RE: Performance enhancement with selegiline

From: gts (gts_2000@yahoo.com)
Date: Thu Jan 30 2003 - 08:20:23 MST


Rafal Smigrodzki wrote:

> ### I know selegiline is a selective MAOI.
> I meant to write "How does it compare to other MAOI's?"
> In other words, since MAOI's suck, and selegiline is a MAOI,
> selegiline sucks, too.

MAOI's don't "suck." Were it not for the risks of hypertensive crises
from tyramine rich foods then MAOI's would still reign supreme as the
best and safest antidepressants in existence. It is only because of
those hypertensive risks associated with certain foods that the
tricyclics and SSRI's and others were developed. But the MAOI selegiline
does not suffer from those risks, Rafal, because as I've stated several
times, at normal dosages it is a selective inhibitor only of *MAO-B*,
and the inhibition of MAO-B does not entail any risks of hypertensive
crises.

In any case, this is not a discussion of the merits of different classes
of antidepressants. The antidepressant effects of selegiline are trivial
in comparison to its other benefits.

> Give me some data supporting the contention that selegiline is "an
> excellent antidepressant", compared to the SSRI's, TCA's, and
> atypicals I mentioned above.

Okay I will offer a few of abstracts below on that subject, but as I
wrote above this is really beside the point. I'm not interested in
defending selegiline only as an antidepressant. Its key value to
transhumanists and others here is that it is a potent neuroprotectant, a
cognitive aid, and a potential agent of life extension.

By the way all of these research abstracts were available for your
perusal at the link I posted originally for you, but which you
apparently never investigated.

-gts

---
Deprenyl and cognition
Lees AJ
Department of Neurology,
Middlesex Hospital, London, UK.
Acta Neurol Scand Suppl 1991; 136:91-4
ABSTRACT 
Selegiline HCl, 10 mg per day has been reported to improve attention and
episodic memory in Parkinson's disease and early Alzheimer's disease.
Selegiline also improves motor reaction times in Parkinson's and
subjective feelings of increased vitality, euphoria and energy.  At
doses of between 10 and 40 mg a day it has also been shown to improve
depression particularly when psychomotor retardation is prominent and
anxiety minimal. 
----
A controlled study of the antidepressant efficacy and side effects
of (-)deprenyl.  A selective monoamine oxidase inhibitor
Mann JJ, Aarons SF, Wilner PJ, Keilp JG, Sweeney JA,
Pearlstein T, Frances AJ, Kocsis JH, Brown RP
Department of Psychiatry,
Cornell University Medical College, New York, NY 10021.
Arch Gen Psychiatry 1989 Jan; 46(1):45-50 1991; 136:91-4
ABSTRACT 
Monoamine oxidase (MAO) inhibitors are effective antidepressants whose
use is limited because of unwanted side effects and the possibility of a
tyramine-induced hypertensive crisis (cheese reaction). (-)-Deprenyl
(the official nonproprietary name for this substance is selegiline), a
selective MAO type B inhibitor, may be safer and have fewer side
effects, but its antidepressant efficacy is uncertain. A double-blind
placebo-controlled study was carried out in depressed outpatients who
were treated with (-)-deprenyl in an MAO type B selective dose range and
at a higher nonselective dose range. (-)-Deprenyl did not have a
statistically significant antidepressant effect after three weeks of
treatment at doses of 10 mg/d. However, after six weeks and at higher
doses (averaging about 30 mg/d for the second three weeks), (-)-deprenyl
was superior to placebo in antidepressant effect with a positive
response rate of 50% vs 13.6% and with a 41% reduction in the Hamilton
Depression Rating Scale mean score vs 10% in the placebo-treated group.
No hypertensive crises were seen.  The rate of occurrence of side
effects with (-)-deprenyl was no greater than with placebo.  It was
concluded that (-)-deprenyl is an effective antidepressant in a dose
range where it is distinguished by the absence of many of the side
effects typical of nonselective MAO inhibitors. 
---
High-dose selegiline in treatment-resistant older depressive patients
Sunderland T, Cohen RM, Molchan S, Lawlor BA, Mellow AM,
Newhouse PA, Tariot PN, Mueller EA, Murphy DL
Section on Geriatric Psychiatry,
National Institute of Mental Health, Bethesda, Md.
Arch Gen Psychiatry 1994 Aug; 51(8):607-15
ABSTRACT
BACKGROUND: We examined the effect of high-dose selegiline in 16
treatment-resistant older depressive patients. We hypothesized that
selegiline, at a dosage of 60 mg/d, would be at least partially
effective but that the higher doses would not maintain the monoamine
oxidase B selectivity observed with the lower doses of selegiline.  
METHODS: Sixteen treatment-resistant subjects (mean [+/- SD] age, 65.6
+/- 9.3 years) entered a double-blind, randomized, crossover study of
placebo vs 3 weeks of selegiline at a dosage of 60 mg/d. Objective
measures of mood and behavior were obtained in all subjects, and 10 of
the subjects underwent repeated lumbar punctures for analysis of
monoamine metabolites in the cerebrospinal fluid. 
RESULTS: Objective measures of mood and behavior revealed significant
improvement in the Hamilton Depression Rating Scale score (37.4%
decrease), the Global Depression score (22.7% decrease), and the Brief
Psychiatric Rating Scale score (19.3% decrease); subjective behavioral
measures, however, did not show significant improvement during the
3-week medication trial. Cerebrospinal fluid values revealed a
statistically significant drop in 3-methoxy-4-hydroxyphenylglycol (51%)
and 5-hydroxyindoleacetic acid (17%) levels, and there was a significant
lowering of systolic blood pressure on standing (15%), but these changes
were not accompanied by clinical side effects. 
CONCLUSIONS: Our results suggest that high-dose selegiline can be an
effective antidepressant in treatment-resistant older depressive
patients.  While the selegiline dose required has nonselective monoamine
oxidase effects and thus would not be free of possible tyramine
interactions, other advantages suggest that further investigations with
selegiline are warranted in this population.
----
Biochemical effects of
L-deprenyl in atypical depressives
Liebowitz MR, Karoum F, Quitkin FM,
Davies SO, Schwartz D, Levitt M, Linnoila M
Biol Psychiatry 1985 May; 20(5):558-65 1991; 136:91-4
ABSTRACT 
To examine the biochemical effects of 10-30 mg/day L-deprenyl,
measurement of 24-hr urinary output of phenylethylamine (PEA), 3-methoxy
4-hydroxy phenylethyleneglycol (MHPG), and L-deprenyl's amphetamine
metabolites were carried out before and during the treatment of atypical
depressives.  Platelet monoamine oxidase (MAO) activity was also
assessed. With L-deprenyl 10-30 mg/day, the expected MAO B inhibition
occurred, as indicated by significant increase in urinary PEA excretion
and virtual disappearance of platelet MAO activity.  Twenty-five to 33%
of the daily dose of L-deprenyl was recovered as urinary methamphetamine
or amphetamine.  Excretion of MHPG was significantly decreased with
L-deprenyl 10-20 mg/day. Overall, the results suggest that L-deprenyl's
antidepressant effects are mediated by some mechanism other than, or in
addition to, MAO B inhibition. 


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