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IBOGAINE | +40 articles

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Ibogaine and the heart: A delicate relation*

Xaver Koenig, Karlheinz Hilber

Ibogaine has shown promising anti-addictive properties in humans as the drug alleviates drug craving and impedes relapse of drug use. Though unlicensed as therapeutic drug, and despite safety concerns, ibogaine is currently used as an anti-addiction medication in alternative medicine clinics worldwide. In recent years, alarming reports of life-threatening complications and sudden death cases associated with the administration of ibogaine have been accumulating. These reactions are hypothesized to be associated with ibogaine’s propensity to induce cardiac arrhythmias. The aim of this review is to recapitulate the current knowledge about ibogaine’s effects on the heart and the cardiovascular system, and to assess the cardiac risks associated with the use of this drug in anti-addiction therapy. The actions of 18-methoxycoronaridine (18-MC), a less toxic ibogaine congener, are also considered.

The mechanisms by which ibogaine exerts its psychoactive effects in the brain are only poorly understood, which is attributable to the alkaloid’s complex pharmacology. Effects on multiple neurotransmitter systems via numerous brain targets have been reported. Among those, ibogaine interacts with neurotransmitter transporters, opioid receptors, sigma receptors, glutamate receptors, and nicotinic receptors in low micromolar concentrations. Long-lasting effects after ibogaine intake are attributed to the alkaloid’s long-lived active metabolite, noribogaine.

Although all efforts to clinically approve ibogaine have failed as yet, NIDA has recently committed financial support for preclinical testing and chemical manufacturing, as well as control work intended to enable clinical trials to develop the synthetic ibogaine congener 18-methoxycoronaridine (18-MC) as a pharmacotherapy for addiction. 18-MC also exhibits anti-addictive effects, and is less toxic in animals than ibogaine.

Ibogaine’s complex pharmacology has a considerable potential to generate adverse effects. Besides neurotoxic actions, ibogaine also affects the cardiovascular system, and, in recent years, alarming reports of life-threatening complications and sudden death cases, temporally associated with the administration of the alkaloid, have been accumulating. It was hypothesised that the above-mentioned sudden deaths cases in humans were related to cardiac arrhythmias. These are most probably associated with ibogaine’s propensity to induce a QT interval prolongation in the electrocardiogram (ECG), which is known to enhance the risk for life-threatening Torsade de pointes (TdP) arrhythmia generation.

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Effects on the cardiovascular system

Several indole alkaloids exert effects on the cardiovascular system, and have been or are still used as therapeutic drugs. Among those reserpine has a history as antihypertensive drug, and ajmaline is still approved as an antiarrhythmic medicine. Cardiovascular effects of iboga alkaloids have been known for many years. For example, Tabernanthine, contained in Tabernanthe iboga root bark extracts, induced bradycardia and hypotension in rats and dogs. Low doses of ibogaine didn't change the resting heart rate or blood pressure, but at higher doses ibogaine decreased the heart rate without affecting blood pressure.

In contrast, a significant decrease in heart rate was found in rats already at low ibogaine doses. 18-MC, even at high doses, did not show any apparent effects on either heart rate or blood pressure. Besides these findings on animals, anecdotal evidence suggests that ibogaine can also slow the heart rate in humans. Mash et al. performed intensive cardiac monitoring in 39 human subjects who received single doses of ibogaine for the treatment of cocain/heroin addiction. With dosages in the range of 500–1000 mg, six out of 39 subjects showed a significant bradycardia, and one subject a significant hypotension.

Ibogaine's effects on heart rate

A drug modulating several neurotransmitter systems, such as ibogaine, may generate effects on the cardiovascular system related to its central nervous activity. Further, ibogaine was shown to inhibit voltage-gated calcium channels in rat sympathetic and parasympathetic neurons via sigma receptor activation. This may influence cell-to-cell signalling in autonomic ganglia, and thus the regulation of heart rate by the peripheral nervous system. Interestingly, compared to ibogaine, 18-MC shows significantly less affinity to sigma receptors. If the heart rate is indeed affected by sigma receptor activation, 18-MC will be less effective in this regard.

Ibogaine’s bradycardic action is often related to stimulatory effects of the drug on the cholinergic system. Here, two possible mechanisms were proposed: (1) inhibition of acetylcholinesterase by the drug; and (2) an agonistic action on muscarinic acetylcholine receptors. 18-MC’s affinity for muscarinic receptors is at least two-fold less than that of ibogaine.

A further postulated mechanism by which ibogaine could induce bradycardia is a blockade of voltage-gated sodium channels. Indeed, ibogaine has low micromolar affinity for sodium channels in the brain, and cardiac sodium channel blockers can exert a bradycardic effect. We recently tested ibogaine’s effects on human cardiac sodium channels heterologously expressed in TSA -201 cells. To our surprise we found that low micromolar ibogaine (18-MC) concentrations did not affect Nav1.5 channel currents at all. Consequently, it is unlikely that cardiac sodium channel inhibition by ibogaine significantly contributes to bradycardia generation. However, in this context, the modulation of ion channels, representing major physiological determinants of the heart rate, deserves special consideration.

Ibogaine's effects on cardiac ion channels

Cases of ibogaine-induced QT interval prolongation and associated life-threatening TdP arrhythmias have been accumulating in recent years. The most common reasons for QT prolongation and arrhythmia induction by drugs are modulatory effects on cardiac ion channels. It is therefore noteworthy to look at ibogaine’s effects on ion channels with major importance for electrical impulse conduction in the heart. In this context, we have recently studied the effects of ibogaine and its congener 18-MC on cardiac sodium, L-type calcium, and "human ether-a-go-go-related gene" (hERG), and we found that cardiac sodium and calcium currents are not significantly modulated by ibogaine and its congener 18-MC in a regime of doses normally used to treat human addicts.

The described effects of ibogaine and noribogaine: prolongation and flattening of the human cardiac AP, and relative selective hERG channel inhibition as triggers of QT interval prolongation must be considered proarrhythmic. Moreover, ibogaine’s effects on in vitro cardiac electrophysiology within the drug’s therapeutic plasma concentration range, closely resemble the cardiac actions of formerly approved drugs like cisapride or astemizole, which have been withdrawn from the market because of their propensity to induce TdP arrhythmias.

Here we want to emphasize that not only QT prolongation itself, but also and especially a flattening of the repolarization phase in the AP is considered a proarrhythmic characteristic. Moreover, ibogaine’s effects on in vitro cardiac electrophysiology within the drug’s therapeutic plasma concentration range closely resemble the cardiac actions of formerly approved drugs like cisapride or astemizole, which are known to be unsafe, and have been withdrawn from the market because of their pronounced propensity to induce TdP arrhythmias. Thus, ibogaine, at the doses currently used in humans, must be classified an unsafe drug! Because of its considerably longer half-life in human plasma, ibogaine’s metabolite noribogaine might represent the major proarrhythmic factor. This clearly challenges the idea of noribogaine being considered a potentially safer alternative to ibogaine for anti-addiction medication development.

Risk factors

Based on the findings of the above described experimental studies and case reports on ibogaine’s cardiovascular actions, this section deals with risk factors and their practical impacts for the future application of ibogaine and 18-MC as anti-addiction drugs. First, application of ibogaine, should be done under strict medical observation and continuous electrocardiographic monitoring for an extended time period, which carefully takes noribogaine’s longevity in human plasma into account.

Secondly, prior to ibogaine application one must carefully consider additional risk factors for drug-induced TdP arrhythmias in a patient including female gender, prolonged baseline QT interval, bradycardia, abnormal electrolyte levels, pre-existing cardiovascular disease, ion channel mutations, drug-drug interactions, and genetic variants influencing drug metabolism.

For anti-addiction treatment with ibogaine, two risk factors deserve special attention: bradycardia and hypokalemia. Ibogaine itself induces bradycardia, and hypokalemia is frequent in drug users. Compared with the large number of people who have received ibogaine treatments over many years worldwide, comparably few fatality cases have occurred or have been reported. In addition, drug safety studies on human addicts performed under well-controlled conditions revealed no significant adverse effects.

Baseline screening should include a medical evaluation, physical examination, ECG recording, blood chemistries, haematological workup, and psychiatric and chemical dependency evaluations. In some cases more extensive evaluations should be performed to rule out cardiac risk factors and to exclude subjects for study entry.

Drug-drug interactions

Addicts often have a long history of substance abuse. Alcohol, heroin, cocaine, benzodiazepines, and methadone are among the abused substances, frequently also combinations thereof. Methadone is also prescribed for opioid substitution therapy. When ibogaine is administered to addicts, the presence of other substances in the patient’s blood plasma is not uncommon. This paves the way for adverse drug interactions.

Concerning the heart, alcohol, cocaine and methadone have been associated with QT interval prolongation. If relevant concentrations of such substances are still residing in the plasma when ibogaine is applied, the drug’s QT prolonging effect, and thus the risk of TdP arrhythmias will be raised. Here, methadone deserves special attention because it additionally has an exceptionally long plasma half-life.

Given that noribogaine has a long half-life in human plasma (1–2 days), the inhibition of its metabolism by other drugs will have strong impacts. Thus, cardiotoxic effects may persist for weeks after intake of a single dose of ibogaine. Therefore, we strongly encourage researchers to determine the pathways involved in the metabolic conversion of noribogaine.

Conclusions

Due to the longevity of noribogaine—ibogaine’s active metabolite—in human plasma, cardiac adverse events may also occur several days, in some cases weeks after intake of a single dose of ibogaine. Noribogaine, on the other hand, may also convey long-lasting anti-addictive efficacy after ibogaine application.

Future administration of ibogaine to treat addiction may be justified by the urgent medical need for an effective anti-addiction drug. Thus, the use of a drug known to prolong the QT interval must be based on risk-benefit analysis in individual patients. Where benefit outweighs risk, QT prolongation should not limit necessary therapy. Recommendations on prevention and guidelines for the management of drug-induced QT prolongation and TdP in hospital settings can be found in. Two things need to be carefully considered:

(1) Ibogaine application should only take place under strict medical observation and continuous electrocardiographic monitoring over a sufficiently long period of time.

(2) Additional risk factors for drug-induced TdP arrhythmias must be clarified prior to ibogaine application. Eventually, informed consent should be received from drug addicts, in which the risk of ibogaine-induced sudden cardiac death is appropriately highlighted. Based on the rapidly accumulating knowledge about the potentially harmful cardiotoxicity of ibogaine, the responsible medical authorities are now requested to define respective standards and exclusion criteria to allow for a safer ibogaine anti-addiction therapy in the future.

*From the study here:
https://www.ncbi.nlm.nih.gov/pmc/art...emss-62840.pdf
 
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What is ibogaine?

by Barb Bauer, MS | Psychedelic Science Review | 22 Jan 2020

Ibogaine is a compound found in the leaves of an African shrub called Iboga. Studies indicate it may have anti-addictive properties.

Ibogaine is one of several chemical compounds found in the plant (shrub) Tabernanthe iboga. The plant is also known by just its species name, iboga. Traditionally, iboga is used in cultural and religious rituals by the indigenous peoples of Central Africa. They also use it in various dilutions for alleviating hunger, fatigue, and thirst. Some of the other compounds found in iboga are noribogaine, tabernanthine, ibogamine, ibogaline, and catharanthine.

The chemistry of ibogaine

Ibogaine was first isolated by Dybowski and Landrin in 1901. The crystalline structure of ibogaine was determined in 1960. It was first synthesized in the lab by Bûchi, and a simplified total synthesis was published in 2012. A detailed summary of ibogaine synthesis is found in Wasko et al., 2018.

Ibogaine crystallizes into prismatic needles from ethanol. In addition to ethanol, it is soluble in ether, chloroform, acetone, and benzene. It is practically insoluble in water. The hydrochloride salt of ibogaine is soluble in water, as well as methanol and ethanol. It is slightly soluble in acetone and chloroform, but practically insoluble in ether.​

What are the some of the effects of ibogaine?

Ibogaine is cardiotoxic at micromolar levels. Specifically, studies have noted a prolongation of the heart’s QTc interval. Ibogaine has also been shown to be neurotoxic in rodents. At higher doses, the effects include tremors, convulsions, nervous behavior, and paralysis of the limbs. However, the doses used in these studies are below what would be used in a clinical setting.

In the early 1960s, subjective reports of the anti-addictive properties of ibogaine began surfacing, most notably from a young heroin addict named Howard Lotsof. Lotsof was born in the Bronx, New York in 1943 and was severely addicted to heroin by the time he was 19 years old. By his own account, the desire of he and six of his friends to take heroin disappeared almost immediately after self-administration of an extract of the T. iboga root. Lotsof became one of the most vocal advocates of ibogaine use for the treatment of addiction. In 1985, he was granted a patent for the treatment of cocaine and heroin addiction using ibogaine.

Research indicates that ibogaine may be effective in treating opiate addiction. The data show that it doesn’t just reduce opioid use, but can result in complete abstinence, along with having “long-term positive psychological outcomes.”

A 2018 study found that the positive effects of ibogaine for treating opioid dependence lasted twelve months. In a 2018 review paper, Mash et al. recommended using a single oral dose of ibogaine during detoxification “to transition drug dependent individuals to abstinence.”​

What receptors does ibogaine use?

In terms of pharmacodynamics, ibogaine shows no clear preferences, having a moderate to a weak affinity for a variety of receptors and transport proteins. As a result, the hallucinogenic effects of ibogaine cannot be attributed to the activation of the serotonin 5-HT2A receptor.

However, ibogaine’s principal metabolite noribogaine has a sub-micromolar affinity as a partial agonist of the kappa opioid receptor. The mechanism of the dissociative effects caused by ibogaine may be similar to that of ketamine and other NMDA (N-methyl-D-aspartate) channel blockers.

Ibogaine also binds in the low micromolar range to the mu opioid receptor, as does noribogaine in the sub-micromolar range. This may explain the ability of ibogaine to decrease self-administration of morphine in rats.

Studies indicate that ibogaine’s anti-opiate effects may be due to its non-competitive antagonist action at nicotinic acetylcholine receptor subtypes including α1ß1 and α3ß4.​

More research needed on the constituents of the iboga plant

Scientists have only begun to scratch the surface to reveal the chemistry, pharmacology, and therapeutic applications of ibogaine and other compounds from Tabernanthe iboga. The early indications for use in treating opioid addiction and alcoholism are encouraging.

Despite what has been learned from studies, much ibogaine’s pharmacodynamics remains a mystery, as research appears to be focusing on its main metabolite noribogaine. Still, there is much to be learned about all the compounds from this naturally occurring source.

Among the many questions that need answering is whether there is an entourage effect with iboga compounds like what is seen with cannabis and the compounds in psilocybin mushrooms (aka magic mushrooms). Clearly, the research and development of iboga compounds is a wide-open area for study.

 
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Ibogaine presents unique challenges in how we approach harm reduction and addiction treatment*

by Jordan May | Psymposia | 4 Dec 2017

This series explores the unique challenges ibogaine presents in how we approach plant medicine, harm reduction, and treatment for addiction, through the lens of ibogaine researchers, providers, patients, and advocates from around the world.

My addiction started when I was 13, with prescription medications. I knew it was over the very first time I took an opiate. It was set, that this was going to be my addiction for a long time.”

There’s a brief silence as the woman sitting across from me takes a moment to swallow the lump in her throat. Her name is Amy. She’s a nurse from Canada, and she’s spent the majority of her life addicted to opioids.

“It developed into a more serious addiction over time, to the point where I was using them intravenously, when I became a nurse and had access to injectable medications. So my use got really, really out of control.”

We’re sitting amidst a hustle and bustle of people as they come and go through the hotel lobby. The sound of excited chatter dominates the space, and despite the heavy undertones of our conversation, you can feel the electricity in the room.

This is the setting for the European Ibogaine Forum, a small conference that took place in Vienna, Austria this past September. The event attracted an unlikely crowd of people from all walks of life. Doctors, researchers, drug users, and hippies from around the world came together for their shared interest in an obscure hallucinogenic alkaloid – ibogaine.

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Tabernanthe iboga

Sourced from the African shrub Tabernanthe iboga, or simply iboga, ibogaine is reputed to have the profound ability to eliminate opioid cravings and withdrawals. And unlike other psychedelics, ibogaine can be fatal. As such, it presents unique challenges in how we approach drug policy and addiction.

Iboga has a long history of use in west-central Africa. Consumption of the root bark, specifically, is intimately tied to the ancient spiritual discipline known as Bwiti, which is believed to have originated with the Babongo people in the Southern forests of Gabon. It’s said that the Babongo shared their knowledge of iboga with a migrant Bantu tribe that settled nearby, the Mitsogho.

Bwiti continued to evolve as the Mitsogho people came into contact with other tribes, such as the Fang, and now exists in the form of many diverse and interconnected syncretic belief systems that use iboga as part of their practice. In these contexts, iboga is typically ingested during initiatory rites of passage, for healing, and to make contact with ancestors.

Iboga and its constituents remained relatively unknown in the West until recent years. Ibogaine was first isolated in 1901, and in 1939 it was marketed in France under the brand name Lambarène for the treatment of depression and fatigue. It wasn’t until 1962, on the streets of the Lower East Side in New York City, that the drug would attract any serious international attention.

Howard Lotsof was only 19 years old when he first tried ibogaine. He was addicted to heroin and willfully experimenting with any substance he could get his hands on. The story goes that he was given ibogaine by a friend of his, who happened to be a chemist. Howard had never heard anything about the strange compound, and he chose to ingest it for no reason other than curiosity. Yet curiously enough, by the time the experience was over, he realized he no longer had any cravings for heroin whatsoever.

He went on to share the drug with his friends, who were also addicted to heroin, and it seemed to have the same miraculous effect on them. From that point on, Howard became a kind of evangelist for the addiction-interrupting potential of ibogaine. Between 1985 and 1992 he was awarded numerous patents for utilizing ibogaine as a rapid method for the interruption of various addictions, and he provided pilot data for a research program that eventually resulted in an FDA-approved Phase I clinical trial for ibogaine in the treatment of addiction.

At the same time, Lotsof also offered underground treatments and provided ibogaine for the Junkie Bond, an advocacy group for drug users. This work served as the foundation for the users-helping-users movement, a treatment modality rooted in harm reduction and self-care.

Howard died in 2010. Ultimately, his crusade involved a small army of devoted individuals, some of whom are featured in this series. Howard’s journey laid the groundwork for a movement that’s been steadily growing since his fateful experiment in 1962. Since his death there has been a tremendous resurgence of interest in psychedelics, and drug-related overdoses have continued to rise at exponential rates around the world. In fact, overdose is now the number 1 leading cause of death in Americans under 50. Given these circumstances, perhaps it’s inevitable that the ibogaine movement has grown so significantly since Lotsof’s passing.

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Howard Lotsof

Though still relatively obscure, the premise that ibogaine can be used for the treatment of addiction is becoming more accepted. Since 2010 there have been over 200 scientific papers about ibogaine published in academic journals, and legislation to legalize it for medical use has been introduced in states like Vermont. With all of this attention, one might wonder why it’s still so unheard of.

Ibogaine is unlike other psychedelics in that it is potentially cardiotoxic and physically dangerous. The National Institute on Drug Abuse abandoned clinical trials with the drug due to safety concerns spurred by neurotoxicity observed in rat trials (however, the doses were substantially larger than equivalent doses that would be given to humans). Ibogaine is also classified as a Schedule 1 narcotic in the United States, and thus individuals seeking to use it must either find it through the black market or travel to foreign clinics in countries where it is not strictly prohibited.

“Because of the unregulated nature of ibogaine treatments, people are playing a lottery as to what kinds of results they will get,” says Hattie Wells of the Beckley Foundation. “Ibogaine clinics range from very good to pretty dangerous, and I wouldn’t recommend people take it without experienced medical supervision and a proper post-treatment program of support in place.”

That it elicits powerful visionary experiences lasting for up to 3 days is yet another factor contributing to the lack of acceptance for ibogaine as a legitimate treatment in the medical world.

“There are examples of licensed medications that carry cardiac risks, but none which also exert long lasting ataxia and a psychedelic trip. It’s not what conventional medicine would call very useable,” Hattie explains.

Ibogaine sits at the intersections of numerous social issues, tossed between movements for drug users advocacy, drug policy reform, and psychedelic research like a political hot-potato. Nobody seems to want to touch it, and yet there seems to be no better option in sight.

Amy was one of several people I spoke with at the Ibogaine Forum who had tried conventional treatments, such as methadone maintenance and 12-step programs, with limited or no success. Desperate, she ultimately turned to ibogaine as a last resort.

This conversational series is an exploration of these stories, a comprehensive look at the use of ibogaine as a medical intervention, a religious sacrament, and a source of misinformation and controversy. Opinions about ibogaine seem to vary from one extreme to the other in virtually every context– its efficacy as a treatment for addiction, its safety, and even whether or not it should be regulated at all are contested by advocates and opposition alike.

I found Amy’s story particularly important to include because of how effectively it highlights the nuances of the ibogaine world. For example, it didn’t really work all that well for her, initially.

“I did a lot of research before going to the clinic in Mexico, but it actually was not a very positive experience,” she told me. “I left the clinic in a wheelchair. I couldn’t even walk. I was still having serious withdrawal that lasted for weeks after the ibogaine experience.”

When I first heard about ibogaine, I was given the impression that it’s a straightforward cure for drug addiction, a kind of magic pill that you take once to solve all your problems forever. Most of the information I could find online seemed to follow this same narrative. Yet quite frankly, there’s nothing straightforward about ibogaine at all.

Many advocates are cautious of how ibogaine may be integrated into a medicalized pharmaceutical framework, with access to it overseen by regulatory agencies with little accountability. Some voices have expressed concerns about the long-term sustainability of international demand for ibogaine, claiming that iboga is becoming scarce due to unsustainable overharvesting. Others believe these claims are politically and economically motivated.

Over the next month, Psymposia will be releasing a series of interviews and conversations featuring key figures in the ibogaine movement. Our goal is to explore diverse, and often conflicting, perspectives on the relevant issues. We spoke with clinical researchers and facilitators, underground providers, activists, policy workers, and of course, individuals who have taken ibogaine for medical, spiritual, and recreational purposes.

Amy did eventually get through withdrawal and her cravings disappeared, temporarily. Her exposure to ibogaine provided a valuable window of opportunity for her to begin making the changes necessary for her recovery.

“I had some serious trauma in my life prior to taking that ibogaine dose, and the experience helped me resolve that trauma in a way I hadn’t been able to with years of counseling. I walked out thinking, once my withdrawal was completely over with and I realized my cravings were gone, ‘This is pretty amazing.’”

The political stigma attached to ibogaine is so strong that I had to agree not to use Amy’s real name in anything published by Psymposia. Amy could lose her job and see the end of her career as a nurse if her employers were to learn that she had ever used ibogaine, despite the fact that it’s a legally prescribed medication in her country.

Like ibogaine itself, there’s much more to Amy’s story than what’s presented here. As we dive into the complexities of the ibogaine world, we’ll revisit Amy on her path to recovery. For now, we’ll start by taking a look at the cultures that have used iboga the longest. Our exploration begins in the heart of the equatorial rainforests of west-central Africa, specifically, in Gabon.

*From the article here :
 
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Former underground provider, Dimitri Mugianis, on the regulation of Ibogaine

by Jordan May | Psymposia | 18 Dec 2017

“Prescription is not about accessibility, by definition it’s about restriction. Unless we start to use psychedelics as a way to tear apart these structures and build new ones in their place, then I think it’s all a revolving door.”

Dimitri Mugianis is well known in the ibogaine world for his work as an underground provider in the early 2000’s, and for his fiery no-nonsense approach to psychedelics, drug policy, and social justice. Dimitri currently works at the New York Harm Reduction Educators and is the founder of We Are The Medicine, a group working to center conversations surrounding spirituality and drug use.

What follows are the highlights of our conversation. Knowing that Dimitri infuses a political praxis into his work, we were particularly interested in his perspective on the regulation of ibogaine in the United States.

So, what’s your relationship with ibogaine?

I first heard about ibogaine probably in 1991 or 1992. I was injecting heroin, getting high with some people, Greta and Adam Nodelman. They were involved with Howard Lotsof in Holland. Adam was American and Greta was Dutch. They were involved in the anarchist movement, the squatters movement, and so forth. They told me about this thing called ibogaine that they had both taken. They said it was a life changing experience. That was the first time I ever heard anything about it.

It took me probably about 10 years before I actually took ibogaine. I was around it in New York, so I ended up contacting Dana Beal and he told me where to go. I went to Holland to do it. At that point I had been using for 20 years, injecting heroin and cocaine. I was also on methadone, so my habit was very big. My pregnant common-law wife had died, many of my friends had died, so I just made the move.

I did the treatment right outside of Amsterdam, and afterwards I never had a desire to use again. It was an incredibly grueling process. I went right off of methadone into the treatment. I took iboga actually, not ibogaine, for the first time. It was a powerful experience. I didn’t go through the process of physical withdrawal that I knew would be associated not only with heroin withdrawal, but methadone withdrawal – which is crushing. I spent the next 3 months in Greece, where my people are from.

I came back to the States and continued in my recovery. I enrolled in 12 steps, but I had a burning desire to help others who didn’t have access to this treatment. So I began to administer ibogaine to people in the underground. For some of that I worked with Eric Taub, one of the pioneers in the ibogaine world, and we handed out fliers in front of methadone clinics. I treated over 500 people and was eventually initiated into Bwiti, in Gabon. I went back 6 times, studying and being involved in ceremony, and eventually I incorporated the ceremonies into my work.

And then in 2011, I was preparing for the last treatment I was going to do in the States before burning out, and I was arrested by the DEA – and that’s a whole other story.

Have you remained in touch with any of the people who you provided treatments for?

I’m still in touch with a lot of them. Many people that I’ve worked with have framed it in a positive light. Not everyone, some of them just say they threw up a lot and saw weird shit, or didn’t see anything.

But I can tell you one story about a guy named Marcus. When I met Marcus he was kicking methadone and in really rough shape. We were doing the treatment and on the 2nd day he ended up running off. This was very early in my practice and we didn’t know how to keep people in, and it was just a bad scene.

Weeks later, I was really worried about him and happened to see him in the park. He was carrying CD’s under his arm, to sell for money, and he was wearing the same t-shirt he was wearing when he ran out. He was greasy and looked tired. And when he saw me he dropped the CD’s, burst into tears, put his arms around me, and told me it had changed his life. But he was still using, and Marcus eventually OD’d and died. He’s been dead maybe 6 years now.

I’ve stayed in touch with a lot of people and some haven’t used. Some have. I think the idea of a linear healing, with sobriety as the final result, produces shame. When people come back from these experiences, there’s all kinds of things that can be learned. Whether it’s around abuse and trauma, identity, sorrow, grief, all those things.
I’ll tell you something. Tomorrow I’m going to the funeral of someone who’s done ibogaine more than anyone I’ve ever met. I mean he probably did ibogaine over 20 times, flood doses. He died from an overdose last weekend, and he was like my little brother.

So I think that yes we need more maintenance. Methadone, Subutex, etc… should be more available. Yes, we need more treatment facilities. Yes, we need 12 step models and alternative models for those folks whom 12 steps doesn’t work for. Yes, we need harm reduction facilities. Yes, we need holistic healthcare. Yes, we need psychedelics.

But this brother did it all. And he still couldn’t stop.

You’ve been on both sides of the coin, so to speak – as someone who’s personally faced addiction and lost friends to it, and as a provider for people who didn’t have access to traditional treatment models. Given your experiences, and your politics, what are your thoughts on the movement to regulate ibogaine in the United States?

I think it’s a really complex question. My first thought is that it could be a helpful drug, but I think the existing medical paradigm is extremely damaging. Not only the medical paradigm, but our economic structure, which I think the psychedelic movement is desperately trying to be a part of. To me, it really shows the limitations of these drugs and these practices. The problem is that we come out of these powerful experiences and we immediately try to find a way to reintroduce them to these destructive paradigms that are destroying life on the planet.

So I think we need to have a structural analysis and approach to any sort of treatment modality. You have to look at what that system is looking for, and that system is not looking for detox – it’s looking for maintenance. There’s a lot of good reasons for maintenance approaches, but we also have to look at the prospect of turning someone into a perpetual consumer.

Many of the proponents of ibogaine are calling it a cure, but they’re looking at it in a linear way – with a beginning, a middle, and an end. In my experience with iboga it simply doesn’t work that way. How many people have actually taken it and changed their lives, or have stopped using drugs permanently? It’s in the thousands. Not the hundreds of thousands, and I don’t even think in the tens of thousands. So the numbers aren’t even there.

And if it were to get through the entire legislative process it would be put into a clinical setting. So what I would ask your readers is, “Why is the best place to take psychedelics with a shrink?”

I think that if you look at it, we’re handing these tools over to folks who have not stood the test of moral authority. I think they failed it drastically. I don’t think that the medical establishment has the moral authority to be the gatekeepers of this or any drug.

Again, when we talk about sobriety as the final result, it produces shame. It produces the same toxic relationship to oneself that brings people into addiction in the first place. I call it “psychedelic gaslighting”, the idea that there’s no such thing as a bad trip. That if you had a bad experience it was because you didn’t “work” hard enough, you didn’t let go. Fuck letting go. It’s just more shaming. We shouldn’t always try to reframe the experience when somebody has a bad time. We should stop the gaslighting.

So do I think it’s a good thing? I think that almost everything that comes out of the system at this point is just poisoned fruit. Say we bring ibogaine into the for-profit medical model we have now, that gives insurance companies the power to decide who gets treated – so who’s got good insurance, who’s got bad insurance, right?
We have to remember that prescription is not about accessibility, by definition it’s all about restriction. Unless we start to use psychedelics as a way to tear apart these structures and build new ones in their place, then I think this is all a revolving door.

You mentioned that someone may only take ibogaine a few times throughout their life, but microdosing is a hot topic right now. How do you feel about microdosing ibogaine, and how does it fit into a regulatory model?

I don’t think we can look at it in a vacuum. Let me just say that microdosing has been happening for thousands of years in Gabon. People take small amounts of it – and it’s great.

I just want to say it out loud. These drugs – psilocybin, MDMA, LSD, iboga, ayahuasca – are drugs that get you high. And they can be fun. I know it’s not politically correct to say that. No matter how many fucking naked Burning Man parties you’ve been to, you’re Protestant and you want to call this shit work. Ibogaine is a great aphrodisiac, it’s great to dance on, and it’s great to just walk around on.

We’re always looking for work. You know, all this shit about LSD helping people in Silicon Valley be more productive; I would hope that the opposite is true. I’d hope that we take psychedelics to be less productive in this system. Again, we’re in a Protestant, capitalist society and we can’t think outside of that.

So what I’d say about microdosing is let’s take the professionalism out of it. Why do we have to professionalize it? You don’t need a professional to microdose. I’ll break it down for you: take a little bit. If it’s not enough, take a little bit more. If it’s too much, take a little bit less next time. End of story. You don’t need a fucking shaman. You don’t need a fucking shrink. You don’t need a doctor, or a social worker, or a corporation to tell you how to do that. Real simple. And if it doesn’t seem to be doing you any good, stop taking it.​

Microdosing done.

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L-R: Dimitri Mugianis, Patrick Kroupa, Margo, Jeffrey Kamlet, Norma Alexander-Lotsof, Howard Lotsof

Do you have any closing thoughts for us?

Although ibogaine can be dangerous, I think the greatest impact from it will come from access without the even more dangerous contact with professionals. I think one reaction to the over-medicalization and high price of boutique ibogaine clinics is that a lot of people are just getting it off the internet to dose themselves. I think this is the most important trend in the movement today, and something that’s not really being talked about – or is only being talked about negatively.

Obviously there are great dangers involved, but there are also benefits. It’s a great failure of the ibogaine community, that we often fall into prohibitionist attitudes such as “Just Say No.”

Collectively, we need to come up with a harm reduction strategy for self-administration. People are taking ibogaine themselves and will continue to do so, so we need to address it.

I’m heartened to see folks being able to buy the drug online and self administer; however, I don’t believe iboga has the potential to significantly impact the so-called heroin epidemic. The plant itself is in great danger – some people are even saying it’s on the verge of extinction – so we need to be mindful that with accessibility comes exploitation.

Yet, despite my misgivings about the medicalization and commodification of ibogaine, the truth is that my life has been transformed, my body transmuted, and my spirit forever changed by this molecule. It set me on a journey of healing that has taken me around the world, even to jail. And it continues to inform me, challenge me, and propel me. I am blessed.​

 
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Ibogaine treatment comes with risks. We had a discussion about safety with medical providers*

by Mike Margolies | Psymposia | 3 Jan 2018

Unlike other psychedelic drugs, ibogaine is known to be potentially cardiotoxic. There are a number of fatalities associated with its use, and anyone considering working with it should be aware of the risks. Read the full series.

Update January 4, 2018: Today, unfortunate news broke that one of the panelists in this article, Anwar Jeewa, was arrested in connection with a fatality at his ibogaine clinic in South Africa. A post-mortem established that the man had overdosed on Xanax, with ibogaine in his system. This underscores the real risks of ibogaine, even with an experienced provider. More information about ibogaine potentiation of benzodiazepines is available in our previous interview with Clare Wilkins.

Unlike other psychedelic drugs, ibogaine is known to be potentially cardiotoxic. There are a number of fatalities associated with its use, and anyone considering working with it should be aware of the risks.

The following are highlights from the safety panel at the European Ibogaine Forum in September. The panel was made up of experts in cardiology, nursing, and ibogaine facilitation.

This conversation is in no way intended to serve as an authoritative guide to safety protocol. What’s presented here is limited in scope and only scratches the surface of factors that should be considered. We strongly encourage anyone thinking about working with ibogaine in any capacity to take the time to do further research. As one resource for more information, you can check out the clinical guidelines established by the Global Ibogaine Therapy Alliance.

Dr. Jeffrey Kamlet is an expert on cardiac safety in ibogaine treatment who has witnessed over 1800 sessions over the past 20 years.

Jamie McAlpin is a nurse and Co-Founder of IbogaSafe, an on-site training service aimed at reducing the amount of adverse events during ibogaine treatment.

Dr. Uwe Maas is a clinical pediatrician who was initiated into the Mitsogho men’s cult in Gabon.

Anwar Jeewa is Director and Founder of Minds Alive Treatment Centre in Durban, South Africa.

Panel moderated by Mike Margolies.

Mike: So let’s kick this off with a straightforward question. I’m afraid to take iboga or ibogaine. Should I be? Can it be done safely?

Jeffrey:
In general, ibogaine is a pretty damn safe drug.

In the healthy population, the mortality [rate] for ibogaine is considered to be about 0.3%, but remember we’re treating a very sick patient population. Patients with HIV, hepatitis, alcoholics — not the healthiest population in the world. Looking at numbers, the mortality rate can be as high, in untrained hands, as 3%.

I have a folder of over 60 ibogaine deaths. Every single one of those could have been avoided. Every single one. These people had severe addictions. Some of them had anorexia, bulimia. Some of them had pre-existing heart conditions.

So how safe is it? I mean if you’re young and healthy and you’ve got a normal EKG, you don’t have congenital prolonged QT syndrome, and you don’t have other drugs on board that are QT prolongers, yeah pretty safe.

Mike: Jamie, you have something to add?

Jamie:
Yeah, I just want to add that the human body can only take a certain amount of metabolic stress, and ibogaine does stress the body on a metabolic level. Detox is very metabolically stressful as well, so those two things in combination tend to potentiate each other a little bit. Several of the cases that I reviewed [showed] signs of metabolic acidosis and other severe metabolic stressors, and that’s something the body can’t really handle.

Jeffrey: Many of our clients come to us addicted to opiates and benzos. [Many] who say, “Well, I was taking Xanax and I took ibogaine, and I never took another Xanax again.”

Well good for you. I’m here to tell you that ibogaine does nothing for benzodiazepine withdrawal. It does not help at all. It’s a different part of the brain, and it just doesn’t work. I’ve seen people on low doses still [experience] horrible anxiety because they missed their benzos. If you don’t realize that your patients are taking benzos and you stop them, or they’re alcoholic, the risk of having a seizure is very high.

Mike: I have a question about microdosing safety. Regarding the classical psychedelics, LSD, psilocybin, etc., which are not known to be cardiotoxic, I’ve read some papers saying there are potential cardiac risks with long-term microdosing. Is that something that could be a concern for ibogaine?

Anwar:
To be very honest with you, it’s about time that we research microdosing. It’s crucial. None of us have the facts yet. If you listen to stories about people microdosing, it’s always different quantities, different sources. [We’re] not getting any consistency in any of the reports, so it’d be wrong for me to give you an answer for something we don’t know yet.

Jeffrey: I very often give boosters after a flood dose. Especially if you’ve been on like, Suboxone for 10 years, you might need some small doses. I’m talking about 100-200mg of ibogaine. You don’t have to be monitored, you can go play on your computer, watch TV. Then maybe 3 days later they get the 100mg and 3 days later 50mg, and now they’re good to go home.

On a related noted, in my opinion using another psychedelic drug 90 days within ibogaine is pure insanity. There [are] clinics now advertising that they give you ibogaine and 7 days later give you ayahuasca. It doesn’t make sense to me. I think it’s disrespectful of the plant; it’s disrespectful to both these substances. It’s scary to me. [Ibogaine metabolite] noribogaine is supposed to last [in the system] for 90 days. Keep that a pure experience.

Jamie: It’s a very disturbing new trend – clinics offering ayahuasca, kambo, DMT, all these things while people still have a lot of noribogaine in their system. It’s not only unsafe, it’s very reckless in this vast uncontrolled experiment that we’re doing. And it’s not ethical. You’re literally turning your patients into human experiments without their consent. So from a legal standpoint, it’s not ethical at all, and it’s a very dangerous and reckless trend.

Anwar: I spend at least 2 hours on orientation and preparation. I think it’s important, especially for medical professionals, that you need to have informed consent. It’s our responsibility to tell the patient everything about ibogaine, the good and the bad. You explain everything and basically give them the worst-case scenario, not to scare them but to prepare them for what can happen.

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Safety panel at the European Ibogaine Forum, Vienna; Dr. Jeffrey Kamlet, Jamie McAlpin, Dr. Uwe Maas, Anwar Jeewa, and moderated by Mike Margolies

Jeffrey: I also wanted to mention something I didn’t before. Don’t stack dosages, ok? As ibogaine is being converted by the liver into noribogaine, you start to see these bizarre T waves, the QT prolonging, the blood pressure going down, and the pulse going low. I’m concerned when I do that baseline EKG and the patient has a QTC baseline of 430 or 460. Whoa, ok not a good candidate for ibogaine.

There’s a blood test you can do, a genetic test, for congenital long QT syndrome. I think it’s 1 per 1000 of the population or something like that [who are born with it]. If you give them ibogaine, you will kill them. If you’re getting a baseline EKG on the patient and their QTC is in the 400’s or above, you better be really careful with that patient or defer to somebody who has a full cardiac setup.

Mike: I’ve got one more question for Uwe, then maybe we’ll open it up for other questions. So it sounds like from everything that’s been said so far, there’s obviously safety concerns around ibogaine and we need more research, but then of course iboga has been used for much longer in Gabon. So my question is, what kind of safety protocol is there in Gabon?

Uwe:
During my initiation, I was told to report constantly about what I was seeing. I was led by about 8 experienced healers, who were sitting around me. They knew everything that was happening to me, and they told me to avoid these people, or open that door, or ask this person something, and things like this.

We were discussing with the Gabonese about the ibogaine treatment that is done in the West, and the only thing that they were really shocked about is that we’re not playing Bwiti music. They said, “Oh that’s very dangerous. They will all die.”

There’s so many things they’re doing for safety. I think the most important of all is that an initiate is never alone. There are always several experienced healers, several initiated people around.

Mike: So, questions from the audience?

Audience member:
Jeffrey said that it’s dangerous to flood and then give another dose, so I wanted to ask the people who’ve been to Gabon if it’s common in Bwiti to keep on feeding iboga? Because I know there are ceremonies happening where [they] keep on feeding [iboga to the initiates] for 3 days.

Süster: Our experience with the Mitsogho tribe is that they were giving test doses and then 14 hours later, the flood dose. That was with the women. [The Mitsogho] never take a flood dose twice, but we know the Fang tribe does it one day after the other. We don’t know how safe this is, and as far as we know, the Mitsogho initiation is the original one.

Jean-Nicolas: In my experience, there are many different ways to do it. You’ve got the Disumba, for example, where the aim is that the Banzi (novice), they have him eat as much iboga as possible until he lies down, and when you pinch him, he won’t feel anything. That’s what they look for.

Anwar: I notice when giving [patients] that small dose initially, they’ve got an hour to play with. We get an idea of their tolerance level because if they feel absolutely nothing, and most of them feel absolutely nothing, then we can give them a bigger flood dose. But if they do feel something, we can drop the flood dose.

I’ve been practicing only one method and my protocol is very standard, but I use it because I find it to be very safe. We do a rough calculation, according to body weight, to get a minimum dose and a maximum dose [for the patient]. We give [the initial dose] depending on the patient’s tolerance level, and then we wait every 2 hours before we give more.

Uwe: I think if you look at the traditional ritual, everything, literally everything, is designed to make the [initiate] feel safe. The fire, the blessings, the drinks for the ones who are helping, everything is designed to make the [initiate] feel safe, and that’s the strong point of the ritual, in my view.

Mike: Any closing thoughts?

Jamie:
I just want to add that providers really need to grasp that this is an extreme responsibility they’re taking on. When you give someone ibogaine, it’s potentially cardiotoxic, and heart patients don’t get sick slow. They get sick very fast, and seconds count. Not minutes, but seconds. So there’s a lot of preparation not only for the patient, but for the provider — to know what to do when the shit hits the fan.

*From the article here :
 
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Ibogaine vs. iboga alkaloids for treating addiction

by Alexandria Jaeger, MSc | Psychedelic Science Review | 11 Jan 2021

Novel chemical variants of ibogaine may offer therapeutic benefits without severe side effects.

Due to its wide net efficiency in intercepting various addictions, ibogaine has been used by shamans in West Africa for many centuries. It is becoming a larger player in the pool of sexy psychedelics to research, due to this rare efficacy and broad use. Isolating the ibogaine alkaloid, found most commonly in the Tabernanthe iboga plant, faces ethical and environmental challenges. Despite its intriguing qualities, this makes it difficult to engage as a viable compound to assist in the epic, wide-range battle of addiction.

There are two ways to isolate an alkaloid like ibogaine: removing the existing molecule from its plant of origin or building the molecule from look-alike alkaloids. Dr. David Olson’s lab at the University of California Davis has been looking into the latter, using Iboga-type alkaloids, hoping to circumvent these extraction challenges faced by the Iboga plant.

Iboga-type alkaloids are structurally and/or neurochemically similar to ibogaine. Hundreds of compounds like voacangine and coronaridine have been identified, yet limitations on synthesis efficiency still remain. Ibogaine has traditionally been extracted from plants found in western parts of Africa. But in the past 10 years, more plants in Mexico, China, and Malaysia that contain Iboga-type alkaloids have been identified. The goal is to use other plants, or series of plants, to mine for these alkaloids.

Why are researchers willing to go to such great lengths to isolate ibogaine?

Ibogaine is unique in its ability to physiologically reduce withdrawal and psychologically initiate neuroplastic changes on broad addictions. The known neurobiological circuitry of ibogaine is confusing, to say the least. Various research has shown its ability to reverse addiction to opiates, stimulants, alcohol, and nicotine. Ibogaine and noribogaine, bind promiscuously with weak strength to a number of receptors across the brain – serotonin, opioid, acetylcholine, sigma, and NMDA receptors, affecting both neurotransmitter release and transport.

The impacts of ibogaine on brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) are lead players in contributing to broad structural brain changes. Ibogaine regulates BDNF and GDNF expression in brain regions involved in the pathophysiology of addiction and has led researchers to hypothesize their involvement with some of the long-lasting effects observed.

Dr. Olson’s lab has been looking into psychoplastogens, small molecules that can quickly regulate larger molecules like BDNF and GDNF expression, upon a single administration, with sustained effects. Ibogaine has been shown to be a promising psychoplastogen, efficient at rewiring characteristically stubborn neural circuits, in a circuit-specific manner. New Iboga-type alkaloids could provide relief to the environmental complications of harvesting the Iboga plant, as well as help characterize unknown biosynthetic pathways.​

What makes a good Ibogalog?

Things get more complicated as the cardiotoxicity of ibogaine is well known to researchers, landing it in the Schedule 1 category of narcotics. Iboga-type alkaloids (ibogalogs) are novel variants on the ibogaine molecule, which may produce similar effects on substance use disorder but lack the health risks to the heart. In addition to easier extraction, the goal is for researchers to identify a group of ibogaine analogs, that produce less of the undesired side effects.

With ibogaine’s mechanism being poorly defined, the understanding of what makes a good molecular structure is missing. Because ibogaine-like effects centered around some difficult to synthesize carbon ring systems (isoquinuclidine ring system, tetrahydroazeepine, and indole rings), it is difficult to allow the function to drive the synthesis of new molecules.

Dr. Olson’s team has started to develop and sift through some of the potential ibogalogs, which vary in their binding affinity profile, thought to be a major contributor to mimicking ibogaine like effects. Few of these have been found and tested, as it is hard to know what to look for in a dark room. The compounds 18-MC and 18-MAC are among some of the more researched ibogalogs, although Olsen’s team poses additional promising structures for research.​

Summary

The unknown mechanistic nature of ibogaine’s effect on the brain, combined with the difficult structural synthesis, impairs the ability to functionally or biomimetically explore Iboga alkaloids at a rapid rate. Despite this difficulty, studying these unique compounds’ ability to work globally on addiction pathways, rather than locally on substance-specific ones, is what drives this research.

Exploring various Iboga alkaloids promotes the beginning of a wave of research that identifies substance use disorder treatment as less substance-specific. This allows Western medicine to search for new and more effective drugs while respecting the ethical boundaries of the source.

 
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Johann Hattingh, with dog Kodak and parents Dirk and Anne, in Brits.

Ibogaine a 'near miracle' therapy for addicts*

by Ufrieda Ho | South Africa Times Live | 8 Sep 2020

The heavens didn't come crashing down on Johann Hattingh's head, more like the blue emptied out of the former photojournalist's sky little by little and left in its place a grey haze. And the grey grew steely with rage and melancholy, guilt and despair.

Hattingh worked on SA newspapers and for the UN, finding angles and bending light with a camera even as he stepped over bodies at crime scenes and cheated death by near misses while embedded with the US military in Iraq.

In 2007 he was diagnosed with PTSD (post traumatic stress disorder), but "I felt like I was born to this job," he says of how easily he ignored the root of his mental illness.

In 2012 he says "the industry spat me out." His couldn't pick up a camera again, his relationship ended and he was forced to move in with his parents in Brits in the North West. He didn't emerge from his cottage for days at a time as the dark hells of remembering and regret turned in pursuit, chasing him to the edge of suicide.

Today Hattingh says it was ibogaine treatment that saved him.

Ibogaine is a psychoactive alkaloid derived from the bark of a plant called iboga, native to Gabon. Hattingh had tried several types of treatments and therapists over the years with little success and had heard about ibogaine four years earlier but couldn't afford the treatment.

There's also scant clinical data on ibogaine and lingering concerns and controversies over its safety. Even though the plant is non-addictive it is toxic in high levels and can cause heart failure. There's also a blurred legal and regulatory framework in which treatment facilities operate. In countries like the US ibogaine is banned outright.

By chance Hattingh found the Magalies Ibogaine Wellness Centre in January. "My dad worked on a labour law issue for them, so we met with the clinical psychologist and I remember just crying my eyes out," says Hattingh.

"It was a like a nuclear bomb was dropped on my head," he says of taking the first dose of ibogaine in a five-day-long supervised treatment. It started a 24-hour trance of visions, looping through emotions and brutal confrontation of Hattingh's truths and lies.

This was followed by a "grey day" of physical weakness and purging.

Next came reflection, but with clarity and compassion, not judgment and guilt, and his treatment ended with re-integration therapy, focusing on coping mechanisms for everyday life.

"It was profound; I feel connected now to myself and everyone around me; I can see beauty in the world again and I have a sense of purpose," says Hattingh, seven months after his treatment.

He continues to microdose intermittently - using a sub-perceptual amount of the iboga root for particularly down days.

He's also become an unapologetic ibogaine treatment evangelist and plans to give talks to help others process trauma and he volunteers at the wellness centre.

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Programme director Anso Taljaard started the
Magalies Ibogaine Wellness Centre in 2013.

Clinical psychologist Anso Taljaard started the centre in 2013. Taljaard says the iboga plant has long been used in Gabon as a healing plant and in traditional initiation ceremonies.

It hasn't had significant uptake in the West because it's never been a club drug and big pharma hasn't seen commoditising potential in a maintenance drug that is used once or maybe twice by a patient and is microdosed intermittently.

"Since 2013 we've had about 1,400 patients, with a relapse rate of about 25%," she says.

Those seeking a psycho-spiritual experience with ibogaine also check in to the centre.

Taljaard says meticulous screening and assessment of patients are essential, so is having an on-site doctor, nursing staff, counselling and integration therapy.

Her centre is in the process of being registered, which Taljaard says will introduce minimum-standard guidelines for all facilities and reduce costs through medical aid coverage.

"Ibogaine is not a magic bullet, it's not for everyone, but patients call it 'a lifetime of therapy in a night' and a 'near miracle'," says Taljaard.

She plays back voice messages on her phone from former patients who arrived with trauma, depression, anxiety and substance abuse.

They speak about a deeper understanding and acceptance of things just as they are, worrying less and loving themselves more. Others speak about being able to "defrag" or "reset" their lives.

Kerryn Matthews (Elske), a therapist at the centre, says this "resetting" is the beauty of ibogaine.

"Psychoactive drugs like ibogaine allow us to alter our default neural mode that can be full of negative programming, trauma and anxiety."

"Ibogaine can actually fix parts of our brain through processes called neural regenesis and neural plasticity; it gives us new chemical pathways and new perspectives to create new realities."


She adds that ibogaine's dissociative power makes visions lucid while being experienced with objective distance.

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Izelle Pitman underwent treatment at the Magalies Wellness Centre in April.

Pitman had buried trauma from abuse she endured till she was 12 years old. Then in 2016, when she was expecting her first child, the emotions came flooding back.

Seeing a psychologist weekly and being prescribed drugs didn't work and when her baby was born, severe post-partum depression set in. Ten years earlier she had been in rehab for alcohol, cat (methcathinone) and cocaine abuse.

"The basics like taking a shower were impossible. I would clench my jaw all day and I was just sad. I had a beautiful baby, a wonderful husband and a gorgeous home but I felt like I wasn't good enough," she says.

Ibogaine treatment turned out to be the alternative she needed, even though she experienced apocalyptic, warlike visions and the purging wiped her out.

"It was hard, but by the third day my head felt lighter, like the files full of negative thoughts were cleaned out and I could start again," she says.

Pitman is expecting a second child and says: "Things haven't been 100% since my treatment; some days are really tough. The point, though, is I'm not depressed about it anymore. I can own my story, I feel connected and I know what I need to do to cope better."

*Brian (identity withheld) had his ibogaine treatment in 2014 with a practitioner in Cape Town. Brian's tik (crystal methamphetamine) addiction took over his life in a matter of months, destroying his relationships and bringing out his most destructive nature.

When he was eventually "ready to not die" he started on microdoses of ibogaine for six weeks before his supervised treatment.

"I would call it an experience, not a trip. It was insane. I remember a presence I call an iboga god sitting on me and I couldn't move".

"Everything slowed down and he showed all the parts of me that needed fixing and told me I had to fix it. I was also shown stuff not worth fixing or stuff I would never be able to fix and told to just throw these away,"
says Brian.

Five years on Brian has successfully changed his career to be involved in lifesaving, as he had wanted to do before his drugging.

"Your craving for the drugs just goes, I eventually even quit smoking. But ibogaine treatment is hard work - it can kill you. I also had to break from the old relationships that took me to drugs in the first place," he says.

For Hattingh, meanwhile, his next chapter is just beginning. On the step at his parents' home he sits down to coffee with them and his dog, Kodak. It's something that hasn't happened for years.

Hattingh's mother, Anne, talks about her own ibogaine treatment that she underwent this autumn after watching her son's transformation. At 70, her victory has been coming off years of anti-depressant medication and setting down anxieties and tiptoeing around others.

She says she's found her voice - she also found her son again.

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THE RESURGENCE OF PSYCHEDELIC DRUGS

Clinical psychologist Jennie Ashwal puts the resurgence of psychedelic drugs and the trend of microdosing on natural healing plants down to humans' eternal questing.

"People are always searching for a richer meaning to life and for psychological wellbeing and good health."

"The likes of ibogaine and psilocybin (magic mushrooms, which are illegal in SA) are showing huge potential and there's an allure to using ancient healing plants combined with modern methods like microdosing."


Ashwal says research is showing that psychoactive plants have positive effects on serotonin and dopamine - the feel-good chemicals in the brain.

"More than a pseudo-spiritual effect, ibogaine and psilocybin can build and change the brain chemically," she says.

"They appear to have long-term effects and unlike club drugs there isn't the after-effect of depleting feel-good chemicals. Ibogaine also appears to be able to tap into early traumas quicker."

Her caution is to do the homework in researching distributors, medical professionals and treatment facilities. As she says, "Ibogaine is not play-play; it's not for fun."

"Conventional therapy has its place, as does supervised ibogaine treatment and microdosing in a world where people need to make sense of incessant rushing, isolation and empty goals,"
she says.

"We need more connection, rapport and love. We need to know that anger, sadness and pain are also healthy feelings and that getting through bad days is how we learn to build resilience and coping skills."

 
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What I learned from treating 400+ patients with ibogaine

by Bruno Gomes, M.A. | March 13, 2017

Since the middle of the 90s, there has been a renewed interest in the possible positive effects of many different plants and substances such as LSD, “magic” mushrooms and psilocybin, ayahuasca or iboga. Many new and rigorous scientific studies have been showing promising evidence that those substances are suitable for the treatment of many diseases and disorders such as obsessive-compulsive disorder, post-traumatic stress disorder, substance abuse or even depression. With so many possibilities, we could easily assume that psychedelics are the new panacea capable of curing any ailment. But, what is this cure? How does it happen? How similar are those curing processes to those of conventional medicine?

I’m a psychologist in Brazil and, after more than ten years working with homeless crack-cocaine users, I got involved with ayahuasca and ibogaine treatments, curious about what they could offer. Could these substances help my patients, who I have been struggling so hard to take care of? Since then, I have studied and assisted a group of recovering homeless individuals using ayahuasca, a brew made with Amazonian plants, most commonly Psychotria viridis and Banisteriopsis caapi. I’ve also treated around 400 patients with problematic drug use by using ibogaine. Ibogaine is a substance derived from the root bark of the African plant iboga (Tabernanthe iboga). Both ayahuasca and ibogaine have intense effects on the user’s perception of the world and oneself.

These substances are classified as entheogens, hallucinogens and plant teachers, depending on how they are used. The ayahuasca treatment I studied integrated the rituals of 2 traditional ayahuasca cultures - vegetalismo, with its purges and diets, and the musical healing rituals of Santo Daime. In this context, the brew is considered a plant teacher: a substance with a spirit that communicates with humanity through its effects. The ibogaine treatment, on the other hand, is much more similar to regular medicine. Ibogaine is extracted from the plant, processed by a pharmaceutical laboratory, and then prescribed by a medical doctor in a hospital.

These contexts affect the use and understanding of the substances, therefore changing what is experienced by the patient. This is even more evident when comparing different ayahuasca rituals. The same ayahuasca decoction in the context of a Santo Daime ritual, with bright light and everyone singing together—and then in a Shipibo indigenous ritual, in complete darkness, guided only by the curandero’s voice—will elicit a very different experience.

Especially interesting in this complex relationship between setting and experience is the element of mystery. Within a medical context, and never having heard about the African traditional cults with iboga, many patients that I’ve given ibogaine to still reported seeing or being visited by the “iboga spirit”; usually an old African woman or ancestral healer.

The reports and testimonials about these 2 substances are very impressive: the intensity of the experiences, as well as the sudden and deep transformations gained through them, attract more users every day; either looking for something new or different, or a spiritual or healing experience. Together with these reports, new scientific research on ayahuasca and iboga shows promising new and effective treatments for problematic drug use and alcoholism. There’s also constantly new data to show psychedelic substances use in treatment of obsessive-compulsive disorder, tobacco dependence and PTSD.

In the context of these reports, patients interested in ibogaine treatment often expect a new and powerful medicine. As aspirin reduces fever, they expect ibogaine to take their drug dependency away; something fast and effective that solves the problem for good. It would be perfect if ibogaine or ayahuasca could cure with the speed of aspirin, no matter the setting. With aspirin, it doesn’t matter where one takes it or if one believes in it, it will still reduce fever. With psychedelics, it’s not like that: the patient’s expectancy, his trust in those responsible for the experience, as well as what happens in the surrounding environment, will exert an intense influence on the experience.

These factors not only affect the experience, but also the outcome. The experience with the substance needs to be part of a process in which certain things happen before and after the experience itself. A recent study at Johns Hopkins' showed the impressive effects of psilocybin sessions in stopping cigarette smoking in patients for more than 6 months. But, psilocybin has this effect when inserted in a process like the one on the study, with sessions of cognitive-behavioral therapy. It’s not as simple as eating psilocybin “magic” mushrooms and then losing the craving to smoke, although it would be wonderful if it were that easy!

How can an intense psychedelic experience lead to important changes in daily life? We need to desire them, and make a determined effort to change. Usually, those kinds of changes are supported in a relationship, be it with a therapist, a doctor, a healer, a shaman, a religious leader, or a group. Each one of the psychedelic substances tested exist within a context: specific ways of understanding the substance use and different ways of dealing with them; sometimes, in a religious, modern or traditional ritual. Those relationships are important for the patient when going through the process, and also to give meaning to the experience.

Many patients arrive expecting a “magic pill,” a new medicine that would solve everything for them, and that has a negative effect on their process. I receive patients in my office before, and after they take ibogaine. Most of the time I can clearly see a difference: they are calmer, it’s easier to face daily challenges and focus on what is important in their lives, and there’s a lack of craving. But it doesn’t mean that the addiction is cured, and not all of them can take advantage of these effects to really overcome their problem.

After ibogaine, many patients are aware of all they need to change in their lives; but really changing their habits is usually harder, as it depends on the patients. If the substance had solved everything for them, why change anything else in their routine? Many of them can’t get out of their established routines, and after, they just go on living in the same way: going to the same bars, meeting the same friends, looking for the same types of pleasures, and one day or another they’ll return to problematic drug use. When we need to change, it will always require effort from ourselves, but if we expect for someone or something to solve our problems for us, it may not be possible.

So, despite the increasing interest in ayahuasca, iboga, ibogaine, psilocybin, and other psychedelics in general, those substances, and the experiences they trigger, are still a new and vast continent to be explored. We are only now beginning to understand the complex interactions between psychedelic substances, psychology, and the setting in which people consume the psychedelic substances. It seems that psychedelics function differently from the traditional Western medicine remedies, and may be better understood as a therapeutic tool.

https://chacruna.net/treating-patients-with-ibogaine-ayahuasca/
 
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The future of medical ibogaine*

Psychedelics Today | Apr 22 2019

Ibogaine is a psychedelic chemical found in the West African shrub Iboga. Bizarre in chemical structure and psychoactive properties, the drug remains mysterious to scientists and psychonauts alike. At high doses, ibogaine causes intense, unforgivingly introspective and dream-like hallucinatory experiences that can last upwards of 24 hours. The African psychedelic might have remained nothing more than a curiosity in the West if not for the discovery of its ability to disrupt physical and psychological drug addiction. Thousands of anecdotal reports and preliminary scientific research provide evidence that a single dose of ibogaine can eliminate both withdrawal symptoms and craving in drug addicts. In the United States, ibogaine remains a schedule 1 drug, and those seeking treatment must pilgrimage to countries that do not regulate it or take a chance with illegal underground treatment centers. What will it take for ibogaine to become medically available in the United States?

New drugs must undergo a rigorous vetting process to move from discovery to the legal market. To become a prescriptible medication, drugs must pass through clinical trials regulated by the Food and Drug Administration (FDA). These trials consist of a pre-testing phase, four clinical phases, and regulatory checkpoints throughout. Advancing to the next phase is predicated on successful completion of the prior phase.

Before moving to clinical trials, researchers must collect extensive pre-clinical data and submit an Investigational New Drug (IND) application to the FDA. Pre-clinical studies use rodent models to determine how effective the drug is for its intended purpose and its safety.

Phase 1 is the first set of studies to determine the safety and efficacy of the drug in humans. If these studies are successful, researchers can proceed to Phase 2, which are well-controlled studies with larger populations. Phase 3 studies test safety and efficacy with different dosages of the drug in even larger populations comprised of various demographics. While the time it takes to move through all phases varies, this process can take many years. After successful Phase 3 trials, the FDA reviews the data and the researchers submit a New Drug Application (NDA). The FDA reviews the NDA and the drug’s labeling to ensure accurate and sufficient information is provided to the consumer and drug-provider. The drug production facility is also inspected by the FDA for health and quality assurance. If the drug is approved, it will be released on the market and available for prescription. Phase 4 trials occur only after the drug has been approved and is publicly available. In Phase 4, the drug manufacturer must continuously monitor the effects of the drug in patients and submit safety reports to the FDA.

For ibogaine to come to market, it must pass through each of these clinical phases of study. Remarkably, ibogaine began the process of becoming an FDA approved therapeutic medication in the early 1990’s. Pre-clinical and Phase 1 trials conducted by Dr. Deborah Mash at the University of Miami supported the anecdotal evidence that patients had significantly reduced drug withdrawal and craving following ibogaine administration. These trials ended prematurely as a result of several factors, including criticism from the pharmaceutical industry, the apparent costliness to continue, and an intellectual property lawsuit between Mash and Howard Lotsof. No clinical trials have been conducted with ibogaine since this preliminary work over 20 years ago.

Another issue facing the medical legalization of ibogaine is that it cannot simply be prescribed in pill form by a doctor. The drug must be administered in a therapeutic setting, potentially as an aid to psychotherapy, as is the case with MDMA. Pre- and post-counseling are vital to ensure proper translation and integration of the psychedelic experience, as well as addressing the underlying problems that contribute to drug abuse. Furthermore, patients must implement changes outside of the clinic to ensure successful treatment outcomes. This means getting away from the external factors that contribute to drug abuse, which can include leaving relationships with friends, family or partners, and/or moving to a new area. While legalization for medical application is important, there must also be infrastructure developed to support proper administration of the drug.

There have been cases of death associated with taking ibogaine. However, none of these cases have been a result of overdose or toxicity. Individuals with certain heart conditions are at a higher risk of cardiovascular-related death after consuming ibogaine, and taking drugs of abuse with ibogaine may cause adverse reactions that can result in death. Rather than supporting the case against legalization, the risk of death for certain patients further evidences the necessity of legalization: unlike some clandestine ibogaine sources, regulated treatment centers would have the resources to screen patients for comorbidities (reasons not to ingest the drug) prior to ibogaine administration.

While the legal status of ibogaine in the US makes research a significant challenge, countries in which ibogaine is unregulated provide the opportunity to study its use in legal clinics. In 2017, the Multi-Disciplinary Association for Psychedelic Studies (MAPS) sponsored two studies investigating the efficacy of ibogaine in Mexico and New Zealand. With abundant data available for legal collection across multiple fields of study, scientists are just beginning to scratch the surface of ibogaine research. Those interested in studying ibogaine should not be discouraged by the barriers in the United States and should look abroad for more opportunities.​

*From the article here:

 
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Ibogaine inhibits hERG channels: A cardiac arrhythmia risk!*

Xaver Koenig, Michael Kovar, Stefan Boehm, Walter Sandtner, Karlheinz Hilber

Ibogaine, an alkaloid derived from the African shrub Tabernanthe iboga, has shown promising anti-addictive properties in animals. Anecdotal evidence suggests that ibogaine is also anti-addictive in humans. Although not licensed as therapeutic drug, and despite evidence that ibogaine may disturb the rhythm of the heart, ibogaine is currently used as an anti-addiction drug in alternative medicine. Here we report that therapeutic concentrations of ibogaine reduce currents through human ERG potassium channels. Thereby, we provide a mechanism by which ibogaine may generate life-threatening cardiac arrhythmias.

In preclinical studies on animals, ibogaine, an indole alkaloid derived from the root bark of the African shrub Tabernanthe iboga, has shown promising anti-addictive properties: ibogaine attenuates opioid withdrawal signs and reduces the self-administration of a variety of drugs including opioids, cocaine, nicotine, and alcohol. The inhibition of dopamine release in the nucleus accumbens as essential part of the brain’s reward systems offers an explanation for ibogaine’s anti-addictive actions. The underlying molecular mechanisms may involve interactions with neurotransmitter transporters as well as opioid and glutamate receptors, effects that have been observed at ibogaine concentrations between 0.1 and 30 uM.

Since ibogaine interacts with numerous different cellular and molecular targets, its potential to generate adverse effects is significant. Besides the expected neurotoxic actions, ibogaine also affects the cardiovascular system. In both animals and humans, high doses of ibogaine decrease the heart rate. Alarming are several reported cases of sudden deaths with unclear cause after ibogaine use, which have been hypothesised to be related to cardiac arrhythmias. In accordance with this hypothesis, a severely prolonged QT interval of the electrocardiogram (ECG), associated with ventricular tachyarrhythmias, was observed in a 31-year-old woman after she had taken a single dose of ibogaine.

Here, we provide the first experimental evidence on the mechanism by which ibogaine may generate life-threatening cardiac arrhythmias: inhibition of human ERG (hERG) potassium channels in the heart. Conducting the rapid component of the delayed rectifier potassium current IKr, hERG channels are crucial for the re-polarisation phase of cardiac action potentials. hERG current reduction, either due to genetic defects or blockade by drugs, delays cardiac repolarisation resulting in QT interval prolongation and in an increased risk for Torsade de Pointes arrhythmias and sudden cardiac death. Consequently, hERG channel blockade has become a common reason for drug failure in pre-clinical safety trials.

*From the article here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888945/
 
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The efficacy of ibogaine in the treatment of drug addiction
STUDY: A mixed-method analysis of persisting effects associated with positive outcomes following ibogaine detoxification - Davis, et al. - 2018
STUDY: A phenomenological analysis of the subjective experience elicited by ibogaine in a drug dependence treatment - Schenberg, et al. (2017)
STUDY: A phenomenological investigation into the lived experience of ibogaine and its potential to treat opioid use disorders - Camlin, et al. - 2018
PAPER: An end to the opioid epidemic: New study suggests ibogaine treatment could be a game changer - Garcia, Barsuglia (2017)
PAPER: An ibogaine treatment protocol - Geerte for Lindesmith Centre
THESIS: Breaking the habit: Ibogaine as a viable treatment for opioid dependence and withdrawal - Matthew Styles (2014)
STUDY: Case studies of ibogaine treatment: Implications for patient management strategies - Lotsof, Alexander (2001)
STUDY: Changes in withdrawal and craving scores in participants undergoing opioid detoxification utilizing Ibogaine - Malcolm et al. 2018
STUDY: Clinical guidelines for ibogaine-assisted detoxification - Dickinson, McAlpin, Wilkins, Fitzsimmons, Guion, Paterson, Greene, Chaves (2016)
STUDY: Detoxification from methadone using low, repeated, and increasing doses of ibogaine: A case report - Wilkins, et al. (2017)
THESIS: Experiences of opioid detoxification using ibogaine in various treatment settings - Jamie Walker (2016)
STUDY: Ibogaine and addiction in the animal model, a systematic review of and meta-analysis - Belgers, et al. (2016)
STUDY: Ibogaine as a potential anti-addictive treatment - Nor Ilyani Mohamed Nazar (2014)
STUDY: Ibogaine as an alternative and efficacious treatment for heroin addiction - Amadon, Roecker
STUDY: Ibogaine detoxification transitions opioid and cocaine abusers between dependence and abstinence - Mash, et al. - 2018
STUDY: Ibogaine effect on cocaine craving and use in dependent patients - Pedro Luis Prior, Sergio Luiz Prior (2014)
STUDY: Ibogaine for opioid use disorder: Can we root out addiction at its source? - Shuang Ouyang (2016)
PAPER: Ibogaine in the treatment of chemical dependence disorders: Clinical perspectives - Howard Lotsof (1995)
STUDY: Ibogaine in the treatment of heroin withdrawal - Mash, Kovera, Pablo (2001)
STUDY: Ibogaine in the treatment of substance dependence - Thomas Kingsley Brown (2013)
THESIS: Ibogaine offers an alternative approach for treating opiate addiction - Christopher Nielsen - 2018
STUDY: Ibogaine treatment outcomes for opioid dependence from a twelve-month follow-up observational study - Noller et al. (2016)
STUDY: Ibogaine: An anti-addictive drug: Pharmacology and time to go further in development - Maciulaitis, Kontrimaviciute, Bressolle, Briedis - 2008
STUDY: Ibogaine: A novel anti-addictive compound - A comprehensive literature review - Freedlander, DiClemente (2003)
STUDY: Ibogaine: A review - Kenneth Alper (2015)
STUDY: Ibogaine: Treatment outcomes and observations - MAPS (2003)
STUDY: Life after ibogaine: An exploratory study of the long-term effects of ibogaine treatment on drug addicts - Ehud Bastiaans (2004)
STUDY: Mechanisms of action of ibogaine: Development of a safer iboga alkaloid congener - Glick, Maisonneuve, Szumlinski (2001)
STUDY: Novel pharmacotherapeutic treatments for cocaine addiction - Daryl Shorter, Thomas Kosten (2011)
STUDY: Receptor binding profile suggests multiple mechanisms of action are responsible for ibogaine's anti-addictive activity - Sweetnam, et al. (1994)
STUDY: Remission of severe opioid use disorder with ibogaine: A case report - Cloutier-Gill, Wood, Millar, Ferris, Socias (2016)
STUDY: Subjective effectiveness of ibogaine treatment for problematic opioid consumption: Short- and long-term outcomes - Davis, et al. (2017)
STUDY: The antiaddictive effects of ibogaine: A systematic literature review of human studies - Dos Santos, Bouso, Hallak (2016)
STUDY: The use of ibogaine in the treatment of addictions - Kenneth Alper, Howard Lotsof (2007)
STUDY: Treating drug dependence with the aid of ibogaine: A qualitative study - Schenberg et al. (2016)
STUDY: Treating drug dependence with the aid of ibogaine: A retrospective study - Schenberg, de Castro Comis, Chaves, da Silveira (2014)
STUDY: Treatment of acute opioid withdrawal with ibogaine - Alper, Lotsof, Frenken, Luciano, Bastiaans (1999)
STUDY: Treatment of opioid use disorder with ibogaine: Detoxification and drug use outcomes - Brown, Alper (2017)
STUDY: Treatment of opioid use disorder with ibogaine_Detoxification and drug use outcomes: Clinical rationale - Brown, Alper (2017)
 
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“A vast, uncontrolled experiment” — Ibogaine, 10 years on

by Loren DeVito, PhD | February 19, 2019

Nearly 10 years ago, I stepped out on a Saturday night to meet a friend for a movie in Davis Square. The movie, I’m Dangerous with Love, was playing as part of a special event. As I settled into the Somerville theater, I wasn’t quite sure what I was in for, or how this documentary would end up informing me of a revolution in medicine to come nearly a decade later.

Living dangerously: clandestine healing

The film followed Dimitri Mugianis, a former musician and recovering addict, as he bounced back and forth between his NYC base to treat people across the nation and in Canada. While the opioid epidemic is all around us in 2019, back then, the vernacular of addiction was still relegated to those taking illicit drugs like heroin. With no medical training, Dimitri set out to heal those addicted to drugs with an alkaloid from a traditional plant native to West Africa: ibogaine.

His clandestine healing sessions intrigued me immediately. This former rocker who treated his addiction using this very method was traveling to people’s homes to administer a plant that, in the majority of cases, almost immediately “cured” people. As a neuroscientist-in-training, every cell in my brain lit up.

How could this plant be so effective? How could no one in the West have heard of this “miracle”?

I watched captivated as Dimitri administered the plant, cared for people as they went through agonizing, albeit, brief detox. Then, as they awoke, he talked them through their new life. Of course, not everyone was able to maintain their abstinence long-term, but most people in the film did get a chance to live without drug dependency for a significant amount of time.

Nevertheless, this treatment was not without harm. In fact, ibogaine can cause severe cardiac side effects, which is extremely dangerous when treating people without a medical license at their homes with a drug that is not exactly mentioned in medical textbooks. After one such case, Dimitri realized he was treating patients without proper knowledge of the plant in its entirety. Therefore, he set out to Gabon to learn more about how the plant is traditionally used to better inform his practice.

After a brief discussion following the movie, I left the theater buzzed. As a good little scientist, I immediately pulled up PubMed (the science version of Google) when I got home to search for studies on ibogaine. While there were many studies using preclinical models, I could find very little information for its use in humans.

I filed ibogaine away as one of the cool things I would study when I had my own lab and could start pursuing (funding permitting) my own research passions, and that’s where ibogaine sat for many years—a paper in the accordion file of my brain—that is, until a few years ago.

Pharmacology of an ancient root

One night, I happened upon a study while numbly scrolling through social media. Researchers found that ibogaine enhances neuroplasticity in the brain. “I knew it!” I exclaimed to no one.

My heart started to race, and images appeared of the movie I had seen years before. Could this be how ibogaine helps people rapidly recover from addiction?

The part of the film that really struck a chord involved a scene with a woman who had taken ibogaine. The day after her treatment, she reported feeling as though her senses were “renewed”: Food tasted different, colors were brighter, and everything had changed overnight.

Neurogenesis occurs in the hippocampus, a part of the brain essential to memory and the region I happened to be studying in graduate school, as well as the olfactory regions in adults. The woman’s report following ibogaine made me think of neurogenesis and neuroplasticity immediately because a supply of new neurons and connections flooding the brain would likely cause these perceptions. Of course, I still didn’t know the first thing about the chemical properties of ibogaine, so I got to work.

Getting to know ibogaine

Ibogaine comes from the roots of Tabernanthe Iboga, a shrub native to West Africa. Lower doses are used to help alleviate fatigue, while higher doses are used in religious ceremonies. Noribogaine is the drug's active metabolite.

Ibogaine works by inhibiting the reuptake of neurotransmitters (brain chemicals), including serotonin, which may induce hallucinogenic experiences similar to other psychedelic substances. As I accidentally discovered one night, ibogaine also contributes to neuroplasticity, which is the brain’s ability to reorganize itself when presented with new information.

A preclinical study showed that ibogaine increases glial cell line-derived neurotrophic factor, a substance that promotes the survival and differentiation of cells in the brain. Additionally, noribogaine changes the structure of brain cells, affecting how they interact with other cells.

Clinical studies have found that a single oral dose of ibogaine can significantly reduce cravings for cocaine and heroin, as well as symptoms of depression, for up to 30 days following treatment. While long-term effectiveness of the treatment varies, a survey of patients who received ibogaine treatment in Mexico showed that 30 percent abstained from opioid use for up to two years, with 41 percent reporting abstinence for more than six months, across a three-year follow-up period. There is also some evidence that ibogaine may help those with alcohol addiction.

A blocked path to progress

While the Food and Drug Administration (FDA) entertained the idea of approving a clinical trial for ibogaine in 1993, they decided against it due to safety concerns, despite the fact that people were getting treated in droves at clinics outside the U.S.

In 2005, a few years before the movie came out, the director of anti-addiction drug development at the National Institute on Drug Abuse (NIDA) referred to ibogaine as a "vast, uncontrolled experiment"—a pretty accurate description then—but times have changed.

Traditional medicines like cannabis and psilocybin finally started to hit the mainstream (i.e., in the West) a few years ago and are making significant strides toward legalization through rigorous clinical trial studies. Essentially, we are finally realizing their potential after thousands of years of anecdotally documented benefits.

Flash-forward to today, and we now have quite a surplus of data on ibogaine. In fact, a current search on ibogaine produces more than 450 hits, a far higher number than when I originally started on my expedition. Yet, it still begs the question of the true effectiveness of ibogaine and, most importantly, its safety.

Unsafe unknowns

While ibogaine remains illegal in the U.S., people continue to travel to clinics throughout the world in an attempt to break the cycle of addiction. Despite a decade of additional research, safety concerns remain significant.

Ibogaine treatment can be deadly. Administration of the drug can cause serious cardiac effects since ibogaine decreases the heart rate. Unfortunately, these effects can come on quite quickly. While a small clinical trial identified the time it takes to clear a small dose of ibogaine from the body, additional study is needed to better understand how to safely dose ibogaine.

While there is evidence that low-dose administration of ibogaine can effectively reduce withdrawal symptoms and cravings, it’s not possible to guarantee the safety of ibogaine treatment. People who take ibogaine do so at their own risk. Ibogaine remains an illegal substance in the U.S., so, is there any hope for ibogaine? Yes, with more research, of course.

A Phase 2 clinical trial is currently underway evaluating ibogaine for alcohol addiction. MAPS has conducted two observational studies in Mexico and New Zealand. U.S. state legislators are also proposing new bills to fund research for ibogaine, and one Republican lawmaker in Iowa just filed a state bill to legalize its medical use.

Ten years later and there is still a lot of work to be done, but I’m Dangerous with Love opened my eyes to the immense potential of using an ancient plant to solve a modern health crisis, and for that, I thank you, Dimitri.

https://prohbtd.com/a-vast-uncontrol...10-years-later
 
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Cardiotoxicity of Ibogaine

STUDY: Acute toxicity of ibogaine and noribogaine - Kubiliene, Marksiene, Kazlauskas, Sadauskiene, Razukas, Ivanov - 2008

STUDY: Anti-addiction drug ibogaine inhibits hERG channels: A cardiac arrhythmia risk! - Koenig, Kovar, Boehm, Sandtner, Hilber (2016)

STUDY: Anti-addiction drug ibogaine inhibits voltage-gated ionic currents: A study to assess the drugs' cardiac ion channel profile - Koenig, Kovar, Rubi, Mike, Lukacs, Gawali, Todt, Hilber, Sandtner (2013)

STUDY: Anti-addiction drug ibogaine prolongs the action potential in human induced pluripotent stem cell-derived cardiomyocytes - Rubi, Eckert, Boehm, Hilber, Koenig (2016)

STUDY: Cardiac arrest after ibogaine intoxication - Steinberg, Deyell - 2018

STUDY: Clinical updates on drug-induced cardiotoxicity - Ashif Iqubal, Mohammad Kashif Iqubal, Syed Ehtaishamul Haque, Sumit Sharma, Mohd. Asif Ansari, Vasim Khan - 2018

STUDY: Distribution of ibogaine and noribogaine in a man following a poisoning involving root bark of the Tabernanthe iboga shrub - Kontrimaviciute, Mathieu, Mathieu-Daud, Vainauskas, Casper, Baccino, Bressolle (2006)

STUDY: Effect of iboga alkaloids on μ-Opioid receptor-coupled G protein activation - Antonio, Childers, Rothman, Dersch, Kuehne, Bornmann, Eshleman, Janowsky, King, Simon, Reith, Alper (2013)

STUDY: Fatal case of a 27-year-old male after taking iboga in withdrawal - Mazoyer, Carlier, Boucher, Peoc, Lemeur, Gaillard (2013)

STUDY: Fatalities after taking ibogaine in addiction treatment could be related to sudden cardiac death caused by autonomic dysfunction - Maas, Strubelt (2006)

STUDY: Fatalities temporally associated with the ingestion of ibogaine - Alper, Stajic, Gill (2012)

STUDY: Herbal Seizures: Atypical symptoms after ibogaine intoxication: A case report - Breuer, Kasper, Schwarze, Gschossmann, Kornhuber, Müller (2015)

STUDY: hERG blockade by iboga alkaloids - Alper, Fowler, Ruan, Bai, Liu, Huang, Priori (2015)

STUDY: Ibogaine neurotoxicity assessment: Electrophysiological, neurochemical and neurohistological methods - Binienda, Scallet, Schmued, Ali (2001)

STUDY: Ibogaine-associated cardiac arrest and death: Case report and review of the literature - Meisner, Wilcox, Richards (2016)

STUDY: Ibogaine-associated ventricular tachyarrhythmias - Pleskovic, Gorjup, Brvar, Kozelj (2012)

STUDY: Ibogaine-related sudden death: A case report - Papadodima, Dona, Evaggelakos, Goutas, Athanaselis (2013)

STUDY: Life-threatening complications of ibogaine: Three case reports - Paling, Andrews, Valk, Blom (2012)

STUDY: Long-QT syndrome induced by the anti-addiction drug ibogaine - Dianne Hoelen (2009)

STUDY: Mechanism of hERG channel block by the psychoactive indole alkaloid ibogaine - Thurner, Stary-Weinzinger, Gafar, Gawali, Kudlacek, Zezula, Hilber, Boehm, Sandtner, Koenig (2014)

STUDY: Opioid treatment and long QT syndrome: A critical review of the literature - Pacini, Maremmani, Dell’Osso, Maremmani (2009)

STUDY: QT interval prolongation and the risk of Torsades de Pointes - Trinkley, Page, Lien, Yamanouye, Tisdale (2013)

STUDY: Pathophysiology of the long QT syndrome - Peter Zimetbaum (2019)

STUDY: Pharmacokinetics of hERG channel blocking - Christina Mair (2016)

STUDY: Predicting drug-induced changes in QT interval and arrhythmias - Lu, Vlaminckx, Hermans, Rohrbacher, Van Ammel, Towart, Pugsley, Gallacher - 2008

STUDY: Predicting the unpredictable: Drug-induced QT prolongation and Torsades de Pointes - Schwartz, Woosley (2016)

STUDY: QTc prolongation by psychotropic drugs and the risk of Torsade de Pointes - Wenzel-Seifert, Wittmann, Haen (2011)

STUDY: The anti-addiction drug ibogaine and the heart: A delicate relation - Koenig, Hilber (2015)

STUDY: The anti-addiction drug ibogaine inhibits cardiac ion channels: A study to assess the drug's pro-arrhythmic potential - Koenig, Hilber (2012)

STUDY: The anti-addictive drug ibogaine modulates voltage-gated ion channels and may trigger cardiac arrythmias - Kovar, Koenig, Mike, Cervenka, Lukács, Todt, Sandtner, Hilber (2011)

STUDY: Toxicokinetics of ibogaine and noribogaine in a patient with prolonged multiple cardiac arrhythmias after ingestion of internet purchased ibogaine - Henstra, Wong, Chahbouni, Swart, Allaart, Sombogaard (2017)
 
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Howard Lotsoff

There are 3 main options for ibogaine treatment (*these are all after a small test dose)

– single administration of 1 high dose ibogaine (with booster doses over the next few days/weeks if needed)
– single day/night of administration of multiple large doses spaced out by a few hours (with booster doses over the next few days/weeks as needed)
– small daily doses of 25-300 mg/day, where the dose is gradually increased each day until it is felt to have been effective for eliminating WDs/cravings (this can be modified quite a bit)

http://www.dialogue.space/ibogaine-help-and-advice/

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Iboga accumulates in the body. It remains in the body for more than 4 weeks. This means that all the drops you take in a 5-week period will accumulate and remain in your body until they slowly wear off. If the dose you take exceeds 10 drops a day, physical and psychological effects, and perhaps even disorientation and ‘trippy’ effects can occur. Be aware that some people respond highly sensitively to a few drops only. It is important to listen to the signs of your body at all times and adjust your dosage accordingly. Do not take the iboga tincture before going to sleep. The plant gives you energy and might cause insomnia.

During self-treatment with iboga, it is advised not to use any drugs and to keep stimulants such as coffee to a minimum, as well as tobacco or certain herbs. Your receptors will become very sensitive and you may have an unexpectedly strong reaction to them. Also, it is strongly discouraged to combine the healing of iboga with ayahuasca or other psychedelic substances. Lastly, iboga should never be combined with anti-depressant medication such as SSRI's, as such a combination would be very dangerous.

https://www.dmt-nexus.me/forum/defau...=posts&t=52279

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Ibogaine has also been given in regimens of small daily doses of 25 to 300 mgs/day and in small daily doses where the dose is increased on a daily basis until the desired interruption of drug dependence is accomplished. These low dose modalities have not been validated for efficacy, however, they can be traced back some decades to the work of Leo Zeff who in the case of a single patient provided ibogaine on an "as needed" basis via nasal administration to a cocaine dependent patient to substitute for his cocaine use. Additionally, reports from Canadian sources indicate multi-week low dose ibogaine therapy 20 mg/day following a therapeutic dose of ibogaine in the treatment of cocaine dependence. Further, reports throughout the ibogaine provider community indicate the use of multiple dosing of varying strength doses over varying time periods in the treatment of opioid dependence. As with all determinations in medicine, decisions must be made based on observations of the patient and knowledge of the disorder(s) and the medication(s) used.

From the "Manual for Ibogaine Therapy Screening, Safety, Monitoring & Aftercare" by Howard S. Lotsof & Boaz Wachtel here: http://ibogainedossier.com/manual.html
 
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Ibogaine’s Unique Impact on Neuroplasticity

by Katie Stone | Psychable

The idea that the human brain can change its physical structure and function in response to changes in environmental input has been around since the late 19th century, but it was only recently that technology allowed us to measure these changes objectively.

It was even more recently when we learned that certain psychedelics support neurogenesis (the growth of new brain cells) and neuroplasticity (the ability for your brain to create new neural pathways and connections). Ibogaine, a psychedelic medicine derived from the iboga shrub native to Gabon, is one of those psychedelics that may be quite beneficial in this regard.

Ibogaine is most well-known for its ability to address opiate withdrawal. While the exact mechanism by which it accomplishes that is unknown, research is finding that ibogaine interacts with the nervous system by activating numerous neurotransmitters that create a wide range of effects in the brain, including neuroplasticity.

Before we get into the specifics about ibogaine’s impacts on neuroplasticity, we’ll dive a little deeper into the science behind it.

What is Neuroplasticity?

For much of the history of psychology, researchers were under the impression that the adult personality is established around age thirty and has very little room for change. There was even a belief that one had a limited number of brain cells and that these cells could not be replaced – a hypothesis that has been disproven.

The discovery of neuroplasticity has changed this view. We now know that the brain can evolve throughout life in response to internal factors and external events or stressors. It is understood that the brain can change throughout life in response to experience, both positive and negative.

There are three significant proteins we will talk about that mediate neuroplasticity in the brain. The first is BDNF (brain-derived neurotrophic factor), the second protein is called GDNF (glial cell-line derived neurotrophic factor), and the third is NGF (nerve growth factor). Ibogaine acts on receptors that modulate the release of all three of these proteins — which makes ibogaine different from other psychedelic compounds.

These proteins are known as neurotrophic factors, and they work together to promote survival, growth, and maintenance of the central nervous system (CNS). It has long been known that these proteins are essential during childhood development, but they have recently been recognized as critical to the adult brain as well.

BDNF and GDNF have also been shown to play a role in modulating addiction behaviors in animal trials.

Ibogaine and BDNF

BDNF is a protein that is released in response to neuronal activity. It stimulates the growth, survival, and differentiation of neurons as well as their connections with each other. These connection points are called synapses. Classical psychedelics like psilocybin increase BDNF by acting on the same receptor as serotonin, the neurotransmitter that regulates mood. Low levels of BDNF have been linked to diseases like Alzheimer’s, Parkinson’s, and Huntington’s disease.

Ibogaine and GDNF

GDNF is a protein that is responsible for maintaining the health and survival of dopaminergic and motor neurons in the brain. GDNF may also stimulate the release of dopamine and other neurotransmitters in synapses, affecting synaptic plasticity. GDNF also plays a role in neurodegeneration, which is thought to be connected to Parkinson’s disease, specifically at the dopamine receptor. As far as we know, ibogaine is the only compound that can stimulate the release of GDNF naturally.

Ibogaine and NGF

NGF works to maintain the health of nerve cells called neurons. NGF is essential for learning and memory, playing a vital role in the preservation of brain cells. It has also been shown to stimulate new neuron growth, which can be beneficial during recovery after a stroke or traumatic brain injury to replace damaged tissue.

Ibogaine Supports Neuroplasticity

Neuroplasticity refers to “the ability of neural networks in the brain to change through growth and reorganization.” One way that brain cells grow is through a process called dendritic branching. Dendrites are the branching roots of the nerve cell that connect to other nerve cells, creating spaces of connection called synapses where neurotransmitters interact and can be taken up into the cell for transport to the appropriate channels of activation.

Once ibogaine is metabolized in the liver into noribogaine, noribogaine then binds to specific receptors and begins to active neurotransmitters that stimulate the release of neurotrophic factors. So while ibogaine is the starter compound, once it has been ingested and metabolized, noribogaine is leading to the resulting neurogenesis.

In one study involving rats, ibogaine was found to catalyze neuroplasticity in a dose-dependent manner. The researchers demonstrated that ibogaine alters the cellular transcription levels of both GDNF and BDNF. This means that ibogaine regulates the rate at which the neurons produce and release these compounds.

The researchers administered ibogaine to rats in a time and dose-dependent manner, analyzing the various neurotrophic factors present in the brain post-mortem. After checking the rats’ brains for variations across dose, time, brain region, and concentration of neurotrophic factors, researchers suggest there could be potential for ibogaine to support neurodegenerative diseases such as Parkinson’s.

It is already well established in the literature that an increase in serotonin transmission results in an increase in BDNF expression. It is further well established that ibogaine and its metabolite noribogaine increase serotonin transmission because both compounds are serotonin-reuptake inhibitors, meaning that they help keep serotonin available for interaction in the synapses.

Ibogaine also interacts with NGF, which may be involved in specific areas of the brain connected to substance-seeking behavior. However,t this protein is less studied than BDNF and GDNF. There is evidence that NGF levels are decreased in the brains of alcohol-treated mice, specifically in the hippocampus and hypothalamus. These conditions were also apparent in the serum of chronic heroin and cocaine users, which might suggest a common relationship between NGF and addictive behavior.

Ultimately, this study revealed that ibogaine administration impacts the expression of three neurotrophic factors: BDNF, GDNF, and NGF, resulting in the production of neuroplasticity. This verifies another study that classified ibogaine as a “psychoplastogen” for its ability to rapidly promote neurogenesis. While these are all promising results, until we have clinical trials to further investigate these effects in humans, we will not know the full impacts of ibogaine on neuroplasticity.

 
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Daily low dosing

It is a very good idea to completely detox from antidepressants before doing a treatment. Personally, I ate small doses (around 1g bark) for about a week before flooding, and received many of the typical benefits (extreme mental and physical calmness, vivid memory recall, personal insight, brain massage feelings, tracers, reduced appetite for food and sleep, changed habits, etc) just from the daily doses before flooding. I think just eating small amounts daily is a viable option, especially if one has any health concerns. Of course flooding does offer a unique transformation, but the small daily doses are very very powerful in themselves. Taking small doses before or even in place of a flood is definitely an option.

10 grams of quality bark is a strong experience for some people. I think there is pretty extreme variation in people's sensitivity that cannot be estimated simply by gender and weight. Usually people who have never eaten iboga are very sensitive at first. Generally, 10 grams is not considered a strong enough dose to get a full reset and break strong opiate addictions.

-rho

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Ibogaine has also been given in regimens of small daily doses of 25 to 300 mgs/day, where the dose is increased on a daily basis until the desired interruption of drug dependence is accomplished. These low dose modalities have not been validated for efficacy to the same extent as have the full therapeutic doses of ibogaine. However, these low dose regimens can be traced back some decades to the work of Leo Zeff who in the case of a single patient provided ibogaine on an "as needed" basis via nasal administration to a cocaine dependent patient to substitute for his cocaine use. Lines of ibogaine were somewhat equivalent to lines of cocaine and the patient ceased cocaine use after a week of this daily self-regulated ibogaine regimen. Additionally, reports from Canadian sources indicate multi-week low dose ibogaine therapy 20 mg/day following a therapeutic dose of ibogaine in the treatment of cocaine dependence. Further, reports throughout the ibogaine provider community indicate the use of multiple dosing of varying strength doses over varying time periods are effective in the treatment of opioid dependence. As with all determinations in medicine, decisions must be made based on observations of the patient and knowledge of the disorder(s) and the medication(s) used.

https://truthtalk13.wordpress.com/20...gaine-therapy/

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Iboga does have dangerous interactions with opioids - when used irresponsibly. What I wanted to relay, specifically, is that at LOW doses (again, 10 - 20mg) the opiate reset effect is fairly minimal - it seemed not so much to reset tolerance as to halt its development, which allowed me to use the chemicals I needed to in a stretch without incurring a massive habit, something that may be INCREDIBLY useful to people in chronic pain management situations. Now, I fully think that anyone taking it at all should probably have the arrhythmia screening - but then again, I also put up to your consideration the sale of lambarine, a 12mg ibogaine pep pill commonly sold in France at the turn of the century, and seems to have no connotation of being dangerous or causing death in the people taking it. But it is a risk calculation. In my particular situation it was "OMG, I'm doing some shit totally beyond the pale of normal human behavior, the end result of which may be completely unmanageable addiction and probably death, or I could try this untested compound in a new way that I have a hunch may just do the trick (I'd done a flood dose before to kick dope)." All I wanted to do is honestly relay, that I feel this compound has saved my life a second time, and that continued low dose usage seems to have compounding positive effects both on my mental state and immune system. I don't know that I want to take it forever, it kind of seems to even mitigate administration of itself along with other chemicals, and as time goes on my drive to take it certainly diminishes. I'm not saying I want to take this stuff forever. I'm saying if I NEED it, I never want to be without it.

-cdin​
 
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The future of medical ibogaine*

Psychedelics Today | 22 Apr 2019

Ibogaine is a psychedelic chemical found in the West African shrub Iboga. Bizarre in chemical structure and psychoactive properties, the drug remains mysterious to scientists and psychonauts alike. At high doses, ibogaine causes intense, unforgivingly introspective and dream-like hallucinatory experiences that can last upwards of 24 hours. The African psychedelic might have remained nothing more than a curiosity in the West if not for the discovery of its ability to disrupt physical and psychological drug addiction. Thousands of anecdotal reports and preliminary scientific research provide evidence that a single dose of ibogaine can eliminate both withdrawal symptoms and craving in drug addicts. In the United States, ibogaine remains a schedule 1 drug, and those seeking treatment must pilgrimage to countries that do not regulate it or take a chance with illegal underground treatment centers. What will it take for ibogaine to become medically available in the United States?

New drugs must undergo a rigorous vetting process to move from discovery to the legal market. To become a prescriptible medication, drugs must pass through clinical trials regulated by the Food and Drug Administration (FDA). These trials consist of a pre-testing phase, four clinical phases, and regulatory checkpoints throughout. Advancing to the next phase is predicated on successful completion of the prior phase.

Before moving to clinical trials, researchers must collect extensive pre-clinical data and submit an Investigational New Drug (IND) application to the FDA. Pre-clinical studies use rodent models to determine how effective the drug is for its intended purpose and its safety.

Phase 1 is the first set of studies to determine the safety and efficacy of the drug in humans. If these studies are successful, researchers can proceed to Phase 2, which are well-controlled studies with larger populations. Phase 3 studies test safety and efficacy with different dosages of the drug in even larger populations comprised of various demographics. While the time it takes to move through all phases varies, this process can take many years. After successful Phase 3 trials, the FDA reviews the data and the researchers submit a New Drug Application (NDA). The FDA reviews the NDA and the drug’s labeling to ensure accurate and sufficient information is provided to the consumer and drug-provider. The drug production facility is also inspected by the FDA for health and quality assurance. If the drug is approved, it will be released on the market and available for prescription. Phase 4 trials occur only after the drug has been approved and is publicly available. In Phase 4, the drug manufacturer must continuously monitor the effects of the drug in patients and submit safety reports to the FDA.

For ibogaine to come to market, it must pass through each of these clinical phases of study. Remarkably, ibogaine began the process of becoming an FDA approved therapeutic medication in the early 1990’s. Pre-clinical and Phase 1 trials conducted by Dr. Deborah Mash at the University of Miami supported the anecdotal evidence that patients had significantly reduced drug withdrawal and craving following ibogaine administration. These trials ended prematurely as a result of several factors, including criticism from the pharmaceutical industry, the apparent costliness to continue, and an intellectual property lawsuit between Mash and Howard Lotsof. No clinical trials have been conducted with ibogaine since this preliminary work over 20 years ago.

Another issue facing the medical legalization of ibogaine is that it cannot simply be prescribed in pill form by a doctor. The drug must be administered in a therapeutic setting, potentially as an aid to psychotherapy, as is the case with MDMA. Pre- and post-counseling are vital to ensure proper translation and integration of the psychedelic experience, as well as addressing the underlying problems that contribute to drug abuse. Furthermore, patients must implement changes outside of the clinic to ensure successful treatment outcomes. This means getting away from the external factors that contribute to drug abuse, which can include leaving relationships with friends, family or partners, and/or moving to a new area. While legalization for medical application is important, there must also be infrastructure developed to support proper administration of the drug.

There have been cases of death associated with taking ibogaine. However, none of these cases have been a result of overdose or toxicity. Individuals with certain heart conditions are at a higher risk of cardiovascular-related death after consuming ibogaine, and taking drugs of abuse with ibogaine may cause adverse reactions that can result in death. Rather than supporting the case against legalization, the risk of death for certain patients further evidences the necessity of legalization: unlike some clandestine ibogaine sources, regulated treatment centers would have the resources to screen patients for comorbidities (reasons not to ingest the drug) prior to ibogaine administration.

While the legal status of ibogaine in the US makes research a significant challenge, countries in which ibogaine is unregulated provide the opportunity to study its use in legal clinics. In 2017, the Multi-Disciplinary Association for Psychedelic Studies (MAPS) sponsored two studies investigating the efficacy of ibogaine in Mexico and New Zealand. With abundant data available for legal collection across multiple fields of study, scientists are just beginning to scratch the surface of ibogaine research. Those interested in studying ibogaine should not be discouraged by the barriers in the United States and should look abroad for more opportunities.

*From the article here :
 
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How safe is ibogaine? We asked Clare Wilkins, who has facilitated over 700 treatments

by Jordan May | Psymposia | 2 Jan 2018

Using ibogaine can be fatal if proper safety precautions aren’t taken.

Clare Wilkins is a former intravenous drug user & methadone patient who shed her chemical dependencies with the aid of ibogaine. As founder of Pangea Biomedics, she has facilitated over 700 treatments and collaborated with MAPS on the Mexico study. Since 2010, Clare has been an active board member of the Global Ibogaine Therapy Alliance (GITA) and is a co-author of the Clinical Guidelines for Ibogaine-Assisted Detoxification. Clare is currently collaborating with ICEERS, developing a clinical trial for methadone for ibogaine-assisted detox.

We’ve mentioned that ibogaine can be dangerous, and we even saw what can happen when proper safety precautions aren’t taken. Here, we take some time to speak with Clare and go more in depth about the risks associated with ibogaine.

While we hope that this interview offers some insight about the safety protocols one should consider before taking ibogaine, we want to stress that in no way should this be considered a thorough safety guide. Simply reading this interview is not adequate preparation, and we strongly encourage anyone thinking about working with ibogaine in any capacity to take the time to do further research.

Would you like to start us off by introducing yourself? What’s your story?

I was an injecting heroin user before switching to methadone. I come from a very traumatic childhood with a lot of violence. I discovered heroin at an Ivy League university, and it seemed to answer every question I ever had.

I spent the next 15 years trying to resolve that answer.

Methadone maintenance treatment worked for a while. It was my lily pad for 9 years. It saved my life. It made me not a criminal, not sick. I had a job, and I was able to get my life together.

Anyway, my sister and I had both been using heroin and she had already detoxed, yet she learned about iboga through Rick Strassman’s work with DMT. It was back when there were just a few clinics in the world. I went to a clinic in Tijuana, which, at that time, was the Ibogaine Association. There, I was freed from the lock of methadone.

After my experience, I saw what may have been lacking in the treatment protocol. I didn’t really have anybody to process with during the experience. I went home, and I was in withdrawal for a month. I couldn’t even do my job. So, I called up the clinic and told them that I’d like to talk to patients who perhaps needed to understand the process from a peer perspective. I was in LA and they were in Tijuana, so I’d take the train down and I’d just sit with people because no one who had taken ibogaine had ever sat with me.

That was the beginning. I volunteered until I was brave enough to purchase the Ibogaine Association name and create Pangea with a full team in a new location. It was a calling, and it seems to be a calling that happens with a lot of people in the drug users’ movement.

Since then, you’ve become prominent in the ibogaine community as a provider and consultant. In your professional opinion, is ibogaine actually safe?

That’s like asking if electricity is safe, in my opinion. You can cook a warm meal, light up a room, or electrocute someone with electricity, as they say.

It’s similar with ibogaine. Ibogaine, in and of itself, is not unsafe. There are both risks and benefits.

Ken Alper, Jeffrey Kamlet, Deborah Mash, Bruno Rasmussen, Roman Paskulin, and Jamie McAlpin are doctors and experts regarding ibogaine safety. There are many published journal articles and presentations of theirs online. To be clear, I’m a lay therapist that’s worked with an integrative team of MDs, naturopathic doctors, psychiatrists, psychologists, and somatic and peer therapists for 12 years.

So, what are some of the specific risks? You mentioned the heart, but could you go into detail about the screenings people should get before they consider taking ibogaine?

Ibogaine increases electricity in the heart, which is one of the reasons reputable clinics do cardiac screenings – to assess how the heart conducts electricity. Ibogaine has some features that require vigilance, and most experts conclude that thorough pre-screening and medical monitoring during the experience is crucial to its safety as a treatment for detoxification.

Ibogaine also induces bradycardia (it lowers heart rate, normally by about 10 beats per minute during a typical dose of 12 – 20mg/kg). The risk of bradycardia is that the heart rate can go very low. If the heart rate stays too low for too long of a period, this can require immediate administration of atropine. This is a serious life-threatening situation that requires medical intervention.

QT prolongation is another major risk with ibogaine. The QT interval is a measure of the heart’s electrical cycle, or the time it takes for the ventricle to get ready from one contraction to the next. During this period, the heart is vulnerable to cardiac arrhythmias and other serious complications. Other legal medications prolong the QT interval, such as methadone. Benzodiazepine and alcohol withdrawal both result in QT prolongation as well, so combining ibogaine with an alcohol or benzodiazepine detox can be extremely dangerous.

Many people who seek out ibogaine for detoxification are poly-drug users. For best outcomes, complete blood and urine panels need to be drawn and analyzed as close to treatment as possible to assess for infection, electrolyte levels, and of course, a toxicology screen. What drugs/medications has this person been taking that they may not have told you about?

Hepatic function and the specific liver enzymes are essential. Many ibogaine patients have liver issues, are diagnosed with hepatitis C, etc. However, this doesn’t preclude them from treatment, in many providers’ experience. Still, the liver enzyme count is crucial to consider. I believe Howard Lotsof’s last patent application was for the use of ibogaine to treat hepatitis C. He had data demonstrating a dramatic decline in viral load counts in those with a diagnosis of Hepatitis C who had taken ibogaine.

Electrolyte count is crucial as well because ibogaine is a potassium hERG channel blocker. Potassium plays an important role in cardiac function, and blocking this channel can lead to prolonged QT intervals, arrhythmias, and insufficient electrolytes for the heart to function as it needs to.

Noribogaine, the metabolite of ibogaine, is an important topic as well. It seems to stay in the system longer than ibogaine, providing the “window of opportunity” we hear about. Noribogaine has similar qualities to ibogaine in terms of decreased self-administration of opiates. According to Ken Alper and others, it’s important to consider the concentration of noribogaine over time, which resembles a curve. Multiple doses of ibogaine in one evening increase the area under the curve, indicating a higher concentration of noribogaine in the system for longer periods of time, which could or could not be predictive of more danger.

In your time as a provider, did you ever have any adverse events?

Pangea had 3 fatalities, on separate occasions, as well as numerous events that required intervention. Thanks to mentors, experts, and teachers, Pangea learned from them. We haven’t had an adverse event since because we do completely different protocols now that have been worked on diligently for the past 8 years.

We don’t just pull the rug right out from under the client upon starting treatment. No need to arrive in withdrawal. Before treatment, we develop specific protocols to treat conditions underlying their dependencies. We continue with this process during treatment.

Our work with ibogaine is done in a specifically timed manner. For example, with opioid dependencies, we give morphine and then ibogaine, then less morphine, and then ibogaine. As the ibogaine accumulates, there’s less and less craving for opioids, and more time to include the adjunct therapies we use. With stimulants, we don’t use the method of co-administration, yet we do use repeated cumulative dosing. It takes an extreme amount of vigilance, but it’s much more successful than anything we ever did before while following the traditional model.

Why did these adverse events occur?

Well first, we were following the traditional model. In the conventional paradigm, you come to treatment in withdrawal and you get ibogaine that night, before trust is developed with the team, soon after an EKG, and usually after a long flight.

We had a staff of 12, including 4 doctors. We essentially had a hospital in a villa; it wasn’t for a lack of equipment or personnel. These were extremely unfortunate and difficult aspects of the learning curve. The fatalities were the result of pulmonary embolism, the presence of residual cocaine in the blood, and hypertrophy. All preventable issues, as we now know.

So, do you think your current model helps prevent adverse events?

Not think, we know.

No deaths and no hospital visits in the 8 years since we have changed our protocols. We’ve had someone who experienced a hypertensive attack, who already had high blood pressure, and we controlled it within an hour. And someone else was vomiting so much they needed an IV, but that would happen almost every week when we administered ibogaine the previous way.

Psychologically, it’s a different story. Clients can regress to their childhoods, start acting child-like, screaming, crying, or behaving violently. Staying in an alternate reality for a prolonged period of time, this comes with safety issues as well.

What’s so different about this alternative protocol?


Well, the traditional treatment model is rapid. Patients come in, they take their ibogaine, and they usually return to their same environment shortly after treatment.

We now emphasize pre-treatment at least a month before they come. Many people focus on aftercare, but nobody seems to talk much about strong preparatory care.

We’ve had numerous clients follow our preparatory protocol who end up not needing to take ibogaine. We worked with naturopaths and developed specific orthomolecular protocols for the 5 most significant physiological issues that occur with drug dependence. Those are depression, pain, anxiety, liver issues, and chronic fatigue.

What we do is called repeated cumulative low dosing, which results in a saturation, or a “flood”, by the end. So instead of giving a single flood dose in one night, we do it over days. What that does is it shows us how someone reacts to the medicine, how they metabolize the drug – versus just going from a blood test result. So how do they react at first? Do they cry? Do they feel nothing? Do they say it feels good? Do they see their dead grandparents? Do they feel calm or anxious at first? Then, as a team, we form a specific protocol based on their body and mind. They teach us.

Is ibogaine safe to take with any other medications?

There are many contraindications. Ibogaine potentiates not just morphine, but it seems to be a potentiator of almost everything. One cup of coffee with a microdose of ibogaine in the morning can feel like 4 cups to some people. Antidepressants and antipsychotics are another category that are restricted with ibogaine. I highly suggest people do a lot of research regarding this issue, as it could take a while to go through all the medications. The GITA Guidelines have information as well.

Working with a physician who supports the use of ibogaine and tapering from other medications, or continued use of them, is strongly encouraged.

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It seems like there’s a lot of controversy and misinformation surrounding ibogaine and benzos. What’s the deal? Is it safe to detox from benzos using ibogaine?

Ibogaine doesn’t work as well for benzos as it does for opioids and stimulants.

Remember, ibogaine electrifies the body. Yes, with the correct dose it can place a person into a para-sympathetic state, where he or she is no longer in fear. Yet it’s extremely dangerous to use ibogaine to decrease the dosage of a benzo, especially rapidly. We refer people to the Ashton manual. Heather Ashton is the world’s expert on benzo tapering.

Of course, one can combine various therapies to detox from benzodiazepines, but we’ve seen that a slow taper, over time, is the safest with long-acting benzodiazepines. Withdrawal from benzos includes QT prolongation, anxiety, fear, insomnia, seizures, and even death. When a person who is dependent on benzos takes ibogaine, they need to be stabilized on a long-acting benzo to keep the QT interval in a safe range. A short acting benzodiazepine can leave the system during a “flood” quickly, increasing the risk of seizures and arrhythmias. It can also stay in the system and be potentiated by the ibogaine.

This all depends on an individual’s body and their metabolism, as well as dosage of the benzos. We don’t know unless we go slowly. There’s debate around this issue, so it would be wonderful if the clinics who work well with benzodiazepine patients can come together and share their knowledge with other providers and patients.

Many people hide their benzo use, even if it’s only occasional, to be accepted to clinics, and this is dangerous. If you look at Ken Alper’s fatality paper, you’ll see benzodiazepines are connected to many of the deaths associated with ibogaine – specifically you’ll see that they weren’t used while in treatment, yet were found in the toxicology report afterward. I call benzos the snipers of ibogaine fatalities.

This subject is controversial because you have a doctor saying one thing and a clinic saying another thing, and so on.

How about other psychedelics? That seems to be a growing trend, taking ibogaine with other visionary substances. How safe is this?

Ibogaine is safe to take with certain psychedelics. And completely unsafe with others.

Dangers seem to occur around the administration of 5-MeO-DMT, kambo, MDMA, and ayahuasca in close proximity with ibogaine. There have been grievances, including a fatality, associated with the use of these medicines alongside ibogaine.

Ayahuasca and kambo are both purgatives, so the issues of dehydration and over-stimulation can be factors in relation to safety with ibogaine treatment. There’s been a surge of the use of these medicines with one another in the past few years. A few practitioners seem to combine the higher risk substances well, with no adverse effects reported. There’s a lot that still needs to be researched.

There’s also debate around using ketamine, which is a dissociative, while taking ibogaine or shortly after. Many clinics have witnessed clients moving from heroin/opioids to ketamine after taking ibogaine, and from stimulants to 5-MeO-DMT and/or DMT as a form of psychedelic substitute. Aside from the physiological complications that may arise from these combinations, there is the psychological component.

Experiences with certain substances can take months, or more, to fully integrate. Often, ibogaine is not enough to get the mission accomplished on its own, to treat years of a chronic condition. It’s essential to use adjunct therapies to create an integrative experience for the client. This, of course, takes time.

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A lot of people are talking about microdosing ibogaine. Are the risks the same as with a larger threshold dose? Should someone still get screened before starting a microdosing regimen?

The risks can be the same, yes. They are far less significant, of course, because the dose is so much smaller than traditional “flood” doses.

Yet, there are people who just simply cannot and should not take ibogaine, period.

Even small doses can exacerbate a heart condition, anxiety, or insomnia. Ibogaine is cumulative, so as it builds up (if you’re microdosing regularly), it eventually saturates the body and it feels like you’ve taken a larger amount that day than you actually have. I know of people who used it daily, with a day of rest per week, and others who had a panic attack with a first dose of only a few milligrams. Although not a microdose, a fatality occurred recently with a dose of only 200mg ibogaine HCl, which is considered less than a “booster dose.”

It’s important to rest, to integrate, to sleep, to dream, and to allow the cascade effect of ibogaine to work its wonders. A guide or facilitator is highly recommended. Others prefer finding their own inner guide – their inner doctor, so to speak. Ibogaine leads us back to the root of our inner voice, which we lose sometimes in this cacophony of modern life.

It seems like there’s a lot of misinformation out there surrounding ibogaine, specifically regarding safety protocol. What do you think are some of the most common misconceptions people have about ibogaine in general?

That they will be liberated from addiction for life. That they will understand the root causes of their dependencies and be able to easily move forward from those realizations. That they’re able to integrate their experience back into their regular life, like it’s easy peasy from there on.

A myth is that everything is fine and perfect after it’s over. With ibogaine, yeah in a night, over the course of a few hours, you’ll be devoid of most withdrawal symptoms and cravings. But after that is when the real work begins.

Those are some of the main ones. Most people don’t know how to integrate what happened to them while taking ibogaine into their life. It’s tough. That’s why if you look on our website, we have a page called ‘The Family’. The family is an organism, and if we notice a family member doesn’t want to talk and be included in therapy, we start to understand that the user may be the scapegoat. Dependency is a family issue that’s complex to traverse.

So all in all, would you say ibogaine is worth taking even despite the safety risks?

Ibogaine is for the person who feels called to it, who resonates with it, just as you do with a food, a country, a friend, a plant, a potential lover, an ally.

One can feel more of the world around them after taking ibogaine, see more clearly, and experience a new awareness of themself that grows or suddenly appears.

We need more people who feel right now. Who see more deeply. It’s urgent. The risk is worth it.​

It certainly has been for me.

 
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New studies confirm ibogaine's effectiveness in stopping opioid addiction*

"In 2015, more that 52,000 people in the U.S. died from drug overdoses. The majority of those deaths were opioid-related. Nationwide, fatal opioid overdoses increased 652 percent from 2000 to 2015, according to CDC statistics, and every indication is that the problem has grown worse in 2016."

The opioid crisis in America has reached epidemic levels and overdose deaths continue to rise. While the destructive effects of heroin and opioids ravage communities and destroy families, the federal government is considering harsh new mandatory sentences for opioid crimes, demonstrating a heart-breaking disconnect from reality when it comes to disrupting dependence on these insanely addictive and deadly drugs.

Opioids in the U.S. are far more deadly than terrorism and even firearms, yet because they fall into the uncomfortable category of addiction and are primarily the result of the legal pharmaceutical industry, the problem is largely ignored by mainstream media, and the government authorized solutions don't help.

Remarkably, there is a natural medicine for treating opioid addiction which immediately stops withdrawals and detoxes opioids from the body, and also produces a deep spiritual experience that helps an addict to stay sober by showing them the source and reason for their addictive behavior and inspiring them to remain clean.

Extracted from the iboga plant, which is native to the equatorial rainforests of West Africa, ibogaine is psychoactive indole alkaloid that has been known for decades to interrupt opioid addiction. Two recent observational studies have now added to the growing body of evidence in support of ibogaine as perhaps the most effective medicinal treatment known.

Brad Burge, Director of Communications and Marketing, MAPS, explains in a recent press release:

"Ibogaine is a psychoactive compound usually extracted from the West African Tabernanthe iboga plant. In animals, a single dose of ibogaine decreases opioid withdrawal and produces sustained reductions in the self-administration of heroin, morphine, cocaine, nicotine and alcohol. Ibogaine is illegal in the U.S., and legal but unregulated in Canada and Mexico."

"New Zealand, South Africa, and Brazil currently authorize the use of ibogaine by licensed medical practitioners. While its mechanism is not yet fully understood, it differs from standard opioid agonist treatments such as methadone and buprenorphine which maintain dependence, and thus may show promise as an innovative pharmacotherapy for opioid addiction."

"The authors of the studies conclude that given the potential demonstrated by ibogaines substantive treatment effect in opioid detoxification, its novel (though not yet fully understood) pharmacological mechanism, and its clinical effect in opioid-dependent subjects who have not satisfactorily responded to other treatments, ibogaine has promise for future research and development as a novel pharmacotherapy for opioid addiction."

"The Mexico study showed that ibogaine administration was associated with substantive effects on opioid withdrawal symptoms and drug use in subjects for whom other treatments had been unsuccessful. 12 out of 30 participants reported 75% reductions in their drug use 30 days following treatment, and 33% reported no opioid use three months later."

"The New Zealand study showed that a single ibogaine treatment could reduce opioid withdrawal symptoms and achieve either cessation from opioids or sustained, reduced use for up to 12 months following treatment. The results indicate that ibogaine may have a significant pharmacological effect on opiate withdrawal. All participants in the study described their ibogaine experience in positive terms.
"

Is ibogaine treatment safe?


Ibogaine is listed as a schedule I drug, which implies that the drug has no medicinal value, however, under properly medically supervised conditions, ibogaine is extremely effective, as further confirmed by these two studies. It is important to note that the drug war ban on ibogaine creates a climate in which treatment with the mysterious alkaloid takes place outside of the proper care of qualified physicians, and that when dealing with opioid addicts ibogaine can indeed be dangerous.

In the New Zealand study one of the participants died while undergoing treatment, and an investigation found that the death was likely related to the ingestion of ibogaine, however, it was also attributed to a failure to properly care for the patient.

"The authors acknowledge the potential shortcoming of ibogaine treatment highlighted by the mortality associated with the therapy, especially in non-medical settings, specifically concerns about potential cardiovascular complications related to ibogaines metabolism in the body." - Brad Burge, MAPS

It needs to be said that there is no magic pill for addiction, as noted by opioid survivor Jeff Cook.

"Iboga is not a magic pill. Iboga is an amazing tool that can free you from the deepest depths of addiction. The spirit of Iboga will teach you everything you need to learn to stay clean, but one must follow these lessons to stay on the right path. Iboga does not change your free will, what Iboga does, is show you the truth. The truth you need to make peace in order to live a happy, drug free life."

Yet, given the deadly nature of the epidemic at hand and the huge and rising numbers of deaths each year, it is past time to give alternative treatments their due and make them available for those who are at risk of succumbing to opioids.

*From the article here :
http://www.wakingtimes.com/2017/06/0...oid-addiction/
 



Dr. Bruno Chaves speaking at MAPS' 2017 Psychedelic Science Conference in Oakland, California

Good afternoon. First of all, I want to thank MAPS for the invitation. Today I will talk about what we are doing in Brazil about bringing ibogaine to be, let's say, [an] above ground treatment to people. So, that's why we ask if finally in Brazil, is ibogaine stepping out from the underground? I am a medical provider of ibogaine since 1994. I am the first medical provider in Brazil, and I think I am the first provider in Brazil, medical or non-medical. I've done more than 1000 treatments.

In Brazil, we don't have too much heroin addiction, we have more stimulent addiction, like cocaine and crack cocaine. So everything that I will talk about our work there, I will be talking about stimulant addiction. We've published some works on ibogaine, a retrospective study, in 2014. I helped to write the clinical guidelines published by GITA, and we've recently published a politative study on treatment, on ibogaine. I'm a former GITA board member.

Brazil has the most rigorous laws about prescription medicines in the world, and this happens because some time ago there were a lot of women who got pregnant after consuming birth control pills containing wheat flour. That was a big scandal in the country, and after that, ANVISA, which is our FDA equivalent, it changed all the regulations about prescription medicines. So it's easier in Brazil for you to get a drug like cocaine or crack than to buy a medicine if you don't have a prescription. This was the birth control pills that were contaminated with wheat flour...it happened in 1998. And after that, they published this law that we call article 273, that says that it's forbidden to sell, or to administer, to use or prescribe or take with you any kind of medicines that are unregistered in the ANVISA, or are from unknown origin. And it is so rigorous that in some situations you get more time in jail for prescribing a non-registered medicine than for a registered one. It's very, very rigorous.

What is a registered medicine in Brazil? It's a medicine that was previously evaluated by the ANVISA, who will analyze the documentation, the clinical trials, the scientific advances. They are more prone to approve a medicine if it's already approved in another country, but there are some medicines that are only approved in Brazil. They see the package, and they see the labels, and if all the requirements are fitted, ANVISA declares that this is a registered medicine. After that, the doctors can prescribe it, and it can be sold, and there are various levels of control on that. Some medicines only need a simple prescription, and others need to be prescribed in special forms that are provided to the clinicians under request.

So it's possible to do the ibogaine legal treatment in Brazil because it's not forbidden, it's not controlled, it's not banned, but it's not registered until now as a prescription medicine. But ANVISA allows people to use non-registered medicines if we meet some requirements that they ask. Basically, we have these two laws that state that non-registered medicines can be used since they are bought in the name of the patient - the medicine must be imported in the name of the patient - in the exact amount of medicine that patient will use, and this importation must be for a single use or for a limited time of use, and the maximum time of 6 months.

This situation doesn't apply to ibogaine because ibogaine normally we use only once, so it fits the law. In Brazil, people are using this law to import a lot of unregistered medicines - medicines for appetite, ibogaine, and medical marijuana preparations. So we import ibogaine to Brazil legally. It arrives in a box that goes through the customs and through ANVISA, and every time they ask a lot of questions, but they allow us to use it. As you can see in the stamp, it's a national agency on sanitary vigilence, "ANVISA liberated" without opening. The first times we imported it 20 years ago, people used the ANVISA at the airport, they used it to open the package and look at the bottle of the medicine, but now they are used to that - they know that we do it - so they are releasing it without opening the box.

But this kind of situation, this kind of importation, has some disadvantages. It takes a lot of time for the medicine to arrive in Brazil and to be released in the airport. The patient must wait all this time. The average time is 30 days, but sometimes it took around 3 months for the medicine to be released. There are costs because you must hire brokers and people to help release the medicine in the airport. If you use an amount that is less than what you bought, you must discard what you didn't use, which makes the patient pay for more than they really need. And ANVISA asks for a medical prescription to accept the importation. So this makes the cost higher than we would like it to be, but at this moment, it's the only way to import it legally.

In 2014 we published a retrospective study on ibogaine, showing a good affect on maintaining a distance from cocaine and crack cocaine. During that year, around 62% of the patients remained clean. And after that, helped by people - activists, psychologists, psychiatrists - people who understand the need for a shift in the treatment of addiction in Brazil - they helped us to talk with the government. We went to the State Council on Drugs Policy, and we went to the National Secretary on Drugs Policy and the Ministry of Justice, and we explained it for the people how ibogaine works, we showed them the study, we asked for more funds for research, and we asked for some kind of facilitation in this regulation - we wanted for regulation not to be so hard for us to try to lower the costs. We showed them that ibogaine really changes the QTc interval and EKG, so the State Council on Drugs Policy - they published some resolutions. It works only for the Sao Paulo state, but anyway, they said :

1. The use of hallucinogenic substances for treatment of problematic use of psychoactive substances should be considered an option that requires scientific research.

2. Scientific research with the use of hallucinogenic substances, including the development of options for treatment of substance abuse, should be encouraged financially by development institutions in order to ensure the realization of quantitative research, qualitative and randomized controlled clinical trials.

3. The semi-synthetic or synthetic compounds based on active principles of Tabernanthe iboga and other species of the genus Tabernaemontana (Aponynaceae family) must have their therapeutic potential in the treatment of problematic psychoactive substance use investigated through scientific research.

4. The semi-synthetic or synthetic compounds based on the active principles of Tabernanthe iboga and other species of the genus Tabernaemontana (Aponynaceae family), particularly ibogaine formulations, can only be administered for the treatment of the abuse of psychoactive substances in a hospital environment, with doctor's supervision and control, given the and good practice of the profession and good recommendations to clinical practice, including rigorous clinical, psychiatric and psychological assessment and psychotherapeutic monitoring.

It was interesting that this decision of the State Council had more repercussion in the U.S. than in Brazil, and in Brazil few people were aware of it, but in the U.S., we saw on the internet some posts talking about this situation, that it opens the door for ibogaine treatment. After that, at the end of 2016, we published a retrospective study - a qualitative study. We saw that the patients improved their quality of life. Even if they relapsed after ibogaine, their relapses were different, and the patients, most of the time, even after relapsing, they said that they felt different, and they felt that this relapse after taking ibogaine was different - that it was easier to get off again and to be clean again. So we measured in a quantitative study the percent, the amount of people that were clean. And in this politative study, we measured how people felt after ibogaine, even if relapsing. Most of the patients relayed that it was different, and even [if] relapsing, they thought that ibogaine had helped them.

So we are at this moment taking the next steps. We are trying to extend this regulation from Sao Paulo to other states. We are trying to somehow register the medicine. It's not easy to because it costs a lot of money - we think about 2 million dollars to register the medicine in ANVISA, because we need to show a lot of documents. We had a signal from ANVISA that maybe they could allow us to have what they said a fast track, which is maybe they will not ask for so many documents that they normally ask because they understand that it's an emergency. We have a lot of people in Brazil dealing with this problem. So it's possible - it's in negotiation at this moment - but it's possible that ANVISA will allow us to register the medicine and give us around 3 or 4 years to use it, and they could wait for this time for us to provide them the documentation. And we are trying to copy the MAPS's model on MDMA - we are trying to negotiate with ANVISA, that ibogaine treatment should be done in a controlled environment, with all the equipment necessary, and all the conditions necessary in the case of emergency.

I need to comment that all these years working with ibogaine, and more that a thousand treatments that I've done, I never saw a real emergency, I never saw a patient die. The worst thing I saw during a treatment was the patient vomiting a little more than the usual, but no problem. I think that this happens because we really [carefully] selected the patients who were going to do the treatment. We do a lot of clinical examinations, we do psychological evaluations, and we only allow people to take ibogaine if they are really in good health. We think that ibogaine treatment works like a minor surgery, so we do some pre-op operating examinations - like in a surgery of the stomach, or of the bladder, or anything in traditional medicine: If the patient is not ok, with blood pressure or with diabetes, for example, the surgery is postponed.

So we do the same thing. We only give ibogaine to the patient if he is really ok, if he is in good shape, in good health. So I think that this explains partially the reason why we never saw complications. We know that other places in Brazil, underground treatments, there was at least one death in Brazil, but it was not in our hospital. The patients that we treated, nothing really important happened. But we really need to convince the government that this is important, that this medicine really works. But what we feel is that the government agencies, they are open to hear us, and they are open to try to make some regulations.

In an ideal world it will be not necessary to be regulated, and people would have their responsibility to give or to take ibogaine, only in a proper situation. But as we see there are a lot of people who are looking more for profits than really worried about the health of the patients. We think that from the first moment, it would be good if we really follow the ANVISA regulations, and we show that it works, and that in the proper conditions, it's safe. And I think that after that, maybe the regulations could be loosened, and it will be more accessible for people.

The fact is that we need to bring ibogaine to the people, with not [such a] high cost, and easier for people to achieve it. It's important for people that they know that there is an option in the end that's a light in the end of the tunnel, and they must seek for a treatment that could be done in a good place, being cared [for] with responsible people, and in a place that they can feel that if anything different or dangerous happens, they will be cared [for]. What we see in some underground treatments in Brazil is that when people start to have some major reactions, normally the people 'put the patient away,' [or] dismiss the patient and say 'go home', like saying 'go and die at home.' And this is exactly what we don't want to happen. We want ibogaine to be seen like a normal treatment, like a lot of other medicines that are hard on the body.

I remember when I was studying medicine we used to treat pulmonary infection with a medicine that was highly cardiotoxic medicine, and the professors used to ask the internists to stay sitting by the patient during all the time that this medicine was dropping into the system of the patient, because we could have some kind of cardiac arrythmias. We want to do ibogaine like that. We want to have the authorization to do ibogaine since there's a person [there] to care for the patient, to be around. If anything different happens, the patient will be protected. And I think from all the treatments that I saw, I think that it's worth the risk. I think it's much more dangerous to take crack in the streets than to take ibogaine in a hospital.
 
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