So how do these psych doctors and pharmacists know that ur typical antipsychotic blocks dopamine in the brain?
What is the precise evidence.
Does anyone know.
And do u have an article, anecdote of a doctor, or journal to back it up with?
Thanks.
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I read an article that apparently, they attach to a different set of dopamine receptors than the ones actually intended to do so, the d1 instead of d2.
As far as the way they know, itâs based on chemistry, they assume the chemical will react with the coresponding places in the gene sequences that produce the chemistry it can attach to. i donât have reference material for what iâm saying; this is just the knowledge i have from back in school
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It was found that with post mortems that there was excess dopamine in people with szâs brains back in the day. It kinda works but these days thereâs better understanding and from what we are seeing now is thereâs probably different interactions involved.
They work. Why they work for like most give or take but why is the question we donât really understand would be how I interpret the latest stuff.
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You canât see the whole paperâs of some (stupid pay walls), but I have access. You can look up âDopamine hypothesis for Schizophreniaâ you can also look up âGlutamate Hypothesis for Schizophreniaâ
https://psycnet.apa.org/record/1992-09301-001
https://www.nature.com/articles/npp2011181
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I am not sure if we can scan or get reports about dopamine levels in our brain in regular basis and not sure how feasible it is for people with Sz or Bipolar as they are already struggling and have constraints. Science is not that developed yet. The proof is the prognosis from psychotic break to sobriety and calmness of the activities that we do and way we talk about our experience. If that makes sense to all parties then we can say meds have worked. Else try different med. It is trial and error approach to advise on meds.
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I watched the 2-minute neuroscience of sz video.
Itâs a good summary and I didnât even know about the issue with glutamate receptors!
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Since I had my full DNA genome sequenced, I have found several issues in my enzyme production for both Dopamine and Glutamate.
For example, my D1-D5 dopamine genes are fast, making a huge uptake in my dopamine receptors. My SLC6A3 genes is slow, which is responsible for recirculating dopamine. Several of my abilities to get rid of my dopamine to urine like MAOA, MAOB, and ALDH2 are bad.
Almost 100% of my Glutamate pathways are shot including GCLC and GSS. When looking at my ability to even make Glutathione (GSH), it is almost zero. As a side note, I personally feel so much better when supplementing with Liposomal Glutathione.
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I was asking my psychiatrist about what the difference is between different antipsychotics
I asked do some antipsychotics block serotonin also because I have depression also
I asked how does abilify work differently at different dosages
My reply was that they are still trying to understand themselves
I dont know how they figured it out, there must have been a way for them to tell which areas of the brain the medication was going to.
I googled and now have the same question, how do they find out that one medication goes to these areas and does this and another goes to different areas and does what it does
I found this article but still am puzzled
Joshi and Panickerâs work relies on transgenic mice called âFosTRAPâ mice, which carry a genetically encoded tool named TRAP (Targeted Recombination in Active Populations), first developed in Professor Liqun Luoâs laboratory at Stanford University. The tool embedded in the mouseâs genome uses a fluorescent protein to permanently âlight upâ cells responding to a specific stimulus. Using these mice, the team were able to identify groups of brain cells that responded to four drugs â the first generation or typical antipsychotics, Haloperidol and Loxapine, and the second generation or atypical antipsychotics, Clozapine and Olanzapine.
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all i know that there is a Technique called âMicrodialysisâ
scientist capable of measuring neurotransmitters in brain of rats using these method.
also they watch the behaviour of rats by doing tests like t-maze test (cognition) and hyperlocomotion test (positive symptoms)
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For me it was trial and error , i tried so many meds i dont even know i think about or more than 10 and side effects not to mention.
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by chance
using chloropromazine for the first cause tranquilizing effect to the body
so why not to use it for scz
and it works!
after some ppl with scz died and seeing their brains they found they have high dopamine in certain parts of their brain so thats the defect they have
then
make drevatives of chloropromazine
and isolating dopamine receptors and trying chemical structures that attach to it
then we have many many AP!
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Please stop pushing a service that is wildly expensive compared to other genetic services.
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Ok, give some alternatives, it really helped me.
I bet it did considering you joined July 4 and have mentioned it 5 times already.
Funny.
Anyway, I donât need to supply alternatives, I only need to make sure no one is spamming the forum.
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Just trying to be of help
Fair enough
Yes, this was big news recently.
https://healthnews.com/news/antipsychotic-medications-dont-function-as-scientists-formerly-thought/
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I was under the impression that, this is why we feel quite paralysed on antipsychotics. thereâs significantly more d1 receptors than the targeted ones
Iâm looking forward to karxt, because apparently somnolence isnât a major issue on it and i believe that is tied to d1 receptors (just because the nervous system has a lot of d1 receptors but obviously iâm just guessing stuff atm)
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The brain is the most complex organ in our body
Psychiatrists learned a whole bunch of theory (science) behind different receptors and such. I see diagrams sometimes when searching and have no idea what it is lol continue scrolling
Nobody has a 100% answer to how it works etc. I believe science is still learning on this subject,
otherwise I think we would ALL be stable by now
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who did you have do it? Any tips / advice for someone who wants to do this?
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