Posted by Conundrum on November 7, 2011, at 13:50:57
In reply to Re: Viibrid Treatment - 20mgs » SLS, posted by joe schmoe on November 7, 2011, at 13:29:28
Good points. I wonder what the effects of activating those serotonergic post synaptic receptors are. I thought the antidepressant response of most SSRIs were in some way mediated through that receptor.
The food thing is interesting as well, there are probably many drugs where taking with or without food makes a big impact on drug availability.
> > > If the binding data on wikipedia are accurate, you probably don't need a high dose of this drug to block transporters/receptors. Too much might make it just like another numbing SSRI. I wonder if you can take 10mg?
> >
> > Thanks. That's great information.
>
>
> Scott did you ever read this post I made, referencing a discussion on another board about the drug's mechanism of action?
>
> http://www.dr-bob.org/babble/20101107/msgs/970202.html
>
> I'll reproduce the relevant part below.
>
> ---
>
> Here is something interesting I ran across on another forum:
>
> "To clarify for those that don't really understand (as I didn't fully up until just a few days ago), these 5-HT1A partial agonists aren't actually enhancing 5-HT1A receptor activity at all, they're decreasing it by blocking/competing with serotonin -- a full agonist --, exclusvely at inhibitory 5-HT1A somatodendritic autoreceptors. This results in increased serotonin release and enhanced activity at 5-HT1A postsynaptic receptors. Note that these drugs have significantly higher affinity for somatodendritic autoreceptors over postsynaptic receptors, as receptors on the cell body and dendrites are much more accessible than those in synapses. Hence, at the low doses in which they're used, they inhibit autoreceptors with little actual action on postsynaptic receptors at all, resulting in therapeutic benefits."
>
> http://www.socialanxietysupport.com/forum/f30/vilazodone-82779/#post1256448
>
> ---
>
> It seems that the reason Vilazodone was not recognized at first as an antidepressant was because too high of a dose was being used, and the drug was "spilling over" into the synapse instead of just being active at the more accessible inhibitory autoreceptors on the dendritic body. If this is true, larger and larger doses would just reduce effectiveness. The sweet spot would be quite a low dose.
>
> My pdoc told me the studies were started with 20mg and later changed to 40mg because it got a better response with some people. I suspect the real therapeutic dosage is 20mg or less. I had to drop back to 20mg when 40mg continued to be too trippy and activating (after taking it for months, the effects weren't going away). Now I wonder if 10 or 15 might be even better.
>
> Note this drug's absorption decreases radically if not taken with food, so I suspect all kinds of doses are being used out there unintentionally depending on how closely people are following the "with food" recommendation. "According to the product labeling, vilazodone blood concentrations in the fasted state can be decreased by approximately 50% compared to the fed state." I wonder if the 40mg dose is really a way to get the right dose (20 mg) to patients who are not always compliant about taking it with food.
this signature | Show by default | Change to hide (next time)Complaints: post-SSRI problems: anhedonia, memory and concentration problems, sexual anhedonia. )
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Currently taking 2.5 mg prozac, Multi B vitamin
poster:Conundrum
thread:994620
URL: http://www.dr-bob.org/babble/20111027/msgs/1001830.html