![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 26. This is the beginning of the thread.
Posted by SLS on January 9, 2007, at 13:47:33
Two Parkinson's Disease Drugs May Cause Valvular Dysfunction CME
Medscape
News Author: Steve Stiles--------------------------------------------------------------------------------
"January 8, 2007 — Two case-control studies published simultaneously in the January 4 issue of The New England Journal of Medicine provide some of the strongest evidence that treatment with the ergot-derived dopamine antagonists pergolide and cabergoline, commonly used in Parkinson's disease, can cause cardiac-valve dysfunction. They also suggest that the adverse effect is not caused by some other prescribed dopamine antagonists, especially those not derived from ergot.According to a perspective by Bryan L. Roth, MD, PhD, of the University of North Carolina in Chapel Hill, that accompanies the 2 studies, the findings support prior clinical and mechanistic evidence for a link between a histologically distinct fibrotic valvulopathy and treatment with drugs that block the serotonin receptor 5-hydroxytryptamine 2B (5-HT2B). Pergolide and cabergoline have that biochemical action in common, whereas the other studied dopamine antagonists do not have significant effects on 5-HT2B, writes Dr. Roth.
The 2 "very careful clinical studies" validate the earlier work and "nail down" 5-HT2B agonism as the mechanism behind the valvulopathy that has been associated with dopamine antagonists and some other drugs, Dr. Roth told heartwire. The observed effects were huge, he said. "They were not minor incidences for a side effect. When you consider that these drugs have been on the market now for decades, you wonder how this could possibly have been missed."
In his article, Dr. Roth describes how earlier research from his group and others had helped define the biochemical mechanisms behind 5-HT2B-related valvulopathy and determine that an active metabolite of fenfluramine is a potent agonist of the receptor. That drug in combination with phentermine constituted the diet pill "fen-phen," which was pulled from the market during the late 1990s after reports that fenfluramine and its isomer dexfenfluramine were a likely cause of valvular disease. The underlying biochemical processes were unrecognized at the time.
An association between 5-HT2B agonism and valve disease, Dr. Roth writes, "has now been seen with drugs for diverse indications.... Clearly, practitioners should avoid prescribing drugs that are potent 5-HT2B-receptor agonists, a growing list of medications that now includes ergot derivatives, dopamine agonists, and amphetamine derivatives" used to treat such disorders as migraines, obesity, and Parkinson's disease..."
http://www.medscape.com/viewarticle/550405_print
- Scott
Posted by ed_uk on January 9, 2007, at 15:23:38
In reply to pergolide, cabergoline: heart pathology via 5-HT2b, posted by SLS on January 9, 2007, at 13:47:33
On the bright side, at least it doesn't apply to Requip and Mirapex.
Ed
Posted by SLS on January 9, 2007, at 15:32:06
In reply to Re: pergolide, cabergoline: heart pathology via 5-HT2b » SLS, posted by ed_uk on January 9, 2007, at 15:23:38
> On the bright side, at least it doesn't apply to Requip and Mirapex.
On the other bright side, it may be that direct receptor agonism is necessary for the valvulopathy, and not an effect secondary to reuptake inhibition or release. I was impressed by the fact that fenfluramine had a metabolite that was a direct agonist.
- Scott
Posted by Phillipa on January 9, 2007, at 17:37:23
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by SLS on January 9, 2007, at 15:32:06
Hey my Daughter took fem fem in Florida with a diet doc should she be concerned as she has been fine since? Love Phillipa
Posted by Emme on January 9, 2007, at 19:28:17
In reply to pergolide, cabergoline: heart pathology via 5-HT2b, posted by SLS on January 9, 2007, at 13:47:33
Aren't pergolide and cabergoline dopamine agonists, not antagonists?
emme
Posted by tessellated on January 9, 2007, at 21:51:00
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by Emme on January 9, 2007, at 19:28:17
> Aren't pergolide and cabergoline dopamine agonists, not antagonists?
>
> emme
QUITE RIGHT!!! I'M UTTERLY CONFUSED.
Posted by SLS on January 9, 2007, at 22:11:33
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by Emme on January 9, 2007, at 19:28:17
> Aren't pergolide and cabergoline dopamine agonists, not antagonists?
>You know, when I read the article, I didn't even notice the mistake. It's funny how the mind works. Obviously, the news author got it wrong.
- Scott
Posted by linkadge on January 10, 2007, at 8:15:18
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by SLS on January 9, 2007, at 22:11:33
>On the other bright side, it may be that direct >receptor agonism is necessary for the >valvulopathy, and not an effect secondary to >reuptake inhibition or release. I was impressed >by the fact that fenfluramine had a metabolite >that was a direct agonist.
Thats what I am afraid of. I don't think that this exonerates serotonin reuptake inhibitors from causing such problems. SSRI's are 5-ht2b receptor agonists plain and simple. Perhaps weaker, but that doesn't mean they aren't causing problem with long term use.
There was one recend study that suggested that cardiac patients who used SSRI's were more likely to die of their disease.
I think what they are "trying" to do is establish that SSRI's don't cause a problem and that 5-ht2b agonists do. They obviously "want" to do that because direct 5-ht2b agonists are much less plentiful than SSRI's.
Could you imagine the implications of such a finding? Thats why I think the research is a little biased, because we have so many SSRI's we don't want them to cause this type of problem.
I'll let time tell.
Remember that study I just posted which showed that mice who were low in the serotonin transporter developed similar cardiac problems later in life.
People just shrug me off, but I'm not the first one to suggest that SSRI's need to be very closly examined.
Thats the problem, drugs are just assumed safe untill proven guilty, but sometimes by the time that happens its too late.
Depression (IMHO) is not due to altered SERT function, it is due to overactive 5-ht autoreceptors expressed in certain parts of the brain. Fixing this would have no effect on cardiac 5-ht function.
Linkadge
Posted by linkadge on January 10, 2007, at 8:16:48
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by SLS on January 9, 2007, at 22:11:33
Doesn't a metabolite of trazodone act as a 5-ht2b agonist? Or is it a 5-ht2b antagonist?
Linkadge
Posted by Quintal on January 10, 2007, at 11:13:00
In reply to Re: metabolite of trazodone ?, posted by linkadge on January 10, 2007, at 8:16:48
>Doesn't a metabolite of trazodone act as a 5-ht2b agonist? Or is it a 5-ht2b antagonist?
I think you're referring to mCPP? It has mixed 5HT2A/2C receptor agonist/antagonist actions.
http://www.drugpreventionevidence.info/web/mCPP322.asp
Q
Posted by linkadge on January 10, 2007, at 12:06:29
In reply to Re: metabolite of trazodone ? » linkadge, posted by Quintal on January 10, 2007, at 11:13:00
Posted by ed_uk on January 10, 2007, at 14:14:00
In reply to Re: metabolite of trazodone ? » linkadge, posted by Quintal on January 10, 2007, at 11:13:00
Hi Quintal
I sent you an email. Did you get it?
Regards
Ed
Posted by Quintal on January 10, 2007, at 15:27:36
In reply to Re: metabolite of trazodone ? » Quintal, posted by ed_uk on January 10, 2007, at 14:14:00
Hi Ed,
I got the email you sent me on 07/01/06 and I sent you one back yesterday. I've just re-sent it, so let me know if you get it?
Q
Posted by psychobot5000 on January 10, 2007, at 21:08:35
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by linkadge on January 10, 2007, at 8:15:18
> There was one recend study that suggested that cardiac patients who used SSRI's were more likely to die of their disease.
>
> Remember that study I just posted which showed that mice who were low in the serotonin transporter developed similar cardiac problems later in life.
>
> Depression (IMHO) is not due to altered SERT function, it is due to overactive 5-ht autoreceptors expressed in certain parts of the brain. Fixing this would have no effect on cardiac 5-ht function.
>
> Linkadge
Probably not relevant, but Tianeptine apparently improves the status of certain cardiac patients, thought from what I read this was thought to be through another pathway than serotonin receptors:"The effects of tianeptine on the glutamate-NO pathway explain the improved cardiovascular status of tianeptine-using patients with ischaemic heart disease. There is a poorly understood association between coronary heart disease and depression; disturbances in nitric oxide production may play a role in both."
__Anyway...I guess I just mean to point out that drugs can have coincidental positive effects on health as well as negative. It's not all bad!
_________________________________________________________
Clinical Efficacy of Tianeptine in Patients With Ischemic Heart Disease and Comorbid DepressionResearch Center for Preventive Medicine; Petroverigsky per., 10; 101953 Moscow, Russia
Ischemic heart disease patients (20 men, 20 women, age 36-72 years) with class II-III effort angina and depression (Beck Depression Inventory - BDI - score >= 19) were randomized to standard therapy were treatment of stable ischemic heart disease (control group) or standard therapy plus tianeptine 37.5 mg/day. After 6 weeks 52% decrease of BDI score occurred in tianeptine treated patients (from 24.9±1.2 to 11.9±1.5, p<0.001). This was associated with decrease of number and severity of cardialgias, better blood pressure control in patients with hypertension, lengthening of exercise time during exercise test (by 3.3±0.9 min, p<0.05), and increase of overall index of quality of life (by 2.6±0.9 points, p<0.01). No dynamics of these parameters occurred in control group.
Posted by SLS on January 11, 2007, at 1:08:47
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by linkadge on January 10, 2007, at 8:15:18
> > On the other bright side, it may be that direct receptor agonism is necessary for the valvulopathy, and not an effect secondary to reuptake inhibition or release. I was impressed by the fact that fenfluramine had a metabolite that was a direct agonist.
> Thats what I am afraid of. I don't think that this exonerates serotonin reuptake inhibitors from causing such problems.Perhaps not, but nor does it exonerate eating crayfish. It's just never been seen. I understand your concerns, though. Note, however, that valvulopathy has developed very quickly with 5-HT2b receptor agonists, and to my knowledge, has yet to be demonstrated with SSRIs after 20 years of usage.
> SSRI's are 5-ht2b receptor agonists plain and simple.
This is not true. That's like saying methylphenidate is the same as bromocriptine. With reuptake inhibitors, my guess is that re-regulation helps to prevent overstimulation of receptors. With a high-affinity direct receptor agonist, however, even with downregulation, occupancy remains high. If the two drugs were the same, Ritalin, a DA reuptake inhibitor, would work as well as DA agonists for Parkinsons. It doesn't.
> There was one recend study that suggested that cardiac patients who used SSRI's were more likely to die of their disease.
Valvulopathy?
That's what we are talking about here with regard to 5-HT2b receptors.
I'd like to see the study, anyway. Were the control subjects people who were depressed who didn't take SSRIs?
> I think what they are "trying" to do is establish that SSRI's don't cause a problem and that 5-ht2b agonists do. They obviously "want" to do that because direct 5-ht2b agonists are much less plentiful than SSRI's.
I wouldn't presume to read the minds of so many scientists who are in agreement about this, but I question your explanation.
> Remember that study I just posted which showed that mice who were low in the serotonin transporter developed similar cardiac problems later in life.Valvulopathy?
I tend to agree with you that dysregulation of neural tone, perhaps autoreceptor-mediated, is a more likely explanation for affective disorders than is a defect in transporter expression.
- Scott
Posted by linkadge on January 11, 2007, at 16:04:08
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by SLS on January 11, 2007, at 1:08:47
Remember that study I just posted which showed that mice who were low in the serotonin transporter developed similar cardiac problems later in life.
>Valvulopathy?
YES!! (see)
Deficiency of the 5-Hydroxytryptamine Transporter Gene Leads to Cardiac Fibrosis and Valvulopathy in Mice.
http://circ.ahajournals.org/cgi/content/abstract/113/1/81
>Note, however, that valvulopathy has developed >very quickly with 5-HT2b receptor agonists, and >to my knowledge, has yet to be demonstrated with >SSRIs after 20 years of usage.
Thats exactly it. When you start a drug and you develop a problem soon after, it is easy to implicate that drug. If you develop heart problems 20 years after starting an SSRI, nobody would suspect it.
>This is not true. That's like saying >methylphenidate is the same as bromocriptine.No, but they will shart a common ability to agonise certain dopamine receptors.
>With reuptake inhibitors, my guess is that re->regulation helps to prevent overstimulation of >receptors.
But, that reregulation occurs with agonists as well. Ie, buspar downregulates 5-ht1a. So if cardiac receptors were protected by downregulation in the presense of uptake inhibitors, then they should be protected by downregulation in the presence of agonists, which they don't seem to be.
>With a high-affinity direct receptor agonist, >however, even with downregulation, occupancy >remains high. If the two drugs were the same, >Ritalin, a DA reuptake inhibitor, would work as >well as DA agonists for Parkinsons. It doesn't.Ritalin is sometimes used for parkinsons, sometimes end stage parkinsons. I think it is not a first line treatment for the same reason it isn't a first line treatment for depression.
One would need to asess comparable doses of 5-ht agonists with uptake inhibitors.
>That's what we are talking about here with >regard to 5-HT2b receptors.
Yeah, I know. But you could have a cardiac event related to this that might not be directly seen as linked to SSRI use for that matter.
>I'd like to see the study, anyway. Were the >control subjects people who were depressed who >didn't take SSRIs?No, but depression was factored into calculations.
Not entirely conclusive, I realize.http://www.news-medical.net/?id=16395
There are also links to maternal use of SSRI's, and development of congenital heart problems to child.
> I think what they are "trying" to do is establish that SSRI's don't cause a problem and that 5-ht2b agonists do. They obviously "want" to do that because direct 5-ht2b agonists are much less plentiful than SSRI's.>I wouldn't presume to read the minds of so many >scientists who are in agreement about this, but >I question your explanation.
There has been a lot about supressed information related to drugs. I wouldn't put it past people to keep potential problems supressed.
Serotonin causes proliferation in a variety of human tissues.
>I tend to agree with you that dysregulation of >neural tone, perhaps autoreceptor-mediated, is a >more likely explanation for affective disorders >than is a defect in transporter expression.
If you mess with the serotonin transporter, you mess with serotonin throughout the body. Ie that is why some people can develop severe GI problems from SSRI use. If there is a serotonin abnormality in depression, I think it is brain specific, and that it could be fixed without altering MAO, or SERT.
Linkadge
Posted by SLS on January 11, 2007, at 16:49:06
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by linkadge on January 11, 2007, at 16:04:08
> > > Remember that study I just posted which showed that mice who were low in the serotonin transporter developed similar cardiac problems later in life.
> > Valvulopathy?> YES!! (see)
> Deficiency of the 5-Hydroxytryptamine Transporter Gene Leads to Cardiac Fibrosis and Valvulopathy in Mice.
> http://circ.ahajournals.org/cgi/content/abstract/113/1/81
That's a pretty incriminating investigation, to be sure.
I found the following particularly salient:
"Although 5-HT1B receptors mediated the 5-HT–induced collagen secretion by human cardiac myofibroblasts, the contribution of this receptor type to valvulopathy was ruled out because double-KO mice deficient in both 5-HTT and 5-HT1B receptors showed the same cardiac alterations as 5-HTT-KO mice."
> > I'd like to see the study, anyway. Were the control subjects people who were depressed who didn't take SSRIs?
> No, but depression was factored into calculations.
> Not entirely conclusive, I realize.
> http://www.news-medical.net/?id=16395It seems to be a well-done study, though.
> There are also links to maternal use of SSRI's, and development of congenital heart problems to child.
This really sucks to hear, Linkadge. Your evidence and logic are convincing. Let't hope that the rate of this adverse event seen clinically turns out to be low.I guess we can let the crayfish off the hook on this one. However, I reserve the right to indict them in the future in the absence of exoneration.
- Scott
Posted by linkadge on January 11, 2007, at 20:10:08
In reply to Re: pergolide, cabergoline: heart pathology via 5- » linkadge, posted by SLS on January 11, 2007, at 16:49:06
>"Although 5-HT1B receptors mediated the 5-HT–>induced collagen secretion by human cardiac >myofibroblasts, the contribution of this >receptor type to valvulopathy was ruled out >because double-KO mice deficient in both 5-HTT >and 5-HT1B receptors showed the same cardiac >alterations as 5-HTT-KO mice."
This says that the vulvopathy is not dependant on 5-ht1b receptors. It doesn't say, however, that 5-ht2b receptors might not be involved.
I think the reason that they started to study these mice was because somebody must have been wanting to know whether pharachological manipulation of the human transporter could affect cardaic function.
There are differences, of course, between 5-htt knockout mice, and people treated with SSRI's. Nevertheless, SSRI's can bring a person pretty close to 5-htt knockout. I remember reading that theraputic doses of sertraline inhibed 5-htt by ~80%.
So, I think there is a possability, and I think only time will tell.
Linkadge
Posted by SLS on January 12, 2007, at 6:02:55
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by linkadge on January 11, 2007, at 20:10:08
> > "Although 5-HT1B receptors mediated the 5-HT–>induced collagen secretion by human cardiac >myofibroblasts, the contribution of this >receptor type to valvulopathy was ruled out >because double-KO mice deficient in both 5-HTT >and 5-HT1B receptors showed the same cardiac >alterations as 5-HTT-KO mice."
> This says that the vulvopathy is not dependant on 5-ht1b receptors. It doesn't say, however, that 5-ht2b receptors might not be involved.Perhaps I misinterpreted it. I thought that since the 5-HT2b KO mice displayed the same pathology, this would indicate that this receptor was not necessary.
> I think the reason that they started to study these mice was because somebody must have been wanting to know whether pharachological manipulation of the human transporter could affect cardaic function.
Well, I hope someone decides to study an SSRI in a similar fashion. I imagine someone has.
I must have missed it, but can you provide the link to the maternal use of SSRI and the congenital heart pathology?
> There are differences, of course, between 5-htt knockout mice, and people treated with SSRI's. Nevertheless, SSRI's can bring a person pretty close to 5-htt knockout. I remember reading that theraputic doses of sertraline inhibed 5-htt by ~80%.
>
> So, I think there is a possability, and I think only time will tell.The evidence you presented is worrisome, though. I spent some time thinking about it last night, and it would indeed be difficult to exclude SSRIs from being a candidate for producing CV adverse effects after long-term use. As you said, time will tell. Hopefully, we haven't missed something obvious, and that the paucity of reported CV effects after 20 years of use reflects a relatively safe CV profile for the SSRIs.
It is unfortunate, but drugs used to treat many different illnesses can display dangerous side effects, even if only rarely. The decision to take these drugs represents a risk versus benefit evaluation. Medicine for many of these other illnesses are almost as archaic as for mental illness (although I would say that the rate of progress is greater for the former), with an incomplete understanding of how the drugs work and a continual discovery of new and serious side effects.
So, what do we do with the SSRIs or any other drug with potent serotonin reuptake inhibition properties? If removed, what else do we have to work with? Is the rate of heart pathology in real life high enough to justify their withdrawal? I guess for now, there is not enough evidence to be able to quantify the risk. I know that for myself, given the severe debilitation and painful existence that my illness produces, at this point in time, I still wouldn't hesitate to take an SSRI.
The decision whether or not to take psychotropic drugs is sometimes difficult and sometimes easy. I guess it becomes easier the more the magnitude of illness drifts towards the mild pole or the severe pole. For those with a moderate depression who remain functional, there is probably more vacillation. Just a guess, though.
Good job putting all of this stuff together, Link.
- Scott
Posted by linkadge on January 12, 2007, at 8:25:27
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by SLS on January 12, 2007, at 6:02:55
>Perhaps I misinterpreted it. I thought that >since the 5-HT2b KO mice displayed the same >pathology, this would indicate that this >receptor was not necessary.
The study uses 5-ht1b knockout mice (I don't think they made a typo). I think that 5-ht1b receptors have also been implicated in some cardiac disturbances, which is why the study chose to study 5-ht1b knockout.
>I must have missed it, but can you provide the >link to the maternal use of SSRI and the >congenital heart pathology?
It may just be paroxetine, but I thought I saw a study regarding sertaline as well.
http://www.congenital-heart-defects.org/pages/antidepressants-birth-defects-paxil-vsd.html
>So, what do we do with the SSRIs or any other >drug with potent serotonin reuptake inhibition >properties? If removed, what else do we have to >work with?
Thats exactly it. It serious data were to be presented about the SSRIs it would take forever to come to light. (for instance SSRI suicide link)
Not sure what would be the step to take. Perhaps such a discovery would change the FDA's propensity to only approve me too uptake inhibitors, and open their minds to other possabilities.
>Is the rate of heart pathology in real life high >enough to justify their withdrawal? I guess for >now, there is not enough evidence to be able to >quantify the risk. I know that for myself, given >the severe debilitation and painful existence >that my illness produces, at this point in time, >I still wouldn't hesitate to take an SSRI.
If it is a time dependant phenomina, Ie taking years to develop, then I don't know how the drug would be dealt with.
>The decision whether or not to take psychotropic >drugs is sometimes difficult and sometimes easy. >I guess it becomes easier the more the magnitude >of illness drifts towards the mild pole or the >severe pole. For those with a moderate >depression who remain functional, there is >probably more vacillation. Just a guess, though.I am just scared that the drugs are (were) dispensed so easily. Heart disease is a lot worse than a bad hair day.
I am putting my hopes on a substance called the 5-ht moduline. It is an endogenious peptide that controlls the sensitivity of the 5-ht1b autoreceptors in the brain. Some researchers believe that synthesizing the 5-ht moduline would provide a brain specific way of altering 5-ht autoreceptor function, and hence sythesis and release of serotonin in specific brain regions like the hippocampus. Possably even free of sexual side effects.
Linkadge
Posted by SLS on January 12, 2007, at 8:58:26
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by linkadge on January 12, 2007, at 8:25:27
> I am putting my hopes on a substance called the 5-ht moduline. It is an endogenious peptide that controlls the sensitivity of the 5-ht1b autoreceptors in the brain. Some researchers believe that synthesizing the 5-ht moduline would provide a brain specific way of altering 5-ht autoreceptor function, and hence sythesis and release of serotonin in specific brain regions like the hippocampus. Possably even free of sexual side effects.
Sounds interesting. Is this a peptide?
For quite a few years, I was focused on presynaptic function as the site of dysregulation responsible for depression. However, the more I learned, the more I was disuaded from looking at this so exclusively. Still, selectively manipulating the tone of the presynaptic feedback loop seems like an elegant way of going about modulating the synthesis and release of neurotransmitter.
- Scott
Posted by corafree on January 12, 2007, at 11:47:11
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by SLS on January 12, 2007, at 8:58:26
Geez .. maybe takin' Lexapro (SSRI?) and Provigil will really beat my heart to death! I just wanna' dump 'em all!
cf
Posted by linkadge on January 12, 2007, at 14:34:03
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by SLS on January 12, 2007, at 8:58:26
Some more information about it here.
http://biopsychiatry.com/5htmoduline.htm
Linkadge
Posted by Larry Hoover on January 21, 2007, at 12:42:59
In reply to Re: pergolide, cabergoline: heart pathology via 5-, posted by linkadge on January 12, 2007, at 14:34:03
Jumping in......
Shows that fluoxetine is considered antagonistic at 5-HT2b, and that trazodone parent overwhelms agonism of mCPP:
http://circ.ahajournals.org/cgi/content/full/102/23/2836
A little off point, but an overview of cardiac/circulatory events even potentially associated with SSRIs does not reveal valvulopathy as an issue.
http://www.theannals.com/cgi/content/full/38/7/1197I also studied the complete 5-HT2b binding affinity table at PDSP http://kidb.cwru.edu/pdsp.php, and found no listed SSRIs with any appreciable agonism at this receptor.
Cabergoline was one of the most potent agonists listed.
Do you have other evidence, link?
Lar
Posted by linkadge on January 24, 2007, at 16:38:50
In reply to Re: pergolide, cabergoline: heart pathology via 5- » linkadge, posted by Larry Hoover on January 21, 2007, at 12:42:59
I didn't really have much "evidence" to begin with, I was just wondering if there could be a possable future association.
The SSRI's will not be listed as 5-ht2b agonists, because the molecules are not. They will be however, indirect agonists at 5-ht2b.
Perhaps the antagonism of fluoxetine will counteract the indirect agonism due to 5-ht reuptake.
I just think it is a potential problem with other SSRI's.
Linkadge
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