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What We Treat›Cocaine & Crack
We require 28 days fully off cocaine before an ibogaine treatment.

Ibogaine treatment for cocaine and crack

Cocaine empties out the reward system until nothing else registers, and the only thing that lifts the flatness is more of it. Ibogaine acts on that system directly rather than on the behavior around it. It also asks something of you first: 28 days completely off, because cocaine and ibogaine interfere with the same channel in the heart.

Treatment is administered by independent licensed Brazilian physicians under their own licenses. See our medical disclaimer.

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The Reality

There is no approved medication for cocaine dependence. Anywhere in the world, there never has been.²⁸

Cocaine does not put you through the kind of withdrawal that lands people in an emergency room. That is exactly why it gets underestimated, and why people who cannot stop are so often told they simply are not trying hard enough.

What cocaine and crack do instead is flatten the reward system until nothing else registers. The crash is not dramatic. It is grey, and it is heavy, and the fastest way out of it is the thing that caused it. That loop is what ibogaine interrupts.

“With cocaine, people do not usually arrive in physical agony. They arrive flat. Nothing works anymore, and that is its own kind of desperate.”

Charles D. Johnston, Co-Founder, Nekawa

How We Help

How ibogaine treatment for cocaine works at Nekawa

The most useful evidence for treating cocaine with ibogaine did not come out of a laboratory. It came out of São Paulo. In 2014 a team led by Eduardo Schenberg, working with the physician Bruno Rasmussen Chaves, published a review of 75 people treated here in Brazil for dependence on alcohol, cannabis, cocaine and crack. Because ibogaine is unregulated in this country, none of it happened underground. It was supervised by a doctor and paired with psychotherapy, which is the whole reason the outcomes are worth anything.³⁴

São Paulo, Brazil, 2014
61%of the 75 were abstinent at follow-up
5.5 monthsmedian, after a single treatment
8.4 monthsmedian, where treatment was repeated
No fatalities and no serious adverse reactions across all 75. Both stretches of abstinence were significantly longer than the same people had managed before ibogaine.
Schenberg, de Castro Comis, Chaves & da Silveira, Journal of Psychopharmacology, 2014

Now the limits, because they matter and we would rather say them than have you find them. The study looked backwards at people who had already been treated instead of assigning anyone at random, and there was no comparison group, so it cannot prove ibogaine caused the abstinence. The abstinence was self-reported. Nearly three quarters were using more than one substance, so this is not a clean cocaine-only result. A controlled trial of ibogaine for cocaine has still never been run anywhere. What this is, is the strongest real-world evidence that exists for stimulants, and it is Brazilian.

The animal work points the same direction. A single dose of ibogaine cut cocaine self-administration in dependent rats for more than 48 hours, and weekly dosing held longer than daily dosing did.³² That is rodent data from 1993, and we mention it because it agrees with what São Paulo saw, not because it proves anything on its own.

What makes that study the right one to build on is that its conditions are our conditions: the same country, the same legal footing, a licensed physician overseeing the treatment, and real psychological work wrapped around it rather than a session sold on its own. Its authors did not conclude that ibogaine cures anything. They concluded that ibogaine given this way can open long stretches of abstinence without serious harm. That is the claim we make too, and what decides whether the stretch holds is the 28 days before it and the months of integration after. How ibogaine works →

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Why This Is So Hard

Why cocaine and crack are so hard to put down

Cocaine works by jamming the door that dopamine normally leaves through. Ordinarily your brain releases dopamine, registers the signal, then clears it away. Cocaine blocks that clearing, so dopamine keeps piling up in the synapse. That flood is the high, and because it is far larger than anything ordinary life produces, the brain reads it as the most important thing that has ever happened.

Then it adapts. Faced with repeated floods, the reward system dials itself down, pruning receptors and cutting its own dopamine output to compensate. The result is a moving target: the same amount does less, and everything that is not cocaine does less too. Food, sex, work, your own children. This is the flatness people describe, and it is a physical change, not a mood.

Crack is the same molecule delivered faster. Smoking it puts cocaine into the brain within seconds rather than minutes, and the sharper the spike, the harder the crash behind it. That is why crack tends to compress the whole cycle into something that runs in hours instead of days, and why it builds a dependency that is harder to interrupt. Chemically it is the same problem. Practically it is a steeper one.

And there is a second thing happening while all of this goes on, quieter and more dangerous. Cocaine is also acting on the heart. It blocks a potassium channel called hERG, one of the channels that resets the heart's electrical charge between beats.³¹ Block it and the reset takes longer, which is what a prolonged QT interval means on an EKG, and a longer QT is a known risk factor for dangerous arrhythmias. Give habitual users cocaine under controlled conditions and you can watch the QTc stretch.²⁹ Crack does the same thing through the same channel, faster.

That is the detail that shapes this entire page, because ibogaine inhibits that same channel.²⁰ Two things pulling on one mechanism in the heart is the risk we are managing, and it is the reason our timeline for cocaine is longer than most. Read how we handle the cardiac side of ibogaine

Withdrawal Timeline

Phase 1

The crash (hours to 3 days)

Exhaustion, enormous appetite, heavy sleep, and a low mood that arrives the moment the last of it wears off. Cravings can be low here, because the system is too depleted to want anything at all.

↳ Ibogaine interrupts here: Not the window for treatment. This is when the heart is still carrying the effects of recent use.

Phase 2

Withdrawal (1–10 weeks)

The long grey stretch. Anhedonia, irritability, poor concentration, disturbed sleep, and cravings that return in waves and get triggered by places, people, and routines rather than by physical need.

↳ Ibogaine interrupts here: The 28 days sit inside this window. The system is stabilizing while the heart clears.

Phase 3

Extinction (months)

Mood and motivation slowly return, but cues still fire. Most relapses happen here, well after the physical part is over, which is why cocaine is so often mistaken for a willpower problem.

↳ Ibogaine interrupts here: The reset lands on a recovered system, followed by months of integration during the Window of Wonder

Your Detox Path

Your 28 days before an ibogaine treatment

Cocaine and crack, in any form

Powder cocaineCrackFreebase
28days fully off cocaine

One pathway, no shorter version. Cocaine and ibogaine both interfere with the same potassium channel in the heart, so the session cannot safely sit close to recent use. Four weeks also gives the reward system time to come up off the floor, so the reset lands on a brain that has already started to recover rather than one still in the crash.

Getting Clear

What the 28 days are actually for

We will be precise about this, because it is the part other centers get wrong in both directions. The cardiac clock is fast: the best longitudinal study on cocaine and the QT interval followed users through monitored abstinence and found QTc came back toward normal during roughly the first week off, with little further change after that.³⁰ So four weeks is not us waiting on your heart, and we verify it with an EKG rather than assume it either way. The 28 days exist for the slower things. The dopamine system takes weeks to come up off the floor, and the reset works better landing on a brain that has started to recover than on one still in the crash. There is also a preclinical signal worth knowing about: in rats, high-dose ibogaine given close to cocaine altered brain electrical activity in a way that has been read as a possible lowering of the seizure threshold.³³ That is animal work at doses well above human treatment levels, and we treat it as a reason for distance rather than proof of anything. Then there is the plain practical one. Cocaine use runs in binges, so four weeks is what actually tells the difference between someone who is clear and someone who is a few days into a gap.

Included in every path

Natural Cleansing & Detox

The same all-natural Ayurvedic preparation protocol is used for every participant. Duration varies by substance and condition.

Sweat Cleansing

Toxin elimination through guided sweat sessions. This clears accumulated residue through the body's most natural purification channel.

Hydrocolonics and Enemas

Deep colon and gut cleansing that removes built-up toxins from the digestive system, restoring the gut-brain connection.

Ayurvedic Nutrition

Fresh cold-pressed juicing, whole-food Ayurvedic meals, and targeted herbal supplementation to nourish and rebuild at the cellular level.

Exercise

Daily movement is part of the protocol, not a break from it. Guided training, hiking, and swimming get the body circulating and clearing, burn off the fat where lingering toxins are stored, and build the strength and resilience you carry into treatment.

Your Program

What's included in your program

  • An ibogaine treatment in hospital, with access to a licensed physician and cardiac monitoring
  • Full cardiac screening, including EKG, before the session is approved
  • Preparation and integration support with psychedelic-experienced psychologists
  • A structured 28-day plan for arriving genuinely clear of cocaine
  • Pre-treatment Ayurvedic cleansing protocol (sweat, colonics, nutrition, exercise)
  • Post-treatment integration support for months, not days, during the Window of Wonder (WoW)
  • Accommodations at our rainforest center for the full program, with nature immersion: rainforest, ocean, and mountain

Suggested Programs

The 28 days off cocaine happen before the session, so the question is how much room you want around it. Most people who come to us for cocaine or crack fit one of these.

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How ibogaine addresses this substance

Ibogaine works across four neurological and psychological dimensions, each specific to how this substance affects the brain.

01

Reward Recalibration

Years of cocaine leave the dopamine system running below its own baseline, which is why everything feels flat without it. Ibogaine acts on that system directly, and most students describe ordinary things registering again afterward: food, music, conversation, mornings.

02

Craving Interruption

Cocaine relapse is driven by cues, not by physical need. A street, a song, a certain hour of the night. Ibogaine disrupts the default-mode-network patterns those associations run on, and the quiet that follows is what gives new routines somewhere to take hold.

03

Root-Cause Clarity

Cocaine is often doing a job: holding up a work life, covering exhaustion, managing something underneath that has never been looked at. The session tends to surface both the original wound and what the drug has cost since. Seeing it plainly does not resolve it, but it changes what you are working with.

04

Neural Repair

Ibogaine stimulates growth factors involved in repairing the pathways that heavy stimulant use wears down. We pair the session with rest, nutrition, and months of integration so that repair has the conditions it needs to hold.

The Tradition

The coca leaf and cocaine are not the same thing

People hear coca and think cocaine. In the Andes it is closer to what coffee is to us, and it has been used that way for thousands of years without producing anything like this.
Charles D. Johnston, Co-Founder, Nekawa
A coca shrub, Erythroxylum coca, in flower, showing pale yellow-white flowers and buds alongside its narrow green leaves
Erythroxylum coca in flower. An ordinary-looking shrub, which is most of the point. Photo: H. Zell, CC BY-SA 3.0
Skeletal chemical structure of cocaine
CocaineAnd this is the part that was taken out, drawn the way chemists draw it. Everything the leaf does gently and slowly, this does at once. That gap is the whole distance between these two pictures.

Coca, Erythroxylum coca, has been grown and used in the Andes for millennia. The leaf is chewed with a little lime or brewed as tea, and it does what a mild stimulant does: steadies you at altitude, dulls hunger on a long day, keeps you working. The alkaloid content of a leaf is under one percent, and it enters the body slowly through the cheek or the stomach. There is no spike, so there is no crash to chase.

Cocaine is what happens when that leaf is stripped down to the single molecule and delivered fast. Isolated in the 1850s, concentrated hundreds of times over, and taken by a route that reaches the brain in minutes or, with crack, in seconds. The plant became a product, and the thing that made it usable for centuries, its slowness, was engineered out of it. Crack is the end of that line: the same molecule, arriving as fast as chemistry allows.

We are not making a romantic point here, and we are not suggesting anyone go looking for coca leaf. The reason it belongs on this page is that it separates the substance from the story people carry about themselves. What has a hold on you is not an ancient plant and it is not a personal failing. It is a concentrate built to hit the reward system harder than the system was ever built to handle.

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Tell us what you have actually been using and for how long, in confidence, and we will tell you plainly whether ibogaine is a fit and what your 28 days would look like. No cost, no pressure.

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Common Questions

Why does Nekawa require 28 days off cocaine when other centers don't?

Because more than one thing has to settle, and only the fastest of them is cardiac. Cocaine blocks the same hERG potassium channel ibogaine blocks, which is how cocaine prolongs the QT interval, and ibogaine prolongs it too. Stacking them is the risk. The best longitudinal study on this followed cocaine users through monitored abstinence and found QTc returned toward normal during roughly the first week off cocaine, with little further change after that, so the cardiac clock is genuinely fast. We still verify it with an EKG rather than assume it. The reason the requirement is 28 days rather than 7 is the rest of it: the dopamine system needs weeks, not days, to come up off the floor, and because cocaine use tends to run in binges, a four-week window is what actually distinguishes someone who is clear from someone who is a few days into a gap. Centers that ask for less are usually looking at the cardiac clock alone.

How do cocaine and crack affect the QT interval?

Cocaine blocks the hERG-encoded potassium channel, which is one of the channels that resets the heart's electrical charge between beats. Block it and that reset takes longer, which shows up on an EKG as a prolonged QT interval, a known risk factor for dangerous arrhythmias. In habitual users given cocaine under controlled conditions, QTc lengthened significantly. Crack is the same molecule and the same channel effect, delivered faster. This matters here because ibogaine inhibits that same channel, so the two should not be anywhere near each other in time. It is worth being clear about where the danger actually sits with cocaine. Stopping it is not physically dangerous the way alcohol or heavy opioid withdrawal can be, and it does not typically produce a medical emergency. The risk is what heavy use has already done to the heart, which is why the screening is thorough and why the 28 days are not negotiable.

Is crack treated differently from powder cocaine?

Same molecule, same 28-day pathway, and the same cardiac question. What differs is severity. Smoking cocaine gets it into the brain within seconds, so the spike is sharper, the crash is harder, and the cycle repeats faster, which usually means a heavier dependency and more cardiac wear behind it. That shows up in screening and in how long a program we recommend, not in the length of the runway.

Does ibogaine actually work for cocaine?

There is real human evidence, and it is Brazilian, but it is not trial evidence and we will not dress it up as such. A 2014 review out of São Paulo followed 75 people treated with ibogaine for alcohol, cannabis, cocaine and crack dependence under a physician and alongside psychotherapy. Sixty-one percent were abstinent at follow-up, with a median of five and a half months after one treatment and eight and a half where treatment was repeated, and there were no fatalities or serious adverse reactions. The caveats are genuine: it looked backwards rather than randomizing, had no control group, relied on self-reported abstinence, and most participants used more than one substance. No controlled trial of ibogaine for cocaine has ever been run. So the honest summary is that the mechanism is well described, the real-world outcomes are encouraging, and the definitive study does not exist yet.

What if I'm using cocaine alongside alcohol or opioids?

Tell us, because it changes the plan. Mixing cocaine and alcohol produces cocaethylene, a compound that is harder on the heart than either one alone, and that affects screening. Opioids on top of cocaine mean a different and usually longer preparation, since opioids carry their own clearing timeline. Combined use is common and it is not a reason to be turned away. It is a reason for us to build the runway around what you are actually taking.

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Citations (8)

  1. [20] Koenig X, Hilber K (2015). The Anti-Addiction Drug Ibogaine and the Heart: A Delicate Relation. Molecules, 20(2), 2208–2228. Read the source →

    Review of ibogaine cardiac risk, including QT prolongation and arrhythmia. Documents a fatality in a 52-year-old man with a 20-year history of alcohol use disorder in whom postmortem examination found hepatic cirrhosis and steatosis alongside coronary artery sclerosis, supporting pre-existing liver disease as a significant risk factor and pre-treatment liver function testing as essential screening.

  2. [28] Substance Abuse and Mental Health Services Administration (2021). Treatment for Stimulant Use Disorders (Treatment Improvement Protocol 33). SAMHSA Publication No. PEP21-02-01-004, Rockville, MD. Read the source →

    There are no FDA-approved pharmacologic treatments for stimulant use disorders, including cocaine. Behavioral approaches, principally contingency management and cognitive behavioral therapy, remain the front-line treatment.

  3. [29] Magnano AR, Talathoti NB, Hallur R, Jurus DT, Dizon J, Holleran S, Bloomfield DM (2006). Effect of acute cocaine administration on the QTc interval of habitual users. The American Journal of Cardiology, 97(8), 1244–1246. Read the source →

    In habitual cocaine users given cocaine under controlled conditions, electrocardiograms showed significant prolongation of the QTc interval after administration (p < 0.001).

  4. [30] Levin KH, Copersino ML, Epstein D, Boyd SJ, Gorelick DA (2008). Longitudinal ECG changes in cocaine users during extended abstinence. Drug and Alcohol Dependence, 95(1–2), 160–163. Read the source →

    Weekly ECGs from 25 chronic cocaine users during up to three months of monitored abstinence on a closed ward. QTc shortened significantly (about 10.5 ms) during the first week of abstinence, with no further significant change afterward, and baseline QTc correlated with how much cocaine had been used beforehand. The authors conclude that cocaine-associated QTc prolongation returns toward normal within roughly the first week off cocaine.

  5. [31] Ferreira S, Crumb WJ Jr, Carlton CG, Clarkson CW (2001). Effects of cocaine and its major metabolites on the HERG-encoded potassium channel. Journal of Pharmacology and Experimental Therapeutics, 299(1), 220–226. Read the source →

    Cocaine and several of its metabolites block the HERG-encoded potassium channel, which governs cardiac repolarization. This is the same channel ibogaine inhibits, and it is the mechanism behind cocaine-associated QT prolongation.

  6. [32] Cappendijk SLT, Dzoljic MR (1993). Inhibitory effects of ibogaine on cocaine self-administration in rats. European Journal of Pharmacology, 241(2–3), 261–265. Read the source →

    A single dose of ibogaine reduced cocaine self-administration in cocaine-dependent rats for more than 48 hours, and weekly dosing across three weeks produced a more pronounced and durable reduction than daily dosing. Preclinical (animal) evidence.

  7. [33] Binienda Z, Beaudoin MA, Thorn BT, Sadovova N, Skinner RD, Slikker W Jr, Ali SF (2000). Application of electrophysiological method to study interactions between ibogaine and cocaine. Annals of the New York Academy of Sciences, 914(1), 387–393. Read the source →

    Electrocorticographic recordings in rats given high-dose ibogaine before cocaine. The combination altered brain electrical activity and dopamine levels in ways that have been read as a possible lowering of the seizure threshold. Preclinical (animal) evidence at doses far above human treatment levels.

  8. [34] Schenberg EE, de Castro Comis MA, Chaves BR, da Silveira DX (2014). Treating drug dependence with the aid of ibogaine: a retrospective study. Journal of Psychopharmacology, 28(11), 993–1000. Read the source →

    Retrospective review of 75 people treated with ibogaine in Brazil for dependence on alcohol, cannabis, cocaine and crack, 72% of them polysubstance users, under physician supervision and combined with psychotherapy. 61% were abstinent at follow-up. Median abstinence was 5.5 months after a single treatment and 8.4 months where treatment was repeated, both significantly longer than the abstinence achieved before ibogaine (p < 0.001). No fatalities and no serious adverse reactions were observed. Retrospective and uncontrolled, with self-reported abstinence, so it is real-world outcome data rather than trial evidence.