Hello.
So, after some research and banging my head against the wall multiple times, here is what I found, and I share it as I feel that it is relevant to be shared for the better future of everything.
If you search a bit about how psychedelics work, it is believed that they do work via activating the 5ht2a receptor. As they are substances that lock into the receptor and activate it.
As you activate a lot of those receptors, at the same time, looks like it causes the psychedelic experience. Keep in mind that usually the 5ht2a and all other 5ht serotonin subtype of receptors are activated by, you guessed it, serotonin.
All these compounds, mimic the structure of serotonin, in such a way that these receptors to speak so, mistake these molecules for serotonin itself.
That means that not only serotonin can enter and activate the receptor, but other compounds as well. To say so, all chemical structures that mimic serotonin in some way, of just have the structure necesary to interact with the receptor, will.
Knowing this, there is something that is not a compound exactly, but it is capable of activating the 5ht2a receptor too.
It is found in our own body, and it is not a substance.
JC virus or also known as Human Polyoma Virus 2, is capable of entering the 5ht2a receptor, and activating it.
This is a benign virus, and usually does not create any problems, people get it at some point in their life, and it will reactivate only in the event of inmunosupression of some sort.
The virus does this, because it uses the receptor to enter the cells.
Now you have to understand that there are 5ht2a receptors in normal cells, like glial cells, oligodendrocites, some cells in the kidneys... and those cells when the virus attaches to the receptor, the cell to say so recognizes the virus as something of its own, and welcomes the virus inside of it. This process is called endocitosis.
But the nerve cells have 5ht2a receptors as well, but when activated, the neuron does not welcome anything inside. Instead, this triggers a signal via depolarization of the cell membrane, to the colindant nerve cells ,kinda like setting current to a cable, so the signal is transmited.
So what do you think would happen if the virus attached to a 5th2a receptor in a neuron?
Well, it would trigger a signal, and in the process, this would make the serotonin level in the intersinaptic cleft/space to deplete. As depletes, the colindant 5th2a receptors are not "filled" with anything. Overtime the receptor closes, and the virus deataches from the receptor. But the other 5th2a receptors that remain open, and these have affinity/attraction for something that triggers them, and the virus gets into them again, and again and again, making a constant impulse/activation of the 5ht2a receptors in that intersinaptic space.
One of the ways that you should de-attach the virus from the receptor is via using an antagonists, hence a substance that blocks the receptor.
For the treatment to be successful, it should be a substance that is not stimulating any other receptors, but only antagonizing.
Cyproheptadine, mitrazapaine, would be good candidates. Antypsychotics... well there are some that barely of almost do not agonize other receptors, but usually do not work as clean as pure antagonists would. These might indeed as some users report, make things worse for a bit, as they usually agonize the 5ht1a receptor. Keep in mind that people get hppd from all kinds of things, or nothing at all, as in the visual snow cases.
The antagonist used for the treatment, should be with high affinity for the 5ht2a receptor, and only having antagonist activity at all receptor sites, it cannot be agonizing at any receptor site nor causing stimulation.
Stimulation, will make the presinaptic neurons to not pull more serotonin in the intersinaptic cleft. Reason why is because as long as the post sinaptic/receiving neuron is getting triggered, there will not be an increase of neurotranmiters. This is a process of neurotransmiter regulation that constantly takes place in our nerves, otherwise if it did not exist we would have moments of abnormal stimulation and such and things wouldn't work as intended up there.
Also, reason why you get hppd after ussage of substances, is due that extraordinary stimulation, makes the serotonin neurotransmiter levels to lower, as such, there is nothing that binds and fills the 5ht2a receptors that remain open. If there is nothing there, this means that whatever that has affinity for that receptor and is near, will enter the receptor. Once the JC virus starts activating the receptor, it creates a vicious cycle, where it cannot unnatach.
Video for reference.
Hope this sheds some light into the issue of HPPD and hopefully inspire your MDs to make better decisions in regards to prescribing medication that suits you well.
Keep in mind that best thing also would be to check what's the cause of the inmunosupression you are going through, so you can fix it and the virus never spreads again to your brain ever again, and what is remaining of it clears itself out thanks to your inmune system, to say so. Otherwise you will be at risk of this again.
Some references that you need to have too:
https://en.wikipedia.org/wiki/Human_polyomavirus_2
The virus is very common in the general population, infecting 70% to 90% of humans; most people acquire Human polyomavirus 2 in childhood or adolescence.[22][23][24] It is found in high concentrations in urban sewage worldwide, leading some researchers to suspect contaminated water as a typical route of infection.[8]
This basically means that you are very likely to have had it at some point. It is benign, and does not cause problems usually, as many other viruses in our bodies do. You need inmunosupression for it to become malignant
Human polyomavirus 2, commonly referred to as the JC virus or John Cunningham virus, is a type of human polyomavirus (formerly known as papovavirus).[3] It was identified by electron microscopy in 1965 by ZuRhein and Chou,[4] and by Silverman and Rubinstein, and later isolated in culture and named using the two initials of a patient, John Cunningham, with progressive multifocal leukoencephalopathy (PML).[5] The virus causes PML and other diseases only in cases of immunodeficiency, as in AIDS or during treatment with immunosuppressive drugs (e.g. in organ transplant patients).[6]
Note the bold "Only". Note that for it to be diesase making, you need your inmune system to be supressed. Now, a heavy inmuno supression would mean that you are at risk of Progressive Multifocal Leukoencephalopathy. A not that hard of inmunosupression, as a flu, or whatever, or partying several days in a row for example, would be a trigger too, not to make a heavy disease, but to provoke visual snow and hppd.
Also important:
Human polyomavirus 2 can cross the blood–brain barrier into the central nervous system, where it infects oligodendrocytes and astrocytes, possibly through the 5-HT2A serotonin receptor.[14] Human polyomavirus 2 DNA can be detected in both non-PML affected and PML-affected (see below) brain tissue.[15]
So this means, that even in seeming healthy people, this virus can enter the brain and infect the 5ht2a rececptor (keep in mind that healthy accoding to these terms, means just functional people, I doubt they have reference of their actual health complaints). Plus these tissues were from dead people where they found this evidence and before dying usually you have a bad healthy state. And how is it that many many HPPDrs have other health issues, usually autoinmune conditions, rashes, and what not. I don't think this is a coincidence. In my case I had lyme disease wich was causing me inmunosupression, and went unnoticed for years before causing major health issues. Then HPPD came in. Wich made things worse, specially sleep wise and this affected everything else healthwise as logic dictates.
Idk, stop the labels, connect the ideas, and solve your problems. Try what makes sense and share your results. But after all, I'm 100% sure this is pretty much the cause of the condition, and an antagonist at all sites is what would heal the condition. Try avoiding anything with an agonist effect at any receptor ( check the charts in wikipedia ) and specially I would say avoid risperidone at all costs too as it usually for some reason can make things worse and that shit is brain sterilizer shit. Avoid any medication with fluoride in it seriously. indeed is a irreversible antagonist to the 5ht7 receptor wich means it will shut it down undeterminatelly ( untill you take something that takes the risperidone molecule awaya from there, some other substance with affinity for that receptor, just ranting a bit, but I can reference everything I'm saying)
Well, that's the end of my rant, just wanted to share some ideas. This is no advice, and anything you do regarding your health consult with a specialst first, but do consult with a good one, because it can be hard finding one smart enough, with enough time and what not for him to be able to assist you accodingly in the best possible manner, having understood all he needs to understand to understand the condition ( and this explanation ).
All other treatment than that, I personally consider symptom managment, althought blocking calcium channels/making the neuron to rest will promote serotonin being pumped in the intersynaptic space again and eventually achieving remission.
If any questions, do not hesitate to post them or DM whatever. Be kind. You deserve it.
This was my 2 cents and just ranting a bit, do not take it too seriously, although this can be helpful, this is me just sharing funny ideas and opinions and nothing shall be taken in any way. Just read this as you read a sci-fi novel. People do say and write things and share them and there is nothing wrong with that alright? I could have not written this wall of text and just mind my business to. Apreciate all and stop taking things for granted.
Much love.
Stay safe y'all
mise à jour Le groupe de participants qui sera sélectionné est en cours de constitution. Nous sommes en avance pour créer l'histoire!
Sounds encouraging! I will monitor the progress
I think around 15 years now. I generally take between 0.75-1.5mg 3 or 4 consecutive days a week, then have 3-4 consecutive days off. I occasionally have a week on if i'm on vacation. I occasionally also have 2 weeks off, to clean the system. I once had 6 weeks off during lock down to really test any signs of addiction/withdrawal... all was ok. So far, no withdrawals and no noticeable tolerance
