![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 19 of 19. This is the beginning of the thread.
Posted by cache-monkey on April 21, 2005, at 12:24:24
Hey all,
So I'm considering trying low-dose selegiline for what I think are a cluster of symptoms related to low dopamine (smoking, ADD, past binge drinking, anhedonia, anergia).
However, selegiline metabolizes into a couple of amphetamites (l-amphetamine and l-methamphetamine). I've heard that these are the "bad" isomers of the drugs. What does that mean in terms of their CNS/periphery effects?
I'm particularly interested in l-methamphetamine, since, according to an in vivo study, this is substantially raised among poor CYP-2D6 metabolizers. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9797797&dopt=Abstract ... I'm an "intermediate" CYP-2D6 metabolizer, which is a lot closer to "poor" than to "extensive"/normal.]
Thanks!
cache-monkey
Posted by cache-monkey on April 22, 2005, at 11:39:39
In reply to Effects of Selegiline's amphetamine metabolites?, posted by cache-monkey on April 21, 2005, at 12:24:24
Posted by Larry Hoover on April 22, 2005, at 16:08:19
In reply to Effects of Selegiline's amphetamine metabolites?, posted by cache-monkey on April 21, 2005, at 12:24:24
> Hey all,
>
> So I'm considering trying low-dose selegiline for what I think are a cluster of symptoms related to low dopamine (smoking, ADD, past binge drinking, anhedonia, anergia).
>
> However, selegiline metabolizes into a couple of amphetamites (l-amphetamine and l-methamphetamine). I've heard that these are the "bad" isomers of the drugs. What does that mean in terms of their CNS/periphery effects?
>
> I'm particularly interested in l-methamphetamine, since, according to an in vivo study, this is substantially raised among poor CYP-2D6 metabolizers. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9797797&dopt=Abstract ... I'm an "intermediate" CYP-2D6 metabolizer, which is a lot closer to "poor" than to "extensive"/normal.]
>
> Thanks!
> cache-monkeyFirst off, the proportion of the selegiline that goes to these amphetamines is tiny. Really tiny. And it occurs over a period of time, so it's also a trickle. A tiny trickle.
I use selegiline myself, and I've also used amphetamines and meth (many years ago). I cannot find the slightest correspondence between the two experiences. Nor am I the least bit concerned about any toxic effects.
That's merely my opinion, of course.
Lar
Posted by christophrejmc on April 22, 2005, at 19:36:43
In reply to Effects of Selegiline's amphetamine metabolites?, posted by cache-monkey on April 21, 2005, at 12:24:24
> However, selegiline metabolizes into a couple of amphetamites (l-amphetamine and l-methamphetamine). I've heard that these are the "bad" isomers of the drugs. What does that mean in terms of their CNS/periphery effects?
L-amphetamine and l-methamphetamine primarily affect the peripheral nervous system (as opposed to the d- isomer which affects the CNS more), leading to side-effects like agitation, insomnia, hypertension, tachycardia, tremor, nausea, and anxiety (I do not know how frequent these side-effects are, you can check rxlist.com). These side-effects usually do not cause problems unless the dose is greater than 5mg.
From my experience, the most pronounced side-effect was insomnia, which did not cause me to discontinue use. The stimulation from the selegiline was comparable to a few too many cups of coffee. You'll want to avoid other stimulants like caffeine, nicotine, and nasal decongestants until you know how the medication will affect you (dietary restrictions are usually not required, but the drug interactions of the traditional MAOIs often apply).
I was smoking before I took selegiline and had no intention to quit, but I couldn't stand smoking while on it. The effect is really quite remarkable.
Good luck,
Chris
Posted by cache-monkey on April 23, 2005, at 13:15:42
In reply to Re: Effects of Selegiline's amphetamine metabolites? » cache-monkey, posted by Larry Hoover on April 22, 2005, at 16:08:19
Thanks Larry,
A few more questions... Are you using selegiline alone as an AD? Low-dose or high dose? What prompted you to go on it, as opposed to others? I'm assuming that your experience with it has been alright, given that you're still on it. But what has it been like for you?
Thanks,
cache-monkey>
> First off, the proportion of the selegiline that goes to these amphetamines is tiny. Really tiny. And it occurs over a period of time, so it's also a trickle. A tiny trickle.
>
> I use selegiline myself, and I've also used amphetamines and meth (many years ago). I cannot find the slightest correspondence between the two experiences. Nor am I the least bit concerned about any toxic effects.
>
> That's merely my opinion, of course.
>
> Lar
>
>
Posted by cache-monkey on April 23, 2005, at 13:23:25
In reply to Re: Effects of Selegiline's amphetamine metabolite » cache-monkey, posted by christophrejmc on April 22, 2005, at 19:36:43
<< L-amphetamine and l-methamphetamine primarily affect the peripheral nervous system (as opposed to the d- isomer which affects the CNS more), leading to side-effects like agitation, insomnia, hypertension, tachycardia, tremor, nausea, and anxiety (I do not know how frequent these side-effects are, you can check rxlist.com). These side-effects usually do not cause problems unless the dose is greater than 5mg. >>
Grr on the side effects. Anxiety, agitation and insomnia are a problem for me as it is. But I'm looking to possibly go on a mood stabilizer that's beneficial for those before starting an AD. Currently on Depakote. Not quite sure what the deal is right now, but if this doesn't work out maybe Seroquel would be a good way to counterbalance the selegiline in the evening.
<< I was smoking before I took selegiline and had no intention to quit, but I couldn't stand smoking while on it. The effect is really quite remarkable. >>
This is good to hear. I think I've been self-medicating a low-grade dysthymia with cigarettes for most of my adult life. I think that other than a mood-stabilizer, I'm looking for a light AD to a) treat my dysthymia and b) help me quit smoking. I didn't like Wellbutrin so much, and my pdoc is receptive to low-dose selegiline...
Anyway, thanks for the input!
Best,
cache-monkey
Posted by Larry Hoover on April 23, 2005, at 14:17:47
In reply to Re: Effects of Selegiline's amphetamine metabolites? » Larry Hoover, posted by cache-monkey on April 23, 2005, at 13:15:42
> Thanks Larry,
>
> A few more questions... Are you using selegiline alone as an AD? Low-dose or high dose? What prompted you to go on it, as opposed to others? I'm assuming that your experience with it has been alright, given that you're still on it. But what has it been like for you?
>
> Thanks,
> cache-monkeyActually, I use it p.r.n.
If I use it continuously, insomnia and acid reflux get too high. It's stimulant, without being buzzy. Antidepressant, yes, but more on the apathy and fatigue and depressed cognitive function.
I'm just bringing it back "online" after starting on gabapentin (for neuropathic pain). I wanted to understand the gabapentin all by itself, so I discontinued selegiline for about a month. So far, the combination is really good for me.
Before I took selegiline, I researched it thoroughly, and I could not find any evidence for anything other than theoretical risk....not in vivo risk.
I just keep my dose really low so I don't have to concern myself with MAO-A inhibition.
Lar
Posted by cache-monkey on April 23, 2005, at 21:55:43
In reply to Re: Effects of Selegiline's amphetamine metabolites? » cache-monkey, posted by Larry Hoover on April 23, 2005, at 14:17:47
Posted by Sarah T. on April 24, 2005, at 1:49:13
In reply to Effects of Selegiline's amphetamine metabolites?, posted by cache-monkey on April 21, 2005, at 12:24:24
Hi cache-monkey. First, I think that a lot depends on how sensitive you are to even minute amounts of medicines. Secondly, as Larry mentions on this thread, the amounts of the various amphetamines are small. Although selegiline does metabolize into several l-isomer amphetamines, they are NOT major metabolites. Contrast this with something like hydroxybupropion, which is a MAJOR metabolite of bupropion and is much more significant than the parent compound as far as effects and side effects are concerned.
Posted by cache-monkey on April 24, 2005, at 23:05:04
In reply to Re: Effects of Selegiline's amphetamine metabolites? » cache-monkey, posted by Sarah T. on April 24, 2005, at 1:49:13
<< Contrast this with something like hydroxybupropion, which is a MAJOR metabolite of bupropion and is much more significant than the parent compound as far as effects and side effects are concerned. >>
Interestingly enough, I had kind of a bad response (agitation, anxiety, ruminations) to Wellbutrin. I'm wondering if this has something to do with hydroxybupropion, which I metabolize slowly (CYP-2D6). Do you know anything more specific about the (side) effects of hydroxybupropion?
Thanks,
cache-monkey
Posted by Sarah T. on April 25, 2005, at 2:16:23
In reply to Re: Effects of Selegiline's amphetamine metabolites? » Sarah T., posted by cache-monkey on April 24, 2005, at 23:05:04
Hi cache-monkey. All I know about buproprion is that I was on it for a long time, and I had terrible insomnia, high blood pressure, palpitations and anxiety, in spite of what the drug company literature advertised at that time. I also know that, among other things, bupropion is a potent inhibitor of the 2D6 liver enzyme, and that hydroxybupropion is a substrate of that same enzyme. In the other words, the drug inhibits its own metabolism! If you happen to have a fairly robust version of that enzyme in your liver, then I guess you can handle the medicine well. On the other hand, if you're like me (a poor metabolizer), then taking a drug that inhibits its own metabolism is going to be very unpleasant, if not downright dangerous.
Posted by chemist on April 25, 2005, at 10:32:29
In reply to Re: Effects of Selegiline's amphetamine metabolites? » cache-monkey, posted by Sarah T. on April 25, 2005, at 2:16:23
> Hi cache-monkey. All I know about buproprion is that I was on it for a long time, and I had terrible insomnia, high blood pressure, palpitations and anxiety, in spite of what the drug company literature advertised at that time. I also know that, among other things, bupropion is a potent inhibitor of the 2D6 liver enzyme, and that hydroxybupropion is a substrate of that same enzyme. In the other words, the drug inhibits its own metabolism! If you happen to have a fairly robust version of that enzyme in your liver, then I guess you can handle the medicine well. On the other hand, if you're like me (a poor metabolizer), then taking a drug that inhibits its own metabolism is going to be very unpleasant, if not downright dangerous.
hello there, chemist here...bupropion is a major substrate of the cyp-2B6 isoenzyme, and a weak inhibitor of 2D6. the 3 active metabolites are reported to exhibit activities rangin from 20% to 50% or the parent compound. the drug does not inhibit its own metabolism, nor does it autoinduce. the majority of drugs are metabolized (those that go the hepatic route) by the 2D6 isoenzyme, and if you are caucasian, there is a 7 to 10% chance your are a poor-metabolizer in re: the 2D6. the metabolic route for bupropion is via phase I, and the hydroxy derivative is half as active as the parent and, further, is metabolized by the 2B6 (not 2D6). given the large difference in K_{i}, it is unlikely though possible that some competitive binding is at play, although a more reasonable scenario is that use of another drug with similar affinity for 2B6 - paroxetine, sertraline, theophylline etc. - is responsible for increased serum concentration of the parent and the adverse effects associated with the increase...all the best, chemist
Posted by cache-monkey on April 25, 2005, at 13:52:05
In reply to Re: Effects of Selegiline's amphetamine metabolite » Sarah T., posted by chemist on April 25, 2005, at 10:32:29
> hello there, chemist here...bupropion is a major substrate of the cyp-2B6 isoenzyme, and a weak inhibitor of 2D6. the 3 active metabolites are reported to exhibit activities rangin from 20% to 50% or the parent compound. the drug does not inhibit its own metabolism, nor does it autoinduce. the majority of drugs are metabolized (those that go the hepatic route) by the 2D6 isoenzyme, and if you are caucasian, there is a 7 to 10% chance your are a poor-metabolizer in re: the 2D6. the metabolic route for bupropion is via phase I, and the hydroxy derivative is half as active as the parent and, further, is metabolized by the 2B6 (not 2D6). given the large difference in K_{i}, it is unlikely though possible that some competitive binding is at play, although a more reasonable scenario is that use of another drug with similar affinity for 2B6 - paroxetine, sertraline, theophylline etc. - is responsible for increased serum concentration of the parent and the adverse effects associated with the increase...all the best, chemist
>Hi chemist,
Thanks for chiming in here. I've read in a couple of places [eg: 1,2] that hydroxybupropion (HB) is or could be a substrate of 2D6.
Further, according to a recent article in Molecular Pharmacology [3]: "bupropion is extensively metabolized to (2S,3R)- and (2S,3S)-hydroxybupropion ... . The concentrations of hydroxybupropion isomers present in cerebrospinal fluid are six times greater than those of the parent bupropion ... . Although it has weak NE-uptake properties, the high levels of the metabolite in brain may be sufficient to produce clinically meaningful blockade of NE reuptake and thereby account for much of the drug's activity. Indeed, plasma levels of hydroxybupropion greatly exceed those of the parent drug, reaching 10 to 100 times the concentration of bupropion ... ."
The authors go on to characterize the affinities of bupropion and the HB metabolites, yielding:
===========================================================
Values given are mean ± S.D., IC50s reported in nMdrug..............[3H]DA.........[3H]NE
Bupropion.........550 ± 65.......1900 ± 12
(2S,3S)-HB........790 ± 11.......520 ± 35
(2R,3R)-HB........>10,000........>10,000
===========================================================
source: [3]Consequently, in steady state the NE effects of HB are likely to dominate the DA effects of BUP+HB. This is potentially bad for people like me (and possibly Sarah T?) who don't like ther NE system to be trucked with. There also seems to be significant inter-individual variation in the ratio of HB to BUP [2]. Finally, adding on a poor CYP-2D6 metabolic status, and the reaction is worse.
Best,
cache-monkey1. http://www.postgradmed.com/issues/1999/11_99/cadieux.htm
2. Pollock BG, Sweet RA, Kirschner M, Reyolds CF. "Bupropion plasma levels and CYP2D6 phenotype." Ther Drug Monit 1996; 18:581-585.
3. M. Imad Damaj, F. Ivy Carroll, J. Brek Eaton, Hernan A. Navarro, Bruce E. Blough, Sadiq Mirza, Ronald J. Lukas, and Billy R. Martin. "Enantioselective Effects of Hydroxy Metabolites of Bupropion on Behavior and on Function of Monoamine Transporters and Nicotinic Receptors." Mol Pharmacol 2004 66: 675-682.
Posted by Sarah T. on April 25, 2005, at 19:53:32
In reply to Re: Effects of Selegiline's amphetamine metabolite » Sarah T., posted by chemist on April 25, 2005, at 10:32:29
Hello, chemist. It's good to see you again. Thanks for the information. I do want to mention, however, that I got the information I provided above from a very reliable source, a drug interaction guide that I read about in a psychiatric journal. This thread is not the first time I have found different information (different liver enzymes) listed for the same drug.
Posted by chemist on April 25, 2005, at 20:31:02
In reply to Re: Effects of Selegiline's amphetamine metabolite » chemist, posted by cache-monkey on April 25, 2005, at 13:52:05
> > hello there, chemist here...bupropion is a major substrate of the cyp-2B6 isoenzyme, and a weak inhibitor of 2D6. the 3 active metabolites are reported to exhibit activities rangin from 20% to 50% or the parent compound. the drug does not inhibit its own metabolism, nor does it autoinduce. the majority of drugs are metabolized (those that go the hepatic route) by the 2D6 isoenzyme, and if you are caucasian, there is a 7 to 10% chance your are a poor-metabolizer in re: the 2D6. the metabolic route for bupropion is via phase I, and the hydroxy derivative is half as active as the parent and, further, is metabolized by the 2B6 (not 2D6). given the large difference in K_{i}, it is unlikely though possible that some competitive binding is at play, although a more reasonable scenario is that use of another drug with similar affinity for 2B6 - paroxetine, sertraline, theophylline etc. - is responsible for increased serum concentration of the parent and the adverse effects associated with the increase...all the best, chemist
> >
>
> Hi chemist,
>
> Thanks for chiming in here. I've read in a couple of places [eg: 1,2] that hydroxybupropion (HB) is or could be a substrate of 2D6.
>
> Further, according to a recent article in Molecular Pharmacology [3]: "bupropion is extensively metabolized to (2S,3R)- and (2S,3S)-hydroxybupropion ... . The concentrations of hydroxybupropion isomers present in cerebrospinal fluid are six times greater than those of the parent bupropion ... . Although it has weak NE-uptake properties, the high levels of the metabolite in brain may be sufficient to produce clinically meaningful blockade of NE reuptake and thereby account for much of the drug's activity. Indeed, plasma levels of hydroxybupropion greatly exceed those of the parent drug, reaching 10 to 100 times the concentration of bupropion ... ."
>
> The authors go on to characterize the affinities of bupropion and the HB metabolites, yielding:
> ===========================================================
> Values given are mean ± S.D., IC50s reported in nM
>
> drug..............[3H]DA.........[3H]NE
>
> Bupropion.........550 ± 65.......1900 ± 12
> (2S,3S)-HB........790 ± 11.......520 ± 35
> (2R,3R)-HB........>10,000........>10,000
> ===========================================================
> source: [3]
>
> Consequently, in steady state the NE effects of HB are likely to dominate the DA effects of BUP+HB. This is potentially bad for people like me (and possibly Sarah T?) who don't like ther NE system to be trucked with. There also seems to be significant inter-individual variation in the ratio of HB to BUP [2]. Finally, adding on a poor CYP-2D6 metabolic status, and the reaction is worse.
>
> Best,
> cache-monkey
>
> 1. http://www.postgradmed.com/issues/1999/11_99/cadieux.htm
> 2. Pollock BG, Sweet RA, Kirschner M, Reyolds CF. "Bupropion plasma levels and CYP2D6 phenotype." Ther Drug Monit 1996; 18:581-585.
> 3. M. Imad Damaj, F. Ivy Carroll, J. Brek Eaton, Hernan A. Navarro, Bruce E. Blough, Sadiq Mirza, Ronald J. Lukas, and Billy R. Martin. "Enantioselective Effects of Hydroxy Metabolites of Bupropion on Behavior and on Function of Monoamine Transporters and Nicotinic Receptors." Mol Pharmacol 2004 66: 675-682.hello there, chemist here...please pardon my jumping in on your thread...the question i have in mind is what you address in noting the selectivity for the diastereomeric pairs (ref [3])...the IC50 values for the (2S,3S) and (2S,3R) HB metabolites in the mol. pharm. article are striking, yet mimic what we see with alpha4beta2 and alpha7 nAChR specificity for nicotine and derivatives (they ``like'' (S)). given the stereospecificity of (excuse my lapse in enzymology here and elsewhere!) almost all enzymes we have categorized, is it likely that your HB diastereomers are ``victims'' of induced fit for the 2D6 after the tert-butyl group is removed? this does leave a nitrogen that is attractive to 2D6, while the bulk of the t-butyl is absent...assuming the beta-hydroxylation is followed by a leaving t-butyl and demethylation, we are looking at something darned close to epi...your thoughts and guidance requested, if you please, as i ought to be set straight and am in the dark at the moment.....thanks much, and all the best, chemist
Posted by chemist on April 25, 2005, at 20:35:21
In reply to Re: Effects of Selegiline's amphetamine metabolite » chemist, posted by Sarah T. on April 25, 2005, at 19:53:32
> Hello, chemist. It's good to see you again. Thanks for the information. I do want to mention, however, that I got the information I provided above from a very reliable source, a drug interaction guide that I read about in a psychiatric journal. This thread is not the first time I have found different information (different liver enzymes) listed for the same drug.
hello there sarah....appears as if i was writing as you were posting...thank cache-monkey, and have a look at my more thoughtful pondering in re: increased affinity by 2D6 after metabolism via 2B6.....do let me (and the others) know, if you please, as i am clearly missing some marbles here! best, chemist
Posted by cache-monkey on April 26, 2005, at 1:16:18
In reply to Re: Effects of Selegiline's amphetamine metabolite » cache-monkey, posted by chemist on April 25, 2005, at 20:31:02
<< hello there, chemist here...please pardon my jumping in on your thread >>
Hi Chemist,
Wouldn't say you were jumping in. Up thread a ways (where I was asking about selegiline) I waved a flag for you!I'm not a pharmacologist, or a chemist for that matter. I'm just starting to get a basic understanding of how the balance between various drugs and their metabolites are going to affect me. (I have to be a little more careful than most since I am an "intermediate" -- a lot closer to "poor" than "extensive" -- CYP-2D6 metabolizer.)
So, unfortunately the rest of your post is a bit above my head. Sorry I can't be of more help!
Best,
cache-monkey
...the question i have in mind is what you address in noting the selectivity for the diastereomeric pairs (ref [3])...the IC50 values for the (2S,3S) and (2S,3R) HB metabolites in the mol. pharm. article are striking, yet mimic what we see with alpha4beta2 and alpha7 nAChR specificity for nicotine and derivatives (they ``like'' (S)). given the stereospecificity of (excuse my lapse in enzymology here and elsewhere!) almost all enzymes we have categorized, is it likely that your HB diastereomers are ``victims'' of induced fit for the 2D6 after the tert-butyl group is removed? this does leave a nitrogen that is attractive to 2D6, while the bulk of the t-butyl is absent...assuming the beta-hydroxylation is followed by a leaving t-butyl and demethylation, we are looking at something darned close to epi...your thoughts and guidance requested, if you please, as i ought to be set straight and am in the dark at the moment.....thanks much, and all the best, chemist
Posted by chemist on April 26, 2005, at 2:25:52
In reply to Re: Effects of Selegiline's amphetamine metabolite » chemist, posted by cache-monkey on April 26, 2005, at 1:16:18
well, your ``basic'' understanding is quite impressive! i just opined in re: your selegiline query...and i do thank you and sarah t. and larry - always! - for setting me straight...all the best, chemist
> << hello there, chemist here...please pardon my jumping in on your thread >>
>
> Hi Chemist,
> Wouldn't say you were jumping in. Up thread a ways (where I was asking about selegiline) I waved a flag for you!
>
> I'm not a pharmacologist, or a chemist for that matter. I'm just starting to get a basic understanding of how the balance between various drugs and their metabolites are going to affect me. (I have to be a little more careful than most since I am an "intermediate" -- a lot closer to "poor" than "extensive" -- CYP-2D6 metabolizer.)
>
> So, unfortunately the rest of your post is a bit above my head. Sorry I can't be of more help!
>
> Best,
> cache-monkey
>
>
> ...the question i have in mind is what you address in noting the selectivity for the diastereomeric pairs (ref [3])...the IC50 values for the (2S,3S) and (2S,3R) HB metabolites in the mol. pharm. article are striking, yet mimic what we see with alpha4beta2 and alpha7 nAChR specificity for nicotine and derivatives (they ``like'' (S)). given the stereospecificity of (excuse my lapse in enzymology here and elsewhere!) almost all enzymes we have categorized, is it likely that your HB diastereomers are ``victims'' of induced fit for the 2D6 after the tert-butyl group is removed? this does leave a nitrogen that is attractive to 2D6, while the bulk of the t-butyl is absent...assuming the beta-hydroxylation is followed by a leaving t-butyl and demethylation, we are looking at something darned close to epi...your thoughts and guidance requested, if you please, as i ought to be set straight and am in the dark at the moment.....thanks much, and all the best, chemist
>
>
Posted by Elroy on April 27, 2005, at 16:48:12
In reply to Re: Effects of Selegiline's amphetamine metabolites? » cache-monkey, posted by Larry Hoover on April 23, 2005, at 14:17:47
Just started selegiline at low dose. Prescription is for 5mg but I'm actually starting at 2.5 mg (half tablet). Testing showed my norepinephrine levels to be really low (like 26 pg/ml with a reference range of 80 - 520). Worse it seems that my body has "adjusted" to those low levels and that any major boost of NE (Effexor, Cymbalta, higher dose tyrosine, higher dose DLPA, intense exercise, etc.) cause a serious increase in anxiety, neuropathy type pains and bring on severe prostatitis type symptoms.
Like Larry, am also on Neurontin for the neuropathy type pains, but am hopeful to get on to Lrica instead if it ever gets released to the US market.
Additionally, am on Ambien for sleep aid and Xanax XR for anxiety.
X
X
X
X
> Actually, I use it p.r.n.
>
> If I use it continuously, insomnia and acid reflux get too high. It's stimulant, without being buzzy. Antidepressant, yes, but more on the apathy and fatigue and depressed cognitive function.
>
> I'm just bringing it back "online" after starting on gabapentin (for neuropathic pain). I wanted to understand the gabapentin all by itself, so I discontinued selegiline for about a month. So far, the combination is really good for me.
>
> Before I took selegiline, I researched it thoroughly, and I could not find any evidence for anything other than theoretical risk....not in vivo risk.
>
> I just keep my dose really low so I don't have to concern myself with MAO-A inhibition.
>
> Lar
This is the end of the thread.
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