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[Contents][Appendix 1]
[Reference 177][Reference 179]

E is for Ecstasy by Nicholas Saunders

Appendix 1: Reference Section

178 Metabolism of 'ecstasy' by CYP2D6) by Tucker et al. published in abstract form in Br. J. Clin. Pharmacol. 36:144P, 1993

This paper suggests that about 8% of Caucasians are genetically deficient in a particular enzyme which helps metabolize MDMA, and that such individuals may be particularly sensitive to its effects and "at increased risk of acute toxicity". However, these same people "may be less susceptible to the chronic neurological effects of the drug".

[I asked two senior American researchers for their opinions on the paper. One commented "I think he has a point". The other said "It is a nice study in terms of showing a pathway of MDMA metabolism that can be applied to the human condition. Unfortunately, we cannot predict whether 'poor metabolizers' will be more (or less) susceptible to acute toxic (i.e. predominantly hyperthermia) much less the chronic neurological effects ('neurotoxicity'), because we do not yet know which metabolites are responsible for the acute and/or neurochemical (neurological) effects of the compound. Tucker et al. allude to this in the final paragraph. The data do show, however, that genetic differences in metabolism or MDMA may be responsible for differences in the response to the drug (toxic or therapeutic effects].

[Contents][Appendix 1]
[Reference 177][Reference 179]
E is for Ecstasy by Nicholas Saunders (
HTMLized by Lamont Granquist (