First Posted 7/28/2013

Ibogaine, a drug long-rumored to treat opioid withdrawal, has become a hot topic for those taking buprenorphine.  Ibogaine is a complex molecule that comes from a group of plants that are known, in West Central Africa, as Iboga.  In native African culture the drug is used to induce psychedelic states that are part of certain rituals.

A reduction in opioid withdrawal from Ibogaine was first described in 1962.  Since that time, anecdotes have been exchanged about the unique properties of Ibogaine, including claims that the drug does far more than reduce the symptoms of opioid withdrawal.  Some users have described trances that they claim effectively ended their addictions to opioids or other drugs.  On the other hand, some people claim to have had no positive effects from ibogaine, and others claim negative effects or bad experiences.  A list of individual experiences with Ibogaine can be found here.

Ibogaine interacts with a number of neurotransmitter receptors, including at least two classes of opioid receptors (kappa and sigma).  Ibogaine’s effects are partially mediated by NMDA receptors (where glutamate acts as neurotransmitter).  The drug also binds to multiple subtypes of serotonin receptors.
Ibogaine has been associated with a number of deaths, most commonly from arrhythmia or heart failure resulting from sympathetic hyperactivity.  There is no treatment for Ibogaine toxicity. The dangers of Ibogaine have led to classification of the drug as Schedule I by the DEA, blocking research into possible therapeutic benefits.  A recent case report in the American Journal of Addictions (Volume 22, Issue 3) highlights the risk of self-treatment with ibogaine:

A 25‐year‐old gentleman with a past medical history of supraventricular tachycardia and chronic heroin addiction decided to try Ibogaine in an attempt at drug cessation. The patient’s mother directly supervised him and indicated that he ingested 2.5 g of Ibogaine over 3 hours. The patient started experiencing hallucinations, ataxia, muscle spasms, weakness, fever, and urinary retention. Most of those symptoms resolved over that day except for muscle spasms and ataxia. He then developed respiratory difficulty followed by cardiopulmonary arrest. He was successfully resuscitated, and brought to the Emergency Department. Physical exam revealed muffled heart sounds and coarse breath sounds bilaterally. Neurologically, the patient was in a decorticate position. A sample of the ingested substance was analyzed by the Poison Control Center, and toxicology results confirmed that Ibogaine was the ingested substance. Despite aggressive care, the patient expired after 2 days from multi‐organ failure.

Because of the heavy interest in the ibogaine, I am adding a section about the drug at SuboxForum, where people can share anecdotes, ask questions, and place links to further information.   I encourage people to approach the discussion with a skeptical mind.  Opioid dependence creates desperation, and desperation makes us eager to chase after anything that is rumored to be a cure.
My opinion?   The whole thing reminds me of laetrile, another wonder drug that the US pharmaceutical industry supposedly withheld from US citizens.   The apricot-pit cancer cure (also known as amygdalin or ‘vitamin B-17’) spawned cancer treatment centers throughout Mexico about 30 years ago.  Steve McQueen was one of the more notable people who died during treatment with laetrile, a drug that the FDA, after decades of study, called ‘a highly toxic product that has not shown any effect on treating cancer’.  Desperate people take desperate measures.

Reducing the severity of opioid withdrawal through actions at multiple neurotransmitters is within the realm of possibility, and could perceivably lead to untold medical benefit if further study was allowed. But the idea that one or two episodes of pleasant psychosis can ‘cure’ opioid dependence sounds, from a neurochemical standpoint, too good to be true.


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