An Iboga Treatment works with what is known as the godfather of all plant medicines, Iboga. Iboga is the inner root bark of a rainforest shrub called Tabernanthe Iboga. It’s been used by West African tribes for thousands of years for its medicinal and spiritual properties as a part of the spiritual tradition Bwiti.
The roots of the herb contain several bioactive alkaloids with the most prominent one being Ibogaine. It was isolated from the plant by Édouard Landrin in 1900 and it’s considered as the main alkaloid possessing psychoactive and therapeutic qualities.
In 1962 it was found that Ibogaine had potent effects on attenuating withdrawal and cravings in individuals addicted to opiates such as heroin and morphine. Case studies also reported effectiveness against cocaine, amphetamine, and alcohol addictions (1).
Ibogaine Therapy and Iboga Treatments have already been employed for healing and as a treatment for addiction in several countries including Portugal, Thailand, Canada, New Zealand, and Mexico.
While both therapies have high success rates, using Iboga Treatments which work with Iboga Root Bark and Iboga TA are more effective due to the combination of several alkaloids which potentiate the benefits of Ibogaine for addiction, mental health, and neurological conditions.
Ibogaine and Iboga Treatment
Ibogaine treatments tend to be very clinical, as they are performed in a hospital setting with little to no spiritual healing, counseling, or integration coaching like you would receive and Iboga Treatment.
What is more, they use a pure single alkaloid extract which misses out on the potential of the whole plant since Ibogaine is not the only active alkaloid in the Tabernanthe Iboga shrub.
In fact, the root and especially the root bark of the herb contains dozens of alkaloids. Apart from ibogaine, other prominent molecules include tabernanthine (13-methoxy ibogamine), ibogamine, coronaridine, ibogaline, and others.
Scientists have investigated the effectiveness of these alkaloids in attenuating drug-seeking behavior in animals, and they have found that tabernanthine, ibogamine, and coronaridine possess potent anti-addictive properties similar to ibogaine (2).
This means that the benefits of ibogaine will be potentiated when used in conjunction with the rest of the alkaloids. Thus, we recommend an Iboga Treatment as a more effective option in attenuating the symptoms of drug craving and withdrawal.
The available Iboga treatments can vary but practitioners usually use Iboga Root Bark, Iboga Total Alkaloid extract (TA), or a combination of the two.
Iboga may be more potent than Ibogaine for other conditions as well, such as alleviating symptoms of depression.
Both ibogaine and tabernanthine activate receptors in the brains called sigma-2 (3). According to the research, activating these receptors can have several benefits for brain function, including antidepressant effects.
There are many different approaches and therapeutic options when it comes to Iboga treatment. We believe the best option is by far the traditional Bwiti ceremonies and retreats that are facilitated by someone who has a proper training from a Bwiti Shaman. This is true because Iboga and Bwiti have been married (in a sense) for thousands of years. Iboga is the sacrament of the Bwiti and it’s spirit has communicated to them directly about how to work with it. The rituals and traditions of a Bwiti focused Iboga treatment were actually given to the Bwiti by the spirit of Iboga itself, enhancing its strength, efficacy, and healing results.
Iboga and Ibogaine for Treating Addiction and Withdrawal
In one study, 33 people with addiction to heroin underwent Ibogaine therapy and were then observed for 72 hours (4).
25 of the patients experienced complete relief of opioid withdrawal within the first 24 hours and the benefits persisted during the observation period.
In the rest of the participants, withdrawal but not drug-seeking behavior was eliminated or significantly reduced.
The participants were tested at 3-, 6-, and 12-months after the dose. Only one subject each at three and six months and two participants at 12 months tested positive for opioids.
Furthermore, a much larger study with 88 opioid-dependent patients also reported long-term effects and up to 30% of the participants achieved complete cessation of drug use (6).
The withdrawal symptoms were suppressed immediately after Ibogaine therapy in 80% of the individuals.
A single dose of Ibogaine appears effective in treating cocaine addiction as well. One study in 27 treatment-seeking cocaine-dependent individuals reported that 800 mg of ibogaine significantly decreased cravings immediately and the effect persisted one month after the dose (7).
Other published scientific observations also confirm the benefits of Ibogaine on cocaine addiction and withdrawal (8).
Another report of 75 previous alcohol, cannabis, cocaine and crack users reveals that a single Ibogaine treatment led to several months of abstinence in 61% of the patients, while additional treatments prolonged the suppressing effects on drug-seeking behavior (9).
Iboga and Ibogaine Benefits for Treating Mental Health Conditions
Depression and anxiety disorders are relatively common amongst drug addicts. In fact, the addiction often occurs in an attempt to cope with psychological symptoms.
With that being said, most of the studies investigating the benefits of Ibogaine for addiction and withdrawal also report significant improvement in symptoms of depression after the treatment (5, 7, 10).
In fact, ibogaine was initially marketed in France in the 1930s as a product for depression and fatigue (11).
Increasing serotonin levels is also one of the main targets of pharmacological therapy with antidepressants.
Furthermore, increasing dopamine may also improve symptoms of depression. If dopamine levels are insufficient, it may lead to mood problems including depressed mood, lack of motivation, and feelings of hopelessness.
In fact, the neurotransmitter is considered to play a central role in the development of the most common type of depression – major depressive disorder (14).
Mood and symptoms of depression may even improve in cases of not-fully successful detoxification with Ibogaine.
Ibogaine also appears effective in certain forms of anxiety, such as PTSD (post-traumatic stress disorder).
According to a study in 51 US veterans, a single oral dose (10 mg/kg) of ibogaine led to a significant reduction in symptoms of depression, anxiety, and PTSD (16). The treatment also led to major reductions in suicidal tendencies and cognitive impairment.
Ibogaine and Iboga Treatment Benefits for Physical Conditions
According to in vitro and animal experiments, Ibogaine may also possess antimicrobial properties, including, antiretroviral, antimycobacterial, and antimycotic effects.
One in vitro study has reported that Ibogaine has activity against the bacteria that causes tuberculosis – Mycobacterium tuberculosis (17).
Furthermore, another in vitro laboratory experiment with human immune cells has revealed that Ibogaine can also block the replication of the Human Immunodeficiency Virus (HIV) that causes AIDS and may stop the spreading of the virus (18).
Both in vitro and animal studies show that Ibogaine is highly effective against one of the most common fungal pathogens – Candida albicans. The fungi are a common cause of infections, especially amongst immunocompromised patients.
In the in vitro trial, the scientists discovered that Ibogaine can inhibit the enzymes that Candida albicans use to infect cells, and thus it can limit the infection(19).
Benefits of Iboga and Ibogaine for Neuroplasticity
Neuroplasticity is the potential of the brain to learn, adapt and recover. It’s the result of the brain cells’ ability to form new connections with each other, reorganize (“cortical remapping” and even form new ones from dormant progenitor cells.
The growth factors in the brain that stimulate this process and ensure the survival of nerve cells are called neurotrophic factors.
According to research, Ibogaine may increase the activity of several neurotrophic factors in the brain, including brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and glial cell-derived neurotrophic factor (GDNF) (21).
According to most experts, the long-term benefits of Ibogaine on symptoms of addiction and drug-seeking behavior are likely due to the activation of some of these factors, especially GDNF (22).
Restoring the normal activity of the neurotrophic factor also ensures the normal function and survival of dopaminergic brain cells.
Potential benefits of Iboga and Ibogaine
The effects of Iboga and its alkaloids such as ibogaine on various receptors and neurotrophic factors in the brain may hide a potential for treating certain neurological conditions.
For example, restoring the activity of BDNF in the brain may boost the recovery of patients with traumatic brain injury (TBI) (28).
TBI is a term describing damage to the brain (such as a concussion) that has occurred due to external force. Severe or repeated injuries can lead to irreparable brain damage and disabilities.
Since Ibogaine stimulates the activity of BDNF in certain areas of the brain, the alkaloid may be able to induce neural regeneration, reconnection, dendritic sprouting, and improved synaptic efficacy.
This in turn may reverse cognitive and emotional deficits in TBI patients. Animal studies support the effectiveness of BDNF activation which was able to cause a complete brain repair after a TBI (29).
Another neurodegenerative condition that may be ameliorated thanks to the effects of Iboga and Ibogaine on neuroplasticity is Parkinson’s. The condition is caused by the death of dopaminergic neurons.
GDNF has been extensively investigated as a possible agent that can prevent the death of brain cells and restore function in the dopaminergic brain cells that are affected by the condition (30).
Studies have shown up to 40% improvement in symptoms after direct GDNF infusion. However, the procedure is invasive, complicated, and inconvenient.
On the other hand, Ibogaine has been proven to upregulate GDNF expression in the same regions which are otherwise affected in Parkinson’s and thus may prove to be an effective and less invasive treatment option (21).
Furthermore, the activation of the sigma-1 receptor by ibogaine and other alkaloids in Iboga may also provide benefits against neurological diseases (31). For example, the activation of the receptor may help patients with Parkinson’s by reducing neuroinflammation (32).
Studies have also shown that the reduction of inflammation in the brain is especially effective in autoimmune neurological conditions such as multiple sclerosis (MS) and autoimmune encephalomyelitis (inflammation of the brain and the spinal cord).
In one experimental animal model of autoimmune encephalomyelitis, sigma-1 activation prevented the accumulation of immune cells and degeneration of neurons which slowed down the progression of the condition (33).
Helping people find clarity in who they are and what they want
An Iboga Treatment should focus on connecting you to who you are and what you want because this is one of the biggest spiritual benefits the treatment offers. In a traditional Bwiti Iboga ceremony, individuals are brought to meet and reconnect with their soul. This connection (and knowing) instills an unwavering sense of confidence, self-love, and clarity to those who truly embrace it. This will then have a profound impact on their perspective and their entire external world. When you leave an Iboga treatment knowing who you are and what you want, there is no stopping you.
While Ibogaine therapy has been studied much more extensively than Iboga, an Iboga Treatment using the isolated alkaloid extract is much more optimal and efficient.
We believe Iboga treatments at our Root Healing retreats offer the best of both worlds, having a medical team and Bwiti trained team on staff, offering comprehensive holistic treatments that work.
- Lotsof, H. S., & Alexander, N. E. (2001). Case studies of ibogaine treatment: implications for patient management strategies. The Alkaloids. Chemistry and biology, 56, 293–313. https://doi.org/10.1016/s0099-9598(01)56020-4
- Glick, S. D., Kuehne, M. E., Raucci, J., Wilson, T. E., Larson, D., Keller, R. W., Jr, & Carlson, J. N. (1994). Effects of iboga alkaloids on morphine and cocaine self-administration in rats: relationship to tremorigenic effects and to effects on dopamine release in nucleus accumbens and striatum. Brain research, 657(1-2), 14–22. https://doi.org/10.1016/0006-8993(94)90948-2
- Popik, P., & Skolnick, P. (1999). Pharmacology of Ibogaine and Ibogaine-Related Alkaloids. Alkaloids: Chemistry and Biology, 52(C), 197–231. https://doi.org/10.1016/S0099-9598(08)60027-9
- Alper, K. R., Lotsof, H. S., Frenken, G. M., Luciano, D. J., & Bastiaans, J. (1999). Treatment of acute opioid withdrawal with ibogaine. The American journal on addictions, 8(3), 234–242. https://doi.org/10.1080/105504999305848
- Noller, G. E., Frampton, C. M., & Yazar-Klosinski, B. (2018). Ibogaine treatment outcomes for opioid dependence from a twelve-month follow-up observational study. The American journal of drug and alcohol abuse, 44(1), 37–46. https://doi.org/10.1080/00952990.2017.1310218
- Davis, A. K., Barsuglia, J. P., Windham-Herman, A. M., Lynch, M., & Polanco, M. (2017). Subjective effectiveness of ibogaine treatment for problematic opioid consumption: Short- and long-term outcomes and current psychological functioning. Journal of psychedelic studies, 1(2), 65–73. https://doi.org/10.1556/2054.01.2017.009
- Mash, D. C., Kovera, C. A., Pablo, J., Tyndale, R. F., Ervin, F. D., Williams, I. C., Singleton, E. G., & Mayor, M. (2000). Ibogaine: complex pharmacokinetics, concerns for safety, and preliminary efficacy measures. Annals of the New York Academy of Sciences, 914, 394–401. https://doi.org/10.1111/j.1749-6632.2000.tb05213.x
- Luciano D. (1998). Observations on treatment with ibogaine. The American journal on addictions, 7(1), 89–90. https://doi.org/10.1111/j.1521-0391.1998.tb00472.x
- Schenberg, E. E., de Castro Comis, M. A., Chaves, B. R., & da Silveira, D. X. (2014). Treating drug dependence with the aid of ibogaine: a retrospective study. Journal of psychopharmacology (Oxford, England), 28(11), 993–1000. https://doi.org/10.1177/0269881114552713
- Mash, D. C., Kovera, C. A., Pablo, J., Tyndale, R., Ervin, F. R., Kamlet, J. D., & Hearn, W. L. (2001). Ibogaine in the treatment of heroin withdrawal. The Alkaloids. Chemistry and biology, 56, 155–171. https://doi.org/10.1016/s0099-9598(01)56012-5
- Goutarel, R., Gollnhofer, O., & Sillans, R. (1993). Pharmacodynamics and therapeutic applications of iboga and ibogaine. Psychedelic Monographs and Essays, 6, 70-111.
- Bulling, S., Schicker, K., Zhang, Y. W., Steinkellner, T., Stockner, T., Gruber, C. W., Boehm, S., Freissmuth, M., Rudnick, G., Sitte, H. H., & Sandtner, W. (2012). The mechanistic basis for noncompetitive ibogaine inhibition of serotonin and dopamine transporters. The Journal of biological chemistry, 287(22), 18524–18534. https://doi.org/10.1074/jbc.M112.343681
- Wells, G. B., Lopez, M. C., & Tanaka, J. C. (1999). The effects of ibogaine on dopamine and serotonin transport in rat brain synaptosomes. Brain research bulletin, 48(6), 641–647. https://doi.org/10.1016/s0361-9230(99)00053-2
- Belujon, P., & Grace, A. A. (2017). Dopamine System Dysregulation in Major Depressive Disorders. The international journal of neuropsychopharmacology, 20(12), 1036–1046. https://doi.org/10.1093/ijnp/pyx056
- Forsyth, B., Machado, L., Jowett, T., Jakobi, H., Garbe, K., Winter, H., & Glue, P. (2016). Effects of low dose ibogaine on subjective mood state and psychological performance. Journal of ethnopharmacology, 189, 10–13. https://doi.org/10.1016/j.jep.2016.05.022
- Davis, A. K., Averill, L. A., Sepeda, N. D., Barsuglia, J. P., & Amoroso, T. (2020). Psychedelic Treatment for Trauma-Related Psychological and Cognitive Impairment Among US Special Operations Forces Veterans. Chronic stress (Thousand Oaks, Calif.), 4, 2470547020939564. https://doi.org/10.1177/2470547020939564
- Rastogi, N., Abaul, J., Goh, K. S., Devallois, A., Philogène, E., & Bourgeois, P. (1998). Antimycobacterial activity of chemically defined natural substances from the Caribbean flora in Guadeloupe. FEMS immunology and medical microbiology, 20(4), 267–273. https://doi.org/10.1111/j.1574-695X.1998.tb01136.x
- Silva, E. M., Cirne-Santos, C. C., Frugulhetti, I. C., Galvão-Castro, B., Saraiva, E. M., Kuehne, M. E., & Bou-Habib, D. C. (2004). Anti-HIV-1 activity of the Iboga alkaloid congener 18-methoxycoronaridine. Planta medica, 70(9), 808–812. https://doi.org/10.1055/s-2004-827227
- Yordanov, M., Dimitrova, P., Patkar, S., Saso, L., & Ivanovska, N. (2008). Inhibition of Candida albicans extracellular enzyme activity by selected natural substances and their application in Candida infection. Canadian journal of microbiology, 54(6), 435–440. https://doi.org/10.1139/w08-029
- Yordanov, M., Dimitrova, P., Patkar, S., Falcocchio, S., Xoxi, E., Saso, L., & Ivanovska, N. (2005). Ibogaine reduces organ colonization in murine systemic and gastrointestinal Candida albicans infections. Journal of medical microbiology, 54(Pt 7), 647–653. https://doi.org/10.1099/jmm.0.45919-0
- Marton, S., González, B., Rodríguez-Bottero, S., Miquel, E., Martínez-Palma, L., Pazos, M., Prieto, J. P., Rodríguez, P., Sames, D., Seoane, G., Scorza, C., Cassina, P., & Carrera, I. (2019). Ibogaine Administration Modifies GDNF and BDNF Expression in Brain Regions Involved in Mesocorticolimbic and Nigral Dopaminergic Circuits. Frontiers in pharmacology, 10, 193. https://doi.org/10.3389/fphar.2019.00193
- Corne, R., & Mongeau, R. (2019). Utilisation des psychédéliques en psychiatrie : lien avec les neurotrophines [Neurotrophic mechanisms of psychedelic therapy]. Biologie aujourd’hui, 213(3-4), 121–129. https://doi.org/10.1051/jbio/2019015
- He, D. Y., & Ron, D. (2006). Autoregulation of glial cell line-derived neurotrophic factor expression: implications for the long-lasting actions of the anti-addiction drug, Ibogaine. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 20(13), 2420–2422. https://doi.org/10.1096/fj.06-6394fje
- Angelucci, F., Ricci, V., Pomponi, M., Conte, G., Mathé, A. A., Attilio Tonali, P., & Bria, P. (2007). Chronic heroin and cocaine abuse is associated with decreased serum concentrations of the nerve growth factor and brain-derived neurotrophic factor. Journal of psychopharmacology (Oxford, England), 21(8), 820–825. https://doi.org/10.1177/0269881107078491
- Pitts, E. G., Li, D. C., & Gourley, S. L. (2018). Bidirectional coordination of actions and habits by TrkB in mice. Scientific reports, 8(1), 4495. https://doi.org/10.1038/s41598-018-22560-x
- Lu,, B. & Figurov,, A. (1997). Role of Neurotrophins in Synapse Development and Plasticity: . Reviews in the Neurosciences, 8(1), 1-12. https://doi.org/10.1515/REVNEURO.19188.8.131.52
- Zigova, T., Pencea, V., Wiegand, S. J., & Luskin, M. B. (1998). Intraventricular administration of BDNF increases the number of newly generated neurons in the adult olfactory bulb. Molecular and cellular neurosciences, 11(4), 234–245. https://doi.org/10.1006/mcne.1998.0684
- Kaplan, G. B., Vasterling, J. J., & Vedak, P. C. (2010). Brain-derived neurotrophic factor in traumatic brain injury, post-traumatic stress disorder, and their comorbid conditions: role in pathogenesis and treatment. Behavioural pharmacology, 21(5-6), 427–437. https://doi.org/10.1097/FBP.0b013e32833d8bc9
- Cacialli, P., Palladino, A., & Lucini, C. (2018). Role of brain-derived neurotrophic factor during the regenerative response after traumatic brain injury in adult zebrafish. Neural regeneration research, 13(6), 941–944. https://doi.org/10.4103/1673-5374.233430
- Gill, S. S., Patel, N. K., Hotton, G. R., O’Sullivan, K., McCarter, R., Bunnage, M., Brooks, D. J., Svendsen, C. N., & Heywood, P. (2003). Direct brain infusion of glial cell line-derived neurotrophic factor in Parkinson disease. Nature medicine, 9(5), 589–595. https://doi.org/10.1038/nm850
- Thompson, C., & Szabo, A. (2020). Psychedelics as a novel approach to treating autoimmune conditions. Immunology letters, 228, 45–54. https://doi.org/10.1016/j.imlet.2020.10.001
- Jia, J., Cheng, J., Wang, C., & Zhen, X. (2018). Sigma-1 Receptor-Modulated Neuroinflammation in Neurological Diseases. Frontiers in cellular neuroscience, 12, 314. https://doi.org/10.3389/fncel.2018.00314
- Oxombre, B., Lee-Chang, C., Duhamel, A., Toussaint, M., Giroux, M., Donnier-Maréchal, M., Carato, P., Lefranc, D., Zéphir, H., Prin, L., Melnyk, P., & Vermersch, P. (2015). High-affinity σ1 protein agonist reduces clinical and pathological signs of experimental autoimmune encephalomyelitis. British journal of pharmacology, 172(7), 1769–1782. https://doi.org/10.1111/bph.13037