A generalized comment here.
A short while back I mentioned that Retigabine seems to somewhat unexpectedly (to our initial speculations anyhow) be a "mood drug"- among other things. I reported how I felt inexplicably positive and upbeat when taking it, etc. and that theme has become clearer as more info has come out lately.
Which is leading me to some pure speculation.....
I don't want to get into the mechanics of this, but enough of us know that classical "anti-depressants" or any "mood drugs" whether they be targeting serotonin, norepinephrine, GABA, dopamine, whatever...are all over the map in how they affect different people in different ways. It's just kind of accepted that a person may have to try three or four classical anti-depressants before 'hitting on the right one'.
Why is that?
Well because when we get into the intricacies of neuro brain chemistry/neurotransmitters and individual genetic makeup of how all those splash around in each unique brain..."it's complicated". Yeah we may have bell curve of "normal" but there's a lot of spread in that. Plus bring in variables like stress levels, dietary variance, social structure, age, gender, lifestyle, and...hell even having a pet can affect "mood"! So yeah, with a little imagination you can see it's a zoo.
So, it seems to me, that if Retigabine is also a mood drug (over an above what we thought it was going to be back on page 5 or so of this thread), then these rather huge variations we are seeing on how it's affecting people, in dose, side effects and variability on tinnitus...is becoming less and less of a surprise to me.
I'm going to hold with my crude analogy of "kicking the doors down" (I guess I like some drama when discussing bio-chemical esoterica), as it is basically a statement of what effective dose is sitting outside the membrane checking out those gates/doors?! Note I said effective dose.
Now it may be that effective dose is not as varied as it could be, though no doubt my "doors" may be welded shut after 58 years of the same tone of T, versus someone who has only had it for 3 months. But that aside, I am thinking here more of how do we know what dose is floating around outside any one individual's neural membranes? Just because Jack took the same dose as Jill (though we don't have any "Jill's" yet) does this mean the same amount of Retigabine is floating around in their intra-cellular space???...You can guess my current answer/supposition to that.
I highly doubt it!
If the "active" part of this Retigabine on tinnitus is coming from the Kv7.2/3 ("we have developed and tested a novel and more specific Kv7.2/3 (KCNQ2/3) activator that works much better than retigabine both for epilepsy and for tinnitus.") which happens to be the part of Retig. that controls "M-current" and "general excitability in the brain and ganglia" [Note! - Not Kv7.4 which affects the cochlea and vestibular hair cells]...then, are you following me here?
This Kv7.2/3 is to me, a much more "generalized function" and all over the brain too!!! So...it's going to be competing with, interacting with, messing with, a whole bunch of other nuro-transmitters in this soup. God knows how much of the active part of Retigabine for tinnitus is getting left over, to "kick at the doors", after it has been through this maze of competitors and distractions along the way. Maybe hardly any?! Maybe a lot for "less distractable" individual brains?!
Thus maybe the reason for some folks getting effects at almost their first pill, and others getting nothing but headaches and missed trams.
Again, if I think of a simplistic, pictorial image modus operandii of why so many "mood drugs" work so incredibly differently for so many people (and there are a lot of mood drugs to cater to this), this kind of scenario I have painted above comes to mind.
So folks...I think "variability" with Retigabine results, doses, methodologies, effects on T, etc., etc. is here to stay.
Best, Zimichael
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