heart and ibogaine molecule

Iboga and Ibogaine Safety

At Root Healing, we take health and Iboga safety very seriously. With our Bwiti training we have learned safety tools and methods developed over thousands of years to help in almost any situation. However, due to the conditions of the modern world, we also include a medical team in our intake, detox and retreat process. As you will learn in this post, Iboga is safe when taken by someone who has no preexisting mental physical factors and is on no contraindicating medications or drugs. Of course there is some prep that can be done to enhance your readiness, but it really comes down to those things. 

In an effort for Harm Reduction around Iboga use, we have asked someone in our medical team to share about the physical concerns, contraindications of medications/drugs, and diet:

Ibogaine Safety and Contraindications

Ibogaine is an alkaloid derived from the Tabernanthe Iboga shrub which has psychoactive effects. The roots of the plant have been used in ceremonies by an African tribe known as the Bwiti, for thousands of years.

Nowadays, more and more research is revealing that Ibogaine is extremely potent in the management of drug addiction and substance abuse. There are reports that even a single dose of the alkaloid can eliminate drug-seeking behavior in some patients.

Ibogaine can be safe and effective in attenuating symptoms of addiction and withdrawal for patients without contraindications as long as it is used under medical control. A team of experienced medical specialists and Iboga providers must examine the health and medical history of all candidates and then strictly supervise the therapeutic process of those approved.

The Potential Health Risks of Ibogaine

Ibogaine therapy has potential health risks because of its effect on the cardiovascular system. The alkaloid blocks the potassium ion channels in the heart (Kv11.1 / hERG) which leads to changes in the cardiac rhythm such as prolonged QT interval [1].

This side-effect slows down the repolarization of the heart muscle and increases the risk of potentially fatal arrhythmia called Torsades de pointes [2].

According to studies, the blockage is temporary but the presence of a prolonged QT interval might last for more than 24 hours [3]. That is due to the long half-life of noribogaine (28-49 h) which is the main metabolite of Ibogaine in the human body. 

Prolonged QT interval poses a significant risk for patients with preexisting cardiovascular conditions, who might be at an already increased risk of arrhythmia. This side-effect is also possible in many prescription medications.

Generally, an increased risk of arrhythmia is present only at high doses of ibogaine and in patients with medical contraindications. 

The main contraindications against Iboga therapy are preexisting medical conditions and various drug therapies that can also affect the QT interval or the liver metabolism of Ibogaine. According to summaries of the reported fatalities that have full medical reports, they were all in either chronically ill patients or because of drug-drug interactions [4].

Other adverse reactions due to high doses of Ibogaine may include nausea, vomiting, dry mouth, and ataxia (problems in coordinating movements) [5]. They are generally mild and temporary.

Physical Contraindications Against Ibogaine Treatment

The main physical contraindication against Ibogaine treatment is any preexisting medical condition related to the heart or the liver. Most heart diseases can be negatively affected by blocking the potassium ion channel which in turn increases the risk of a potentially fatal arrhythmia or heart failure.

Furthermore, Ibogaine therapy slows down the heart rate so patients with bradycardia or tachycardia are not good candidates. Patients with hypertension or hypotension are also excluded from Ibogaine therapy.

Ibogaine is metabolized in the liver by a group of enzymes called cytochrome P450, more specifically CYP2D6 [6].

If the liver is not functioning properly then Ibogaine is not going to be broken down and neutralized effectively. This increases the active dose of Ibogaine and elevates the risk of cardiovascular side effects such as arrhythmia and heart arrest. 

In fact, there are reports of fatal cases in patients with serious liver damage due to alcohol abuse [7].

Furthermore, patients with schizophrenia, mania, psychosis, or dementia are not good candidates for the therapy because in some cases Ibogaine can lead to worsening of their symptoms [8].

Foods to Avoid During Iboga Therapy

Ibogaine therapy requires proper preparation, which includes a somewhat specific diet. There are some foods which should be avoided for Ibogaine safety.

Foods such as grapefruit and pomelo must be avoided before and during Ibogaine therapy. These fruits are known for blocking some of the liver enzymes from the P450 family, including CYP2D6 [9].

Blocking these enzymes stops the breakdown of Ibogaine and elevates its blood concentrations to dangerous levels. Thus, consumption of pomelo and grapefruit is strictly prohibited as it can lead to an increased risk of side-effects such as arrhythmia.

Tonic water and Bitter lemon drinks must be avoided as well due to the content of quinine [10]. Quinine is the ingredient that contributes to the bitter taste. 

It is also a type of medication, used for the treatment of malaria and some autoimmune disorders. Unfortunately, it is a strong inhibitor of CYP2D6 and it will block Ibogaine breakdown leading to elevated concentrations and side-effects.

Alcohol can also lead to dangerous interactions with ibogaine. Patients should not consume any alcohol for at least 3-7 days before Ibogaine administration and liver enzymes should not be significantly elevated.

Contraindicated Medications and Drug-Interactions

Medications that may block the liver metabolism or prolong the QT interval are strongly contraindicated during ibogaine therapy and should be tapered off at least a week before the treatment.

Most of the drugs act both on the liver metabolism by interacting with CYP2D6 and prolong the QT interval by affecting the potassium ion channel. The list of drugs that affect either or both includes [11].

  • Antidepressants, especially SSRIs
  • Antiarrhythmics
  • Antifungal
  • Anti-HIV
  • Quinine
  • Cannabidiol (CBD)
  • Antacids
  • Antipsychotics
  • Antibiotics
  • Opioids and methadone
  • Beta-blockers
  • Diuretics

Antidepressants such as Selective serotonin reuptake inhibitors (SSRIs) have the strongest inhibitory effect on CYP2D6 as well as a QT-prolonging effect on the heart muscle [12]. Combinations with Ibogaine are extremely dangerous.

Ibogaine is used to treat addictions with opiates and narcotics but it should not be taken together with these drugs. They are also metabolized in the liver and which may slow down the breakdown of both substances [13]. This increases the risk of side-effects and can lead to a potentially lethal overdose.

How to Minimize Possible Ibogaine Risks

Ibogaine is safe for those patients who do not have any physical contraindications, safely taper off their medications, and prepare with a proper and healthy diet.

To minimize the risks, Ibogaine therapy must involve medical supervision by a team of experienced doctors, nurses, and pharmacists. Furthermore, there are several medical tests and procedures that patients should undergo to ensure the success and safety of the therapy, such as:

  • Blood tests (potassium levels, etc.)
  • ECG
  • Heart, kidney, and lung function
  • Liver enzymes
  • Complete medical history of infections, surgeries, and chronic conditions

The preparation before ibogaine therapy includes tapering off your medications and following a specific diet. Always consult with a medical doctor for more information on how to safely stop your medications and prepare for the therapy. 


  1. Koenig, X., Kovar, M., Boehm, S., Sandtner, W., & Hilber, K. (2014). Anti-addiction drug ibogaine inhibits hERG channels: a cardiac arrhythmia risk. Addiction biology, 19(2), 237–239. https://doi.org/10.1111/j.1369-1600.2012.00447.x 
  2. Sanguinetti, M. C., & Tristani-Firouzi, M. (2006). hERG potassium channels and cardiac arrhythmia. Nature, 440(7083), 463–469. https://doi.org/10.1038/nature04710 
  3. Glue, P., Lockhart, M., Lam, F., Hung, N., Hung, C. T., & Friedhoff, L. (2015). Ascending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability. Journal of clinical pharmacology, 55(2), 189–194. https://doi.org/10.1002/jcph.404 
  4. Alper, K. R., Stajić, M., & Gill, J. R. (2012). Fatalities temporally associated with the ingestion of ibogaine. Journal of forensic sciences, 57(2), 398–412. https://doi.org/10.1111/j.1556-4029.2011.02008.x 
  5. Brown T. K. (2013). Ibogaine in the treatment of substance dependence. Current drug abuse reviews, 6(1), 3–16. https://doi.org/10.2174/15672050113109990001 
  6. Koenig, X., & Hilber, K. (2015). The anti-addiction drug ibogaine and the heart: a delicate relation. Molecules (Basel, Switzerland), 20(2), 2208–2228. https://doi.org/10.3390/molecules20022208 
  7. Papadodima, S. A., Dona, A., Evaggelakos, C. I., Goutas, N., & Athanaselis, S. A. (2013). Ibogaine related sudden death: a case report. Journal of forensic and legal medicine, 20(7), 809–811. https://doi.org/10.1016/j.jflm.2013.06.032 
  8. Houenou, J., Homri, W., Leboyer, M., & Drancourt, N. (2011). Ibogaine-associated psychosis in schizophrenia: a case report. Journal of clinical psychopharmacology, 31(5), 659. https://doi.org/10.1097/JCP.0b013e31822c6509 
  9. Girennavar, B., Poulose, S. M., Jayaprakasha, G. K., Bhat, N. G., & Patil, B. S. (2006). Furocoumarins from grapefruit juice and their effect on human CYP 3A4 and CYP 1B1 isoenzymes. Bioorganic & medicinal chemistry, 14(8), 2606–2612. https://doi.org/10.1016/j.bmc.2005.11.039 
  10. Brasić J. R. (1999). Should people with nocturnal leg cramps drink tonic water and bitter lemon?. Psychological reports, 84(2), 355–367. https://doi.org/10.2466/pr0.1999.84.2.355 
  11. Nachimuthu, S., Assar, M. D., & Schussler, J. M. (2012). Drug-induced QT interval prolongation: mechanisms and clinical management. Therapeutic advances in drug safety, 3(5), 241–253. https://doi.org/10.1177/2042098612454283 
  12. Ereshefsky, L., Riesenman, C., & Lam, Y. W. (1995). Antidepressant drug interactions and the cytochrome P450 system. The role of cytochrome P450 2D6. Clinical pharmacokinetics, 29 Suppl 1, 10–19. https://doi.org/10.2165/00003088-199500291-00004 
  13. de la Torre, R., Yubero-Lahoz, S., Pardo-Lozano, R., & Farré, M. (2012). MDMA, methamphetamine, and CYP2D6 pharmacogenetics: what is clinically relevant?. Frontiers in genetics, 3, 235. https://doi.org/10.3389/fgene.2012.00235 

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