Mike

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About Mike

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  1. Damn dude, sorry it didn't work out, quick
  2. 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.
  3. 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
  4. 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 low dose for a month or two or maybe even longer that then it starts to "slow the train down" like a crest or something, then maybe like a cool down period so it gets use to being in a normal state. Everybody probably has a different I guess "goldilocks zone" so to speak and you have to "hit the brakes" a different amount of time for whatever person. But hypothetically, your trying to take an amount lower than the amount that causes extrapyrimadal side effects(or I guess very minimal). That I imagine would be a good indicator because if your activating other receptors, I.e. Dopamine. I guess one good thing is that if anything, most people with this are in a relative steady state(you don't have Parkinson's), but I'm not a doctor but if you have other Health problems, you should not ignore them, just throwing that out there. If anybody listened to the podcast by the doctor that wrote the "Post Lsd Syndrome" book, he was using the lowest possible dose of Zyprexa(2.5 mg) of all things and sometimes that was too much so people I guess cut them in half if you can, half to listen again sometime. Was reading though that Zyprexa effects 5ht2a and 5ht2c,ect at a much higher level than dopamine, which may be why the guy that wrote the "post lsd" book got more benefit from it than others. Maybe an easier way to find a middle ground with it. But I guess the thing about Nuplazid is it bypass having to do most of this because it doesn't mess with a lot of other receptors other than 5ht2a(strongly) and much less more 5ht2c, it just may be a challenge of getting a script and even then getting it paid for. I know they have free 30 day sample packs out. I guess nobody knows how long it would take to work if it did since nobody's given it a real run yet, might take awhile might not, everybody's different. I would think if you had a good relationship with your doc and you showed him some literature a light would go off in their head. Either way both avenues are worth exploring. Yeah so in short. Nuplazid or Low dose antipsych in a "goldilocks zone" good luck
  5. 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.
  6. 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.
  7. 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.
  8. 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.
  9. 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 it has been used in research settings for quite some time. Hopefully if it's remarkably effective, it will not need to be used very long term. Maybe paired up with klonopin or something.
  10. 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, also sold as a gel that is related to Nuplazid(primavanserin). It seems to come up a lot when researching this area. It seems like researchers are aware of its LSD blocking capabilities and effects on seretonin, however, it's only I guess shown to stop the effects of lsd when taken prior to ingestion??? Though I have never heard of anybody using it for this condition before this article was recently published. Not sure about availability. https://www.theverge.com/2017/1/26/14388034/lsd-acid-neuroscience-trip-meaning-research-science
  11. 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 can occur without an agonist; that is called basal activity. If you have an agonist, that stimulates a receptor and increases the activity of that receptor. Then there are drugs called antagonists. Antagonists block the agonist, but they permit the ongoing basal activity. Then you have inverse agonists. Inverse agonists suppress basal activity. So, with NUPLAZID, you are suppressing the basal activity of some serotonin receptors in the brain. It’s thought that the effect of NUPLAZID is a result of a combination of an inverse agonist and antagonist activity at serotonin receptors.- See more at: http://www.ajmc.com/journals/supplement/2016/understanding-the-burden-and-management-of-hallucinations/a645-article/P-4#sthash.O13qeyGg.dpuf so even if your antagonizing the receptor your still activating it in a sense, antagonism returns it to it "baseline". But if it's stuck being hyperactive so to speak, inverse agonism depresses it, it's different, a lower baseline. The "volume" is what needs to be lowered.
  12. 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 are not being stimulated, even when you don’t have an agonist bound to that receptor. Signaling can occur without an agonist; that is called basal activity. If you have an agonist, that stimulates a receptor and increases the activity of that receptor. Then there are drugs called antagonists. Antagonists block the agonist, but they permit the ongoing basal activity. Then you have inverse agonists. Inverse agonists suppress basal activity. So, with NUPLAZID, you are suppressing the basal activity of some serotonin receptors in the brain. It’s thought that the effect of NUPLAZID is a result of a combination of an inverse agonist and antagonist activity at serotonin receptors.- See more at: http://www.ajmc.com/journals/supplement/2016/understanding-the-burden-and-management-of-hallucinations/a645-article/P-4#sthash.O13qeyGg.dpuf
  13. 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 DLB and PDD." With a diagram. Give it a look. http://labiotech.eu/axovant-sciences-bermuda-dementia/ Best