Correspondence |
Departments of Psychiatry and Neurology, New York University School of Medicine, New York, NY 10016, USA.
Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, New York, USA
Correspondence: E-mail: kral{at}nyu.edu
EDITED BY KIRIAKOS XENITIDIS and COLIN CAMPBELL
The recent review by Werneke et al (2006) contains substantive errors and omissions regarding the iboga alkaloid ibogaine and its synthetic congener 18-methoxycoronaridine (18-MC). The review cites a single paper published in 1994 consisting of seven case reports and overlooks two larger studies on the use of ibogaine for the treatment of opioid withdrawal in 32 (Mash et al, 2001) and 33 patients (Alper et al, 1999). These were retrieved on Medline using the search terms stated by Werneke et al. The authors incorrectly state that clinical trials of ibogaine were abandoned because of cerebellar toxicity: this has been limited to the rat at higher doses than those that diminish drug self-administration and opioid withdrawal, and has not been evident in primate or mouse models (Alper, 2001). In 1993 the US Food and Drug Administration authorised Phase I clinical studies in which humans were given ibogaine. These studies were halted only because of a contractual dispute among the study sponsors and not because of safety issues.
Table 6 of Werneke et als review states that 18-MC
binds to the NMDA [N-methyl-D-aspartate] receptor
and that this is because of its putative anti-addictive mechanism of action.
Mash et al (1995) is
cited but this paper makes no mention of 18-MC, which lacks significant
affinity for the NMDA receptor but is a potent antagonist at the
3ß4 nicotinic receptor
(Maisonneuve & Glick,
2003). The statement that ibogaine blocks the dopamine
response in general is inaccurate, as ibogaine does not have the
properties of a dopamine receptor antagonist and does not decrease dopamine
release in all brain regions (Maisonneuve
et al, 1991).
Werneke et al stated that All recovered papers were reviewed for further relevant references, which would have led, among other sources, to an entire volume devoted to ibogaine of the Medline-indexed serial The Alkaloids (Alper & Cordell, 2001) and the additional references cited here. Systematic implementation of the stated search strategy and careful and accurate reading of the papers that were retrieved would have provided a far more credible evidence basis regarding the use of iboga alkaloids for the pharmacotherapy of addiction.
REFERENCES
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