![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 22 to 46 of 52. Go back in thread:
Posted by psychobot5000 on December 22, 2008, at 10:56:32
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl, posted by linkadge on December 21, 2008, at 22:34:13
Hi Link,
>
> I wonder if a 5-ht2c agonist antidepressant would have psychedelic properties?Like in that pilot study indicating psilocybin had a positive acute effect on OCD symptoms? I knew a guy with severe OCD who continually self-medicated with psilocybin mushrooms, by the way. At least that was my interpretation of his situation...
> A 5-ht2c agonist might have more application in depression associated with hyperactive frontal cortex function (for instance OCD/Depression). A 5-ht2c agonist might also work well with atypical depression depression that is associated with overeating etc.
So is OCD thought to be related to frontal cortex overactivity? (I have both OCD and severe difficulty with executive function...so I'm very curious...) It's worth mentioning, that (I read in one article) some patients find Remeron (5HT2c antagonist, no?) highly effective for OCD symptoms. I also found this to be the case from my personal experience. Any ideas what might explain the (apparent) paradox that both 5HT2c agonists and antagonists can be effective on OCD? Granted, mirtazipine (like most antidepressants) takes several days to have its positive effects, whereas presumably psilocybin gives its benefits almost immediately, when the user takes them, leaving open the question of whether mirtazipine's positive effects are due to some sort of re-regulation... But should one look to the medications' effects on other targets as well (i.e. 5HT-2a)? How well understood is the 5HT-2c link?
(and if frontal cortex activation is bad for OCD...what is someone like myself with both OCD and cognitive dysfunction/executive dysfunction supposed to do, I wonder?)
I'd be very curious to hear any insight anyone might have, of course. I suppose the practical answer to such questions is: take agomelatine and see what happens. But it sure is all confusing.
Psychbot
Posted by desolationrower on December 22, 2008, at 12:32:52
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » linkadge, posted by psychobot5000 on December 22, 2008, at 10:56:32
IIRC 5ht2c also exhibits downregulation in the face of both agonism and antagonism. I think there was some evidence some of the psychedelics exhibit functional agonism at 5ht2a at least; my suspicion is that a number of drugs acting at ht52 receptors have these complicated actions; it woudl explain some of the contradictory findings. So i'd be quite wary of drawing conclusion of what one drug will do based on what another one does at this receptor. It doesn't seem this set of recptors is very well understood yet. lots of clues, not many real maps. Lots of info in this thread.
-d/r
Posted by linkadge on December 22, 2008, at 14:05:59
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » linkadge, posted by psychobot5000 on December 22, 2008, at 10:56:32
>So is OCD thought to be related to frontal >cortex overactivity? (I have both OCD and severe >difficulty with executive function...so I'm very >curious...)
Generally yes, but it may depend on the nature of the OCD. If it is more rumanative, then there may not be frontal hyperactivity. If your OCD involves repetitive motor behaviors then perhaps this is associated with hyperactivity.
OCD and attention problems can certainly coexist and then it is probably more complex.
I do know that 5-ht1a receptor stimulation apparently has some anti-OCD effects. Remeron indirectly increases 5-ht1a receptor activity through the alpha-2 antagonism which may mediate some effects in OCD. I do know that in some studies potent and selective 5-ht2a/c antagonists can abololish or greatly reduce the anti OCD effects of SSRI's.
>It's worth mentioning, that (I read in one >article) some patients find Remeron (5HT2c >antagonist, no?) highly effective for OCD >symptoms. I also found this to be the case from >my personal experience.Remeron is not generally a first line OCD medication, but you are right there are case reports of it both improving (and worsening OCD). Remeron can have strong anxolytic effects which may indrectly improve OCD. Also, the enhanced 5-ht1a receptor stimulation could underly a theraputic effect in OCD.
>(and if frontal cortex activation is bad for >OCD...what is someone like myself with both OCD >and cognitive dysfunction/executive dysfunction >supposed to do, I wonder?)Again its hard to say. Activating the frontal cortex can actually supress certain limbic activity. I think there are probably subtle different neurobiological underpinnings of varients in OCD.
Do you mind me asking if your OCD is more classic (i.e. specific obsessions with associated specific behaviors indented to prevent the behaviors) or more ruminative?
Linkadge
Posted by psychobot5000 on December 22, 2008, at 19:27:55
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl, posted by linkadge on December 22, 2008, at 14:05:59
> Again its hard to say. Activating the frontal cortex can actually supress certain limbic activity. I think there are probably subtle different neurobiological underpinnings of varients in OCD.
>
>
> Do you mind me asking if your OCD is more classic (i.e. specific obsessions with associated specific behaviors indented to prevent the behaviors) or more ruminative?
>
>
> Linkadge
>
>Not at all, and thanks for all your thoughts. I suppose my personal OCD symptoms are mixed, including both behavioral and ruminative aspects--and both entangled with other anxiety symptoms. A bit of a mess, like many of us here, of course.
But, re 5HT2c and frontal cortex dopamine, I've decided to take some heart from the fact that stimulants (dexamph and methylphenidate) never made my OCD worse. So perhaps in my case increased stimulation of the frontal cortex would be fine, and there would be no conflict with improving executive function.
I didn't know that remeron/mirtazipine made some patients' OCD worse. Perhaps it's as you say, that Remeron only helps largely by reducing anxiety in-general (it did do that in my case). I wonder if ritanserin might have had similar beneficial effects on anxiety, without some of Remeron's drawbacks (sedation etc)--I suppose we'll never know). But with any luck, pharmacologists will get some helpful tools from the small slew of 5ht2 affecting meds in the pipeline.
Psychbot
Posted by linkadge on December 22, 2008, at 20:55:59
In reply to Re: 5HT(2c), remeron and etc » linkadge, posted by psychobot5000 on December 22, 2008, at 19:27:55
Remeron has some opioid like effects. Opiates also have some anti-ocd effects.
Here's one study with ritanserin reversing some ocd effects of fluvoxamine.
http://www3.interscience.wiley.com/journal/109711247/abstract
A study demonstrating an upregulation of 5-ht2c receptors in OCD.
http://www.leaddiscovery.co.uk/articles/18533183
[Although, as mentioned, some 5-ht receptor antagonists also downregulate 5-ht receptors]
You've probably seen this article on psilocybin in OCD:
http://www.maps.org/research/psilo/azproto.html
There is a high density of 5-ht2a/c receptors in the caudate neucleus which acts as a gate between the frontal cortex and hypothalamus. OCD may be associated with less grey matter in this region to regulate crosstalk and that 5-ht receptor modulators somehow improve the functionality of this circuit.
Low doses of risperidal reduce OCD but higher doses increase it. Some effect on 5-ht2 receptor saturation?
http://www.springerlink.com/content/bdqt1fde2jqgf4h0/
Anyhow, there are only leads. There is nothing conclusive.Linkadge
Posted by SLS on December 23, 2008, at 7:16:15
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » SLS, posted by Marty on December 21, 2008, at 15:08:00
Hi Marty.
Interesting.
http://www.nature.com/npp/journal/v28/n2/full/1300057a.html
To produce a treatment - whether monotherapy or polypharmacy - that will inhibit the reuptake of 5-HT and simultaneously antagonize 5-HT2a and 5-HT2c receptors in the absence of DA antagonism might be ideal to treat depression.
I hate when researchers feel it necessary to search for a single molecule that will combine all the relevant mechanisms of action. Just give us multiple drugs that are highly specific, complementary, and synergistic.
- Scott
Posted by Marty on December 23, 2008, at 9:14:46
In reply to Re: 5HT(2c), remeron and etc, posted by linkadge on December 22, 2008, at 20:55:59
Linkage is in fire or what ? :) Very interesting collection of abstract Link, I'm bookmarking some for latter.What is your opinion regarding antagonizing 5-HT2a and 5-HT2c at the same time (without -DA) ? I think you find it counter intuitive, right ?
/\/\arty
Posted by linkadge on December 23, 2008, at 9:35:47
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » Marty, posted by SLS on December 23, 2008, at 7:16:15
Theres more than that which could be considered ideal.
For instance, there are some compounds with 5-ht uptake inhibition and 5-ht1a/b autoreceptor antagonism which apprently bypass the need for long term drug administration to desensitize these receptors.
If you take into acount the mood modulating effects of all 5-ht receptors you'd have some agent which might do the following:5-ht1a/b post synaptic agonism
5-ht1a/b autoreceptor antagonism
5-ht2a/c antagonism
5-ht3 antagonism
5-ht4 agonism
5-ht7 antagonism+ 5-ht uptake inhibition (or not)
etc. etc.
(but I still don't think that 5-ht uptake inhibition is at all relatant to the antidepressant effects of SSRI's.Linkadge
Posted by SLS on December 23, 2008, at 9:38:23
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » Marty, posted by SLS on December 23, 2008, at 7:16:15
> Interesting:
> http://www.nature.com/npp/journal/v28/n2/full/1300057a.html
> To produce a treatment - whether monotherapy or polypharmacy - that will inhibit the reuptake of 5-HT and simultaneously antagonize 5-HT2a and 5-HT2c receptors in the absence of DA antagonism might be ideal to treat depression.Oops.
I managed to overlook the role that 5-HT2c receptors are suggested to play. The authors conclude that 5-HT2c agonism, and not antagonism, can act as a synergist to SRIs.
Geodon is an interesting drug. I didn't think much of it as an antidepressant augmenter when it first appeared. However, I have come to believe that it possesses an array of properties, including selective 5-HT2a receptor antagonism, that serves to explain its antidepressant properties. It really is the most antidepressant-like of the neuroleptic antipsychotics. I've seen it work wonders in TRD when added to a combination of Lexapro and Wellbutrin.
Antidepressant properties of Geodon:
5-HT1a agonist ++
5-HT1d antagonist
5-HT2a antagonist +++
NE reuptake inhibition
5-HT reuptake inhibition
- Scott
Posted by linkadge on December 23, 2008, at 9:42:05
In reply to Oops., posted by SLS on December 23, 2008, at 9:38:23
I made a typo in the following:
>Apparently 5-ht2c agonism decreases the >responsiveness of postsynaptic 5-ht2b receptors >which are involved in reward function and >certain spatial memory functions.
Which should read:
Apparently 5-ht2c agonism decreases the responsiveness of postsynaptic *5-ht1b* receptors which are involved in reward function and certain spatial memory functions.
Posted by Marty on December 23, 2008, at 9:51:29
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » Marty, posted by SLS on December 23, 2008, at 7:16:15
> Interesting.
>http://www.nature.com/npp/journal/v28/n2/full/130>0057a.htmlYes, great paper indeed. Makes me think the team who develop Trazodone were on a good track: 5-HT2a antagonist, 5-HT2c agonist (via m-CPP) AND some SRI. If it wasn't of the side effects, in particular the hangover, and if the SRI was stronger it could be an awesome antidepressant if you embrace the thesis discussed in your paper.
That, said I wonder if my Agomelatine/Trazodone combo isn't working against each other in some way s while being completive in others. That paper suggest it would somehow, or did I badly interpret ? (I just woke up, my eyes are still glued)
Something happened yesterday that made me wonder even more: I took Agomelatine and .25mg Clonazepam but forgot to take my other meds (Trazo, Wellbutrin, Lamictal, Chromium).. 1 hour later I feel good and go to bed. Time pass by and I'm still not sleeping completely (unusual for me) but I wasn't caring because I was feeling GREAT.. even better than since I started Agomelatine. After a while I got up to go to the bathroom and realized how terrific I was feeling and when going back to my bed I saw on my desk the pills I forgot to take... and so I took them. This morning I wake up feeling not that great.. just normal hangover from Trazo and while I want to go out of the bed and do something of my day (this wasn't the case before Agomelatine) I don't feel excited about life like I do when I take Agomelatine alone...
While I strongly believe the thesis of the paper you sent me, my beliefs in my Ago/Trazo combo are shaky right now. I'm wondering if I should try reducing Trazodone .. in the last 3 days I realized my Agomelatine miracle wasn't 'constant' (consistency of Ago effect is a recurring theme in discussion between people who are currently on it BTW)
I scratch my head over this today. If you have an opinion whatsoever, even if the strong, I'm interested.
> To produce a treatment - whether monotherapy or >polypharmacy - that will inhibit the reuptake of >5-HT and simultaneously antagonize 5-HT2a and 5->HT2c receptors in the absence of DA antagonism >might be ideal to treat depression.I think it's a great strategy for a lot of people. But I'm still not sure about which are the best complement to 5-HT2a antagonism.. 5-HT2c antagonism OR agonism ? Linkage seems to eat for breakfast the right kind of papers lately to express an interesting opinion. I've ask him in my last post on this thread. What about yours ?
> I hate when researchers feel it necessary to
>search for a single molecule that will combine
>all the relevant mechanisms of action. Just give
>us multiple drugs that are highly specific,
>complementary, and synergistic.So do I. I wish our 'drug palette' would be more complete and specific. I feel the day we'll have the likes of 5-HT5/6/7 agonists, for example, developed and marketed is far, far away.
/\/\arty
Again, sorry for the long post.. hope you're good are reading diagonally. ;)
Posted by SLS on December 23, 2008, at 10:30:08
In reply to Re: Oops., posted by linkadge on December 23, 2008, at 9:42:05
> Apparently 5-ht2c agonism decreases the responsiveness of postsynaptic *5-ht1b* receptors which are involved in reward function and certain spatial memory functions.
Hmm.
Are these heteroreceptors?
- Scott
Posted by linkadge on December 23, 2008, at 11:14:25
In reply to Re: Oops. » linkadge, posted by SLS on December 23, 2008, at 10:30:08
No, I don't think so.
http://www.ihop-net.org/UniPub/iHOP/pm/718965.html?nr=2&pmid=8863849
Linkadge
Posted by linkadge on December 23, 2008, at 11:16:40
In reply to Re: Oops. » linkadge, posted by SLS on December 23, 2008, at 10:30:08
Here's another study:
http://www.ihop-net.org/UniPub/iHOP/pm/7983944.html?nr=4&pmid=7935328
You can probably find more info too on ihop.
http://www.ihop-net.org/UniPub/iHOP/gs/89250.html
Linkadge
Posted by desolationrower on December 23, 2008, at 11:18:32
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » Marty, posted by SLS on December 23, 2008, at 7:16:15
> Hi Marty.
>
> Interesting.
>
> http://www.nature.com/npp/journal/v28/n2/full/1300057a.html
>
> To produce a treatment - whether monotherapy or polypharmacy - that will inhibit the reuptake of 5-HT and simultaneously antagonize 5-HT2a and 5-HT2c receptors in the absence of DA antagonism might be ideal to treat depression.
>
> I hate when researchers feel it necessary to search for a single molecule that will combine all the relevant mechanisms of action. Just give us multiple drugs that are highly specific, complementary, and synergistic.
>
>
> - Scottit sort of goes to many parts of the industry - fda wants a drug that is more effective than other treatments, not just part of a an effective coctail. And doctors want to prescibe one drug not polypharmacy. And the pharm companies don't want a drug that only works when taken with their competitor's drug.
also marty, how has the agometaline affected weight/appetite/metabolism?
I hope researchers beging to look at conditional effects of recptors more as i don't think the always have simple linear reltaionship: MORE agonism=MORE activation or whatever. I would like if there was a wiki database of research - as a researcher publishes their study, they must update the encyclopedia - less to create articles, but to have references to the relevant research. I'm sure there are many problems with such an idea.
-d/r
Posted by psychobot5000 on December 23, 2008, at 12:08:43
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » Marty, posted by SLS on December 23, 2008, at 7:16:15
>
> To produce a treatment - whether monotherapy or polypharmacy - that will inhibit the reuptake of 5-HT and simultaneously antagonize 5-HT2a and 5-HT2c receptors in the absence of DA antagonism might be ideal to treat depression.
>
> I hate when researchers feel it necessary to search for a single molecule that will combine all the relevant mechanisms of action. Just give us multiple drugs that are highly specific, complementary, and synergistic.
>
>
> - ScottI agree (for what that's worth)--that would allow for more flexible and specific treatment for those of us who are resistant, while presumably also making drug development easier. However, I would suggest that almost any agent with significant serotonin reuptake inhibition would not be 'ideal,' (even assuming Linkadge is wrong and it -is- a significant AD mechanism), simply because the mechanism causes so many damned side-effects.
Posted by linkadge on December 23, 2008, at 12:17:13
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl, posted by desolationrower on December 23, 2008, at 11:18:32
These drugs are still more discovered than designed.
Linkadge
Posted by psychobot5000 on December 23, 2008, at 12:23:31
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » SLS, posted by Marty on December 23, 2008, at 9:51:29
>
> > Interesting.
> >0057a.html" target="_blank">http://www.nature.com/npp/journal/v28/n2/full/130>0057a.html
>
> Yes, great paper indeed. Makes me think the team who develop Trazodone were on a good track: 5-HT2a antagonist, 5-HT2c agonist (via m-CPP) AND some SRI. If it wasn't of the side effects, in particular the hangover, and if the SRI was stronger it could be an awesome antidepressant if you embrace the thesis discussed in your paper.
>This is all sort of above my head, of course, but isn't nefazodone pretty much what you're describing: trazodone, only with less sedation/hangover, and a (modestly) stronger SRI effect?
Posted by psychobot5000 on December 23, 2008, at 16:46:37
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl, posted by linkadge on December 23, 2008, at 9:35:47
> Theres more than that which could be considered ideal.
>
> For instance, there are some compounds with 5-ht uptake inhibition and 5-ht1a/b autoreceptor antagonism which apprently bypass the need for long term drug administration to desensitize these receptors.
>
>Suppose we take this in a slightly different direction: What might be the properties of an 'ideal' agent (acting on 5HT receptors) to be combined with a serotonin-reuptake -enhancer-, rather than an SSRI? 5HT1a agonism? Something else? Mightn't one make a more effective or targeted drug combination by -reducing- synaptic serotonin, and then targeting certain specific receptor subgroups for -increased- action, rather than the reverse?
(disclaimer: I am a tianeptine loyalist)
Posted by iforgotmypassword on December 24, 2008, at 4:33:31
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » Marty, posted by psychobot5000 on December 23, 2008, at 12:23:31
and i was hoping that the nefazodone SRI effect was weak enough that i wouldn't have to worry about it.
(sorry i just realized my whole post from here on in was my babbling about me and my nefazodone rx i hope to fill in the states, but want to post it to see if anyone finds it relevant and has a response.)
i have suspicions my problems are of the hyperserotonergic-hypodopaminergic domino effect type, and exacerbated by previous SSRI use. i am worried about increasing serotonin, i worry that i either have too much of it, or i am hypersensitve, or that i have receptor or transpoter genotypes i could benefit knowing more about, if it were possible.
i was under a faint impression that not only did 5-HT1a autoreceptor agonism decrease serotonin (an increase catecholamines), but that 5-HT2a antagonism did this as well (decrease serotonin, increase NE DA) and that 5-HT2c seemed to as well, but that it has complexities with regards to executive function (that it seemed to be the opposite of 5-HT2a in some ways).
i guess they may all be different in where their action is prominent. if i remember correctly (i may not), buspirone's anti-bruxism effect was due to its serotonin depleting and dopamine enhancing effect in the VTA. i *think* they tagged the mesocortical tract as being implicated in bruxism.
the final effect of nefazodone, and increase or decrease in serotonin, i am not sure of, and it bothers me. i know that the drug paradoxically increases REM by a small amount, whereas trazodone decreases REM, i think. i don't know the significance of this, if any, in determining what the broad chemical effect of nefazodone is.
both the hard to figure out SRI effect, and the 5-HT2c and mCPP issue bother me a lot. as does the 5HT-2b agonist property of mCPP, and how it's levels may depend on certain liver enzyme genotype(s) one has. (i think there was one or two enzymes that may be specifically relevant.)
the occupancy* of 5-HT2a by nefazodone is lower than i would have expected, making me wonder if it the recognition of nefazodone "having an effect" relied significantly on other properties of the drug, like its mCPP metabolite, or a possibility that it's SRI effect wasn't that weak at the dosage range that the drug ended up being rx'd at. but then again, i do not know what levels of antagonistic occupancy of 5-HT2a is associated with which types of responses.
i do not know anything about what type of occupancy profile trazodone has. it would be interesting to know how it compares, and which drug metabolizes into more mCPP at the dosage ranges that are used clinically.
* a single dose of 200mg nefazodone apparently creates ~39% occupancy of 5-HT2a receptors, and "less than 50% after 6 weeks of treatment with an average dose of approximately 450mg"
Posted by psychobot5000 on January 22, 2009, at 14:53:54
In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl, posted by linkadge on December 22, 2008, at 14:05:59
For those few who might be interested in 5ht(2c) and its effects on OCD, here's a brief account of 5ht(2c) antagonist Agomelatine's effects on my symptoms thus far...
I has had dramatic effects. And yet, I am not entirely certain I would recommend it to someone else. The ruminative components of my OCD are gone or severely reduced. Concerns with things like, say, handwashing, are more or less gone. However, a certain -feeling of obsessive urgency- has arisen or been magnified, and it's connected to a certain physical obsessiveness...repetitive and unnecessary movements, like winking (not at someone--just on my own). Thinking back, this reaction is somewhat similar to my reaction to Remeron, though more dramatic. It's probably less unpleasant than the previous incarnation of my OCD, but it's always present, and disrupts my ability to work without distraction.
Problematic. I have no idea what it means in neurobiological terms, but I thought I'd throw it out there, for those with an interest in this stuff: ruminative symptoms largely eliminated, physical obsessiveness much increased. Patient claims subjective similarity to previous experience with Remeron.
(incidentally, I more recently added low-dose nefazodone to my regimen, but I attribute most of the change to Agomelatine, as it started before the second drug was added)
Psychbot
Posted by SLS on January 22, 2009, at 15:05:21
In reply to Re: Agomelatine effects on OCD..., posted by psychobot5000 on January 22, 2009, at 14:53:54
How about adding Luvox for the OCD? Prozac might aggravate things with its 5-HT2c antagonism.
- Scott
Posted by desolationrower on January 23, 2009, at 1:43:13
In reply to Re: Agomelatine effects on OCD..., posted by psychobot5000 on January 22, 2009, at 14:53:54
that sounds a bit like tics, more than OCD?
-d/r
Posted by SLS on January 23, 2009, at 2:45:48
In reply to Re: Agomelatine effects on OCD..., posted by desolationrower on January 23, 2009, at 1:43:13
> that sounds a bit like tics, more than OCD?
That's a great observation.
Often OCD and tics go together. Maybe the melatonin receptor agonism has muted the OCD and left the tics? Just a guess.
I found no evidence that 5-HT2c receptors are involved in either OCD or tics. Investigations designed to look for this concluded that there was no association with either one.
- Scott
Posted by psychobot5000 on January 23, 2009, at 12:07:18
In reply to Re: Agomelatine effects on OCD..., posted by desolationrower on January 23, 2009, at 1:43:13
> that sounds a bit like tics, more than OCD?
>
> -d/r
Mmm. Good thought, d/r--Now, I don't know how ironclad this is, but as I understand it, there is a distinction between tics and 'tic-like' behaviors in OCD, and I think my behavior falls into the latter category. Tics are supposed to be involuntary, whereas OCD repetitive movements are ultimately under voluntary control. In my case, the movements are easily suppressed, and are the result of a feeling of...compulsion, which can manifest in a variety of ways. Its that -feeling- that's the root problem, as far as I can tell, and it can manifest in other irritating behavioral compulsions.Still, I'd like to know how well-established the distinction is. They say tics involve dysfunction in the same brain-regions as OCD, and some articles seem to lump them together, though perhaps this is just sloppy terminology.
Psychbot
PS - Scott, thanks for your note on 5HT-2c and OCD etiology. That's good to know. I'm not at all convinced that this won't ultimately work out somehow. Maybe nefazodone and its 5ht-2a effects could even be the actual cause...
Go forward in thread:
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.