I have definitely read case reports of euphoria and even addiction to MAOIs. It seems to be a possibility. It makes sense. You're increasing levels of all three 'major' neurotransmitters, not just in the synaptic cleft but extracellular too. I think cocaine does something similar, although certainly to a larger extent.
How do you think that works spaceboy? I understand that, to a certain level you can inhibit MAO but I would guess that higher doses (e.g. 120mg Nardil/phenelzine) aren't inhibiting MAO anymore than lower doses (e.g. 60mg), since your body only makes so much MAO. I think? So, maybe it's an interaction between the MAO inhibition and a metabolite? Interesting to think about.
FDA indication for Parnate is 30-60mg, but I have read about people on as much as 200mg, in combination with stimulants (clinically). Not as abuse - this is for severe
low-energy depression and a very skilled doctor. (It may also have to do with people being fast metabolizers.) Hmm, drugs are complicated like that.
I am bipolar. I wondered about MAOI use and mania. It would appear that there is not necessarily a higher incidence of mood destabilization on MAOIs - if anything, perhaps lower, compared to other antidepressants. Emphasis added:
Tranylcypromine versus imipramine in anergic bipolar depression
Himmelhoch JM, Thase ME, Mallinger AG, Houck P
Department of Psychiatry,
University of Pittsburgh School of Medicine, PA.
Am J Psychiatry 1991 Jul; 148(7):910-6
OBJECTIVE: This investigation compared the efficacy of the monoamine oxidase inhibitor (MAOI) tranylcypromine with that of the tricyclic imipramine in the treatment of anergic bipolar depressive illness. METHOD: A controlled, double-blind comparison was used to study 56 outpatients who met operationalized criteria for anergic bipolar depression. Patients with bipolar I and II depression were equally distributed between comparison groups. Outcome was measured by the patient-rated Beck Depression Inventory and the clinician-rated Hamilton Rating Scale for Depression, Raskin Mania and Depression Scales, Clinical Global Impression Scale, and the Pittsburgh Reversed Vegetative Symptom Scale. Twenty-eight patients were treated with tranylcypromine and 28 with imipramine. Seventy-three percent of bipolar depressive patients screened for the study met criteria for anergic depression, consistent with previous findings from studies in bipolar illness that stretch back over 100 years. RESULTS: Tranylcypromine produced statistically significant superior outcome in terms of lower attrition, greater symptomatic improvement, and higher global response without increased risk of treatment-emergent hypomania or mania.
CONCLUSIONS: The authors propose that the apparently superior efficacy of tranylcypromine in bipolar depression is specifically linked to anergia and reversed neurovegetative symptoms. Bipolar I and bipolar II patients had comparable outcomes, but bipolar I patients had a significantly greater risk of treatment-emergent mood swings. Although the relatively poor showing of imipramine warrants close scrutiny, these findings provide further documentation of the utility of MAOIs in patients presenting with anergia, motor retardation, hyperphagia, and/or hypersomnia.
Antidepressant-associated mania: a controlled comparison with spontaneous mania.
Stoll AL, Mayer PV, Kolbrener M, Goldstein E, Suplit B, Lucier J, Cohen BM, Tohen M.
Bipolar and Psychotic Disorders Program, Mailman Research Center, McLean Hospital, Belmont, Mass.
Am J Psychiatry. 1994 Nov;151(11):1642-5.
OBJECTIVE: Antidepressants have been associated with the induction of mania and rapid cycling. This study examined whether antidepressant-associated manic states differ in any way from spontaneous mania. METHOD: Forty-nine consecutive inpatients with antidepressant-associated manic states were compared with 49 matched inpatients with spontaneous mania in a blind, retrospective chart review. RESULTS: Across virtually every clinical measure examined, the patients with antidepressant-associated manic states experienced milder and more time-limited manic episodes than the patients with spontaneous mania. The patients with antidepressant-associated manic states were subject to frequent checking by nurses and hall restriction for a significantly shorter period of time than the patients with spontaneous mania. The patients with antidepressant-associated manic states also had significantly less severe levels of delusions, hallucinations, psychomotor agitation, and bizarre behavior, according to a standard rating instrument, than the patients with spontaneous mania. For further study the patients with antidepressant-associated mania were divided into subgroups taking four individual classes of antidepressant drugs: tricyclics (N = 19), fluoxetine (N = 13), monoamine oxidase inhibitors (MAOIs) (N = 8 ), and bupropion (N = 6); three patients taking combinations of drugs were not included in these analyses. The patients with MAOI- and bupropion-associated mania had a slightly lower overall rating of severity of psychopathology at admission than the subgroups with fluoxetine- and tricyclic-associated mania. CONCLUSIONS: Antidepressant-associated mania appears to be a milder and more time-limited syndrome than spontaneous mania and may represent a distinct clinical entity. MAOIs and bupropion may be associated with milder manic states than either tricyclic drugs or fluoxetine.