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  1. Kind of a shame, too bad it's so expensive or inaccessible. Would sort of fill the gaps as to why the other meds missed. Still think there might have been something to the low dose anti-psych, but people with this condition might have other comorbids that would negate a low dose anti-psych run. Still think nuplazid should have gone somewhere. Maybe even a low or lower dose run of nuplazid would have yielded some type of positive result. Well, best of luck.
  2. I wrote a post about Nuplazid way back. In theory it should be helpful. There's another that I guess is in the pipeline that I guess should be more effective, Vitolenserin??? Idk, I don't feel like looking it up right now. Buuuuttt... There is an antidepressant in the same category that's available in Europe that's been around awhile called Mianserin that's doesn't look like it has a bad profile and is thought to be an inverse agonist on 5HT receptors, so just I guess if you are over there, figured I'd throw that put there.
  3. Want to just throw out there that if anybody hopefully tries the low dose antipsych and hits some kind of wall, that that shouldn't disqualify Nuplazid in any way seeing that it's something for the most part completely different. At least with the antipsych deal, your taking such a low dose that your shouldn't be dealing with side effects.
  4. Here's a link to part of that guys book(post lsd syndrome) if your interested https://books.google.com/books?id=KKYh00o69TUC&pg=PA58&lpg=PA58&dq=thiothixene+lsd&source=bl&ots=TzolEssc07&sig=q6EOTJuaH09Ok7CWdScOWTQn3co&hl=en&sa=X&ved=0ahUKEwiA3_PN8rTUAhWG6iYKHbeIDKYQ6AEIRTAD#v=onepage&q=thiothixene lsd&f=false
  5. It's essentially less is more. When you start increase the dosage of these drugs you start activating all these other receptors and they interact and start bouncing off each other. For lack of a better example, I guess kind of like finding a "goldilocks zone". Kind of like slowly bringing the train to a halt as opposed to slamming the brakes and having the wheels fall off. Also, just hypothetically, I wonder if there's kind of a "breaking point" so to speak, were you keep enough "pressure" on the point(5ht2a), and Things start to normalize. Like if you take X antipsych at a
  6. Got a feeling if the low dose antipsych deal worked, it would take a some time, just throwing that out there. Your trying to get the over activity at 5ht2a down, that's basically the premise and what the guys in North Carolina were trying to tell you and maybe what the guy that wrote the post led syndrome book wrote.
  7. I think the bigger thing there might be the low dose of antipsych's. It seems like it's kind of mixed if remeron an inverse agonist at 5ht2a. A lot of pages say it's an antagonist. I think if people would have gotten better off remeron it would have been found by now. Think it helps to a point. Not trying to bring you down. Sure some records on this page.
  8. Yeah trazadone is an antagonist, this med is an inverse agonist, it's different. It's mechanism is to lower the activity or hyperactivity of 5ht2a receptors.
  9. Also kind of wonder about the low dose of Zyprexa or antipsych meds the one doctor had success with, whether that actually holds up or if they act differently when not causing so much stimulation.
  10. If anything, if you have a good relationship with your doctor and you explain it to them, you may be able to get a free 30 day sample pack. It is being tested as an add on for psychiatric problems as well but when it gets through trials is anybodies guess, it may be another year or so until it is officially labeled as such. I guess it's something you have to ask your doctor if it being covered for right now. Chances are, it will become a wildly popular medication due to the fact that it lowers the amount of other psych meds that people have to take thus lowering the side effect profile, and
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