Originally published at: https://www.propeciahelp.com/androgen-driven-covid-19-pandemic-and-the-post-finasteride-syndrome/
Deregulated Androgen Receptor in PFS In our recent online publication: Post-Finasteride Syndrome as an Epigenetic Post-Androgen Deprivation Syndrome: A potential pathological link between Drug-Induced Androgen Receptor Overexpression and Polyglutamine Toxicity we suggested that site-specific epigenetic changes induced by androgen deprivation as a result of 5AR inhibition may result in a pathological AR upregulation, which in…
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Awor, could you please clarify if, in your opinion, we all have hypersensitive AR or some have hypersensitive ones and some have silenced AR ?
If I understand correctly, our AR would have had epigenetic changes that made them up-regulated or maybe down-regulated is that correct ?
No need for a long answer, I know your time is precious. Just a few words to shed some light would help me understand more and give me guidance on the direction the epigenetic repair regime I’m experimenting with should take.
Thank you for you time !
Hi Greek.
Do you happen to have an answer ? What’s your opinion ?
Thank you
If you refer to the paper that Axo and Awor wrote it hypothesizes overexpressed AR, not “hypersensitive” or silenced AR. This has now been confirmed by Baylor.
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Thank you for your answer !
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Shouldn’t overexpression lead to hypersensitivity and make you hypersexual ?
It seems to be a U shaped curve. Basically having to much, or to little is both detrimental.
I’m not a stupid guy but this isn’t at all my forte.
All I keep asking myself is after this study came out and ppl either have a better understanding of what this is OR it confirmed hat some already knew…
Can this thing eventually be treated?
It’s all I wanna know is if it’s possible
The simple answer is, we really don’t know. Baylor was useful in terms of showing us that we’re on the right track, and that the hypothesis of Axo and Awor was correct - that our AR is overexpressed. However, the study was always limited in its design to study just that, and not to look at possible mechanisms involved or propose pathways for treatments.
The next steps for us are to do the work to understand both the predisposition to this disease - highly likely to be genetic - and the mechanism of action that occurs during onset. Our group have been consulting with researchers for some time, with the support of the PFSF, to bring opportunities to the table for fundraising and we hope to have updates soon. I posted recently about why these are held up currently and we apologise for the delay.
Once we’ve done that work, we may have an idea of what possible treatments look like. As Axo posted in his commentary on the Baylor results thread, this could be through gene editing technology such as CRISPR (which is accelerating much faster than many predicted), or through existing technology. It’s really too early to say.
Don’t give up hope - we’re all working hard and need every patient in this fight with us.
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No need to apologise - we know you and the crew are doing your utmost to get research off the ground.
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