Psycho-Babble Medication Thread 16095

Shown: posts 1 to 20 of 20. This is the beginning of the thread.

 

nardil vs. parnate

Posted by JIM on December 2, 1999, at 18:17:36

I have taken nardil for several years and had good results. The weight gain was a problem though and it increased my blood pressure. After stopping nardil my depression became horrible. I have since started parnate but the side effects(headache, nausea, fatigue and sleep disturbance are a concern). After several weeks I wonder if I should switch back to Nardil?? Has anyone tried both these medications??? What has been your experiences??

 

Re: nardil vs. parnate (Celebrity Death Match)

Posted by Elizabeth on December 2, 1999, at 20:34:59

In reply to nardil vs. parnate, posted by JIM on December 2, 1999, at 18:17:36

> I have taken nardil for several years and had good results. The weight gain was a problem though and it increased my blood pressure. After stopping nardil my depression became horrible. I have since started parnate but the side effects(headache, nausea, fatigue and sleep disturbance are a concern). After several weeks I wonder if I should switch back to Nardil?? Has anyone tried both these medications??? What has been your experiences??

Your experiences are more important than anyone else's for your decision! But anyway, have you tried any other ADs besides the MAOIs? What about Marplan?

 

Re: nardil vs. parnate (Celebrity Death Match)

Posted by JIM on December 2, 1999, at 22:29:00

In reply to Re: nardil vs. parnate (Celebrity Death Match), posted by Elizabeth on December 2, 1999, at 20:34:59

> > I have taken nardil for several years and had good results. The weight gain was a problem though and it increased my blood pressure. After stopping nardil my depression became horrible. I have since started parnate but the side effects(headache, nausea, fatigue and sleep disturbance are a concern). After several weeks I wonder if I should switch back to Nardil?? Has anyone tried both these medications??? What has been your experiences??
>
> Your experiences are more important than anyone else's for your decision! But anyway, have you tried any other ADs besides the MAOIs? What about Marplan?
Ihave tried other AD's without success. Too many side effects/no results. I have not tried Marplan.

 

Yes, I've tried Nardil, Parnate, Marplan, and Sele

Posted by JohnB on December 2, 1999, at 22:33:31

In reply to nardil vs. parnate, posted by JIM on December 2, 1999, at 18:17:36

Hi, I've tried three of the non-reversible, non-selective MAO inhibitors, as well as another MAO inhibitor which loses its selectivity above 10-15 mg/day. What I can tell you are primarily my personal experiences and what I've read in the research. Please keep in mind that many effects, both therapeutic and side effects, vary greatly from individual to individual.

Regarding Nardil, I found it extremely effective for my social phobia, but only at doses of 60 mg/day and above. I did not find therapeutic benefit at so-called "maintenance" doses of 30 to 45 mg/day. Further, I am not aware of any research (or any pscyhopharmacologist, for that matter) which suggests a lower dose does not result in decreased efficacy. Unfortunatelyl, I also experienced fairly significant weight gain - about 12 lbs. For me, that's alot, as my metabolic rate is fairly high, and I don't crave carbohydrates. My carbohydrate craving on Nardil was my biggest problem - I couldn't pass up a donut or ice cream, or anything else for that matter. Sexual dysfunction, both erectile and orgasmic dysfunction, were pretty severe. Unfortunately, my psychodoc and I did not try any antidotes other than Periactin, which I found of no benefit. I understand that certain dopamine agonists are used as antidotes to both of these problems, such as amantadine or bromocriptine (hopefully I've spelled these correctly), but I imagine there use is contraindicated in the official drug literature. My psychdoc, who is a good psychopharmacologist, prescribed bupropion, which has a dopaminergic effect, while I was taking parnate and looking for additional efficacy. Unfortunately, I have not tried Bupropion (Wellbutrin) while I've been on Nardil. Again, this is contraindicated in the drug literature, but experienced and knowledgable psychopharmacologists believe they can cautiously manage this combination with some patients. Bottom line, I have yet to return to Nardil, but am toying with the idea. It's really hard to resist it's efficacy. If it weren't for the side effects, I'm sure it would be one of the top medications for anxiety disorders.

Regarding Parnate, I found it much less effective than nardil, but without the weight gain and complete sexual dysfunction. I did experience an annoying dry mouth, as well as some cognitive dysfunction - mostly a slowing down in my speech (not a slurring, which would suggest possible serotonin syndrome or hypertensive crisis). My voice mail messages became notoriously slow, and difficult to wade through, even when listeners used the "speed up" feature. I also found insomina to be a problem, if I titrated the dosage too quickly. You need to start very slowly, in the a.m., and stop your caffeine intake. Bottom line on Parnate, not enough efficacy for its somewhat tolerable side effects, at least for me.

Marplan - I'm still waiting for therapeutic benefit at 80 mg/day. No weight gain and very limited sexual dysfunction so far - about 1 month. I've just recently worked my way up to 80 mg/day - so I'll give it another few weeks or so, hoping the efficacy will "kick-in." In the meantime, I've noticed a pleasant side effect, in which my normally patient personality is even more patient. Almost nothing is able to irritate me. This suggests, to me, a strong serotonin effect (which 5HT subtypes - I haven't a clue), though I do understand that a serotonin deficit may lead to aggressive behavior. I am hoping that the efficacy will be equivalent to Nardil, as both are hydrazine (indicating a GABA effect), as well as non-selectible (for MAO-A or MAO-B) and irreversible.

Selegiline, another MAOI, I tried at 60 mg/day. It loses its selectivity for MAO-B above 10-15 mg/day. It's a non-hydrazine. As such, I was hoping for some benefit in the range of parnate, or, possibly, somewhat more, but without parnate's side effects. I experienced no unpleasant side effects. In fact, my sexual urge was increased to the point that it was frequently difficult to focus on certain work issues. On second thought, this was an unpleasant side effect, though it's hard to think of it that way. I also felt somewhat increased coginitive functioning, but this could have been a placebo effect, or just the absence of cognitive dysfunction, which is common among all central nervous system depressants - but to varying degrees. Bottom line here - no efficacy, very, very unfortunately.

Lastly, I can emphasize enough how these are just my experiences. I've heard and read of people who actually lose weight on Nardil. Further, I've never seen any side effects as occuring 100%, though some do seem to go under-reported vs what I see in the "official" drug literature.

Good luck.

JohnB :)

 

Re: nardil vs. parnate (Celebrity Death Match)

Posted by JIM on December 2, 1999, at 22:36:57

In reply to Re: nardil vs. parnate (Celebrity Death Match), posted by Elizabeth on December 2, 1999, at 20:34:59

> > I have taken nardil for several years and had good results. The weight gain was a problem though and it increased my blood pressure. After stopping nardil my depression became horrible. I have since started parnate but the side effects(headache, nausea, fatigue and sleep disturbance are a concern). After several weeks I wonder if I should switch back to Nardil?? Has anyone tried both these medications??? What has been your experiences??
>
> Your experiences are more important than anyone else's for your decision! But anyway, have you tried any other ADs besides the MAOIs? What about Marplan?
>
> I have tried other AD's without success.Too many side effects/no results. I also suffer from social phobia and anxiety. I have not tried Marplan

 

You never know-Nardil vs. Parnate

Posted by S. Suggs on December 3, 1999, at 6:24:44

In reply to nardil vs. parnate, posted by JIM on December 2, 1999, at 18:17:36

It just goes to show that different meds work differently for different people. I have been on parnate for 3 wks and currently taking 50mg a day. While this has not been 4 wks or greater, I have noticed a big difference. My sleep is fantastic at night, I have a tremendous amount of energy during the day, no significant sexual side effects, weight gain is not a problem and there seems to be an increase in my comfort level with social situations etc...

I just hope it continues, but for me 50 mg (20 mg at rising, 20 mg before lunch and 10 after lunch or so) is a wonder. Thanks to Elizabeth for the suggestion of taking the last dose before 3p.

You just never know.......

Blessings,

S. Suggs

 

Re: You never know-Nardil vs. Parnate

Posted by Elizabeth on December 4, 1999, at 9:29:24

In reply to You never know-Nardil vs. Parnate, posted by S. Suggs on December 3, 1999, at 6:24:44

> It just goes to show that different meds work differently for different people. I have been on parnate for 3 wks and currently taking 50mg a day. While this has not been 4 wks or greater, I have noticed a big difference. My sleep is fantastic at night, I have a tremendous amount of energy during the day, no significant sexual side effects, weight gain is not a problem and there seems to be an increase in my comfort level with social situations etc...
>
> I just hope it continues, but for me 50 mg (20 mg at rising, 20 mg before lunch and 10 after lunch or so) is a wonder. Thanks to Elizabeth for the suggestion of taking the last dose before 3p.

You're welcome. It's the same recommendation I've always heard for caffeine. (Parnate's half-life -- not relevant for MAO inhibition since it's irreversible, but may be useful to keep in mind when considering its stimulant properties -- is 2 hours or so...so if you take your last dose at 3pm, less than 10% is still around by 11pm.)

Glad to hear the Parnate is helping. I wish I could figure out a way to go above 30mg/day -- it was a good drug for me other than that.

 

Re: You never know-Nardil vs. Parnate

Posted by Scott L. Schofield on December 5, 1999, at 12:24:44

In reply to Re: You never know-Nardil vs. Parnate, posted by Elizabeth on December 4, 1999, at 9:29:24

> Glad to hear the Parnate is helping. I wish I could figure out a way to go above 30mg/day -- it was a good drug for me other than that.

What prevents you from going above 30mg/day ?


- Scott

 

Re: You never know-Nardil vs. Parnate

Posted by Elizabeth on December 6, 1999, at 1:20:55

In reply to Re: You never know-Nardil vs. Parnate, posted by Scott L. Schofield on December 5, 1999, at 12:24:44

> > Glad to hear the Parnate is helping. I wish I could figure out a way to go above 30mg/day -- it was a good drug for me other than that.
>
> What prevents you from going above 30mg/day ?

Spontaneous (non-food-related) hypertensive crises whenever I took more than 10mg in a single dose. Because it's a stimulating drug, I didn't want to be taking it late in the day, so I found 3 divided doses was the most I could do.

I'm told this is a rare-but-not-unheard-of side effect. At first I kept trying to figure out what I'd eaten to cause it...was frustrating!

 

Re: You never know-Nardil vs. Parnate

Posted by Adam on December 6, 1999, at 12:11:30

In reply to Re: You never know-Nardil vs. Parnate, posted by Elizabeth on December 6, 1999, at 1:20:55

A while ago, I "spontaneously" experienced this weird sensation for about a week; I had this
feeling of levity in the front of my head, as if it were trying to lift off from the rest of
my body. It felt worse if I sat down, and better if I got up and walked around. Bizarre.
Anyway, I thought it might be connected to b.p. somehow, since orthostasis gave some relief.
I went to see my doctor, got checked out by Dr. Bodkin instead, and had a little discussion
about spontaneous hypertension (the weirdness went away on its own-maybe just a bug). He said
spont. hyp. was almost exclusively a "Parnate effect", and was related to the stimulant
properties of tranylcypromine metabolites. Essentially the drug can have adverse interactions
with itself. He also said that they've "thrown everything but the kitchen sink" at selegiline
to try to get the same thing to occur, and the conclusion was that spont. hyp. "simply does
not happen" with that drug.

Of course there was no time for in-depth discussion, so I've been trying to figure this out. I
can understand (sort of) the explanation of the Parnate parent compound/metabolite interaction:
the metabolite(s) resemble amphetamine in form and function, they behave as a sympathomimetic,
cause release of too much NE (in some people, at least), you get the "cheese effect." In the
case of selegiline, the metabolites not only look like amphetamines, they ARE amphetamines. I
imagine the key may lie in the fact that selegiline metabolites are the L-enantiomers. Perhaps
they are not only "weaker" than their dextro siblings. In the case of some bioactive organics,
a particular enantiomer might not only be weaker or inactive compared to the other, it might
even interfere with the action of the other due to antagonistic competition.

I came across a curious statement afterward in the PDR about selegiline. I don't have it in
front of me, but what was written, if I remember correctly, was that, while there was no
clinical evidence that selegiline at MAO-B-specific doses should require dietary restrictions,
they shoud still be observed. Part of this statement contained, parenthetically, a suggestion
that selegiline actually might protect against the "cheese effect". So I guess I'm wondering,
could selegiline metabolites somehow inhibit NE release (which is why you never see spont. hyp.
in people taking it), and could it even be an antidote to spont. hyp.? Could a low dose of
selegiline be combined with Parnate to prevent this from occuring?

I know, ridiculous idea, probably, but something I figured I'd ask.
>
> I'm told this is a rare-but-not-unheard-of side effect. At first I kept trying to figure out what I'd eaten to cause it...was frustrating!

 

Re: You never know-Nardil vs. Parnate

Posted by Elizabeth on December 6, 1999, at 20:14:56

In reply to Re: You never know-Nardil vs. Parnate, posted by Adam on December 6, 1999, at 12:11:30

>...Anyway, I thought it might be connected to b.p. somehow, since orthostasis gave some relief.

Huh - did you try taking your BP?

> I went to see my doctor, got checked out by Dr. Bodkin instead, and had a little discussion
> about spontaneous hypertension (the weirdness went away on its own-maybe just a bug). He said
> spont. hyp. was almost exclusively a "Parnate effect", and was related to the stimulant
> properties of tranylcypromine metabolites. Essentially the drug can have adverse interactions
> with itself.

Yup, that's what he told me too.

> He also said that they've "thrown everything but the kitchen sink" at selegiline
> to try to get the same thing to occur, and the conclusion was that spont. hyp. "simply does
> not happen" with that drug.

...which is terribly interesting given selegiline's pharmacokinetic profile (I tested positive for amphetamines at one point when I was on it). I wonder about the d and l forms too; may look that up later on....

> So I guess I'm wondering,
> could selegiline metabolites somehow inhibit NE release (which is why you never see spont. hyp.
> in people taking it), and could it even be an antidote to spont. hyp.? Could a low dose of
> selegiline be combined with Parnate to prevent this from occuring?

Oh god. Don't go there...at least not in humans!

> I know, ridiculous idea, probably, but something I figured I'd ask.

Kids, don't try this at home! :)

 

Re: Ask a silly question...

Posted by Adam on December 7, 1999, at 0:38:30

In reply to Re: You never know-Nardil vs. Parnate, posted by Elizabeth on December 6, 1999, at 20:14:56

> >...Anyway, I thought it might be connected to b.p. somehow, since orthostasis gave some relief.
>
> Huh - did you try taking your BP?
>

Nope. Don't have a b.p.-cuff yet. I should get one. My b.p. connection: Getting up temporarily
alleviated the weird lightheadedness. Then it came back. Dr. B. took my b.p. It was low, both
sitting and after getting up. It didn't change. I have no clue what was going on. Nobody else
does either. File under "must be a bug."

>
> ...which is terribly interesting given selegiline's pharmacokinetic profile (I tested positive for amphetamines at one point when I was on it). I wonder about the d and l forms too; may look that up later on....
>

Here's what I found...

"Pharmacol Biochem Behav 1976 May;4(5):575-82

Catecholamines and self-stimulation: evidence suggesting a reinforcing role for
noradrenaline and a motivating role for dopamine.

Herberg LJ, Stephens DN, Franklin KB"

"Eur J Pharmacol 1979 Aug 1;57(2-3):127-33

Norepinephrine elevations in cerebrospinal fluid after d- and l-amphetamine.

Ziegler MG, Lake CR, Ebert MH"

Above two abstracts suggest there is no differential effect btw. amphetamine enantiomers and NE
release. D-amp. is much a much more potent stimulator of DA release.


"Pharmacol Biochem Behav 1976 May;4(5):545-9

Differential actions of d- and 1-amphetamine on the metabolism of 3H-norepinephrine in
rat brain.

Peterson DW, Sparber SB"

Authors demonstrated d- and l-amp. have a stereoselective effect on the production of a certain
metabolite, (methoxyhydroxyphenylethylene-glycol). There seems to be no other info. out there
about this metabolite (none I could find anyway), so I have no idea if this is of any importance.


"J Cardiovasc Pharmacol 1982 Mar-Apr;4(2):326-9

Cardiovascular effects of methamphetamine in dogs treated chronically with the amine.

Vidrio H"

"J Auton Pharmacol 1983 Jun;3(2):79-88

Involvement of presynaptic alpha 2-adrenoreceptors in the depressor response produced
by repeated administration of dextro-methamphetamine."

Both abstracts describe the antihypertensive effects of chronic methamphetamine treatment.
L-methamphetamine is a major metabolite of l-selegiline, so _maybe_ there's the answer.
The first abstract suggests that l-methamp. doesn't give this antipressor effect, however.


"Neurology 1997 Mar;48(3):662-7

Selegiline diminishes cardiovascular autonomic responses in Parkinson's disease.

Turkka J, Suominen K, Tolonen U, Sotaniemi K, Myllyla VV

Department of Neurology, University of Oulu, Finland."

In a nutshell, selegiline, at doses indicated for Parkinsons, has sympatholytic properties.


"Br J Clin Pharmacol 1998 Jun;45(6):551-8

Comparison of the effects of moclobemide and selegiline on tyramine-evoked mydriasis in
man.

Bitsios P, Langley RW, Tavernor S, Pyykko K, Scheinin M, Szabadi E, Bradshaw CM

Department of Psychiatry, University of Nottingham, UK."

This one is cool. They use pupil dilation as a model for MAOI/tyramine interactions.
Found that moc. permits tyramine-induced dilation, while selegiline (at MAO-B specific
dose) does not. This would suggest that MAO-B is not involved in protecting against
the effect of tyramine, which seems to contradict the notion that moc. is safe because it
spares MAO-B. Anyway, both drugs actually cause contraction of the pupil alone, and the
authors interpret this as evidence of sympatholytic properties of both sel. and moc.


"Psychopharmacology (Berl) 1985;86(4):432-7

Tyramine pressor sensitivity changes during deprenyl treatment.

Sunderland T, Mueller EA, Cohen RM, Jimerson DC, Pickar D, Murphy DL"

This one demonstrates selegiline is about as bad as tranylcypromine at non-MAO-B
specific doses in increasing sensitivity to the tyramine pressor effect.


So, it seems that selegilne has some sympatholytic properties, but they are
either insufficient to protect against tyramine, or are lost at higher doses.
Whatever this sympatholytic property is derived from, l-amp. and l-methamp. are
unlikely candidates. It would appear, though, that selegiline can protect
against some of its own amphetamine properties. ???? :-\ ????

>
> Oh god. Don't go there...at least not in humans!
>
> > I know, ridiculous idea, probably, but something I figured I'd ask.
>
> Kids, don't try this at home! :)

I know the combo. is strictly contraindicated in "the literature", but so are a
number of combos which turn out to be relatively safe. What, do you suppose,
would be the problem with low-dose selegiline+tranylcypromine? Still a risk
of serotonin syndrome? Too stimulating? Bad CYP450 stuff?

 

Re: Ask a silly question...Addendum

Posted by Adam on December 8, 1999, at 0:22:55

In reply to Re: Ask a silly question..., posted by Adam on December 7, 1999, at 0:38:30


Check it out:


J Affect Disord 1985 Sep;9(2):137-41

Attempts to attenuate the 'cheese effect'. Combined drug therapy in depressive illness.

Pare CM, Al Mousawi M, Sandler M, Glover V

Although earlier results, employing intravenous tyramine challenge, had indicated that a tricyclic antidepressant plus monoamine oxidase inhibitor drug
combination might be free from the 'cheese effect', the experiments reported here, involving oral tyramine challenge during the combined therapy, showed
that relaxation of a tyramine-free diet during such a drug regimen might be unsafe. Preliminary observations indicated that combined (-)-deprenyl plus
nonselective monoamine oxidase inhibitor therapy might lead to an unacceptable degree of orthostatic hypotension without reduction in tyramine sensitivity.

PMID: 2932486, UI: 86034975


Looks like somebody has tried my idea 15 years ago (not for tranylcypromine-associated spontaneous hypertension specifically, but the use of
selegiline as an antidote to hypertension in combination with non-selective irreversible MAOIs). It would seem the adverse effect was hypotension.


Here's another interesting abstract:

Acta Physiol Hung 1990;75(4):321-36

The effect of various monoamine oxidase (MAO) inhibitors on the response of blood
pressure of rats and cats to tyramine.

Abdo-Rubo A

Department of Pharmacology, Semmelweis University of Medicine, Budapest, Hungary.

The "cheese effect" is the clinically most important side effect of structurally different MAO inhibitors. It occurs mainly as a result of the interaction of
MAO inhibitor with tyramine in foodstuffs. Anaesthetised rats and cats were used in order to investigate and compare the influence of the effect of
tyramine by selective MAO type-B inhibitors with that produced by non-selective and A-selective MAO inhibitors on the one hand, and on the other hand,
different MAO-B inhibitors with (-)deprenyl. (-)Deprenyl was the only one which inhibited the effect of tyramine in the experimental animals used, while
other MAO inhibitors potentiated the tyramine effect. Therefore this study indicates that not only non-selective and A-selective inhibitors potentiate the
effect of tyramine but selective inhibitors of B-type MAO as well. The inhibition of tyramine uptake by (-)deprenyl is a remarkable exception from the
rule.


Appears selegiline really is an antipressor drug. Maybe the combined effects of MAO-A inhibition and tyramine overwhelm its sympatholytic properties,
and that's why high-dose selegiline and low-dose selegiline+MAOI aren't protective against the "cheese effect". But maybe it might work for less potent
sympathomimetic stimuli. Perhaps Parnate+low dose selegiline as an antidote isn't completely out of the question.

Just a thought.

 

Re: You never know-Nardil vs. Parnate

Posted by Scott L. Schofield on December 8, 1999, at 10:46:18

In reply to Re: You never know-Nardil vs. Parnate, posted by Elizabeth on December 6, 1999, at 1:20:55


> > What prevents you from going above 30mg/day ?
>
> Spontaneous (non-food-related) hypertensive crises whenever I took more than 10mg in a single dose. Because it's a stimulating drug, I didn't want to be taking it late in the day, so I found 3 divided doses was the most I could do.
>
> I'm told this is a rare-but-not-unheard-of side effect. At first I kept trying to figure out what I'd eaten to cause it...was frustrating!

Have you ever tried selegiline (l-deprenyl)? I was surprised to see how many people posted who described a robust antidepressant effect from it. Perhaps your reaction is due to the amphetamine metabolites of Parnate. With l-deprenyl the amphetamine metabolites are l-amphetamine and l-methamphetamine. These enantiomers are significantly less potent than their dextrorotary isomers.

Check out the abstract below. Of significance are the differences in the metabolism between oral versus transdermal administration.

-----------------------------------------------------------

Biopharm Drug Dispos 1997 Oct;18(7):567-84

Integrated pharmacokinetic and metabolic modeling of selegiline and metabolites after transdermal administration.

Rohatagi S, Barrett JS, DeWitt KE, Morales RJ
Somerset Pharmaceuticals, Tampa, FL 33607, USA.

Selegiline (SEL) is a selective, irreversible inhibitor of MAO-B, used in the treatment of Parkinson's disease, either alone or as an adjunct to L-DOPA. Selegiline hydrochloride (HCl) undergoes significant first-pass metabolism following oral administration. Transdermal delivery avoids the first-pass effect and provides greater and more prolonged levels of unchanged SEL and reduced levels of metabolites (N-desmethylselegiline (DES), L-amphetamine (AMP), and L-methamphetamine (MET) compared to the oral regimen. An integrated pharmacokinetic-metabolic model which predicts plasma concentrations of SEL and metabolites following a single 24 h application of a selegiline transdermal system (STS) is proposed. The model is based on the metabolic conversion of SEL to DES and MET and subsequently to AMP. The input function is described by a zero-order constant for the delivery of SEL from the STS system based on in vitro studies of penetration of SEL across human skin. The elimination-non-metabolic constants for each analyte account for the urinary elimination. Plasma concentration data from a pilot pharmacokinetic study in which six healthy male volunteers were administered single 24 h applications of a 1.8 mg cm2, 10 cm2 STS were used to examine this model. The coefficient of determination was 0.98 and model selection criterion was 3.4 for mean data fits, supporting the goodness of fit of the model. The pharmacokinetic parameters obtained by non-compartmental analysis were comparable to those predicted by a compartmental model. The model also predicted urinary recoveries for AMP and MET and negligible recovery for SEL and DES consistent with recent studies with the STS in which urine was collected. The metabolic conversion constant from SEL to DES was significantly lower than the conversion constant from SEL to MET, indicating that metabolism of SEL is primarily driven towards MET following transdermal administration. The metabolic conversion from MET to AMP was less than the conversion from DES to AMP. This simultaneous prediction of the SEL and metabolites is essential as the metabolic ratios have been linked to the neuroprotective effects of SEL. These findings support the proposed regional delivery advantage attributed to the transdermal route compared to the conventional therapy with the oral tablet. Future model applications may also help identify significant covariates (i.e. age, gender, and disease state) in upcoming clinical trials.

Publication Types:


Clinical trial
PMID: 9330778, UI: 97471837

 

Re: You never know-Nardil vs. Parnate Scott L. Schofield

Posted by FredPotter on October 13, 2009, at 17:48:56

In reply to Re: You never know-Nardil vs. Parnate, posted by Scott L. Schofield on December 8, 1999, at 10:46:18

Another metabolite seems to be melatonin. Is this what causes the drowsiness? As melatonin is acetylated 5HT the drowsiness should get worse as the amount of available serotonin increases

 

Re: You never know-Nardil vs. Parnate

Posted by SLS on October 14, 2009, at 5:09:43

In reply to Re: You never know-Nardil vs. Parnate Scott L. Schofield, posted by FredPotter on October 13, 2009, at 17:48:56

> Another metabolite seems to be melatonin. Is this what causes the drowsiness? As melatonin is acetylated 5HT the drowsiness should get worse as the amount of available serotonin increases

Hi Fred.

I am confused. Which drug are we talking about?


- Scott

 

Re: You never know-Nardil vs. Parnate SLS

Posted by FredPotter on October 14, 2009, at 15:51:04

In reply to Re: You never know-Nardil vs. Parnate, posted by SLS on October 14, 2009, at 5:09:43

sorry Parnate

 

Re: You never know-Nardil vs. Parnate

Posted by SLS on October 15, 2009, at 5:07:47

In reply to Re: You never know-Nardil vs. Parnate, posted by SLS on October 14, 2009, at 5:09:43

Hi Fred.

Regarding Parnate (tranylcypromine):

> > Another metabolite seems to be melatonin. Is this what causes the drowsiness? As melatonin is acetylated 5HT the drowsiness should get worse as the amount of available serotonin increases

I was unaware that Parnate increases the amount of melatonin released into the blood stream. You may have found the answer to an otherwise bewildering question.


- Scott

 

Re: You never know-Nardil vs. Parnate SLS

Posted by FredPotter on October 15, 2009, at 15:05:51

In reply to Re: You never know-Nardil vs. Parnate, posted by SLS on October 15, 2009, at 5:07:47

Hi Scott I did a google search on parnate+melatonin and came up with several papers in journals that said Parnate produced melatonin. In addition I get that awful restless legs feeling, like a tickling in the bones, only in arms as well, everywhere really. Just a guess, but melatonin+amphetamine-like metabolite might cause the distressing feeling of sleepiness+agitation. Ken Gillman suggests that propanolol should get rid of this but I haven't tried it yet.

I think too many people think of the effect of the drug, whereas the true picture is given by the drug+all metabolites, complicated in the case of Parnate by the reaction between the drug and one of its metabolites (I'm told).

Apparently the effect of Nardil is complicated by its requirement for MAO to metabolise it. So the less MAO the more Nardil hangs around until presumably it builds up to high levels.

Ken Gillman's theory about Parnate is that after bringing MAO down by 80% one can go on to a maintenance dose of 10mg on alternate days. This assumes it takes about 4 weeks for MAO to be build up to the previous level. I would think that the decline in MAO would have a decaying exponential shape so Parnate gets less efficient at disabling MAO as MAO levels drop, possibly because unsullied MAO molecules are harder to "find". So I think this 10mg alt die is too low.

Something else that interested me in the changeover from Nardil to Parnate was that in using virtually no washout period I expected Parnate to work even faster than stated. Then I thought that the position on the MAO molecule (a great 3 dimensional protein) where Nardil blocks, is vanishingly unlikely to be the same position where Parnate blocks it. So much of the Parnate is wasted at first as it blocks MAO molecules already blocked by Nardil. Hence the onset isn't that quick after all.

The fact that I don't mention MAO A and B shows I don't really know what I'm talking about.

Ken Gillman took my remark about melatonin and is now looking into it
Fred

 

Re: You never know-Nardil vs. Parnate

Posted by desolationrower on October 16, 2009, at 4:54:43

In reply to Re: You never know-Nardil vs. Parnate SLS, posted by FredPotter on October 15, 2009, at 15:05:51

melatonin is metabolised by MAO just like 5ht is. i think it is why some people have noticable drwosyness on MAO inhibitors

-d/r


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