First Posted 12/28/2013

I’ve always assumed that stories about ibogaine curing opioid dependence were fabricated or exaggerated.  But I’ve read more about ibogaine since the drug popped up on an episode of Homeland.  The scene made me wonder how and when the hoopla over ibogaine began, and why it ended.  After all, people treat addiction with all sorts of things that don’t work—so why ban ibogaine?

Ibogaine for opioid addiction

In the era of the internet, the answers are easy to find.  Ibogaine was used for religious rites in Africa for at least 200 years.  Since the 1930’s the drug, brand-named Lambarène, was used to treat depression and improve energy in France.   The usefulness of ibogaine for treating opioid addiction was described by Howard Lotsof in 1962.  But Lambarene was removed from the market in the 1960s, when the World Health Assembly classified ibogaine as ‘a substance likely to cause dependency or endanger human health.’  A few years later the DEA moved ibogaine to Schedule I—a class of drugs deemed to have ‘no value as medicine.’ Marijuana is schedule I, by the way.

In lack of formal study, several authors have recorded clinical outcomes after ibogaine treatment in non-standard environments.  Carl Waltenburg wrote about treating addicts with ibogaine in a squatters’ village in Denmark in the early 1980’s. Lotsof described a series of patients treated for addiction in a patent awarded for that use of ibogaine in 1985.  In the 1990’s the NIDA funded research of ibogaine treatment of opioid dependence, but that funding was cut in 1995 when a review of early outcome data revealed the death of a young woman treated with ibogaine.  The woman’s death was not clearly attributed to ibogaine, since her belongings were found to include heroin paraphernalia after her death.  But as we all know, attitudes toward medications in the addiction field are subject to emotion and politics, and the death of a young woman during study of a schedule I drug was all it took for NIDA to pull the grant and spend the money elsewhere.

Reports of the efficacy of ibogaine for treating addiction are interesting, and I encourage readers to dig into discussions about the drug with a healthy dose of skepticism.  Remember that scientific truth never comes from one study, or even from a few studies.  Rather, results must be replicated by a number of scientists, preferably with a wide range of bias and perspectives.  In the 1985 patent application for the use of Ibogaine for opioid dependence, Lotsof summarized impressive findings (which are in the public domain and copied below).  Keep in mind, though, that someone applying for a patent is not going to use the application to report their failures!


It is a principal object of the present invention to provide an improved method for the treatment of opiate addiction.

Another object of the present invention is to provide an improved method for interrupting the physiological and psychological aspects of the heroin addiction syndrome.

Still another object of the present invention is to provide a method of the above nature characterized by its high degree of success, the absence of the great pain and discomfort accompanying earlier treatments, the ease and convenience of application the absence of undesirable or persistent side effects and the persistent effectiveness of the treatment.

The above and other objects of the present invention will become apparent from a reading of the following description which sets forth preferred embodiments thereof.

A feature of the present invention is based on the discovery that an alkaloid of the family Apocynaceae and its therapeutically active derivatives and salts, particularly, ibogaine and its therapeutically active, non-toxic derivatives and salts for example, ibogaine hydrochloride and other non-toxic salts of ibogaine, possess the unexpected unique ability to disrupt the heroin addiction syndrome. Examples of other salts of ibogaine which may be used are ibogaine hydrobromide, and any other non-toxic salt of ibogaine.

For the purpose of definition, the heroin addiction syndrome is meant to consist of all the symptomology demonstrated by addicts in their use of and search for heroin. The interruption of the syndrome was accomplished in five out of seven (71%) of the test subjects who were addicted to heroin. None of the test subjects were seeking to terminate their habits, and all seven were enamored with narcotics.

A single treatment with ibogaine or ibogaine HCl of doses ranging from 6 mg/kg to 19 mg/kg administered orally, disrupted the subject’s use of heroin for about six months.

A treatment lasts about thirty hours during which time ibogaine exerts a stimulant effect. Apparently, an abreactive process is involved during ibogaine therapy but is not noticeable until the patient wakes from natural sleep occurring after primary and secondary effects of ibogaine are diminished. When effective, ibogaine left the addict with no desire to use heroin and no noticeable signs of physical withdrawal. Subjects appeared relaxed, coherent, with a sense of direction and feelings of confidence. 

(Note: abreaction is defined as ‘the release of emotional tension achieved through recalling a repressed traumatic experience.)

Ibogaine was one of five substances we studied. The other four–mescaline, psilocybin, LSD and DMT though different in duration of action and intensity–have similar psychotropic effects that are well documented and will not be discussed here. Ibogaine, unlike the others, is not a euphoriant hallucinogen and did not leave the subjects open to swells of emotion. While under the influence of ibogaine, emotional responses to traumatic repressed thoughts and feelings appeared to be negated.

Another effect of ibogaine administration that was found interesting was that even after twenty-six to thirty hours of wakefulness, subjects slept three to four hours and awoke fully rested. This pattern continued, diminishing slowly, over a three to four month period.

The effects of oral administration of ibogaine are first noticed in fifteen to twenty minutes. Initially, a numbing of the skin is accompanied by an auditory buzzing or oscillating sound. Within twenty-five to thirty-five minutes the auditory transcends across the sensory mechanisms to include the visual: objects appear to vibrate with great intensity. It is at this time that the dream enhancement or hallucinatory effects begin. In many cases an acute stage of nausea follows the hallucinatory phase. The visions end abruptly and the numbness of the skin begins to abate.

This is followed by six to eight hours of a high energy state during which the subjects see “lightening” or flashes of light dance about them. Thoughts which seem to amplify the meaning of the visions seen during the primary phase of ibogaine intoxication continue during this period.

Between twenty-six and thirty-six hours, the level of stimulation diminishes and the test subject falls asleep.
Thus, three stages of ibogaine intoxication have been observed. First, a hallucinatory period lasting for three to four hours during which time the person receiving ibogaine manifests repressed material visually. Second, a high energy period accompanied by flashes of light, the appearance of a vibration to all objects, and the awareness of thoughts appropriate to the visual material seen by the subject. Third, a diminishing energy period free of vibration or light flashes and culminating in sleep.

In the administration of acceptable dosage forms, any one of a variety of preparations may be compounded, for example: capsules, tablets, pills, powders, solutions, etc. In addition to the active agent, there may be present additional substances used in the manufacture of pharmaceutical preparations such as binders, fillers and other inert ingredients.

The entire patent application, including case reports, can be found at the web site of the US Patent Office.

Assignment of a substance to Schedule I creates significant barriers to formal study, at least in the United States.  But US Schedule I status has not prevented the establishment of ibogaine treatment centers in other parts of the world, including Mexico and Canada.  The data pieced together over the years suggests that ibogaine could be a remarkable medication for some people.  But like any medical treatment, there are significant risks to ibogaine treatment.  One particular concern is cerebellar damage in rats treated with doses of ibogaine greater than 100 mg/kg.  Proponents of ibogaine point out that the dose used for treating human opioid dependence is about 50% lower, hardly a reassuring margin of safety.  Best estimates, taken from limited data, suggest an overall fatality rate of 1 in 300 people treated with ibogaine for opioid dependence, with higher death rates in people with certain comorbid conditions.

I’m skeptical of the claims of permanent, positive treatment outcomes from ibogaine.  Addiction to opioids creates a complicated, interconnected collection of physical and psychological dispositions that favor eventual relapse.  I have a hard time believing that one dose of abreactive insight, no matter how profound or intense, can selectively eliminate the desire to use opioids…. while leaving unaffected the desires for all of the normal, good things that humans enjoy.   But then again, opioid dependence is an often-fatal condition.  The significant risks in the risk/reward equation create scenarios where Ibogaine treatment may be appropriate.  I’d be interested in hearing and sharing first-hand accounts from anyone who has been through ibogaine treatment—without need to share your personal identity, of course.


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