Ibogaine has been used therapeutically for several indications, particularly detoxification from opiates. It has been shown to decrease the self-administration of stimulants, opiates and alcohol, as well as to significantly reduce the withdrawal symptoms from opiates after a single administration.1 Other research shows a reduction of developed tolerance to opiates2 and alcohol,3 and a significant decrease in cravings for opiates and cocaine for an extended period of time after treatment.4
Ibogaine therapy has also been used for other indications, such as in the treatment psychological disorders like depression and post-traumatic stress disorder. Its psychological effects have been reported to help people to view difficult experiences in an objective way, and to help facilitate the closure of unresolved emotional conflicts.5
There is also anecdotal evidence, and a theoretic framework, to suggest that ibogaine can have therapeutic benefits in the treatment of Parkinson’s disease and similar disorders. Ibogaine has been shown to be neuro-protective,6 and also stimulate increased levels of glial cell line-derived neurotrophic factor (GDNF) in the brain,7 which stimulates the growth of new neurons, and has been shown to have a strong benefit for Parkinson disease in animal models.8 People have found benefits from ibogaine therapy for these and other reasons applications, including increasing fertility, the reduction in viral load counts for Hepatitis C, and the cessation of symptoms of Tourette’s syndrome.
Outside of its potential medical benefits, ibogaine is used by many who wish to explore its potential for personal and spiritual growth. Many have made reference to the nature of addiction described in Buddhist practice, as clinging to the world, to life events, or to aspects of personal identity, and suggest ibogaine has helped to relax the “existential grasp.”
Ibogaine therapy consists of a safety screening protocol, a structured and comfortable treatment environment under the case of an experienced guide and sufficient continuing care after treatment. In September, 2015, GITA published the 1st edition Clinical Guidelines for Ibogaine-Assisted Detoxificiation that outlines clinical risk management protocols in detail.
Popik P, Glick S. Ibogaine, a putatively anti-addictive alkaloid. Drugs of the Future. 1996; 21:pp 1109-1115. ↩
Trujillo KA & Akil H, Inhibition of Morphine Tolerance and Dependence by NMDA Receptor Antagonist MK-801, Science, 2512:85-87, 1991. ↩
Khanna JM, Kalant H, Shah G, Chau A, Effect of D-cycloserine on Rapid Tolerance to Ethanol, Pharmacology Biochemistry & Behavior 45(4):983-986, 1993. ↩
Dao-Yao He, Nancy N.H. McGough, Ajay Ravindranathan, Jerome Jeanblanc, Marian L. Logrip, Khanhky Phamluong, Patricia H. Janak, and Dorit Ron. Glial Cell Line-Derived Neurotrophic Factor Mediates the Desirable Actions of the Anti-Addiction Drug Ibogaine against Alcohol Consumption. The Journal of Neuroscience, Jan. 19, 2005, Vol. 25, No. 3, p. 619. ↩
NMDA Antagonist Properties of the Putative Antiaddictive Drug, Ibogaine. Popik, P., Layer, R.T., Fossom, L.H., et al. J Pharmacol Exp Ther 275:753-760, 1995. ↩
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. The FASEB Journal, 20, 2420-2422. ↩
Gill, S. S., Patel, N. K., Hotton, G. R., O’Sullivan, McCarter, R., Bunnage, M., Brooks, D. J., Svendsen, C. N. and Heywood, P. (2003) Direct brain infusion of glial cell-line derived neurotrophic factor in Parkinson disease. Nature Medicine, 9, 589-595. ↩