drug craving for extended periods of time. The purported efficacy of ibogaine for the treatment of drug dependence may be due in part to an active metabolite. The majority of ibogaine biotransformation proceeds via CYP2D6, including the O-demethylation of ibogaine to 12-hydroxyibogamine (noribogaine). Blood concentration-time effect profiles of ibogaine and noribogaine obtained for individual subjects after single oral dose administrations demonstrate complex pharmacokinetic profiles. Ibogaine has shown preliminary efficacy for opiate detoxification and for short-term stabilization of drug-dependent persons as they prepare to enter substance abuse treatment. We report here that ibogaine significantly decreased craving for cocaine and heroin during inpatient detoxification. Self-reports of depressive symptoms were also significantly lower after ibogaine treatment and at 30 days after program discharge. Because ibogaine is cleared rapidly from the blood, the beneficial aftereffects of the drug on craving and depressed mood may be related to the effects of noribogaine on the central nervous system.

hAddress for correspondence:
Deborah C. Mash, Ph.D., Department of Neurology (D4-5).
1501 N.W. 9th Avenue, Miami, Florida 33136.
Tel.: (305) 243-5888; fax: (305) 243-3649.


Ibogaine is a naturally occurring indole alkaloid derived from the roots of the rain forest shrub Tabemanthe iboga. Ibogaine is used in low doses by indigenous peoples of western Africa to combat fatigue, hunger and thirst, and in higher doses as a sacrament in religious rituals. The use of ibogaine for the treatment of drug dependence has been based on anecdotal reports from American and European addict self-help groups that it decreased the signs of opiate withdrawal and reduced drug craving for cocaine and heroin for extended time periods.1 Although ibogaine has diverse effects on the central nervous system (CNS), the pharmacological targets underlying the physiological and psychological actions of ibogaine are not completely understood. The purported efficacy of ibogaine following single-dose administrations may be due to the formation of an active metabolite.2,3 Ibogaine is O-demethylated to 12-hydroxyibogamine (noribogaine) by the activity of liver enzymes. Noribogaine appears to have a slow clearance rate in humans, suggesting that some of the aftereffects of ibogaine may be due to the actions of the metabolite.3,4

Medications for the treatment of addictions are intended to reduce or eliminate drug use, reduce harm to the patient, and/or modify high risk behaviors.5 Potential drug candidates for the treatment of cocaine and opiate dependence have been considered based on pharmacological approaches. The neurobiological similarities between depression and drug dependence have led to a self-medication hypothesis.6 Based on this association, drug abusers may self-medicate with opioids or psychostimulants in an effort to improve their dysphoric mood. Chronic drug abuse leads to adaptations at neural systems that mediate drive, motivation, and affect.7 Discontinuation of drug use leads to alterations in these motivational systems, placing more incentive value to the abused drug than to nondrug stimuli, thus leading to a loss of control over drug use.8This hypothesis is supported by clinical observation that drug dependence is characterized by an intense desire to administer the drug to the exclusion of other reinforcement. We report here that single-dose administrations of ibogaine to drug-dependent individuals resulted in fewer self-reports of craving for cocaine and opiates, and significantly improved depressive symptoms. These preliminary observations provide evidence for an improvement in clinical status following detoxification with ibogaine.


Subjects were self-referred for inpatient detoxification and met inclusion/exclusion criteria. All individuals were deemed fit and underwent treatment following a physician’s review of the history and physical examination. Participants did not have histories of stroke, epilepsy or axis I psychotic disorders. Results of the electrocardiogram and clinical laboratory testing were within predetermined limits. All subjects signed an informed consent for ibogaine treatment. Participants included 27 treatment-seeking opioid- and cocaine-dependent men (n = 23) and women (n = 4). The mean age was 34.6 +/- 1.9 years old for the opiate group and 37.5 +/- 2.9 years old for the cocaine group. Mean education level was 14.0 +/- 0.5 years. All participants met DSM-IV criteria for cocaine or opioid dependence and had positive urine screens at entry to the study. Individuals participated in a 14-day inpatient study to determine the safety and effectiveness of ibogaine as a potential medication treatment for drug dependence. Participants were assigned to one of three fixed-dose (500, 600, or 800 mg) ibogaine HCl treatments under open-label conditions. Ibogaine and 12-hydroxyibogamine (noribogaine) were measured in whole blood specimens by full-scan electron impact gas chromatography/mass spectrometry (GC/MS) as described previously.2 Subjects were genotyped for the CYP2D6 alleles (3, 4, 5, and wildtype alleles) as described previously.9

On admission, participants were administered the Addiction Severity Index10 and received structured psychiatric evaluations before and after ibogaine treatment (SCID I and II). In cases where the participant’s responses were deemed questionable due to intoxication or withdrawal signs, portions of all interviews were reconducted later, as necessary. Additional information about substance use history, as well as past and current medical condition(s), was gathered and later cross-referenced for accuracy through a separate comprehensive Psychosocial Assessment.

Participants were required to complete a series of standardized self-report instruments relating to mood and craving at three different time points during the study and at one month following discharge from the treatment program. Subjects were asked to provide ratings of their current level of craving for cocaine or opiates using questions from the Heroin (HCQN-29)11 and Cocaine (CCQN-45) Craving Questionnaires.12 Self-reported depressive symptoms were determined by the Beck Depression Inventory.13 Subjects’ scores were subjected to repeated measures analyses of variance with primary drug of abuse (opiates versus cocaine) as the between-subjects factor and treatment phase (pre-ibogaine, post-ibogaine, and discharge) as the within-subjects factor for the total score from the Beck Depression Inventory and the HCQN-29 and CCQN-45 subscales.


 illustrates representative pharmacokinetic measures of the levels of parent drug and metabolite following oral doses of ibogaine. We have demonstrated previously that ibogaine is metabolized by cytochrome P4502D6 to an active metabolite noribogaine.14 In this study, the proportion of homozygous and heterozygous CYP2D6 extensive metabolizers (EM) were not significantly different between opioid- and cocaine-dependent groups (data not shown). None of the subjects was identified as a poor metabolizer (PM) genotype. The CYP-2D6-mediated metabolism of ibogaine resulted in significant levels of noribogaine in blood for male and female subjects. Ibogaine was well tolerated by both opiate- and cocaine-dependent subjects, in agreement with our previous findings.4FIGURE 1. Pharmacokinetics of ibogaine and noribogaine over the first 24 h after oral doses of ibogaine. Data shown are from representative male (800 mg) and female (500 mg) subjects. Values for parent drug and desmethyl metabolite were measured in whole blood samples at the times indicated.

Subjects reported clinically significant levels of depressive symptoms (i.e., Beck depression score of 11 or more) at program entry.13 Opiate- and cocaine-dependent subjects did not differ significantly on the Beck depression scores. TABLE 1 summarizes the effects of ibogaine treatment on depressive symptoms following ibogaine detoxification from opiates and cocaine. The results demonstrated lower levels of self-reported depressive symptoms during inpatient ibogaine treatment. Beck depression scores were significantly lower at one month after program discharge as compared to those measured at program entry. This observation suggests a lasting effect of single-dose adminstration of ibogaine on mood and depressive symptoms.

TABLE 3 summarizes the results for selected categories from the HCNQ-29 and CCNQ-45 craving questionnaires. These instruments inquire about specific aspects of drug craving, including urges (category scale Desire to Use), as well as thoughts, about drug of choice or plans to use the drug (category scale, Intention to Use). The instruments incorporate questions about dynamics thought to be important for the reinstatement of drug-taking behavior by referencing the positive reinforcing effects of drugs or the expectation of the outcome from using a drug of choice (category scale, Anticipation of Positive Outcomes), or the alleviation of withdrawal states (category scale,Relief of Negative States). Perceived lack of control over drug use also was included (category scale, Lack of Control), because it is a common feature of substance abuse disorders and is most operative under conditions of active use, relapse, or for subjects at high risk.

Subjects undergoing opiate detoxification reported significantly decreased drug craving for all of the HCQN-29 scales at 36 h post-treatment mark, and mean scores remained significantly decreased at program discharge (TABLE 2). Subjects undergoing cocaine detoxification also reported significantly decreased drug craving at post-treatment and at discharge for three of the five category scales of the CCQN-45. Similar to the results of the HCQN-29, the lower mean scores for Intention to Use at program entry may reflect participants’ inpatient circumstances and motivation for treatment. These results demonstrate an immediate and lasting attenuation of craving while the subject remained in treatment. At one month following discharge from the program, subjects’ responses indicated that they still experienced diminished craving for cocaine and opiates (data not shown).


The results of this study revealed that levels of self-reported depressive symptoms and craving were significantly decreased following ibogaine administration. A limitation of the study is that it is based on findings in only 27 subjects; thus, replication is needed in future studies to determine the stability of the findings. Furthermore, it is not known whether the symptoms experienced in the treatment setting are unique. However, subjects were evaluated at one month after program discharge, having returned to their normal environment or following entry to residential sober living in a community setting. Future research efforts will be aimed at determining an association between CYP2D6 metabolizer status, depressive symptoms, drug craving, and relapse rates.

The concept of drug craving is believed to play a crucial role in the dynamics of relapse, although it has proven to be an elusive and difficult construct to measure. In part, this is due to its transient nature and its variable expression in addicts’ subjective reports. Tiffany and co-workers12 have suggested that many investigations involving objective measures of craving have utilized unidimensional instruments (consisting of only one or a few items) that have not been adequately tested for validity or reliability. Therefore, it has been proposed that craving might best be captured by asking sets of multidimensional questions with terms that may be more familiar to addicts and that represent distinct conceptualizations of processes that may lead to craving.12,15 To our knowledge, this study represents the first attempt to confirm ibogaine’s purported therapeutic effects on drug craving in well-characterized cohorts of opiate- or cocaine-dependent subjects.

After treatment with ibogaine, opiate-dependent subjects were less likely to anticipate positive outcomes from heroin (or other opiate) use, less likely to believe that heroin (or opiate) use would relieve withdrawal/dysphoria, and more likely to believe in their control for abstaining or stopping their drug use. Ibogaine treatment also decreased participants’ desire and intention to use heroin. Cocaine-dependent subjects were less likely to anticipate positive outcomes from cocaine use, less likely to believe that cocaine use would relieve withdrawal/dysphoria, and more likely to believe in their control in abstaining or stopping their drug use at post-ibogaine and discharge assessments than at the pre-ibogaine assessment. Treatment did not seem to affect participants’ desire to use cocaine nor their intent to use cocaine, in part because of floor effects at pre-ibogaine assessments and because of the small sample size.

Drug dependence results from distinct but interrelated neurochemical adaptations, which underlie tolerance, sensitization, and withdrawal. The apparent ability of ibogaine to alter drug-taking behavior may be due to combined actions of either the parent drug and/or its active metabolite at key pharmacological targets that modulate the activity of drug-reward circuits.16 Noribogaine is longer lasting and has a unique spectrum of neurochemical activities as compared to the parent compound. Recent studies have suggested that noribogaine’s efficacy as a full û-opioid agonist may explain ibogaine’s ability to block the acute signs of opiate withdrawal and its suppressive effects on morphine self-administration.17 Preclinical evaluation ofnoribogaine’s anti-cocaine medication effects in a rat model of cocaine self-administration demonstrated that noribogaine antagonized cocaine-induced locomotor stimulation and reinforcement.18 Since ibogaine is cleared rapidly from the blood, the extended aftereffects on drug craving, mood, and cognition may be related to the actions of metabolite noribogaine. Medication development of a slow-release formulation of noribogaine for opiates and psycho stimulants dependence deserves further consideration.


This work was supported in part by the Addiction Research Fund. We extend our appreciation to the staff of the Healing Visions Institute for Addiction Recovery, Ltd., St. Kitts, W.I. and Holistic Counseling, Inc., Miami, Florida. We thank the Centre for Addiction and Mental Health. Ms. Ewa Hoffmann provided excellent technial assistance with the performance of the genotypying for CYP2D6 alleles.


1. SHEPARD, S.G. 1994. A preliminary investigation of ibogaine: case reports and recommendations for the further study. I. Subst. Abuse Treat. 11: 379-385.

2. HEARN, W. L., I. PABLO, G. HIME & D.C. MASH. 1995. Identificaion and quantitation of ibogaine and an O-demethylated metabolite in brain and biological fluids using gas chromatography/mass spectrometry. I. Anal. Toxicol. 19: 427-434.

3. MASH, D.C., I.K. STALEY, M. BAuMANN, R.P. RoTHMAN & W.L. HEARN. 1995. Identification of a primary metabolite of ibogaine that targets serotonin transporters and elevates serotonin. Pharmacol. Lett. 57: 45-50.

4. MASH, D.C., C.A. KOVERA, B.E. BucK, M.E. NoRENBERG, P. SHAPSHAK, W.L. HEARN & J. SANCHEZ-RAMos. 1998. Medication development of ibogaine as a pharmacotherapy for drug dependence. Ann. N. Y. Acad. Sci. 844: 274-292.

5. KLEIN, M. 1998. Research issues related to development of medications for treatment of cocaine addiction. Ann. N. Y. Acad. Sci. 844: 75-91.

6. MARKOU, A., T.R. KOSTEN & G.F. KOOB. 1998. Neurobiological similarities in depression and drug dependence: a self-medication hypothesis. Neuropsychopharmacology 18(3): 136-174.

7. KOOB, G.F. & F.E. BLOOM. 1988. Cellular and molecular mechanisms of drug dependence. Science 242: 715-723.

8. MARKOU, A., F. WEISS, L.H. GOLD, S.B. CAINE, G. SCHULTEIS & G.F. KOOB. 1993. Animal models of drug craving. Psychopharmacology 1l2: 163-182.

9. HElM, M.H. & U.A. MEYER. 1990. Genotyping of poor metabolizers of debrisoquine by allele specific PCR amplification. Lancet 336: 529-532.

10. McLELLAN, A.T., H. KUSHNER, D. METZGER, R. PETERS, I. SMITH, G. GRISSOM, H. PETTINATI & M. ARTGERIOU. 1992. The fifth edition of the Addiction Severity Index. I. Subst. Abuse Treat. 9: 199-213.

11. SINGLETON, E.G. 1996. The HCQN-29: a short version of the Heroin Craving Questionnaire. Unpublished research. Available from the Clinical Pharmacology and Therapeutics Research Branch, Intramural Research Program NIDA, 55 Nathan Shock Drive, Baltimore, MD 21224, USA.

12. TIFFANY, S.T., E. SINGLETON, C.A. HAERTZEN & I.E. HENNINGFIELD. 1993. The development of a cocaine craving questionnaire. Drug Alcohol Depend. 34: 19-28.

13. BECK, A.T., C.H. WARD, M. MENDELSON, I. MOCK & I. ERBAUGH. 1961. An interview for measuring depression. Arch. Gen. Psychiatry 4: 561-571.

14. OBACH, R.S., I. PABLO & D.C. MASH. 1998. Cytochrome P4502D6 catalyzes the 0-demethylation of the psychoactive alkaloid ibogaine to 12-hydroxyibogamine. Drug Metab. Dispos. 25(12): 1359-1369.

15. CARTER, B.L. & S. TIFFANY. 1999. Meta-analysis of cue-reactivity in addiction research. Addiction 94(3): 327-340.

16. STALEY, I.K., Q. OUYANG, I. PABLO, W.L. HEARN, D.D. FLYNN, R.B. ROTHMAN, K.C. RICE & D.C. MASH. 1996. Pharmacological screen for activities of 12-hydroxyibogamine: a primary metabolite of the indole alkaloid ibogaine. Psychopharmacology 127: 10-18.

17. PABLO, I. & D.C. MASH. 1998. Noribogaine stimulates naloxone-sensitive (35S]GTPyS binding. Neuroreport 9:109-114.

18. MASH, D.C. & S. SCHENK. 1996. Preclinical screening of an ibogaine metabolite (noribogaine) on cocaine-induced hyperlocomotion and cocaine self-administration. Soc. Neurosci. Abstr. 22: 1929.

Taking the Cure – by Andy Craft

March 21, 2012


(from Black Book magazine, Spring 2000)

The government doesn’t want you to know about a rainforest shrub that cures “the great twentieth-century malaise” after one dose. But who’s really keeping Ibogaine from the people who need it?

I wake up and the bed is all wet. It’s 8am. I haven’t pissed in it and neither has she. I move and the bedclothes peel away from my sweaty body, letting in a bit of cold air. It’s freezing. She gets up and deals with the kids, who are watching TV. I can’t stand the TV in the mornings. She puts the kettle on, turning up all the rings of the stove so it will heat up the kitchen. Makes the veins stand out a bit better.

I want the relief and the warmth now. I need to smell it behind my nose and feel the heat behind my eyes now. I keep pushing the plunger and it all goes in. I wonder whether to flush it, to try to wash every last particle of smack out of the works with blood and shove it into me.

I try once and I don’t lose the vein. I don’t feel stoned, none of that comforting thickness in my throat. Just a little smacky hint. She bundles the kids off to school. I turn the TV off and she turns it back on again. I can see myself in the mirror on the mantelpiece.A week’s growth, a really stupid haircut I used to be so good-looking I can’t stand to look. I used to have some potential I don’t know where it went I used to have some prospects. I turn away from the mirror.

For this man and his problem, there is a God – in a gelatin capsule. The “magic bullet” solution to this man’s problem might be Ibogaine. Derived from Tabernanthe iboga, a plant which grows in the rainforests of Gabon and western central Africa, Ibogaine is a naturally psychoactive alkaloid which has two extraordinary properties: Firstly, for the 300 persons who have tried Ibogaine over the past decade, of those who used the drug to detox off of opiates, 99 percent reported that the drug removes almost entirely the withdrawal symptoms of addiction to all the major opiates. Approximately 10 percent of those suffering from dependencies on cocaine, alcohol, methamphetamine, and tobacco reported an interruption of chemical dependence with one treatment of Ibogaine.

The remainder needed three or four treatments over approximately a two-year period.

Ibogaine’s other property, however is profound enough to challenge the paradigm governing a good chunk of Western medical science: Ibogaine is also a powerfully psychoactive drug, inducing, at therapeutic doses, hallucinations or visions unlike any produced by LSD, psilocybin, STP, or mescaline. While under the influence of Ibogaine, the patient has an experience that can only be described as transcendental, after which the proverbial “craving monkey” is off the addict’s back for months. A second dose keeps it off, and follow-up care seems to keep it at bay. The visionary experiences for Ibogaine users are strikingly familiar, even alarming. Lives that were consistent paragons of destruction, degradation, and agony have now, after a shared experience the like of which they could not possibly have imagined, dramatically turned around.

Much has been written about Ibogaine, and the most common route taken by journalists, in the hope of rendering their story sensational, is to try to prove that the government is doing its utmost to stymie the efforts of scientists involved in Ibogaine research. Dana Beal is the man who organizes the marijuana marches down Broadway to Battery Park, and the co-author of a book called The Ibogaine Story, a confusing tome which brings in the CIA, the FBI, Hitler the Black Panthers, and the Knights Templar.

He alleges that The Establishment doesn’t like psychedelic drugs, The Establishment wants to keep the war on drugs going, and The Establishment is in bed with the pharmaceutical giants. There might be some truth in these allegations. It is true that the pharmaceutical companies have no interest in Ibogaine, since it is only used once or twice. Scott Reines, MD of Merck Research Laboratories, in his recommendation to NIDA (National Institute on Drug Abuse), said they should not proceed with human testing of Ibogaine and that the rationale for use of the drug would appear to be insufficient to justify the necessary resources.

It’s hard to find much in the way of substance or sense from conspiracy theorists. The truth, as it were, can only be approached by balancing between those who have used the cure-all, and those who would like their names to be synonymous with the cure for the great twentieth century malaise.

It is impossible to talk about Ibogaine without talking about Howard Lotsof, an erstwhile hippie who was involved with the Berkeley Free Speech Movement (and later, in the ’70s’ Rock Against Racism). From 1962-63 he was part of a focus group composed of students studying the effects of hallucinogens. Lotsof eventually got into heroin the same way that most people do, it was exciting, it felt great, and addiction was something that happened to other people. It was not until after a few months that he noticed he had a habit. As he was working his way through the usual pharmacopoeia, he was introduced to Ibogaine. He took some and emerged from a 32-hour experience noticing that not only was the physical desire to use heroin completely absent, but the psychological desire had vanished, too. The craving monkey was gone.

Lotsof is not a scientist. He graduated from NYU film school and thought he was going to be an artist, but since 1982 he has been involved in addiction research and treatment in one alternative capacity or another It was Lotsof who brought Ibogaine to the attention of NIDA. It was Lotsof who brought it to the attention of scientists like Stanley Glick, from the University of Albany, whose work testing Ibogaine on rats conclusively demonstrated efficacy in animals (Glick says that rats are very much like humans and love to self-medicate).

By 1986, Lotsof, supported by his friends and family got busy with his own Ibogaine research. He formed a company (NDA International, and because Ibogaine has been a class-one drug [in the US] since the ’60s, began flying addicts to Holland, where they were given Ibogaine in hotel rooms. All his “patients” reported similar experiences: “seeing” their lives spinning out before them like a video and the perception of an absolute reality beyond addiction and the ego. When they came out of the hallucinogenic trance, all withdrawal symptoms, and more significantly all desire for drugs, had vanished. It was during this time that three important things happened: Lotsof managed to patent the use of Ibogaine and any of its derivatives, known or unknown, to treat chemical dependence: a woman he was treating died while under the influence of the drug, thus ending the Dutch operations, and he met Dr Deborah Mash, a professor of neurology from the University of Miami.

Ultimately, all three incidents did more to hinder the development of the wonder drug than any purported government sponsored obstruction.

The death of the Dutch woman scared everybody at NIDA away from Ibogaine and tainted much of the research being done. Mark Molliver, a neuroscientist at Johns Hopkins University of Medicine, found that injecting massive doses of Ibogaine directly into the brains of rats caused damage to their nervous system. Lotsof’s total lack of academic credibility, and his association with Dana Beal and the movement to legalize marijuana, did not help. But more damaging than anything was the relationship which developed, flourished, then dramatically deteriorated between Deborah Mash and Howard Lotsof.

Dr Mash, after watching Lotsof treat people in Dutch hotel rooms, had been very impressed, even astonished. In 1992, she and Lotsof arranged a deal wherein Lotsof would supply the Ibogaine and all the research he had done, or caused to be done; while Mash’s connections at the University of Miami would supply the addicts, the expertise, and facilities to do the phase-one dose escalation studies, which had been approved by the FDA. These are studies in which humans were given tiny gradually increasing doses of Ibogaine in order to observe the exact mechanism and safety of the drug.

The deal could have been lucrative for both. Most of the money would have gone to Lotsof and most of the fame would have gone to Mash. Then the problems started.

During ’93 and ’94, Mash submitted four grants to NIDA to fund various aspects of Ibogaine research, each of which was refused. In August 1996, she submitted a grant to NIDA for $1.5 million to underwrite a team of 22 researchers. This was blocked by the peer review (a committee consisting of ten scientists appointed by NIDA to review the work upon which her application for the grant was based). She was rejected by the team with the blithe and unexplained verdict “Not For Further Consideration,” which was a damning indictment. A government that wages war on drug users via legislation like “three strikes and you’re out” is unlikely to be sympathetic to the use of a rainforest psychedelic to treat addicts from the inner city.

Conversations with Dr Reese Jones, a professor of psychiatry at the Langly Porter Institute in California who performed research in the ’60s with LSD, and Herbert Kleber, a professor of psychiatry at Columbia University and former advisor to Bill Bennett (Bush’s drug czar and author of such timeless classics as The Children’s Book of Virtues), reveal something much less sinister but much more petty: Scientists routinely dismiss one another’s work, often hacking to pieces the reliability of the methodology and the veracity of every little piece of data, and this often out of infantile jealousy. Dr Jones admits to having done this, Kleber says it has been done to him many many times, and Frank Vocci of NIDA says that even if a scientist’s work is 80 percent funded, the rejection of the other 20 percent can be “…a clobbering, like, ‘Why d’you even come here with that?”‘ Despite FDA approval for phase-one dose escalation in August 1993, NIDA continues to reject the funding of Ibogaine research in humans. Mash said such a trial would cost around $300,000. With an annual budget of $80 million, Mash’s need for approximately $300,000 does seem relatively manageable, but the reasons are the same today as they were four years ago: the research upon which all grant submissions rest must be deemed meritorious by the peer review committees.

Such intransigence and obduracy of Mash’s NIDA colleagues, and the deaths of two more addicts while under the influence of Ibogaine, led to the total breakdown of all communication 4 between Lotsof and Mash. About three years into their alliance, each had set up 1 offshore treatment facilities of their own; with Lotsof’s retreat in Panama, and Mash based on the Caribbean island of St Kitts. Mash’s operation survived, while Lotsof’s center without luck or capital, works under contract with hospitals in Panama. They are now suing one another, and the lawsuits are pending. Lotsof blames the failure of his Panama operation on the publicity accorded Mash’s facility via the Internet, and sites Mash’s connections and ruinous lawsuits against him as the reason for the devise of his facility. (Mash’s husband Joe Geller, as well as being her business partner and attorney is the Democratic Party chairman of Dade County. It is true that the couple invited a group of private investors to help fund the Healing Visions Institute For Addiction Recovery Ltd on St Kitts. It is also true that Mash’s suit against Lotsof alleges that he did not diligently pursue the securing of a patent for an Ibogaine derivative she discovered, asserting that this was grounds for nullification of the contract between them. She also brought suit against him in the Netherlands for the death of the woman mentioned earlier. That suit was thrown out of the Dutch courts, and Lotsof was exonerated (Mash is attempting to bring the case to court in Germany).

Mash cites Lotsof’s lack of academic credibility as the reason for the failure of the Panama operation, but it could be that his prices were a bit steep: one of Mash’s patients who had first approached Lotsof was quoted a cure-all figure of $35,000. (Lotsof is still referring patients to another facility called the Panama Ibogaine Project.) “There’s too much shit going on around here,” proclaims Dr Deborah Mash, scurrying about the endless, chilly corridors of the University of Miami’s School of Medicine. She’s all high heels and hairdo, organizing a million things at once. She’s a formidable lady, extremely sure of herself and says she has treated 78 people on St Kitts since her facility opened in 1996. Patients are charged on a sliding scale, with a high end of $12,000. She reckons it works out to about half the cost of the average treatment center. I ask her what this meant in terms of the demographics of her clientele and she describes them as being mostly the Hazelden and Betty Ford failures. She calls them her “Iboganauts” which, though corny is fair enough because they have all been out there in space.

A 29-year-old man we’ll call Anthony remembers his Ibogaine journey. “I was in a chair, watching scenes from my life, like a video, but of my life. From all life, from the beginning of time, in full color. And above me was this presence. I mean it was God. Definitely a holy presence, like the omnipresence of everything that encompasses energy and all of life, but it was looking through my eyes. I knew the Ibogaine was my friend, that it wouldn’t hurt me, that it was going to work with me, show me what I needed to know. I saw myself in the womb, growing into a man. I saw a medicine man on a horse and he winked at me.

When he winked I knew, I just knew at this time that everything was 0K, that this is who I am, and that everything was going to be 0K.” Anthony had been using heroin for 6 years, and 80 milligrams of methadone a day for 3 years, when he found Deborah Mash. “Other treatments…” he recalls, “nothing ever got a hold of me. I mean I’ve cried with my family, with therapists. I’d feel good after but later it was just like another thing I did. I went straight out and got high, without even knowing why. I’ve been to five rehabs, spent thousands of dollars.” Post-treatment, Anthony has been clean for a year and says that the idea of using is repellent to him.

Another man who was opiate addicted says he could feel “…a spirit of Ibogaine. That there is some conscious direction going on there. I don’t feel it is just some random chemical reaction going on, but that there is this purpose and meaning and direction and guidance. I’ve been trying to get away from dope for seventeen years.

Nine, ten treatment programs, AA, NA…. I feel like a new man. I don’t wanna do dope…I’m completely free of narcotics for the first time in 25 years.” It has been suggested that the Ibogaine experience is very similar to the fourth step of the AA program, in which the alcoholic makes a “searching and fearless moral inventory” of him- or herself. The Iboganauts who had done a fourth step in AA or NA have said that the Ibogaine experience was nothing like sitting at a desk with a pen and paper, writing down a laundry list of good and bad. They all emphatically agreed that their lives were shown to them in totality and that it was as brutal and choiceless as it was penetrating and revealing, with a scope and intensity beyond their wildest expectations. Ibogaine gives you a glimpse of what is possible, but the rest is work.

Aftercare is an important part of the process. Even the cravings will return after a few months if issues are left unaddressed. Subsequent doses of Ibogaine are sometimes given, but it is imperative that patients take care of themselves. Anthony sees a shaman every three months. Some go to AA. Most go to weekly support-group meetings. They are, after all, members of a fairly exclusive club.

However, the Iboganauts all regard Ibogaine as an indispensable tool. Alastair a man of nearly 50, had been using heroin for 25 years. When he turned up at Deborah Mash’s door he had one foot in the grave and said it wouldn’t have taken much to push him over. He claims that Ibogaine is the most valuable tool for recovery. “You have to do your recovery,” he says, “but Ibogaine gives you the best leg up you can possibly have.” Ibogaine is obviously of scientific interest. In November, Dr Kenneth Alper of New York University’s School of Medicine organized the first-ever international Ibogaine conference. While the event was well-attended and touched off a flurry of publicity, it remains to be seen whether it will have any affect upon the obduracy of the dreaded peer review committee. Most in the scientific community are biological reductionists, and as such, defenders of the unassailable importance of the chemical nuts and bolts, and the scientific method. They revere the sanctity of skepticism and the need, at the costs of their all-important reputations and livelihoods, to remain dispassionate about their subject matter. I asked Mash about the fact that she is studying the numinous while wearing her biological reductionist’s hat, and she told a story of a conversation with a colleague about Ibogaine almost a decade ago. He shook his head at her and advised her, in his professorial wisdom, to let it go, that it was not something she should pursue in her lifetime. She said, “I have seen this very powerful transformation that occurs in these people, that enables them to get at the root causes of their self-destructive patterns of addiction. He shook his head and said, ‘Come on. Deborah, that’s Paul on the road to Damascus,’ meaning (that was the patient’s) conversion, his sudden belief. Well, I’ve seen that on the island.”

Mash is also working on synthesizing a metabolite created by the liver after the use of Ibogaine, which she believes is chemically responsible for keeping the craving at bay. She is looking for someone to be her partner in going after that metabolite. She adds, in her defense, that this is what the government wants, what the biological reductionists want, and that since she can talk biological reductionism with the best of them, a metabolite like that could be of more interest than a profound hallucinatory experience. A metabolite like this would be developed in the form of a transdermal patch. Could these be marketable? One cannot help but wonder.

Still, it remains that a man with no scientific qualifications discovered the drug’s miraculous and beneficent effects. Lotsof holds the worldwide patents to its use, but is in fierce litigation with a woman who, with her own ambitions to develop a patch that could be sold by the millions, is suing him for $50,000 more than he has. Each has tried separately and together to convince a jealous scientific establishment whose members serve the interests of politicians who pay their wages that they hold the keys to the kingdom of heaven. Both have been met with skepticism and resistance. Without any keys to copy, it seems, everyone wants a piece of the gate.