Depression during methadone withdrawal: no role for beta-phenylethylamine.

Abstract

An atypical depression, resembling beta-phenylethylamine (PEA) deficiency states, frequently complicates methadone withdrawal. We undertook a study of 24-h urinary free PEA excretion in steady-dosed and withdrawing methadone patients, hypothesizing that abstinent patients would excrete less PEA than controls and that methadone would show a dose-dependent effect on PEA turnover. As hepatic dysfunction, frequent in methadone patients, might affect PEA turnover, we also evaluated liver chemistries, [13C]aminopyrine excretion, 2-hydroxylation of estradiol, and 'blind', global severity ratings in each subject. PEA excretion did not significantly differ between eight fully detoxified methadone patients (median 4.76 micrograms/24 h) and seven normal controls (median 5.80 micrograms/24 h). Moreover, PEA excretion bore no relation to methadone dosage among 24 steady-dosed subjects. PEA excretion in seven withdrawing subjects each receiving 4-8 different doses of methadone similarly showed no relation to dose. Despite significant liver disease, several measures of impairment did not correlate with PEA excretion. These findings argue against a role for PEA deficiency in withdrawal depression.