Related Chapters:
Treatment for Substance Use Disorders
Addictive Properties of Various Drugs

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11. Growth of Ibogaine Subculture

"The estimated number of participants in the ibogaine subculture increased fourfold relative to the prior estimate of 5 years earlier, an average yearly rate of growth of approximately 30%."

Alper, Kenneth R.; Lotsof, Howard S.; and Kaplan, Charles D., "The ibogaine medical subculture," Journal of Ethnopharmacology (Cagliari, Italy: International Society for Ethnopharmacology, January 2008), Volume 115, Issue 1, p. 20.

12. Ibogaine Subculture Contrasted With Other Drug Subcultures

"The clinical focus on the treatment of opioid withdrawal distinguishes the ibogaine subculture from subcultures associated with psychedelic or other illegal drugs. The reason for taking ibogaine was more frequently to alleviate the symptoms of opioid withdrawal than to pursue spiritual or psychological goals. In the US, the expansion of the ibogaine subculture coincides temporally with a substantial increase in the public health impact of opioid use disorders (Compton and Volkow, 2006). The incidence of opioid-related deaths in the US doubled between 1999 and 2004 (Fingerhut, 2007), with methadone and oxycodone accounting for most of this increase. In contrast to trends regarding opioids, there was no increase in use of hallucinogen and MDMA among young adults in the US between 2002 and 2005 (Substance Abuse and Mental Health Services Administration, 2006), suggesting that the recent expansion of the ibogaine subculture is not an epiphenomenon of popular interest in psychedelic drugs and the availability of psychoactive substances on the Internet (Schifano et al., 2006)."

Alper, Kenneth R.; Lotsof, Howard S.; and Kaplan, Charles D., "The ibogaine medical subculture," Journal of Ethnopharmacology (Cagliari, Italy: International Society for Ethnopharmacology, January 2008), Volume 115, Issue 1, p. 18.

13. Rat Studies of Ibogaine

"18-MC [18-methoxycoronaridine], a novel iboga alkaloid congener, reduces intravenous methamphetamine and nicotine self-administration in rats. These and previous results with morphine, cocaine and alcohol indicate that 18-MC warrants further development as a potential treatment for multiple forms of drug addiction."

Glick, S.D., Maisonneuve, I.M., and Dickinson, H.A., "18-MC Reduces Methamphetamine and Nicotine Self-Administration in Rats," Neuropharmacology, Vol. 11, No. 9, June 26, 2000, p. 2015.

14. Rodent Studies of Ibogaine

"Studies also suggest that ibogaine attenuates drug- and ethanol-induced behaviors in rodents. For example, ibogaine reduces operant self-administration of heroin in rats, as well as naloxone-precipitated withdrawal in morphine-dependent rats (Glick et al., 1992; Dworkin et al., 1995). Administration of ibogaine decreases cocaine-induced locomotor activity and reduces cocaine self-administration in rats (Cappendijk and Dzoljic, 1993) and mice (Sershen et al., 1994)."

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.

15. Ibogaine and Glial Cell Line-Derived Neurotrophic Factor (GDNF)

"In summary, repeated administration of drugs of abuse and alcohol induces a common pattern of changes in gene expression and protein levels selectively in the VTA [ventral tegmental area]. A subset of these changes is reversed by intra-VTA GDNF [glial cell line-derived neurotrophic factor], as are some of the drug-induced behavioral effects. Endogenous GDNF systems appear to inhibit drug related behaviors, while repeated drug administration appears to inhibit GDIVF signaling itself. Based on these studies, we propose that GDNF is an endogenous anti-addiction agent. This possibility is directly supported by the finding that the activity of the anti-addiction drug, ibogaine, on alcohol consumption is mediated via increased expression of GDNF in the midbrain and the subsequent activation of the GDNF pathway."

Ron, Dorit, and Janak, Patricia H., "GDNF and addiction," Reviews in the Neurosciences, Vol. 16, No. 4, 2005, p. 281.