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The Cause of HPPD and Possible Treatments.


Fawkinchit

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On 1/21/2023 at 6:12 AM, Fawkinchit said:

If per say that the neurons are not lost, then the mitochondria can repair and replenish. Unfortunately its just not known whether or not we have lost neurons.

Hey man - I know it's a while since you've posted in this thread - but did you get any further with your thoughts on the etiology of it all?

Would you still recommend your niacin stack - or do you think there's potentially less chance of it working if neurons are lost? or do you think it might help to regrow axons (going from the interneuron loss theory)?

I've been taking the stack - it seems to help with my mood, it seems to have subdued some of the trippier elements of my visuals but not the more recalcitrant long lasting symptoms...it's only been a week though.

Anyway just wondering if you're still confident that based on your most recent reading if you think it's still likely a good treatment.

Oh - and love all your work mate. I'm sure I can say for everyone here that you're incredibly appreciated.

Joe

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  • 2 weeks later...
On 7/18/2023 at 2:45 AM, joegives said:

Hey man - I know it's a while since you've posted in this thread - but did you get any further with your thoughts on the etiology of it all?

Would you still recommend your niacin stack - or do you think there's potentially less chance of it working if neurons are lost? or do you think it might help to regrow axons (going from the interneuron loss theory)?

I've been taking the stack - it seems to help with my mood, it seems to have subdued some of the trippier elements of my visuals but not the more recalcitrant long lasting symptoms...it's only been a week though.

Anyway just wondering if you're still confident that based on your most recent reading if you think it's still likely a good treatment.

Oh - and love all your work mate. I'm sure I can say for everyone here that you're incredibly appreciated.

Joe

Hey Joe!

Haven't really made much more progress on anything lately, just have been working a lot and trying to find ways to maybe make some money to do research on the matter and test some of the ideas, or at least do some studies that show with evidence certain causes of the condition.

The niacin regimen I am not entirely sure of, one thing that I have been aware of and has certainly been proven true is that there are vitamin complexes in foods, and typically the singular vitamin extracted is scarcely as effective without the complex. Synthetically produced vitamin C for example in comparison to a comparable amount of camu camu is almost completely ineffective, as shown by studies, there are other examples as well, but too profuse to elaborate on for the time being. I think a natural sourced vitamin c complex would be better than niacin in its self, and maybe a natural b complex better also.

If the problem is neuronal loss however, I don't believe these will help much. Though a c complex would be better than nothing. 

And thank you I appreciate the support very much. 

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  • 1 month later...

Thought this was really interesting, seems like its saying that downregulation of 5ht2a receptors are long term...

Edit: Realizing that I think they mean while still on the antagonists. Although I do want to state that there may be unknown variables in the premise of downregulation/upregulation that may have not been fully explored yet. Maybe there are permanent changes that can possibly occur. 

Its extremely interesting as well, that, as I think I have brought up before, that schizo/OCD/and other conditions appear to be linked to 5ht2a receptor dysfunction, which alternatively I suppose may also be the case with HPPD. If I remember correctly there is consistency with HPPD and previous mental health conditions of the same lines. Even I personally have had mild OCD. 

It is strange as they state as well that the antagonist induce downregulation, instead of upregulation, which is quite paradoxical as they state. 

Functional regulation of 5-HT2A

The functional regulation of 5-HT2A involves desensitization and re-sensitization, which differentiates 5-HT2A from conventional GCPRs (e.g. the B2 adrenergic receptor) and prevents overstimulation.1 At the molecular level, desensitization and re-sensitization of the receptor are controlled via clathrin-mediated receptor internalization and recycling.1 This dynamin-dependent internalization can be triggered by antagonists or agonists of the receptor and exists to allow the recuperation of signaling competence.1 Long-term use of 5-HT2A antagonists has been shown to downregulate 5-HT2A expression1 and, while the mechanism of this "paradoxical regulation" is unknown, it is likely due to functional regulation.

https://www.reprocell.com/blog/biopta/5ht2a-serotonin-receptor#:~:text=5-HT2A receptor location,ligand binding experiments in rats.

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On 9/10/2023 at 1:15 AM, Fawkinchit said:

Thought this was really interesting, seems like its saying that downregulation of 5ht2a receptors are long term...

Edit: Realizing that I think they mean while still on the antagonists. Although I do want to state that there may be unknown variables in the premise of downregulation/upregulation that may have not been fully explored yet. Maybe there are permanent changes that can possibly occur. 

Its extremely interesting as well, that, as I think I have brought up before, that schizo/OCD/and other conditions appear to be linked to 5ht2a receptor dysfunction, which alternatively I suppose may also be the case with HPPD. If I remember correctly there is consistency with HPPD and previous mental health conditions of the same lines. Even I personally have had mild OCD. 

It is strange as they state as well that the antagonist induce downregulation, instead of upregulation, which is quite paradoxical as they state. 

Functional regulation of 5-HT2A

The functional regulation of 5-HT2A involves desensitization and re-sensitization, which differentiates 5-HT2A from conventional GCPRs (e.g. the B2 adrenergic receptor) and prevents overstimulation.1 At the molecular level, desensitization and re-sensitization of the receptor are controlled via clathrin-mediated receptor internalization and recycling.1 This dynamin-dependent internalization can be triggered by antagonists or agonists of the receptor and exists to allow the recuperation of signaling competence.1 Long-term use of 5-HT2A antagonists has been shown to downregulate 5-HT2A expression1 and, while the mechanism of this "paradoxical regulation" is unknown, it is likely due to functional regulation.

https://www.reprocell.com/blog/biopta/5ht2a-serotonin-receptor#:~:text=5-HT2A receptor location,ligand binding experiments in rats.

And if this is the answer,what treatment would be good?

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  • 2 weeks later...

Just posting this study that shows that there are increases of glutamate in the prefrontal cortex from LSD. It states an increase or 206% from the second drugs tested but seems to bypass the percent increase from LSD.

I think i looked in to this once and the increase wasn't as substantial with LSD, no where near in range to suspect possible glutamate cascade toxicity. But I will look in to it again incase I can find anything else or incase I missed anything.

https://www.sciencedirect.com/science/article/abs/pii/S0006899304011813

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On 10/3/2023 at 7:43 AM, Siren001 said:

These are all great theories.

 

Too bad nobody here is capable of testing them.

 

I would actually be capable if I had the time and money for the equipment.

That's actually what I have been working on a lot in the last few years, which is why I haven't posted here as much. So far no success yet. But, there is still time. 

Edited by Fawkinchit
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