Ah right, gotcha.
bloods are in
LH below range
testosterone below range
shbg below range
e2 above range
dht top of the range
this explains why i was shedding like crazy
also estrogen has a negative impact on hypothalamus and LH so @DHT might be on the right track with the aromatase inhibitor, what is your DHT to testosterone ratio?
@MOONCHILD
i think time off would need a lot of luck relying on homeostasis if the gene is really silenced
in my case 5ar and aromatase seem to be upregulated as bloods point out, for the estrogen it’s simple just add some exemestane with the test
however i think it’s not enough to cause the shift in genic expression we need
enters nandrolone
All of these years no body checked my DHT level… but, i suspect that it is low because i kept my hair 7 years after secession of finasteride which is impossible because i had less hair before the treatment when i was 25 years old also, i suspect that some how my prostate crashed.
That explains a lot with reduced and watery ejaculate also, i have really weird sensation started in my genitals after the 3rd or 4th day of aromatase inhibition. I cannot define it properly but, it is like you are about to come and having orgasm at any time, it is the kind of feeling at the start of orgasm. Then this feeling increased and i start to feel it between my legs and almost like inside of my rectum. I researched and it that it might come from male g spot which happens to be prostate gland. May be it is generating some how it was 14cc before the arimidex which is quite small for a late 30`s man.
And this makes me think about this might be the case for some of us, we reduced prostate which is main dht producer in body and it did not recovered later may be because our bodies high estrogen some how induce a permanent pressure on dht actions on prostate and when dht recovers a bit it reduce our testosterone further down (remember finasteride kills 5-ar pathway around 66 percent only way available for testosterone is aromatase pathway to estrogen) even with high estrogen we had high testosteron but, after secession of finasteride for at least some of us powerful estrogen suppression on hypothalamus bounces recovery.
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@DHT 5ar is not “killed” it recovers in a few days after fina, thats what caused the silencing in first place
don´t know why but im surprised that all my blood markers reaffirm the AR silencing theory
remember me to sue merck when i get prostate cancer
just calculated my free test and it came in at 50% above the range, another reason we can´t rely on testosterone to manipulate our biochemistry and revert this, too many variables like shbg, dht etc
I agree but i do not understand why i still have a small prostate. By killing i mean finasiteride kills it when you are using it not after of course it comes back but now some of testosterone goes to dht while estrogen was still high so total T goes down despite dht estrogen keeps pressure on dht.
Maybe dht goes high for a period but it is not enough to recover prostate or like you said ar is become unresponsive but, if thats the case by taking out aromatase i am pushing dht and testosterone production to maximum if it is a silencing issue i have to crash after a month or so.
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aromatase inhibitors also lower shbg so going by that line it´d be counterproductive
like i said testosterone adds too many variables, better keep an eye on bloodwork, after 3 weeks you should get an idea where things are going
----Edit----
im getting hopeful since i started pinning last week my penis tumescence is back, erection quality got better today, let’s see with the aromatase inhibitor if i can get random boners like the old days
@VinnyG check my story too i got my random boners at first day also sensitivity came back. Then I lost boners I got unbelievable fatigue . That point I understand that I took too much then, I reduced the dosage boners came back fatigue dissipated. I deliberately experimenting fatigue because, after that fatigue, I got that funny sensation in my genitals or prostate and man, it is really make you want sex and offload your load.
I really want to try an aromatase inhibitor like you but multiple people have gotten worse and committed suicide
Well my theory on that is when you take out estrogen you also takeout all serotonin and most people with pfs are vulnerable to mental disorders because finasiteride messes with nerostreoid ratios. Estrogen has neroprotective effects also it modulates serotonin without it and you will have anxiety. it might increase extremely and make you suicidal.
Think you have panic attacks and suddenly you hit by extreme fatigue and it did not dissolves quickly if you do not expect this it will cause further panic and deplete serotonin you got huge depression on your hand.
I already took 10mg methylfolate and 10mg trintellix plus 20 mg methylphenidate last one really protects me from crash.
Anyway aromatase inhibitors are dangerous.
I start to use it because at my last crash if was not a believer, I might really choose to end it…
I really considered it.
I was quitting methylphenidate even I know the cause, I was alone and couldn’t find a way out I immediately start back methylphenidate crash went away in 4 days then, I went to urologist he told me that finasiteride by some unexplained way accelerated natural aging of my androgenic system, and add this; if you would not use it you probably experienced these same symptoms at very late age.
That moment, I understand, I have nothing to loose and started this.
If I lost these gains I do not know what I do. I understand what I lost now. Man satisfaction from orgasm came back, for that alone, worth living for…
My recommendation for you brothers give me time for a month we will all see what will happen.
I can easily say that I am living best two weeks of my life since I hit by PFS.
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obviously you don´t want to crash your estrogen with something like letrozole, come on
people need to keep things in context, and to not create theories but work on those already stablished, otherwise we lose continuity and keep repeating things…if i was on this forum for
more than a year i´d be nuts and giving up already
@DHT which one are you using? exemestane is best, anastrozole rebounds like crazy and letrozole crash is no joke
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I am afraid of exemestane It has crazy half life so, i started with anastrozole after checking these studies
https://academic.oup.com/jcem/article/89/3/1174/2844209
You can check my progress from here:
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@AnhedonicApe , Decitibine (5-aza-2’-deoxycitidine ) was used to successfully demethylate a gene involved in erectile dysfunction that was intentionally methylated by feeding rats an over-abundance of a methyl donor precursor:
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Thought you might be particularly keen on reading the study also:
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One has to question the health of the rats after going through this and whether such a treatment favors abnormally methylated genes; although, I don’t see a reason why it would.
Also raises the question as to why our PAS/PSSD symptoms were severely exacerbated by treatment with methyl donors. Would a non-PAS/PSSD patient experience the same symptoms from excessive methyl donor consumption?
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bicalutamide is an AR blocker tho
Hey dude. My mom who seems to have similair genes as i do, overthinking etc. I look and act a lot like here. She also took the betaine while I did. She noticed nothing. I know the rat study btw`!
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did zadig (RIP) and the other guy even use azacitidine? zadig mentioned he would try it this summer, but i dont remember him reporting using it
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Zadig never took it. I think @AnhedonicApe is in contact with the other guy (Nasibi) you can also find him on the pssd forum
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Does anyone in forum tried azacitidine?
So everyone. A while ago I spoke about nilotinib, its now trialed in parkinson patients because they benefit from it. It works in a different way then demethylating agents like AZA or DECA @awor @axolotl what would ur opinion be on this substance when it comes to demethylating (which i think for me is the case since my very very very bad reaction to a simple methyl donor) I found this out: ‘’ Nilotinib suppresses DNMT expression, induces DNA hypomethylation, and impairs AML patient cell expansion ex vivo and in vivo. A-G, AML patient (Pt) primary cells (n ¼ 3) were treated for 24 hours with 0, 10, or 30 mmol/L nilotinib’’
Also the parkinson stuff: https://gumc.georgetown.edu/news-release/cancer-drug-improved-cognition-and-motor-skills-in-small-parkinsons-clinical-trial/
ALSO. U guys tend to think OVERexpresion is the case. Wouldn’t demethylating be useless for this? I know I crashed on a methyl donor, so I tend to say at least in my PSSD case i have to go for demethylating. But i was wondering if u guys think demethylating would be of any use since u think the AR is overexpressed.
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Which one?
Changes in gene methylation status can cause over/under expression of other genes. No, I don’t generally think it’s useless, but here again, we need to know what to target. The problem with HDACi’s is that they are not very specific.
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