heart and ibogaine molecule

Iboga (Ibogaine) Science Resources

Science Resources

The main active alkaloid in Iboga is called Ibogaine and it has been shown to be beneficial in a number of scientific studies. Scientific studies report that it has powerful effects on attenuating drug-seeking behavior and withdrawal symptoms. It can help individuals suffering from heroin, cocaine, morphine, oxycodone, amphetamine, nicotine, and alcohol addictions. Ibogaine medicates these effects by affecting several neurotransmitters in the brain. By increasing serotonin levels, also has benefits for patients with depression, anxiety, and post-traumatic stress disorder. Furthermore, the alkaloid activates neurotrophic growth factors in the brain which have neuroprotective and anti-inflammatory effects. Therefore, Ibogaine may have potential application in the therapy of several neurodegenerative and autoimmune conditions, especially Parkinson’s.

How does Iboga Work?

Ibogaine has a complex effect on the brain by affecting the activity of several neurotransmitters. By increasing dopamine levels and blocking N-acetylcholine receptors, the alkaloid can restore the normal biochemistry of the brain and attenuate symptoms of addiction (1, 2). By increasing serotonin levels in the brain, Ibogaine also improves symptoms of depression and anxiety (3). The psychedelic effects of the drug are due to blocking the NMDA receptors in the brain (4).

  1. 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 
  2. Glick, S. D., Maisonneuve, I. M., Kitchen, B. A., & Fleck, M. W. (2002). Antagonism of alpha 3 beta 4 nicotinic receptors as a strategy to reduce opioid and stimulant self-administration. European journal of pharmacology, 438(1-2), 99–105. https://doi.org/10.1016/s0014-2999(02)01284-0
  3. Baumann, M. H., Rothman, R. B., Pablo, J. P., & Mash, D. C. (2001). In vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in rats. The Journal of pharmacology and experimental therapeutics, 297(2), 531–539.
  4. Popik, P., Layer, R. T., Fossom, L. H., Benveniste, M., Geter-Douglass, B., Witkin, J. M., & Skolnick, P. (1995). NMDA antagonist properties of the putative antiaddictive drug, ibogaine. The Journal of pharmacology and experimental therapeutics, 275(2), 753–760.

 

Neuroplasticity

Ibogaine can rewire the brain by activating several neurotrophic growth factors: Brain-derived neurotrophic factor (BDNF), Nerve Growth Factor (NGF), and Glial Cell-Derived Neurotrophic Factor (GDNF) (1). They have neuroprotective and neuro-remodeling effects (2). The combined effect on the various nerve growth factors is likely the key to the long-term effect of Ibogaine on attenuating drug and alcohol addictions (3). BDNF might also stimulate the formation of new neurons in parts of the adult brain that still retain stem cells (4).

  1. 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
  2. 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.1997.8.1.1
  3. 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
  4. 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

 

Treating Mood, Depression, and Anxiety

Ibogaine has antidepressant effects thanks to its serotonin-increasing activity (1). Several studies report that symptoms of depression are significantly reduced (2, 3).

These benefits for mood are likely limited to people with depression, anxiety, or other related psychiatric problems and do not extend to healthy people (4).

  1. Mash, D. C., Staley, J. K., Baumann, M. H., Rothman, R. B., & Hearn, W. L. (1995). Identification of a primary metabolite of ibogaine that targets serotonin transporters and elevates serotonin. Life sciences, 57(3), PL45–PL50. https://doi.org/10.1016/0024-3205(95)00273-9
  2. 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
  3. 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
  4. 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

 

Treating DETOX and Withdrawal Symptoms

There are multiple case reports and clinical trials which reveal successful treatment of heroin, cocaine, morphine, amphetamine, and alcohol addictions (1, 6, 7, 8, 9, 10, 11, 12). The biologically active metabolite of the antiaddictive drug ibogaine is Noriobogaine. It works by affecting several neurotransmitters and neurotrophic growth factors in the brain (2, 3, 4, 5).

  1. 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
  2. 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
  3. 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.1997.8.1.1
  4. 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
  5. 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
  6. Mash, D. C., Duque, L., Page, B., & Allen-Ferdinand, K. (2018). Ibogaine Detoxification Transitions Opioid and Cocaine Abusers Between Dependence and Abstinence: Clinical Observations and Treatment Outcomes. Frontiers in pharmacology, 9, 529. https://doi.org/10.3389/fphar.2018.00529
  7. 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
  8. Alper, K. R., Lotsof, H. S., & Kaplan, C. D. (2008). The ibogaine medical subculture. Journal of ethnopharmacology, 115(1), 9–24. https://doi.org/10.1016/j.jep.2007.08.034
  9. Maciulaitis, R., Kontrimaviciute, V., Bressolle, F. M., & Briedis, V. (2008). Ibogaine, an anti-addictive drug: pharmacology and time to go further in development. A narrative review. Human & experimental toxicology, 27(3), 181–194. https://doi.org/10.1177/0960327107087802
  10. Srivastava, A. B., Mariani, J. J., & Levin, F. R. (2020). New directions in the treatment of opioid withdrawal. Lancet (London, England), 395(10241), 1938–1948. https://doi.org/10.1016/S0140-6736(20)30852-7
  11. Baumann, M. H., Pablo, J. P., Ali, S. F., Rothman, R. B., & Mash, D. C. (2000). Noribogaine (12-hydroxyibogamine): a biologically active metabolite of the antiaddictive drug ibogaine. Annals of the New York Academy of Sciences, 914, 354–368. https://doi.org/10.1111/j.1749-6632.2000.tb05210.x
  12. Brown, T. K., & Alper, K. (2018). Treatment of opioid use disorder with ibogaine: detoxification and drug use outcomes. The American journal of drug and alcohol abuse, 44(1), 24–36. https://doi.org/10.1080/00952990.2017.1320802

 

Treating PTSD with Iboga

Post-Traumatic Stress Disorder (PTSD) is a common psychological condition that can be improved by Ibogaine (1). Studies reveal that therapy amongst US veterans leads to major reductions in suicidal tendencies, cognitive impairment, depression, anxiety, and PTSD symptoms (2).

  1. Olszewski, T. M., & Varrasse, J. F. (2005). The neurobiology of PTSD: implications for nurses. Journal of psychosocial nursing and mental health services, 43(6), 40–47. https://doi.org/10.3928/02793695-20050601-09
  2. 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. https://doi.org/10.1177/2470547020939564

Treating Viruses and Bacterial Infections with Iboga

Preliminary evidence such as laboratory experiments and animal studies reveal that Ibogaine may have antibacterial (1), antiviral (2), and antifungal properties (3, 4).

  1. 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
  2. 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
  3. 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
  4. 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

 

Treating Parkinson’s

Ibogaine may be a potential treatment for Parkinson’s. Parkinson’s disease is a chronic debilitating condition that’s expected to affect more and more people every year (1). It is caused by the death of dopamine-producing brain cells in the midbrain (2, 3, 4, 5). Ibogaine can activate a neurotrophic factor in the brain called Glial Cell-Derived Neurotrophic Factor (GDNF) (10, 11, 12). The factor plays a major role in ensuring the survival of dopamine-producing neurons and its activation in the brain may lead to up to 40% improvement in the symptoms of Parkinson’s (6, 7, 8, 9).

  1. Kowal, S. L., Dall, T. M., Chakrabarti, R., Storm, M. V., & Jain, A. (2013). The current and projected economic burden of Parkinson’s disease in the United States. Movement disorders : official journal of the Movement Disorder Society, 28(3), 311–318. https://doi.org/10.1002/mds.25292 
  2. Davie C. A. (2008). A review of Parkinson’s disease. British medical bulletin, 86, 109–127. https://doi.org/10.1093/bmb/ldn013 
  3. Schaser, A. J., Osterberg, V. R., Dent, S. E., Stackhouse, T. L., Wakeham, C. M., Boutros, S. W., Weston, L. J., Owen, N., Weissman, T. A., Luna, E., Raber, J., Luk, K. C., McCullough, A. K., Woltjer, R. L., & Unni, V. K. (2019). Alpha-synuclein is a DNA binding protein that modulates DNA repair with implications for Lewy body disorders. Scientific reports, 9(1), 10919. https://doi.org/10.1038/s41598-019-47227-z 
  4. Sulzer, D., Alcalay, R. N., Garretti, F., Cote, L., Kanter, E., Agin-Liebes, J., Liong, C., McMurtrey, C., Hildebrand, W. H., Mao, X., Dawson, V. L., Dawson, T. M., Oseroff, C., Pham, J., Sidney, J., Dillon, M. B., Carpenter, C., Weiskopf, D., Phillips, E., Mallal, S., … Sette, A. (2017). T cells from patients with Parkinson’s disease recognize α-synuclein peptides. Nature, 546(7660), 656–661. https://doi.org/10.1038/nature22815 
  5. Lindestam Arlehamn, C. S., Dhanwani, R., Pham, J., Kuan, R., Frazier, A., Rezende Dutra, J., Phillips, E., Mallal, S., Roederer, M., Marder, K. S., Amara, A. W., Standaert, D. G., Goldman, J. G., Litvan, I., Peters, B., Sulzer, D., & Sette, A. (2020). α-Synuclein-specific T cell reactivity is associated with preclinical and early Parkinson’s disease. Nature communications, 11(1), 1875. https://doi.org/10.1038/s41467-020-15626-w 
  6. Peterson, A. L., & Nutt, J. G. (2008). Treatment of Parkinson’s disease with trophic factors. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 5(2), 270–280. https://doi.org/10.1016/j.nurt.2008.02.003
  7. Oo, T. F., Kholodilov, N., & Burke, R. E. (2003). Regulation of natural cell death in dopaminergic neurons of the substantia nigra by striatal glial cell line-derived neurotrophic factor in vivo. The Journal of neuroscience : the official journal of the Society for Neuroscience, 23(12), 5141–5148. https://doi.org/10.1523/JNEUROSCI.23-12-05141.2003
  8. 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 
  9. Love, S., Plaha, P., Patel, N. K., Hotton, G. R., Brooks, D. J., & Gill, S. S. (2005). Glial cell line-derived neurotrophic factor induces neuronal sprouting in human brain. Nature medicine, 11(7), 703–704. https://doi.org/10.1038/nm0705-703 
  10. Carnicella, S., He, D. Y., Yowell, Q. V., Glick, S. D., & Ron, D. (2010). Noribogaine, but not 18-MC, exhibits similar actions as ibogaine on GDNF expression and ethanol self-administration. Addiction biology, 15(4), 424–433. https://doi.org/10.1111/j.1369-1600.2010.00251.x 
  11. 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 
  12. 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 
  13. Dustin R., Mandel Ronald J. “The Future of GDNF in Parkinson’s Disease” Frontiers in Aging Neuroscience VOLUME 12 2020 PAGE 388  https://www.frontiersin.org/articles/10.3389/fnagi.2020.593572/full

Treating Auto-Immune Disease

Ibogaine may be a potential treatment for Autoimmune Disease. Ibogaine is a potent agonist of the sigma-1 receptors (Sig1R) in the brain (3).  Activating the receptor may provide benefits for neuroinflammation and help the management of autoimmune neurological diseases (1, 2). Currently, it has shown potential for the management of Parkinson’s, brain injury, stroke, and Multiple Sclerosis (MS).

  1. 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
  2. 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 
  3. 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