Psycho-Babble Medication Thread 9748

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Re: Parnate information wanted

Posted by Mark on November 29, 1999, at 3:47:48

In reply to Re: Parnate information wanted, posted by carole on November 29, 1999, at 2:05:16

Carole, was Parnate good for your social anxiety, if you have it?

 

Re: Parnate information wanted

Posted by carole on November 29, 1999, at 21:49:24

In reply to Re: Parnate information wanted, posted by Mark on November 29, 1999, at 3:47:48

> Carole, was Parnate good for your social anxiety, if you have it?
I did not have a social anxiety. More of a situational "misery". A combination of "sorry Life Events" left me feeling very sad and hopeless. Parnate took me from feeling like "I hate the world, why me?" to "this is pretty cool, I really love people after all!!" in a matter of a week! Not what you normally see with antidepressants. The "euphoria" leveled off however, and I just felt damn NORMAL again. Less emotional, more energy. I expect that my "kiss-my-butt-confidence" is boosted by the "wonder drug". The med had same effect on my brother who had suffered serious clinical depression complete with the expected social "phobia" that one developes after years living with a chronic disableing disease. He turned his life around. BUT... the drug seemed to lose it's effectiveness after 4-5 years and he slid back into a severe depression with some psychotic features.Parnate IS a wonderful medication. Much education is needed so that clinicians will not avoid trying patients on it when other meds just dont work. The benefits FAR outweigh the risks in many cases!We dont withhold the toxic cancer drugs from patients who need them as the only treatment available to extend life. Mental illness requires the same aggressive treatment sometimes.

 

Re: Parnate information wanted

Posted by JAIME on December 7, 1999, at 8:27:36

In reply to Parnate information wanted, posted by Lynne on August 7, 1999, at 20:36:10

>IN response to the original questions:
1. Yes for me works against social phobia
2. if is better than nardil I can say that are different. Because Parnata acts as a Anphetamine and Nardil not. I prefer Nardil because it works better for me.
3. Yes both cause weight gain.
4. I dont follow any dietary resatriccions and I am on nardil + parnate.
5. I use NARDIL + Parnate and really are fantastic combined.

I am going to start taking Parnate soon. I have Social Phobia and Atypical Depression. Any thoughts or information on Parnate would be deeply appreciated!

 

Re: Parnate information wanted

Posted by Scott L. Schofield on December 12, 1999, at 12:27:31

In reply to Re: Parnate information wanted, posted by JAIME on December 7, 1999, at 8:27:36

> 4. I dont follow any dietary resatriccions and I am on nardil + parnate.
> 5. I use NARDIL + Parnate and really are fantastic combined.


You have taken Parnate and Nardil at the same time? I have never heard of this, but I have often thought of it. My doctor feels that it is necessary to allow two weeks between discontinuing one and beginning the other.

1. How did you go about beginning the combination treatment?
Did you begin both at the same time or add one while already taking the other?
2. Do you know if this combination has been used by others?
3. Why did you discontinue it if it was working so well?

This seems like an exciting treatment option for those of us who are treatment-resistent. It would be greatly appreciated if you could provide any documentation or other sources to support the safety of this combination.

Much Thanks.


- Scott

 

Parnate: sleep & weight

Posted by Zeke on December 13, 1999, at 6:27:06

In reply to Re: Parnate information wanted, posted by lynne on August 9, 1999, at 9:03:32

Parnate is structurally related to amphetamine. You may experience some sleep difficulty transiently at first (or at first at a certain dose). This is reportedly the most common side effect. You should become tolerant to that if it happens. Re weight gain, the med may cause some weight gain but also by virtue of being an amphetamine-cogener also weight loss effects.

A adverse effect of both medications is orthostatic hypothension -- dizziness or fainting when for example going from laying to standing. Since it is a side effect of both drugs, that may be more likely to occur. Because of that and other MAOI interatcions (in general, not necessarily with Desyrel per se) your doc will likely be more cautious than in using Parnate alone.

You might wish to look at: http://www.mentalhealth.com/drug/p30-p01.html
Also see the section on monoamine oxidase inhibitors in the Merck Manual: http://www.merck.com/pubs/mmanual/section15/chapter189/189b.htm

Had you previously taken any SSRIs?

 

Carole: MAOIs and the Serotonin Syndrome

Posted by Zeke on December 13, 1999, at 7:28:00

In reply to Re: Parnate information wanted, posted by carole on November 29, 1999, at 2:05:16

Between being lectured and being a nurse, I'm certain you've heard about the Serotonin Syndrome -- a sudden buildup of serotonin in the body. This syndrome is a special hazard from MAOI interactions and has reportedly caused 15 deaths (eg, Libby Zion: phenelzine and meperidine). This syndrome may be easily overlooked in diagnosis. Combined with the fact that MAOIs are much less used, since the SSRIs etc have become available, most physicians are inexperienced in treating patients taking MAOIs, though academically aware of the potential dangers. I imagine the role of serotonin in the Phen-Fen matter, also increases the concern. So from a doctor's perspective, the Hippocratic Oath as well as malpractice suits (eg, Libby Zion again), must come to bear.

That doesn't make your situation easier, but it's an explanation!

See:
http://www.hospitaldoc.com/serotoni.htm
http://www.vh.org/Providers/Lectures/EmergencyMed/Psychiatry/MedEmergSerotonin.html
http://www.ozemail.com.au/~ouad/SERO0001.HTM
http://www.ozemail.com.au/~ouad/MONA0001.HTM

 

Re: Parnate: sleep & weight

Posted by Elizabeth on December 13, 1999, at 7:36:24

In reply to Parnate: sleep & weight, posted by Zeke on December 13, 1999, at 6:27:06

> Re weight gain, the med may cause some weight gain but also by virtue of being an amphetamine-cogener also weight loss effects.

AFAIK Parnate has *never* been reported to cause weight gain in the literature.

 

On behalf of Lucifer...

Posted by Zeke on December 13, 1999, at 7:52:39

In reply to Re: Parnate information wanted, posted by carole on November 29, 1999, at 21:49:24

> Much education is needed so that clinicians will not avoid trying patients on it when other meds just dont work. The benefits FAR outweigh the risks in many cases! We dont withhold the toxic cancer drugs from patients who need them as the only treatment available to extend life. Mental illness requires the same aggressive treatment sometimes.

Since it works for you witout severe untoward reaction, it's a wonderful drug.

No we don't withhold (some) toxic compounds in cancer therapy. But we are cautious about using them. We also withdrawl some drugs that have non fatal toxicities: thalidomide and fenfluramine.

I know you're venting, but just playing the devil's advocate...

Besides, have all other meds failed? Have all the SSRIs been tried? other newer antidepressants? Have they been augmented with Synthroid or pindilol or stimulants or... This may or may not be safer than an MAOI but sounds like it would cause less physician anxiety and hassle for you (in the long run).

 

Liz: Parnate: weight gain, & the literature

Posted by Zeke on December 13, 1999, at 8:28:53

In reply to Re: Parnate: sleep & weight, posted by Elizabeth on December 13, 1999, at 7:36:24

> > Re weight gain, the med may cause some weight gain but also by virtue of being an amphetamine-cogener also weight loss effects.
>
> AFAIK Parnate has *never* been reported to cause weight gain in the literature.

I beg to disagree -- see references. (I have to refrain from saying, "not in the literature, just in people.")

However since we're speaking of Parnate, note that the weight gain seems to occur much moreso with Nardil than Parnate. As Bernstein says, "...an amphetamine-like structure of tranylcypromine may explain its lesser ability to stimulate appetite and weight gain than the appetite and weight effects observed with phenelzine."

Bernstein JG
Induction of obesity by psychotropic drugs.
Ann N Y Acad Sci 1987;499:203-15
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2886102&form=6&db=m&Dopt=b

Remick RA, Froese C, Keller FD
Common side effects associated with monoamine oxidase inhibitors.
Prog Neuropsychopharmacol Biol Psychiatry 1989;13(3-4):497-504
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2748873&form=6&db=m&Dopt=b

Cantu TG, Korek JS
Monoamine oxidase inhibitors and weight gain.
Drug Intell Clin Pharm 1988 Oct;22(10):755-9
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3068037&form=6&db=m&Dopt=b

On the otherhand, some evidence exists for a weight loss effect from Parnate(tranylcypromine).

Dulloo AG, Miller DS
Thermogenic drugs for the treatment of obesity:
sympathetic stimulants in animal models.
Br J Nutr 1984 Sep;52(2):179-96
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6477859&form=6&db=m&Dopt=b

(Importantly, this article also rejects the common notion that stimulant type drugs reduce weight purely through reducing appetite.)

So its a mixed bag...

 

Re: Liz: Parnate: weight gain, & the literature

Posted by Adam on December 13, 1999, at 9:32:08

In reply to Liz: Parnate: weight gain, & the literature, posted by Zeke on December 13, 1999, at 8:28:53


> I have to refrain from saying, "not in the literature, just in people."

Why refrain? Individual responses to ADs can diverge quite dramatically from the average response.
'Not to say "the literature" has no value, it just doesn't account for everything.

 

Adam: My sarcasm missed!

Posted by Zeke on December 13, 1999, at 10:00:58

In reply to Re: Liz: Parnate: weight gain, & the literature, posted by Adam on December 13, 1999, at 9:32:08

> Why refrain? Individual responses to ADs can diverge quite dramatically from the average response.
> 'Not to say "the literature" has no value, it just doesn't account for everything.

I was being more sarcastic than literal. I didn't want to be hurtful to Elizabeth however. (Literally, weight gain is documented in (Parnate in) the medical journals.)

 

Re: Adam: My sarcasm missed!

Posted by Adam on December 13, 1999, at 10:53:49

In reply to Adam: My sarcasm missed!, posted by Zeke on December 13, 1999, at 10:00:58

I seem to have a special talent for failing to recognise sarcasm, or even mild irony. You didn't miss, I did.

> > Why refrain? Individual responses to ADs can diverge quite dramatically from the average response.
> > 'Not to say "the literature" has no value, it just doesn't account for everything.
>
> I was being more sarcastic than literal. I didn't want to be hurtful to Elizabeth however. (Literally, weight gain is documented in (Parnate in) the medical journals.)

 

Parnate: weight gain, & the literature - Zeke

Posted by Elizabeth on December 13, 1999, at 13:06:51

In reply to Liz: Parnate: weight gain, & the literature, posted by Zeke on December 13, 1999, at 8:28:53

> > AFAIK Parnate has *never* been reported to cause weight gain in the literature.
>
> I beg to disagree -- see references. (I have to refrain from saying, "not in the literature, just in people.")

:-) Well I *did* say "AFAIK." You can't argue that I knew of documented weight gain with Parnate! :-)

> However since we're speaking of Parnate, note that the weight gain seems to occur much moreso with Nardil than Parnate.

Tell me about it! (50 lbs - more than 40% of my original weight - on Nardil, none on Parnate.)

> As Bernstein says, "...an amphetamine-like structure of tranylcypromine may explain its lesser ability to stimulate appetite and weight gain than the appetite and weight effects observed with phenelzine."

I *really* wonder about the stimulant-like properties of Parnate (a psychopharm consultant first mentioned this to me in 1997 and I was intrigued).

> Bernstein JG
> Induction of obesity by psychotropic drugs.
> Ann N Y Acad Sci 1987;499:203-15
> http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2886102&form=6&db=m&Dopt=b

I can only view abstracts at this time, but I saw no reference to any specific case of Parnate-associated weight gain.

Also as an aside, remember there is a big confound in the claim that Parnate might "cause" weight gain: Parnate has been used, historically, mainly for atypical depression in which weight gain is already a feature of the depression!

> Remick RA, Froese C, Keller FD
> Common side effects associated with monoamine oxidase inhibitors.
> Prog Neuropsychopharmacol Biol Psychiatry 1989;13(3-4):497-504
> http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2748873&form=6&db=m&Dopt=b

Okay, here is a specific report. However, the abstract, at least, doesn't document the cases adequately to convince me the weight gain was *caused* by the Parnate (were they on other drugs? were they already gaining weight prior to taking the Parnate? etc.).

> Cantu TG, Korek JS
> Monoamine oxidase inhibitors and weight gain.
> Drug Intell Clin Pharm 1988 Oct;22(10):755-9
> http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3068037&form=6&db=m&Dopt=b

Uhh... "There are no cases of tranylcypromine-induced weight gain in the literature that are clearly associated with the drug." (This was after the drug had been approved in this country for nearly 30 years.)

> On the otherhand, some evidence exists for a weight loss effect from Parnate(tranylcypromine).
>
> Dulloo AG, Miller DS
> Thermogenic drugs for the treatment of obesity:
> sympathetic stimulants in animal models.
> Br J Nutr 1984 Sep;52(2):179-96
> http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6477859&form=6&db=m&Dopt=b
>
> (Importantly, this article also rejects the common notion that stimulant type drugs reduce weight purely through reducing appetite.)

No doubt the appetite reduction helps, though my appetite increased on Parnate (probably secondary to remission of depression!).

 

Re: Parnate: weight gain, & the literature - Liz

Posted by Zeke on December 14, 1999, at 1:39:09

In reply to Parnate: weight gain, & the literature - Zeke, posted by Elizabeth on December 13, 1999, at 13:06:51

> > > AFAIK Parnate has *never* been reported to cause weight gain in the literature.
> >
> > I beg to disagree -- see references. (I have to refrain from saying, "not in the literature, just in people.")
>
> :-) Well I *did* say "AFAIK." You can't argue that I knew of documented weight gain with Parnate! :-)
>

You're a tough sell -- probably from Missouri -- but I respect that!

General references like the PDR and the Merck Manual (and especially the watered down popular books) tend to generalize the MOAIs and use the same profile for all. What we can certainly agree on is that while Parnate and Nardil are similar, they have important differences. This is true of others, my pet peeve being the 'sameness' attributed to Ritalin and Dexedrine (the amphetamines in general). For example, there has been reluctance to treat epileptics with ADD because of Ritalin's proconvulsant effect, and this then is assumed for amphetamine. But the literature demonstrates an antiseizure property of amphetamines. But somehow this has been all but forgotten aboutand replace with the simple notion that amphetamines were used just to offset the sedative effects of phenobarbital. Fortunately, the therapeutic differences in stimulants is becomeing more appreciated by those who treat ADD.

> > However since we're speaking of Parnate, note that the weight gain seems to occur much moreso with Nardil than Parnate.
>
> Tell me about it! (50 lbs - more than 40% of my original weight - on Nardil, none on Parnate.)
>
> > As Bernstein says, "...an amphetamine-like structure of tranylcypromine may explain its lesser ability to stimulate appetite and weight gain than the appetite and weight effects observed with phenelzine."
>
> I *really* wonder about the stimulant-like properties of Parnate (a psychopharm consultant first mentioned this to me in 1997 and I was intrigued).

Well among other things, the DEA is keeping an eye on Parnate and its derivatives for abuse potential.
http://rhodium.lycaeum.org/chemistry/future_drugs.html
(Interestingly, is the Surgeon General's report documenting people not seeking help for psychiatric disorders. Gee guys, we take away the tools and what do you expect. We've already removed the promising application of MDMA in psychotherapy because of morally biased research.)

>
> > Bernstein JG
> > Induction of obesity by psychotropic drugs.
> > Ann N Y Acad Sci 1987;499:203-15
> > http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2886102&form=6&db=m&Dopt=b
>
> I can only view abstracts at this time, but I saw no reference to any specific case of Parnate-associated weight gain.
>
> Also as an aside, remember there is a big confound in the claim that Parnate might "cause" weight gain: Parnate has been used, historically, mainly for atypical depression in which weight gain is already a feature of the depression!

That's a good point. Further confounding is the fact that SSRIs are more frequently used in atypical depression with efficacy. Conversely here, weight loss is reported in the atypicals.

IMHO Parnate is also mainly for refractory depression:

"Tranylcypromine in high doses (20 to 30 mg po bid) is often effective for depression refractory to sequential trials of other antidepressants; it should be administered by physicians experienced in the use of MAOIs."
--The Merck Manual

>
> > Remick RA, Froese C, Keller FD
> > Common side effects associated with monoamine oxidase inhibitors.
> > Prog Neuropsychopharmacol Biol Psychiatry 1989;13(3-4):497-504
> > http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2748873&form=6&db=m&Dopt=b
>
> Okay, here is a specific report. However, the abstract, at least, doesn't document the cases adequately to convince me the weight gain was *caused* by the Parnate (were they on other drugs? were they already gaining weight prior to taking the Parnate? etc.).

Don't know - just pointing to evidence in the literature.

>
> > Cantu TG, Korek JS
> > Monoamine oxidase inhibitors and weight gain.
> > Drug Intell Clin Pharm 1988 Oct;22(10):755-9
> > http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3068037&form=6&db=m&Dopt=b
>
> Uhh... "There are no cases of tranylcypromine-induced weight gain in the literature that are clearly associated with the drug." (This was after the drug had been approved in this country for nearly 30 years.)

With emphasis on the word 'clearly.'


>
> > On the otherhand, some evidence exists for a weight loss effect from Parnate(tranylcypromine).
> >
> > Dulloo AG, Miller DS
> > Thermogenic drugs for the treatment of obesity:
> > sympathetic stimulants in animal models.
> > Br J Nutr 1984 Sep;52(2):179-96
> > http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6477859&form=6&db=m&Dopt=b
> >
> > (Importantly, this article also rejects the common notion that stimulant type drugs reduce weight purely through reducing appetite.)
>
> No doubt the appetite reduction helps, though my appetite increased on Parnate (probably secondary to remission of depression!).

Remember that increased appetite (especially carbo cravings) are a symptom of atypical depression, just as weight gain is!

You might find this one interesting

Richard J. Wurtman and Juidith J. Wurtman
Carbohydrates and Depression
SCIENTIFIC AMERICAN January 1989
http://www.sciam.com/0189issue/0189wurtman.html

 

Re: Parnate: weight gain, & the literature - Liz

Posted by Elizabeth on December 14, 1999, at 4:44:22

In reply to Re: Parnate: weight gain, & the literature - Liz, posted by Zeke on December 14, 1999, at 1:39:09

> > :-) Well I *did* say "AFAIK." You can't argue that I knew of documented weight gain with Parnate! :-)
> >
>
> You're a tough sell -- probably from Missouri -- but I respect that!

Not even close - Boston. :)

> General references like the PDR and the Merck Manual (and especially the watered down popular books) tend to generalize the MOAIs and use the same profile for all.

Yeah, I know. Among my many flames about such references. :)

> Well among other things, the DEA is keeping an eye on Parnate and its derivatives for abuse potential.

I guess they wonder about it too. There *have* been reports of that in the literature (and in people, too!).

> http://rhodium.lycaeum.org/chemistry/future_drugs.html

> (Interestingly, is the Surgeon General's report documenting people not seeking help for psychiatric disorders.

I can't find this...happen to have a URL?

>Gee guys, we take away the tools and what do you expect. We've already removed the promising application of MDMA in psychotherapy because of morally biased research.)

You know, I really don't think that opposing use oof certain types of drugs has anything to do with morality. Maybe that's just my own moral bias, though!

> IMHO Parnate is also mainly for refractory depression:
>
> "Tranylcypromine in high doses (20 to 30 mg po bid) is often effective for depression refractory to sequential trials of other antidepressants; it should be administered by physicians experienced in the use of MAOIs."
> --The Merck Manual

True, that's what I use MAOIs for (haven't given tricyclics an adequate trial due to side effects, though).

> > Uhh... "There are no cases of tranylcypromine-induced weight gain in the literature that are clearly associated with the drug." (This was after the drug had been approved in this country for nearly 30 years.)
>
> With emphasis on the word 'clearly.'

I think that's what I'd require to consider it real evidence that Parnate "causes" or "induces" weight gain.

> > No doubt the appetite reduction helps, though my appetite increased on Parnate (probably secondary to remission of depression!).
>
> Remember that increased appetite (especially carbo cravings) are a symptom of atypical depression, just as weight gain is!

Well yeah, I thought that was where the weight gain came from! Eating junk food, especially at night.

> You might find this one interesting
>
> Richard J. Wurtman and Juidith J. Wurtman
> Carbohydrates and Depression
> SCIENTIFIC AMERICAN January 1989
> http://www.sciam.com/0189issue/0189wurtman.html

Oh god, not the Wurtmans!

 

Re: Parnate: weight gain, & the literature - Liz

Posted by Zeke on December 14, 1999, at 11:25:55

In reply to Re: Parnate: weight gain, & the literature - Liz, posted by Elizabeth on December 14, 1999, at 4:44:22

> > (Interestingly, is the Surgeon General's report documenting people not seeking help for psychiatric disorders.
>
> I can't find this...happen to have a URL?
>

http://www.nytimes.com/library/politics/121399mental-health.html


> >Gee guys, we take away the tools and what do you expect. We've already removed the promising application of MDMA in psychotherapy because of morally biased research.)
>
> You know, I really don't think that opposing use oof certain types of drugs has anything to do with morality. Maybe that's just my own moral bias, though!
>

I'm not talking about people taking ecstasy every weekend at the local rave -- though that's the reason it's schedule 1. I'm talking about limited clinical use to augment therapy just as pindolol augments Prozac. When I say morality, I mean the government passing along research that supports its view and withholding research that doesn't, or even preventing research in the first place. I get upset when they rant that 'MDMA destroys serotonin neurons," but never mention that administration of an SSRI four hours later will block the uptake and damage. I'm sorry, I just get upset when moral prejudice strongarms block scientific discovery. And remember that many of these folks would like to cast all psych meds in to the sea -- ' and by God, you should just pull yourself up by your bootstraps!'

> > IMHO Parnate is also mainly for refractory depression:
> >
> > "Tranylcypromine in high doses (20 to 30 mg po bid) is often effective for depression refractory to sequential trials of other antidepressants; it should be administered by physicians experienced in the use of MAOIs."
> > --The Merck Manual
>
> True, that's what I use MAOIs for (haven't given tricyclics an adequate trial due to side effects, though).

Despite all the bliss, I think the side effects of SSRIs cause many to drop those too. I can't deal with higher doses of Luvox but use a lower dose and pindolol.
>
> > > Uhh... "There are no cases of tranylcypromine-induced weight gain in the literature that are clearly associated with the drug." (This was after the drug had been approved in this country for nearly 30 years.)
> >
> > With emphasis on the word 'clearly.'
>
> I think that's what I'd require to consider it real evidence that Parnate "causes" or "induces" weight gain.
>

OK, with emphasis on no case being clear to this particular researcher.

> > > No doubt the appetite reduction helps, though my appetite increased on Parnate (probably secondary to remission of depression!).
> >
> > Remember that increased appetite (especially carbo cravings) are a symptom of atypical depression, just as weight gain is!
>
> Well yeah, I thought that was where the weight gain came from! Eating junk food, especially at night.
>
> > You might find this one interesting
> >
> > Richard J. Wurtman and Juidith J. Wurtman
> > Carbohydrates and Depression
> > SCIENTIFIC AMERICAN January 1989
> > http://www.sciam.com/0189issue/0189wurtman.html
>
> Oh god, not the Wurtmans!

If I'd only know you were from Boston! (Besides, RW's a good guy -- Now if I'd have said John Mack... Beam me up Scotty!)

 

Re: Parnate: weight gain, & the literature - Liz

Posted by Adam on December 14, 1999, at 22:06:45

In reply to Re: Parnate: weight gain, & the literature - Liz, posted by Zeke on December 14, 1999, at 11:25:55

>
> I'm not talking about people taking ecstasy every weekend at the local rave -- though that's the reason it's schedule 1. I'm talking about limited clinical use to augment therapy just as pindolol augments Prozac. When I say morality, I mean the government passing along research that supports its view and withholding research that doesn't, or even preventing research in the first place. I get upset when they rant that 'MDMA destroys serotonin neurons," but never mention that administration of an SSRI four hours later will block the uptake and damage. I'm sorry, I just get upset when moral prejudice strongarms block scientific discovery. And remember that many of these folks would like to cast all psych meds in to the sea -- ' and by God, you should just pull yourself up by your bootstraps!'
>
I had the opportunity to take MDMA not too long ago which I thankfully declined. Anyway, what I read lead me to believe that it takes very high doses of MDMA or chronic use to kill
brain cells. However, axonal damage might still be a problem at lower doses, and even though axons can grow back, it's tough to know how they will grow back, and in the mean time
the cell is out of comission. MDMA also stimulates excessive dopamine release, and reactive oxygen species produced during metabolism of dopamine by MAO have been implicated in
neurotoxicity. Addition of an SSRI might offer some protection, but its difficult to know how much and what neurons.

This may all be really nitpicky, though. I've become very casually aquainted with a couple fairly regular users, and it's hard to tell if "Adam" (gotta love _that_ nickname) is doing
them any real harm or not.

> > > IMHO Parnate is also mainly for refractory depression:
> > >
> > > "Tranylcypromine in high doses (20 to 30 mg po bid) is often effective for depression refractory to sequential trials of other antidepressants; it should be administered by physicians experienced in the use of MAOIs."
> > > --The Merck Manual
> >
> > True, that's what I use MAOIs for (haven't given tricyclics an adequate trial due to side effects, though).

I wonder what it takes before some people decide you are "refractory" enough and insist you consider an MAOI. I had one doctor keep me on Serzone for more than two months even though
I knew it wasn't working and started rapidly spiraling the drain while on it. I guess a quivering, weeping, suicidal state of frenzy is "refractory."

>
> Despite all the bliss, I think the side effects of SSRIs cause many to drop those too. I can't deal with higher doses of Luvox but use a lower dose and pindolol.
> >

I never got anywhere near bliss on an SSRI, but had a couple fun side effects for my troubles: a spare tire around the waist, anorgasmia, and loss of libido. Perhaps if I had
tried Prozac I could have been thin, asexual, and depressed. Will MAOIs never be a first or even second-line treatment again?

 

MAOIs - Adam

Posted by Elizabeth on December 15, 1999, at 10:06:46

In reply to Re: Parnate: weight gain, & the literature - Liz, posted by Adam on December 14, 1999, at 22:06:45

> I wonder what it takes before some people decide you are "refractory" enough and insist you consider an MAOI. I had one doctor keep me on Serzone for more than two months even though
> I knew it wasn't working and started rapidly spiraling the drain while on it. I guess a quivering, weeping, suicidal state of frenzy is "refractory."

Actually I think it's just "nonresponse to other stuff." :-)

> I never got anywhere near bliss on an SSRI, but had a couple fun side effects for my troubles: a spare tire around the waist, anorgasmia, and loss of libido. Perhaps if I had
> tried Prozac I could have been thin, asexual, and depressed. Will MAOIs never be a first or even second-line treatment again?

I think they should be put ahead of tricyclics in some cases actually, at least.

 

Re: Parnate: weight gain, & the literature - Liz

Posted by Elizabeth on December 15, 1999, at 10:24:21

In reply to Re: Parnate: weight gain, & the literature - Liz, posted by Zeke on December 14, 1999, at 11:25:55

> I'm not talking about people taking ecstasy every weekend at the local rave -- though that's the reason it's schedule 1. I'm talking about limited clinical use to augment therapy just as pindolol augments Prozac.

Yes, I know what you're talking about, although I really don't see *either* use as being morally wrong.

> When I say morality, I mean the government passing along research that supports its view and withholding research that doesn't, or even preventing research in the first place.

Now *that's* morally wrong. God I hate the War on Some Drugs!

> I'm sorry, I just get upset when moral prejudice strongarms block scientific discovery.

Nothing to be sorry about!

> And remember that many of these folks would like to cast all psych meds in to the sea -- ' and by God, you should just pull yourself up by your bootstraps!'

The government (NIDA etc.), or just random anti-med people?

> Despite all the bliss, I think the side effects of SSRIs cause many to drop those too. I can't deal with higher doses of Luvox but use a lower dose and pindolol.

How is pindolol for you? I'm using it with Marplan - had a fast response, now have really low BP and insomnia! (Like, even more insomnia than I had before. Which is a lot.)

> OK, with emphasis on no case being clear to this particular researcher.

We'd have to comb through the literature for ourselves to make a real decision, of course.

> If I'd only know you were from Boston!

I'm not just from Boston...I went to MIT!

> (Besides, RW's a good guy -- Now if I'd have said John Mack... Beam me up Scotty!)

:-)

 

Re: Parnate: weight gain, & the literature - Adam

Posted by Zeke on December 15, 1999, at 10:26:36

In reply to Re: Parnate: weight gain, & the literature - Liz, posted by Adam on December 14, 1999, at 22:06:45

> >
> > I'm not talking about people taking ecstasy every weekend at the local rave -- though that's the reason it's schedule 1. I'm talking about limited clinical use to augment therapy just as pindolol augments Prozac. When I say morality, I mean the government passing along research that supports its view and withholding research that doesn't, or even preventing research in the first place. I get upset when they rant that 'MDMA destroys serotonin neurons," but never mention that administration of an SSRI four hours later will block the uptake and damage. I'm sorry, I just get upset when moral prejudice strongarms block scientific discovery. And remember that many of these folks would like to cast all psych meds in to the sea -- ' and by God, you should just pull yourself up by your bootstraps!'
> >
> I had the opportunity to take MDMA not too long ago which I thankfully declined. Anyway, what I read lead me to believe that it takes very high doses of MDMA or chronic use to kill
> brain cells. However, axonal damage might still be a problem at lower doses, and even though axons can grow back, it's tough to know how they will grow back, and in the mean time
> the cell is out of comission.

I don't want to beat this subject to death but one more ecstatic respone!

I am referring to limited, controlled use of entactogens (eg, MDMA) in psychotherapy, in persons where fear and anxiety are roadblocks to insight and expression. I think two factors must be considered:

1. A protocol of giving the entactogen and several hours later giving an SSRI (and perhaps deprenyl) would aloow for the beneficial effects but minimize possible neurotoxicity. Use of the levo isomer of MDMA appears safer as it excludes delayed damage -- loss of uptake sites. SSRIs may offer no protection from this toxicity, but again is is stereospicific.

2. Lack of effective treatment (often) allows for high levels of glucocorticoids (eg, cortisol) which also have documented neurotoxicity. This toxicity however, has been more clearly linked with behavioral deficits and abnormalities.


> MDMA also stimulates excessive dopamine release, and reactive oxygen species produced during metabolism of dopamine by MAO have been implicated in
> neurotoxicity.

(And you're taking deprenyl right?!!!)

Yet I think you'd agree that the significant toxicity is to 5HT processes, and this seems to occur when MDMA is carried inside the neuron, and thus the protective effect of an SSRI. I susbect that MDMA competes with 5HT for entry so initially there is very little MDMA uptake and damage.

As for free radical damage, there are MAOis but also other central antioxidants.

> Addition of an SSRI might offer some protection, but its difficult to know how much and what neurons.

I agree it is complex and damage may occur at different times. But documentation of the damage (immediate vs. delayed) suggests that testing SSRI interactions whould be one of the next steps.


> This may all be really nitpicky, though. I've become very casually aquainted with a couple fairly regular users, and it's hard to tell if "Adam" (gotta love _that_ nickname) is doing
> them any real harm or not.

Not nitpicky at all, and this observation is typical. Correlation between reported damage and obvious behavioral changes have been the exception, to my knowledge.

>
> > > > IMHO Parnate is also mainly for refractory depression:
> > > >
> > > > "Tranylcypromine in high doses (20 to 30 mg po bid) is often effective for depression refractory to sequential trials of other antidepressants; it should be administered by physicians experienced in the use of MAOIs."
> > > > --The Merck Manual
> > >
> > > True, that's what I use MAOIs for (haven't given tricyclics an adequate trial due to side effects, though).
>
> I wonder what it takes before some people decide you are "refractory" enough and insist you consider an MAOI. I had one doctor keep me on Serzone for more than two months even though
> I knew it wasn't working and started rapidly spiraling the drain while on it. I guess a quivering, weeping, suicidal state of frenzy is "refractory."
>

But who knows what else may have worked in you.
> >
> > Despite all the bliss, I think the side effects of SSRIs cause many to drop those too. I can't deal with higher doses of Luvox but use a lower dose and pindolol.
> > >
>
> I never got anywhere near bliss on an SSRI, but had a couple fun side effects for my troubles: a spare tire around the waist, anorgasmia, and loss of libido. Perhaps if I had
> tried Prozac I could have been thin, asexual, and depressed. Will MAOIs never be a first or even second-line treatment again?

I meant the bliss ABOUT them, not from them! But I hear you. A spare tire from an SSRI --- really?

I think selective MAO inhibitors will be their resurrection. Side effects and interactions are few(er) and rare, and efficacy in depression is being demonstrated. What do you think?

 

Re: Parnate: weight gain, & the literature - Adam

Posted by Adam on December 15, 1999, at 11:45:04

In reply to Re: Parnate: weight gain, & the literature - Adam, posted by Zeke on December 15, 1999, at 10:26:36

> I am referring to limited, controlled use of entactogens (eg, MDMA) in psychotherapy, in persons where fear and anxiety are roadblocks to insight and expression.

I understand that. I was acting as one of those minions of Satan you referred to above, mostly. This is, I believe, one of the early clinical uses of MDMA (after it lost favor as an appetite supressant), yes?

I think two factors must be considered:
>
> 1. A protocol of giving the entactogen and several hours later giving an SSRI (and perhaps deprenyl) would aloow for the beneficial effects but minimize possible neurotoxicity. Use of the levo isomer of MDMA appears safer as it excludes delayed damage -- loss of uptake sites. SSRIs may offer no protection from this toxicity, but again is is stereospicific.
>
> 2. Lack of effective treatment (often) allows for high levels of glucocorticoids (eg, cortisol) which also have documented neurotoxicity. This toxicity however, has been more clearly linked with behavioral deficits and abnormalities.
>

There are probably all kinds of potential sources of neurotoxicity associated with use of MDMA, and from what I can see, the subject is still open to debate. That significant neurotoxicity even occurs from recreational use is a point of debate, it appears.

> (And you're taking deprenyl right?!!!)

Yes. Um, I'm not sure what this statement means. Perhaps you are referring to this: taking deprenyl means exposure to l-methamphetamine (some similarities to MDMA) and l-amphetamine. To be honest, I find it rather difficult to understand why people, especially on high oral doses of selegiline, don't have more problems than they do. Serotonin syndrome and spontaneous hypertension seem like obvious potential problems, and yet nobody gets these things with high-dose selegiline monotherapy. I read about selegiline, and it seems like the magic molecule. It protects against oxidative stress by upregulating expression of things like superoxide dismutase. It has antipressor properties that not only protect against its own sympathomimetic metabolites, but even other pressor stimuli like tyramine (IF you take it in small doses). People say it enhances memory and sex drive. What doesn't deprenyl do?

> Yet I think you'd agree that the significant toxicity is to 5HT processes, and this seems to occur when MDMA is carried inside the neuron, and thus the protective effect of an SSRI. I susbect that MDMA competes with 5HT for entry so initially there is very little MDMA uptake and damage.
>
> As for free radical damage, there are MAOis but also other central antioxidants.
>
I am frankly a bit confused by the things I read about MDMA and how it causes neuron damage. Excitotoxicity? Oxidative stress? Neither, both, other things?

I've seen references to use of deprenyl and SSRIs in protecting against MDMA-induced neurotoxicity. In the clinical setting, use of deprenyl at any dose within the time frame needed to give this supposed protective effect would be a tough sell indeed. Not to say you're wrong. I honestly don't know.


> I think selective MAO inhibitors will be their resurrection. Side effects and interactions are few(er) and rare, and efficacy in depression is being demonstrated. What do you think?

I'm sure they are efficacious. I don't think they will replace the old, non-selective MAOIs, though. The doctors I am working with right now seem rather unimpressed with the RIMAs, and that appears to be the consensus, in this country at least. What excites me is the transdermal delivery system. It gives the benefits of an MAOI with fewer side effects and no dietary restrictions. I'm not certain why this approach isn't being explored with other MAOIs besides selegiline. I think the head of the study I am participating in mentioned something about Parnate, at least, being a little "too toxic" for this, but I'm not sure what that means (skin irritation?) Maybe its just money, since the patents ran out on the big three a long time ago. But other MAOIs could conceivably be developed, maybe some that are more tolerable in general than the older ones, for transdermal delivery too. This is way, way cool if you ask me.

 

Adam: dangling threads from Parnate

Posted by Zeke on December 15, 1999, at 20:53:30

In reply to Re: Parnate: weight gain, & the literature - Adam, posted by Adam on December 15, 1999, at 11:45:04


> > (And you're taking deprenyl right?!!!)
>
> Yes. Um, I'm not sure what this statement means. Perhaps you are referring to this: taking deprenyl means exposure to l-methamphetamine (some similarities to MDMA) and l-amphetamine. To be honest, I find it rather difficult to understand why people, especially on high oral doses of selegiline, don't have more problems than they do. Serotonin syndrome and spontaneous hypertension seem like obvious potential problems, and yet nobody gets these things with high-dose selegiline monotherapy. I read about selegiline, and it seems like the magic molecule. It protects against oxidative stress by upregulating expression of things like superoxide dismutase. It has antipressor properties that not only protect against its own sympathomimetic metabolites, but even other pressor stimuli like tyramine (IF you take it in small doses). People say it enhances memory and sex drive. What doesn't deprenyl do?
>

You were referring to MDMA increasing dopamine & dopamine metabolism and in turn which free radicals toxic to the dopamine neurons. And it came to mind that you are taking deprenyl, which of course is an antioxiant specific to dopamine! (Coincidence perhaps but also suggests in part your knowledge in this area.)

I'm glad you responded and said what you did. In sannning MedLine this morning about the 5HT axon damage issue, I learned that this occurs in part because 5HT uptake pumps occur not just at terminals, but all along the axon as well. I guess some reading this will say so what, but I think you will appreciate how this contrasts with what we were taught. It's like recent findings about neurogenesis, about electrical transmission without chemical transmitters, and about the greater importance of the cerebellum. (Actually Robert Heath alluded to this but he has been discounted because of his 'mad science' -- putting active electrodes in human subjects.)


> > Yet I think you'd agree that the significant toxicity is to 5HT processes, and this seems to occur when MDMA is carried inside the neuron, and thus the protective effect of an SSRI. I susbect that MDMA competes with 5HT for entry so initially there is very little MDMA uptake and damage.
> >
> > As for free radical damage, there are MAOis but also other central antioxidants.
> >
> I am frankly a bit confused by the things I read about MDMA and how it causes neuron damage. Excitotoxicity? Oxidative stress? Neither, both, other things?
>
> I've seen references to use of deprenyl and SSRIs in protecting against MDMA-induced neurotoxicity. In the clinical setting, use of deprenyl at any dose within the time frame needed to give this supposed protective effect would be a tough sell indeed. Not to say you're wrong. I honestly don't know.
>
>

The thing that jumped out at me, is that both +MDMA and -MDMA are entactogens, but -MDMA lacks the delayed damage of +MDMA, and the immediate damage is what can be blocked (to whatever degree) by SSRIs and deprenyl.

The one thing that I don't see mentioned re MDMA is an effect on endogenous opioids (ie, enkephalins) which are intermediate between 5HT and dopamine neurons. And the flood of dopamine you mention is supposedly caused by the massive release of 5HT.

> > I think selective MAO inhibitors will be their resurrection. Side effects and interactions are few(er) and rare, and efficacy in depression is being demonstrated. What do you think?
>
> I'm sure they are efficacious. I don't think they will replace the old, non-selective MAOIs, though. The doctors I am working with right now seem rather unimpressed with the RIMAs,

is RIMA: Reversible Inhibitors of MonoAmine oxidase? or what???

> and that appears to be the consensus, in this country at least.

I'm glad you said "in this country at least" as European researchers seem to be way out in front on the possibilities (eg, derivatives of deprenyl with even more specific properties and applications.)

> What excites me is the transdermal delivery system. It gives the benefits of an MAOI with fewer side effects and no dietary restrictions. I'm not certain why this approach isn't being explored with other MAOIs besides selegiline. I think the head of the study I am participating in mentioned something about Parnate, at least, being a little "too toxic" for this, but I'm not sure what that means (skin irritation?) Maybe its just money, since the patents ran out on the big three a long time ago. But other MAOIs could conceivably be developed, maybe some that are more tolerable in general than the older ones, for transdermal delivery too. This is way, way cool if you ask me.

You know, my mother died of Alzheimer's last year. I unsucessfully tried to get the doctors to try deprenyl -- the last one seemed fearful of psychotic reactions. (They seemed to like the idea of neurolepticss widespite the toxicity of those drugs. BTW she had much less than typical agitation and positive symptoms.) Anyway, you mention transdermals and I think that one other possibility we considered was the nicotine patches used for smoking cessation.

 

Re: Parnate: weight gain, & the literature - Zeke

Posted by Elizabeth on December 15, 1999, at 21:10:30

In reply to Re: Parnate: weight gain, & the literature - Adam, posted by Zeke on December 15, 1999, at 10:26:36

> 1. A protocol of giving the entactogen and several hours later giving an SSRI (and perhaps deprenyl) would aloow for the beneficial effects but minimize possible neurotoxicity. Use of the levo isomer of MDMA appears safer as it excludes delayed damage -- loss of uptake sites. SSRIs may offer no protection from this toxicity, but again is is stereospicific.

Even excluding the slight problem of illegality of MDMA (yes I am opposed to this, but it is a difficulty nevertheless!) I think you would have a nigh-impossible time convincing most pdocs to do this, between the speculative uses of SSRI and selegiline, and the mixing of the three. Indeed, I believe more research needs to be done before this is done clinically, and the patient would have to be very well monitored.

That said, though, interesting idea. Can you explain (on a psychological level) the mechanisms whereby MDMA might aid with this kind of "blocking?" Never experienced the stuff myself.

> As for free radical damage, there are MAOis but also other central antioxidants.

I hope you just mean selegiline (you *do* know what happens when you take a nonselective MAOI with MDMA, right? do we actually know this won't happen with selegiline? especially with an SSRI too?).

> I think selective MAO inhibitors will be their resurrection. Side effects and interactions are few(er) and rare, and efficacy in depression is being demonstrated. What do you think?

Not that you asked :), but I thought selegiline was much more difficult to tolerate than the nonselective MAOIs (I took it at high (nonselective) doses, though). It also did not work - doh. As for moclobemide, it has a rep in countries where it's used for not being particularly effective in the people who would be trying the irreversible MAOIs (those who've already tried a lot of other stuff). I also don't think, based on the stories I've heard from patients who've tried it, that it's really all that much more tolerable than the irreversible MAOIs.

Does anyone know what happened to clorgyline, though? Was it ever marketed for clinical use?

But anyway, I think it's more likely that the nonselective MAOIs will be resurrected as the "stigma" surrounding them (re the dietary restrictions, which it turns out have been overblown) vanishes.

 

Re: dangling threads from Parnate

Posted by Elizabeth on December 15, 1999, at 21:24:31

In reply to Adam: dangling threads from Parnate, posted by Zeke on December 15, 1999, at 20:53:30

(this subject: line makes it sound like the dangling threads were a side effect of Parnate!)

> is RIMA: Reversible Inhibitors of MonoAmine oxidase? or what???

Exactly.

> You know, my mother died of Alzheimer's last year. I unsucessfully tried to get the doctors to try deprenyl -- the last one seemed fearful of psychotic reactions. (They seemed to like the idea of neurolepticss widespite the toxicity of those drugs. BTW she had much less than typical agitation and positive symptoms.)

ARGH!!!!! I'm very sorry to hear this. (Misuse of neuroleptics in demented elderly patients is a big pet peeve of mine.)

> Anyway, you mention transdermals and I think that one other possibility we considered was the nicotine patches used for smoking cessation.

*Very* jittery for a nonsmoker!

 

Re: Hanging from a thread - E, Z...

Posted by Adam on December 15, 1999, at 22:44:55

In reply to Re: Parnate: weight gain, & the literature - Zeke, posted by Elizabeth on December 15, 1999, at 21:10:30

> I hope you just mean selegiline (you *do* know what happens when you take a nonselective MAOI with MDMA, right? do we actually know this won't happen with selegiline? especially with an SSRI too?).

Here's a review that addresses some of those issues:

Drug Saf 1998 Jul;19(1):11-22

Safety of selegiline (deprenyl) in the treatment of Parkinson's disease.

Heinonen EH, Myllyla V
Orion Pharma, CNS Drugs, Turku, Finland.

Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson's disease. As the first MAO-B inhibitor approved for the treatment of Parkinson's disease, concerns were raised about the safety of the drug based on the adverse effect profiles of older, nonselective MAO inhibitors. Unlike the nonselective MAO inhibitors, selegiline does not significantly potentiate tyramine-induced hypertension (the 'cheese effect') at the dosages (5 to 10 mg daily) used for the treatment of Parkinson's disease. Selegiline has been well tolerated when given alone. The most frequent adverse events seen during monotherapy have been insomnia, nausea, benign cardiac arrhythmias, dizziness and headache. When combined with levodopa, selegiline can potentiate the typical adverse effects of levodopa, if the dose of levodopa is not reduced sufficiently. Thus, the most common adverse effects associated with this combination are nausea, dizziness, fatigue, constipation and insomnia. At the later stages of Parkinson's disease when fluctuations in disability occur, peak dose dyskinesias, psychiatric complications like hallucinations and insomnia, and orthostatic hypotension are further potentiated by selegiline. Mortality was recently reported to be increased when selegiline and levodopa were given together in comparison with treatment with levodopa alone, but a large meta-analysis of 5 long term studies and 4 separate studies did not support this conclusion. Selegiline seems to be generally well tolerated in combination with other drugs. However, when pethidine (meperidine) has been given to patients who are receiving selegiline therapy, severe adverse effects have been reported. Thus, the concomitant use of these drugs is not recommended. A low tyramine diet is recommended if selegiline is used together with nonselective MAO inhibitors or the selective, reversible MAO-A inhibitor, moclobemide. Several adverse effects have been reported when fluoxetine and selegiline have been used together. A recent survey revealed that the incidence of a true serotonin syndrome is, however, very low with this combination. Concomitant use of selegiline and other selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors (SSRIs) like citalopram, which have generally less interactions than fluoxetine, seems to be well tolerated. Nevertheless, caution is advised when combining a SSRI or a tricyclic antidepressant and selegiline.


It seems like a lot of this talk about combining low-dose selegiline with MAOIs, RIMAs, SSRIs, etc., comes out of Finland. Maybe the habit of sitting in a 50+ deg. C sauna for as long as one can stand it, then jumping naked into a snow bank heightens their overall sense of adventure. Anyway, one particularly bad drug interaction that I've come across here and a couple other places is with meperidine (Demerol). I don't know if MDMA-induced 5-HT release is of the order caused by meperidine, but I get the feeling that even low-dose selegiline+MDMA could be unacceptably risky. I can't find any specific cases to support this, though. I don't imagine there are very many Parkinson's sufferer's doing E.


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