PFS an adaptation to a higher androgen environment

I took cyproterone to lower my testosterone, since that time I have pain all over my body (scalp, eyes, bladder, bones, joints,…).
But if some guys want to try what I did, fine, I’m curious what will be the outcome. We need more guinea pigs.
Or just don’t try anything reckless, because it could make your case even worse.

Hey can I ask why you took Cyproterone and was it Dutasteride that caused you to get Post Finasteride Syndrome

I took Cyproterone because of gender disorder.
Before that I had PFS because of Lupron or Dutasteride. But my main issue was only no sex drive at all, it was not a big deal, just sometimes frustrating.
I took Lupron in 2009 for a year after almost a year of Cyproterone then I stopped for Dutasteride (my endo told me it was a light AA, I was not aware of what it is exactly). My testosterone came back and still no libido. I was intrigued.
In 2017 when I took back Cyproterone and Lupron (again) my sex drive came back for a while, but pain appeared with it. That’s when I realized I might have androgen receptors upregulation. But all docs I met made fun of me because of that theory. On propeciahelp it was a commun shared theory, so I knew it was definitely FPS. I tried a lot of stupid things. But I truly think now the best way to be cured is to do nothing at all… if you try something, you can never know what’s going to happen because no one really understands what’s going on.
Sometimes I also think its not only androgen receptors upregulation, because when I had 0 testosterone and stopped estradiol I had strange feelings in my breasts, I could feel more feminine, like my estrogen receptors were also upregulated. I cannot prove it but it made sense to me at that time. I just wanted to add that. And I also think maybe PFS is the opposite of PSSD (androgen receptors downregulation, I cannot prove it, just an intuition from was I read).
So pease be careful, don’t try anything foolish. I was stupid to no giving up.

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Finasteride and minoxidil both affect the androgen receptors although the mechanism is different in each cases

But it just proves that changing serum dht levels won’t do crap…

Changing serum dht is the action which triggered the mechanism of AR alteration , if we didn’t touch that hormone , things would’ve been normal for us , some poeple got the same condition by lowering their estradiol serum via armidex , the interesting part is the role of E2 in every pfs case , i think we need to investigate more about that

Minoxidil does not change serum DHT levels and it brought me here.

It can lower your androgen activity in somme tissue but not in your blood , most people on this forum have a normal androgen activity in their blood level but may suffer from a lack of androgen activity in the genital area ; here’s a study showing that Minoxidil acts as anti-androgen https://pubmed.ncbi.nlm.nih.gov/30064598/

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Yes but it’s not lowering DHT like you said, it’s suppressing androgen receptors.

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That’s true , however lowering temporarily the hormones may have played the most prominent role in the alteration of the androgen receptors because some people (generally for a bodybuilding purpose ) got similar symptoms to us by lowering their estradiol level via armidex alone

So how many years did you go without libido and forgive me if I picked this up wrong but are you saying that when you were put on Lupron and Cypoterone in 2017 that your libido came back with pain?

8 years without libido because of lupron or dutasteride
Came back when I took Cyproterone, but was never consistant. Now I have some sex drive twice a week, sometimes more sometimes less.

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I have had this same thougth a lot of times, lowering our androgens to see if the “signal” improves, also because before PFS I became hyperandrogenic with 1mg finas.

After aprox 4 years with PFS I started taking finas again several times in different doses with this goal without any change, better or worst, still take time to time. Aprox one month ago I tried 3 days of cypro (1/8 50mg each day), but I scared and stopped, did not feel anything during thouse days. For me the most promising but also danger would be to try bicalutamide, not just lowering the androgens, to block the receptor and pray to recover the normal signaling after the blocking, crazy but who knows …

Other thing that just recently tried is nitroglycerin to improve nitric oxide, but I will open other topic about this for not mixing different issues.

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Interesting. Thank you

I have seen Bicalutamide mentioned here before not aware of any users experimenting with it. If lowering androgens and keeping them chronically low don’t work then I’m at an absolute loss how this can be reversed, it makes sense in my mind but who knows how methylation, histone acetylation, chromatin remodelling can be reversed in site specific tissues if that’s actually what’s happening.

butyrate crashed you?

is that what moonchild took to recover as he claims?

Wenn sich minoxidil negativ auf die androgenrezeptor wirkt könnte man es wohl kaum als Bart wuchs mittel verwenden soweit ich weiß stimuliert es die Follikel kann aber zu Blutdruck schwankung führen. Oder sehe ich das falsch ?

Hey guys! I think bicalutamid is not advisable, sometimes people after withdrawal see a further decrease in PSA and regression of prostate cancer suggesting induction of androgen resistence which is what has brought us here.
But I think adaption can go the opposite way reversing our condition. Maybe the key is to deprive androgen receptors for a certain time to resensitize them as you theorized yet, but the key point would be to avoid the androgen rebound at any costs which is responsible for androgen receptor signalling downregulation. Maybe a combination of a 5ARI together with HPA axis shutdown could realise this to make sure after 5AR come back online they dont have immediately testosteron to convert.

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I have had a few theories on this platform but this one makes the most sense to me. Our receptors were unable to recalibrate properly leaving us in a diseased state. The androgen receptor is permanently downregulated in tissues because it is sensing that there is too much androgens so long as we our producing them they will remain that way acting like a safety switch. The reason why taking Finasteride again won’t work is because it increases Testosterone and both have an affinity for the androgen receptor. What we need to do in my opinion is drag Testosterone right down and let the receptors upregulate again, if this disease is epigenetic then it means it is not permanent, our cells adapt to changes in the environment and should theoretically change given the right stimulus. I also believe this because my body tried to shut down Testosterone levels to 8nml I felt much better when it was chronically low.

Two questions that need to be asked?
Why do men feel like they get better with time, is it because Testosterone decreases by 1% every year after the age of 30?

Is it because methylation decreases with age?

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I’d like to know if there’s any truth to what you said about taking cyproterone and intentionally lowering your Testosterone and why you did it in the first place. Thanks

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