Posted by linkadge on October 24, 2008, at 6:29:15
In reply to Re: Beauty and sadness » linkadge, posted by Marty on October 23, 2008, at 19:33:33
>There's something interesting in this discussion >ONLY if your response is worst on Prozac than on >the other (more typical) SSRIs. Is it the case >or not ?
Like I said, they all suck for me. I can't really tell much of a difference.
>It's not. What I'm saying is more like if >aspirin induce migraine each time Joe the >plumber is taking one then Joe may have >something biologically different that's causing >this atypical response...I don't know if I'd call my responce to prozac atypical. The drug is known to cause all shades of akathesia and dysphoria upon start up. It is known to cause early symptomatic worsening and suiciadiality in many pepople. I stopped blaming myself for not responding to a particular drug a long time ago.
The aspirin example was a bad one because SSRI response rates are much poorer than what common belief dictates. They are much more poorly tolerated than aspirin.
If you are saying that the neurobiology of responders is different than the neurobiology of nonresponders then yes, of course. But, I certainly wouldn't lable this difference as something that makes the individual more sick, (unless you measure the degree of sickness by the degree to which something can be treated)
Basically, I refuse to think that there is something "wrong" with me for not responding to SSRI's. I think the drugs are garbage, and it is ultimately their fault for not targetting what is wrong with unresponsive patients.
(Some studies suggest that no more than 50% of patients takin SSRI's actually get a meaningful improvement)
>IF you feel way worst on Prozac than on other >SSRIs, it COULD be because of the 5-HT2c >antagonistic properties of Prozac since it's >about the only -relevant- difference between >Prozac and others.
There are differences to prozac than just 5-ht2c antagonism. Prozac has effects on MAO-a and b. It also has a longer halflife which may pose more problems for neuroendocine regulation, sleep wake cycle etc.
>It matters because 5-HT2c antagonism very >typically makes people feels better.
Thats very hard to say because we have no clinically avaiable seletive 5-ht2c antagonsts.
>and so, while it doesn't tell you more about the >precise etiology of your disorder, it gives you >the opportunity to tweak something that may end >up improving your condition.
I've tweaked everything. Now I am a little tweaked.
>1. More/different 5-HT2c antagonism with no SRI >action: Agomelatine (already out there) or low >dose Geodon (pre-DA antagonistic dose = 5-HT2c >antagonism)
>2. Light (Not LSD strong) 5-HT2c agonism: low >dose mCPP could do the trick. One of Trazodone >metabolite happen to be mCPP. SRIs properties of >Trazo is pretty weak and it's 5-HT2a >antagonistic properties are good for emotions. >To see how 5-HT2c agonism makes you feel only 1 >or 2 days of Trazo would be enough to see.. you >take it before bed and a couple hours after you >wake up you'll feel it. No need for clinically >active dose.
I fail to see the strength in your logic. Just because drug x doesn't work, doesn't mean anti-x will. I.e. just because 5-ht2c antagonism makes me feel worse, doesn't mean that 5-ht2c agonism will make me feel better.(If there is nothing wrong with that particualr system to begin with, then any chemical modulation of it could have the propensity to make me feel worse).
Linkadge
poster:linkadge
thread:857746
URL: http://www.dr-bob.org/babble/20081016/msgs/859062.html