Ibogaine Research Update: Summer 1992

Ibogaine Picture

Summer 1992 Vol. 03, No. 3 Building on Common Ground

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Last year, the Medications Development Division (MDD) of the National Institute on Drug Abuse (NIDA) began a research initiative to evaluate the use of ibogaine as an anti-addiction agent. Since then, numerous articles have appeared in sdentific journals, both in the US and abroad, which show promising results.

Spearheading the research efforts are the Pharmacology and Toxicology Department of Albany Medical college, headed by Dr. Stanley D. Glick. His department published no fewer than six papers in little over a year. Other New york research institutions evaluating ibogaine include the Nathan S. Kline Institute for Psychiatric Research, a fadlity of the New York State Office of Mental Health affiliated with NYU Medical Center, and the City University of New York Medical School.

Claims that ibogaine is effective as a treatment for both cocaine and opiate narcotics were at first widely viewed with scepticism. Cocaine is, after all, a stimulant while opiate narcotics have an opposite effect, that of sedating the user. What they do share in common, however, is that use of either substance increases dopaminergic (DA) activity in the brain’s mesolimbic system, and / or mesocortical pathways. This triggers the reward mechanism, which is associated with the reinforcing effects of drugs of abuse. Researchers thus began looking at the relationship of ibogaine to the DA system.

In early 1991, Dr. Broderick of CUNY Medical School submitted an abstract to the College on Problems of Drug Dependence (CPDD), The African Alkaloid, Ibogaine, Alters Cocaine-Induced Accumbens Dopamine Neurotransmission: In Vivo Voltametric Studies in the Conscious Brain. She reported that ibogaine reduced cocaine induced DA increases, but without complete depletion, and observed, "These data have clinical implications because pharmacotherapeutic medications which decrease DA neurotransmission without a complete DA block could drcumvent the reported anhedonia often associated with some cocaine treatment modalities." Her finalreport, presented at the CPDD’s 53rd annual scientific meeting, concludes, "Thus, ibogaine’s effects are consistent with current views regarding rational strategies for cocaine treatment." (NIDA Research Monograph Series, 119: 285,1992.)

At the same time, researchers at the Division of Neurochemistry at the Nathan Kline Institute in Orangeburg, NY were examining the relationship between ibogaine and cocaine in mice. Hertry Sershen, et. al., reported this year that lbogaine Antagonizes Cocaine-Induced Locomotor Stimulation in Mice (Life Sciences, Vol. 50, No. 15, pp. 1079-1086. 1992). "The results," he states, "suggest that ibogaine may have induced a selective change in the dopaminergic system that results in a decrease in responsiveness to cocaine that persisted for at least one week." He further concluded that "The above results are not in conflict with the proposed uses of ibogaine in the treatment of cocaine abuse, since increased dopamine neurotransmission has been shown to be associated with the locomotor-stimulant and reinforcing effects of cocaine. Attenuation of these effects by ibogaine could possibly reduce the craving for cocaine."

Additional work involving ibogaine and cocaine was accomplished by m.P. Dzolic, of Erasmus University in Rotterdam. An abstract submitted to the CPDD, Effects of Ibogaine on Cocaine Self-Administration in Rats, showed promising results, and compared favorably to uncontrolled clinical observations. "All this is encouraging," said Dzolic, "since it supports the idea that ibogaine is a potential long lasting interrupter of both cocaine and morphine dependency."

Ibogaine Picture

Figure 106. Tabemanthe iboga. From A. Landrin, De l’Iboga a de l’lbogaine, 1905.

In June, 1992, Dzolic made an oral presentation to the CPDD at the 54th annual scientific meeting in Keystone, Colorado. The significance of his findings are twofold. Firstly, heretofore the interruption of cocaine self-administration with a non-toxic substance was unheard of. In a number of widely-reported studies, animals, when given the ability to self-administer cocaine did so continuously, ignoring food, water, and sex, until they died. Secondly, Dzolic’s findings are consistent with those of S.D. Click, et. al., Effects and Aftereffects of lbogaine on Morphine Self-Administration in Rats. (European Journal of Pharmacology, 195: 341-345, 1991).

Glick found that not only would ibogaine interrupt morphine self-administration, but that it continued to do so long after the ibogaine was eliminated from the body. Citing two US patents (4,499,096; and 4,587,243) which describe the potential efficacy of ibogaine in treating opiate and cocaine addiction, Glick concludes, "though far from addressing the full extent of the claims presented in the patents, the results of this study suggest that such claims should be taken seriously, and that further investigation is warranted."

In a study entitled, Interactions between lbogaine, a Potential Anti-Addictive Agent, and Morphine: An In Vivo Microdialysis Study (European Journal of Pharmacology, 199:35-42, 1991) I. M. Maisonneuve et. al. found that "It appears that ibogaine affects brain DA systems for a period of time that exceeds its elimination from the body, and during this time, alters the responses of these systems to morphine by preventing the increase in dopaminergic transmission induced by morphine in the nucleus accumbens, ibogaine may decrease the reinfordng efficacy of morphine. Thus, although a definitive mechanism underlying the claims regarding ibogaine’s therapeutic effects cannot be specified yet, the results of the present study indicate that such mechanisms merit investigation."

Maisonneuve and Glick published two other papers addressing the dopamine question, Interactions between Ibogaine and Cocaine in Rats: An In Vivo Microdialysis and Motor Behavior (European Journal of Pharmacology, 212:263-266, 1992); and Acute and Prolonged Effects of lbogaine on Brain Dopamine Metabolism and Morphine-Induced Locomotor Activity (Brain Research, 575, 69-73,1992).

Glick then turned his attention to another claim that ibogaine will suppress the multiple symptoms of narcotic withdrawal. The daim that ibogaine attenuated many, but not all, symptoms of withdrawal was first reported by Dzolic et. al., Effect of Ibogaine on Naloxone-Precipitated Withdrawal of Chronic Morphine Dependent Rats (Archive of International Pharmacodynamics, 294, 64-70. 1988). Two years later, Aceto, Bowman and Harris at the Medical College of Virginia reported that ibogaine suppressed withdrawal signs in morphine dependent monkeys (NIDA Research Monograph 95; 578,1990). A controversy was created when Sharpe and Jaffe refuted those findings, stating that ibogaine failed to reduce the majority of withdrawal signs in naloxone precipitated withdrawal in morphine dependent rats (NeuroReport 1, 5-7,1990). However, Sharpe and Jaffe conceded that such discrepandes were possibly the result of methodological differences. "Despite all these differences," observed Glick, "some aspect of the opiate withdrawal symptom was ameliorated in all three studies."

Glick prepared a study to re-examine the possibility that ibogaine might attenuate morphine withdrawal. His results indicate that ibogaine significantly decreased the intensity of many withdrawal signs (Effects of Ibogaine on Acute Signs of Morphine Withdrawal in Rats: Independence from Tremor, Neuro-pharmacology, Vol. 31, No. 5, p. 497-500,1992). "Exactly how ibogaine might attenuate opiate withdrawal is, at this point, open to conjecture," Glick states. "Regardless of the explanation," he concludes, "the present results indicate that the potential usefulness of ibogaine in treating acute manifestations of opiod dependence should be further investigated."

Editor’s note: Howard Lotsof is trying to develop ibogaine through the use of a for-profit corporation, the opposite approach of MAPS to MDMA. For more information, contact Howard Lotsof:

Howard Lotsof
NDA International
46 Oxford Place
Staten Island, NY, 10301
(718) 442-2754