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
poster:linkadge
thread:720797
URL: http://www.dr-bob.org/babble/20070107/msgs/721013.html