Edit: I don’t know how to make the fancy link with the fancy title and frame layout.
Is PNMT variation part of the 23 and me raw data that was submitted to mods? Would be interesting to see if a lot of us have similar genotypes
No clue, don’t ask me, tag the mods.
Sorry I just meant in general for anyone reading that. @Greek
Does this give hope for cure?
‘there is always hope’ - aragorn
Can anyone shed any light on the findings? It’s way too heavy for me. What does this all mean and does it bring us any closer to a cure?
I think a problem over here now is that we miss central leading figures like Awor and Mew. Smart people with a lot of knowledge and a helicopter view about all what’s going on. People who can put all puzzle parts together and give a further direction for Investigation. People who understand this kind of studies and who can link this to other findings.
Too much armchair dr’s (with good intentions) and too much fragmatised info.
Bump, what is the conclusion of this study is this the missing piece of the puzzle or just one more part. @Awor
All valid points
But what is stopping you or I from finding out if 23 and me tests genes that encode the PNMT enzyme ? Yes it’s work but just saying
Mew disappeared long ago, Awor only occasionally resurfaces. Seems like the right answer would be to have the PFS Foundation review this report and try to interpret it for those of us who can’t understand it. Unfortunately the foundation seems to have given up on the research end of PFS. Not sure what our options are but glad to see Dr. Melcangi is still interested in our cause. It looks like a ton of work went into this research paper.
You can interpret it but it’s a lot of work .
Which is why I’m guessing no one wants to do it
My understanding is that FIN irreversible bound to PNMT and destroyed norepinephrine to epinephrine conversion. Googling PNMT inducers shows glucorticoids induce PNMT…
That is not exactly what it stated.
They found out Fin did bind to PNMT.
This is likely not a constant state and should to back to normal when Fin is out of the system.
Although they discuss how these changes in neurosteroids could affect gut microbiota, which may be harder to restore.
Also it could be that these changes would induce a new level of homeostasis. But it’s not discussed in the study.
I wish they would have discontinued the drug and looked at the levels after a wash out period but sadly they didn’t.
So two different neurotransmitter paths to explore further . Fin’s impact on the
PNMT enzyme and the impact on norepinephrine to epinephrine conversion. And the impact of temporarily lowering Allopregnanolone and the returning of Allopregnanolone on the GABA receptors .
I did not take fin. I took Dut and then Saw P later after Dut. But my prediction is neurotransmitters will be the explanation for a lot of this.
Neurotransmitters/neurosteriods go hand to hand with a lot of this stuff. I think we are on a promising path