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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 7 of 7. This is the beginning of the thread.
Posted by g_g_g_unit on April 27, 2012, at 2:34:49
if there's anyone who happens to be reading who found benefit on Parnate for ADHD, did this occur at a certain dose? everyone in the archive seemed to be mega-dosing, i.e. 90+mg
Posted by g_g_g_unit on May 1, 2012, at 3:47:09
In reply to parnate and adhd, posted by g_g_g_unit on April 27, 2012, at 2:34:49
Scott, I've seen a couple of people in the archives (including Chairman_MAO) referring to Parnate's 'amphetamine-like' metabolites becoming active at a certain dose (I think 100mg+). Are you aware of any data backing this up, and how these metabolites might differ to the stimulant effect experienced at lower doses?
I feel like I'm at a bit of a crossroads. My psychiatrist is really happy that I'm experiencing an improvement in ADHD on Parnate, but from what I understand (according to board members etc. and also Dr Gilman), this 'stimulant' effect is more than likely going to disappear. The maximum he'll prescribe is 60mg and he won't co-administer a stimulant. Financially and logistically, trying to reach a 100mg+ dose on my own seems impossible. I e-mailed that TRD specialist and asked if he uses high-dose Parnate, but he has yet to reply.
Right now, I'm taking 40mg. I've been thinking about trying to add in Memantine to see if I can preserve the stimulant effect before I reach my target dose, but I am a little bit concerned about the moral conundrum of self-medicating. Is this something you have had to endure?
My other option would be to increase, slowly, to 60mg, under my psychiatrist's guidance and let him attend to the loss of any gains on the ADHD-front, though that thought leaves me somewhat depressed.
Posted by SLS on May 1, 2012, at 8:43:41
In reply to question for SLS, posted by g_g_g_unit on May 1, 2012, at 3:47:09
> Scott, I've seen a couple of people in the archives (including Chairman_MAO) referring to Parnate's 'amphetamine-like' metabolites becoming active at a certain dose (I think 100mg+).
Parnate (tranylcypromine) does a few things at higher dosages that it does not do at lower dosages. For instance, only high dosages downregulate 5-HT2a receptors - those that are blocked by amitriptyline, nortriptyline, Remeron, and atypical antipsychotics. It also downregulates tryptamine receptors. However, I don't know of anything that would suggest that high-dosage Parnate produces an amphetamine effect. It may. I found one report of Parnate overdose indicating that amphetamine was found in the blood stream. There has been a debate regarding the possibility of Parnate having amphetamine metabolites since its introduction in the 1960s. I don't know if there is a consensus yet.
I tried Parnate at higher dosages. I felt somewhat more energized and my head was clearer. I worked up to 150 mg/day and subsequently added d-amphetamine to it while also taking desipramine. Actually, adding desipramine to Parnate 60 mg might produce both an antidepressant effect and an anti-ADHD effect. Not too many doctors would be willing to do this.
> I feel like I'm at a bit of a crossroads. My psychiatrist is really happy that I'm experiencing an improvement in ADHD on Parnate, but from what I understand (according to board members etc. and also Dr Gilman), this 'stimulant' effect is more than likely going to disappear.
They might be talking about the subjective sense of activation rather than the persistence of an anti-ADHD effect. Do you feel activated when you take amphetamine chronically? If not, then perhaps the subjective feeling of activation is not necessary for Parnate to produce an enduring therapeutic effect. Unfortunately, there isn't much data using adults as subjects. Zametkin et al (1985) used it for children and found Parnate to be effective. In another study, Zametkin reported an immediate therapeutic effect of Parnate for ADHD and theorized that this indicated that it was the result of a different mechanism than that mediating antidepressant effects. I wish that I still had access to Len Adler. I could have asked him about Parnate for you.
If the anti-ADHD effects of Parnate poop-out on you, perhaps you could have your doctor look at guanfacine coadministration. It might produce some dizziness as a side effect, although this might abate over time. "On paper", the combination should not be toxic. However, I cannot know for sure as I could not find any evidence that the combination is ever used. Neither I could find any suggestions that the combination is unsafe. The PI makes no mention of MAOIs as a contraindicated substance.
- Scott
Posted by g_g_g_unit on May 2, 2012, at 8:35:49
In reply to Re: question for SLS » g_g_g_unit, posted by SLS on May 1, 2012, at 8:43:41
> Parnate (tranylcypromine) does a few things at higher dosages that it does not do at lower dosages. For instance, only high dosages downregulate 5-HT2a receptors - those that are blocked by amitriptyline, nortriptyline, Remeron, and atypical antipsychotics. It also downregulates tryptamine receptors. However, I don't know of anything that would suggest that high-dosage Parnate produces an amphetamine effect. It may. I found one report of Parnate overdose indicating that amphetamine was found in the blood stream. There has been a debate regarding the possibility of Parnate having amphetamine metabolites since its introduction in the 1960s. I don't know if there is a consensus yet.
Interesting. I just figured it would be worth keeping in mind as an option, permitting there was someone willing to prescribe it, and given my failure to respond to traditional psychostimulants. I think Dr Gilman told me that (working in a different state of Australia to the one I reside in) the highest dose he ever prescribed was approx. 120mg.
I suppose, though, that as with traditional amphetamine hypomania and/or tolerance is always a risk.
> I tried Parnate at higher dosages. I felt somewhat more energized and my head was clearer. I worked up to 150 mg/day and subsequently added d-amphetamine to it while also taking desipramine. Actually, adding desipramine to Parnate 60 mg might produce both an antidepressant effect and an anti-ADHD effect. Not too many doctors would be willing to do this.
Unfortunately, desipramine isn't available in Australia.
>
> > I feel like I'm at a bit of a crossroads. My psychiatrist is really happy that I'm experiencing an improvement in ADHD on Parnate, but from what I understand (according to board members etc. and also Dr Gilman), this 'stimulant' effect is more than likely going to disappear.
>
> They might be talking about the subjective sense of activation rather than the persistence of an anti-ADHD effect. Do you feel activated when you take amphetamine chronically? If not, then perhaps the subjective feeling of activation is not necessary for Parnate to produce an enduring therapeutic effect.Wow! You make a really interesting point. I tend to associate activation with attentional improvements, but I do know that my psychiatrist has said that tolerance to the sympathetic activity of d-amphetamine should develop relatively quickly, whereas cognitive benefits (and anxiety) remain.
Unfortunately, I never responded very well to d-amphetamine. It improved my 'focus', but left me feeling cloudy-headed in a way - like my thought processes were being suppressed. Today - 8 days on 40mg of Parnate - I noticed likewise that the sympathetic activation seems to have died down, but I experience a similar phenomenon involving a kind of 'cloudy' focus, if that makes sense. When highly activated/anxious, I am more alert, which tends to have more of a beneficial effect on my ADD symptoms. I've always suspected I'd respond well to Adderall, which I believe is more noradrenergic than d-amphetamine, but sadly it isn't available here.
>Unfortunately, there isn't much data using adults >as subjects. Zametkin et al (1985) used it for >children and found Parnate to be effective. In >another study, Zametkin reported an immediate >therapeutic effect of Parnate for ADHD and >theorized that this indicated that it was the >result of a different mechanism than that >mediating antidepressant effects. I wish that I >still had access to Len Adler. I could have asked >him about Parnate for you.
Well, that gives me some room for hope. Maybe higher doses - i.e. 60mg - will offer even more benefit. I'm very flattered by your offer. I suppose I should ask MY psychiatrist if he knows anything about MAOIs and ADHD, since he is an ADHD specialist; but he primarily trained with children, so I always suspected he never used MAOIs much.
>
> If the anti-ADHD effects of Parnate poop-out on you, perhaps you could have your doctor look at guanfacine coadministration. It might produce some dizziness as a side effect, although this might abate over time. "On paper", the combination should not be toxic. However, I cannot know for sure as I could not find any evidence that the combination is ever used. Neither I could find any suggestions that the combination is unsafe. The PI makes no mention of MAOIs as a contraindicated substance.
>
Unfortunately, Guanfacine isn't available here. However, Reboxetine is - and is completely safe to combine with Parnate, from what I understand.I did order some Memantine last night, regardless. Now I just have to wrestle with my own guilt over whether to try it or not without my psychiatrist's knowledge.
Posted by psychobot5000 on May 4, 2012, at 17:01:38
In reply to Re: question for SLS » SLS, posted by g_g_g_unit on May 2, 2012, at 8:35:49
Not that you asked, but in my opinion, there is no moral conundrum concerning self-medicating. Just health and safety conundrums, though it probably speaks well of you that you're still concerned about the ethics of it after dealing with the problem all this time.
Have you read this post on tranylcypromine and selegiline by Chairman MAO, from about six years back?
http://www.dr-bob.org/babble/20060304/msgs/617798.htmlYou're in rough straits over there for ADD--they won't co-prescribe a stimulant...and guanfacine and desipramine are both unavailable! Damn! What to do! Beyond reboxetine, one other thought is protriptyline, if they have it? It's supposed to be even more activating than desipramine, though I don't know that it's been vetted for ADD.
For what it's worth, I found tranylcypromine to have some activating and stimulant-like properties even at low doses like 30mg per day--and that was in marked contrast to phenelzine. Those stimulant properties never disappeared, though as my MAO inhibition increased, I ran up against the fuzzy, brain-fog feeling that all MAOis give me and which worked at cross-purposes to it. From your words about cloudiness, it sounds like you may be experiencing a small version of this phenomenon. If you deem this likely, my tentative advice would be to back off the dose before your active MAO levels go even lower, and the problem gets worse (as it did for me). In my experience, it seemed to be directly related to the level of [presumed] MAO inhibition in my body.
But, yeah, apologies for the meandering and unsolicited response. And protriptyline might be helpful with attention and activation. Its serotonin reuptake inhibition ought to be low enough they won't give you sh*t about serotonin syndrome when combining the two. There's some literature out there about that.
Posted by g_g_g_unit on May 6, 2012, at 8:20:55
In reply to Re: question for SLS, posted by psychobot5000 on May 4, 2012, at 17:01:38
> Not that you asked, but in my opinion, there is no moral conundrum concerning self-medicating. Just health and safety conundrums, though it probably speaks well of you that you're still concerned about the ethics of it after dealing with the problem all this time.
For what it's worth, I've one run self-directed trial (with Stablon), though I wasn't under the care of a psychiatrist at the time. I think the fact that I'm currently engaged in psychodynamic therapy with my psychiatrist - which emphasizes unfettered self-disclosure - might make the decision more difficult in this case. I don't feel like I'm betraying him as a psychiatrist, but I do feel like I'm betraying him as a therapist.
> Have you read this post on tranylcypromine and selegiline by Chairman MAO, from about six years back?
> http://www.dr-bob.org/babble/20060304/msgs/617798.htmlNo, I hadn't seen that.. very informative, thank you, and it also seems to provide due justification for exceeding 80mg as far as ADHD is concerned.
>
> You're in rough straits over there for ADD--they won't co-prescribe a stimulant...and guanfacine and desipramine are both unavailable! Damn! What to do! Beyond reboxetine, one other thought is protriptyline, if they have it? It's supposed to be even more activating than desipramine, though I don't know that it's been vetted for ADD.I just checked and it seems like protriptyline was discontinued several years back.
>
> For what it's worth, I found tranylcypromine to have some activating and stimulant-like properties even at low doses like 30mg per day--and that was in marked contrast to phenelzine. Those stimulant properties never disappeared, though as my MAO inhibition increased, I ran up against the fuzzy, brain-fog feeling that all MAOis give me and which worked at cross-purposes to it. From your words about cloudiness, it sounds like you may be experiencing a small version of this phenomenon. If you deem this likely, my tentative advice would be to back off the dose before your active MAO levels go even lower, and the problem gets worse (as it did for me). In my experience, it seemed to be directly related to the level of [presumed] MAO inhibition in my body.My experience echoes yours, i.e. phenelzine lacked anything in the way of psychostimulation. However, I simply found 30mg of Parnate to be too anxiogenic and never noticed any improvement in mood, other than the mysterious gains at night.
How long did you remain on higher doses of Parnate? Do you think it's possible the fogginess may have passed?
One interesting discovery - I've been using cyproheptadine as a sleep-aid for the past 2-3 nights. I believe it behaves as an antagonist at certain serotonin receptors (5-HT2a, 5-HT2b, 5-HTc). Through some mechanism - either improved sleep, or synergy between the Parnate and cyproheptadine - I've noticed a distinct return of the psychostimulant effect. Unfortunately, this is accompanied by an increase in compulsive behavior (due to the Serotonin antagonism, I presume?), so probably wouldn't be ideal as a long-term option, but it's made me question what's precisely causing the fuzziness.
>
> But, yeah, apologies for the meandering and unsolicited response. And protriptyline might be helpful with attention and activation. Its serotonin reuptake inhibition ought to be low enough they won't give you sh*t about serotonin syndrome when combining the two. There's some literature out there about that.
>
No need to apologize! I didn't find your post meandering or unsolicited and appreciate your input.
Posted by psychobot5000 on May 6, 2012, at 13:07:27
In reply to Re: question for SLS » psychobot5000, posted by g_g_g_unit on May 6, 2012, at 8:20:55
I've never actually used cyproheptadine. My surmise about these things, built from experience (with Geodon, Remeron, and agomelatine), a bit of research, and what other posters have told me, here, has indicated that while 5HT-2a antagonism can be good for mood, 5ht-2c activation seems to be sort of pleasantly stimulating in the short run, but is indeed bad for OCD after a few days. I generally found the body's response to its positive effects to attenuate during that period, also, presumably as it got used to the extra neurotransmission :(
Re: parnate, it's been a few years since I had my long trial with it. I went up and down a few times, but I don't really recall how long I stayed at 60 (I don't believe I went any higher). However, from long experience with it and with selegiline (as well as a briefer trial with phenelzine), I came to the conclusion that there was zero chance the cloudiness would ever abate, at least until I got off the medication or moved to a dose that was too small to be useful.
For what it's worth, the selegiline brain-fog was lighter and felt different--probably because I didn't take it in doses reputed to give substantial MAO-A inhibition. But that's getting farther afield.
This is the end of the thread.
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