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Everything posted by Mike

  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
  11. Been looking all of this up again I guess for whatever reason. A doctor apparently treated this condition with a VERY LOW DOSE of Zyprexa. I'm talking 2.5 mg or lower, not even therapeutic. Apparently when he went higher he got an opposite effect, doesn't sound like many people were helped by Zyprexa, quite the opposite, but not sure they were on a low dose. He even wrote a book about it the condition if that means anything, The Post-LSD Syndrome. http://www.blogtalkradio.com/powerful-patient/2012/04/13/curing-the-post-lsd-syndrome Ketaserin is an older hypertensive agent,
  12. I haven't looked into this in quite awhile but this to me is very interesting. In other words they seem to be implying is that inverse agonist bring down the basal activity, think of basal activity as "baseline activity". From the way this doctor describes it : Dr Kremens: NUPLAZID is a selective serotonin inverse agonist. To understand this, you have to understand how receptors in the brain work. Many receptors in the brain are capable of initiating signals even when they are not being stimulated, even when you don’t have an agonist bound to that receptor. Signaling
  13. Nuplazid is already available in the US, seems interesting, was reading some more about it. It's a new class of antipsych that fills a need none of the others were. Previous post is from another drug with a similar profile in the pipeline. This was from another website that explained how it worked and in way, why maybe others are having difficulty treating symptoms. Dr Kremens: NUPLAZID is a selective serotonin inverse agonist. To understand this, you have to understand how receptors in the brain work. Many receptors in the brain are capable of initiating signals even when they
  14. This is a related drug "in the model of" the drug mentioned above that has not made it through the drug approval pipeline yet, probably a couple more years if not fast tracked. I bring it up because the chart on this website kind of simply explains the mechanism of this new class. It is literally described as .... "The candidate, nelotanserin, targets the 5HT2A receptor for serotonin in cells from the central nervous system. Its activation is the basis of psychedelic drugs such as LSD. Nelotanserin does the opposite, blocking its activity to reduce hallucinations in patients with
  15. This is interesting.... Was browsing some medical things today and came across this med that came out recently. It made me think it may be beneficial to this underserved area due to its unique mechanism of action. It's essentially an add on antipsychotic BUT it doesn't work like any other antipsychotic on the market. It targets 5HT2A almost exclusively as an inverse agonist and to a much lower extent at 5HT2C. You guys probably know that LSD, psychedelics, ect, target 5HT2A as an agonist, this is essentially a down regulator at that site in other words calming overexcitab
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