View Single Post
Anonymous59893
Guest
Anonymous59893 has no updates. Edit
 
Posts: n/a
Default Apr 30, 2018 at 01:53 PM
 
Quote:
Originally Posted by Sometimes psychotic View Post
All of those are possibilities but here is my logic for thinking it’s the meds. A partial agonist at d2 is still less than native dopamine so it still blocks dopamine and actually binds more efffectively than any other AP because it’s a partial agonist. So it’s still dopamine blockade which is how APs all work. The meds for add/adhd function by increasing dopamine, they are basically speed, that suggests that adhd is in part caused by too low of dopamine. This is why I think it could be the meds.
One of the good things about not taking meds for over a year is that you know that whatever's going on is probably not down to meds anymore (well, except for the tardive myoclonus, which I figure is permanent now after 8 years of it) :/ But I remember trying in vain to figure out what was meds and what was 'me' back when I was on meds

Obviously, to preface all of this, what we understand about the brain and dopamine systems and what the meds are actually doing in there is limited. But the theory is that the striatal and frontal dopamine levels are linked by a mesocortical feedback loop. So high striatal dopamine levels in psychosis push down the frontal dopamine levels.

Regular D2 antagonists are theoretically going to push down the striatal dopamine signalling, which should increase frontal dopamine signalling in response. BUT they're 'dirty' in the sense that they don't just act on the mesolimbic pathway areas, so they're probably undermining that in the frontal area by antagonising D2 there too.

But D2 partial agonists, like aripiprazole (and brexpiprazole, and I believe that cariprazine is a partial agonist too?? Neither of those are out in the UK yet though) should theoretically increase the frontal dopamine signalling. They might not decrease the striatal signalling as much as the antagonists do to activate the frontal feedback loop as much, but they should also be working in the frontal lobe to actively increase dopamine signalling too.

Aripiprazole is the only AP with evidence for use in combination with another AP as it can improve negative and cognitive symptoms, whereas all of the other combos just increase side effects with limited/no benefits. So, IMO, aripiprazole shouldn't be causing you as much issues with impulsivity and cognition as the standard D2 antagonists might. I'm honestly leaning towards it being negative and cognitive symptoms. But that's jmo and who really knows what's actually going on in reality: it's all just theories!

Anyway, it occurred to me last night that you must really be struggling if you are considering taking sarcosine and other stuff. I know how concerned you were about supplements before, so I figure that things must be bad if you're willing to try them, and I'm sorry about that

I know that you are even more scared about messing with the aripiprazole, and I don't blame you when it has worked for you so well for so long. But maybe it would be worth trying something else if the supplements don't do everything that you hope? Cognitive and negative symptoms are the hardest to treat though, as you well know, but everyone responds differently to the meds, and only trial and error will show if there's a better option for you out there.

Anyway, I know that it really sucks, and so I just wanted to offer my support

*Willow*
  Reply With QuoteReply With Quote