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
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.
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.
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
@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:
Thought you might be particularly keen on reading the study also:
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?
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. 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.
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.
By HDACI-bicalutamide I assume they mean a combination of an HDAC inhibitor and bicalutamide? It’s confusing that they didn’t mention which HDAC inhibitors they used.
It seems like PFS, PSSD and all other conditions are caused by very low levels of androgens, however bicalutamide shouldn’t cause low levels of androgens because it simply blocks the androgen receptor. Do you guys think this would have the same effect as inducing low levels of androgens? Or perhaps this could be a seemingly paradoxical cure.
5-alpha reductase type 2 (SRD5A2) , an enzyme that is critical for prostatic development and growth, is utilized as an inhibitory target by finasteride for patients with bladder outlet obstrution secondary to BPH. However, we have found that many aging benign prostate tissues do not express the enzyme. Since the SRD5A2 promoter contains a CpG island, we hypothesized that somatic methylation of the promoter would be regulated by DNA methyltransferases leading to suppression of SRD5A2.
We found that methylation of SRD5A2 was regulated by DNA methytransferase 1 (DNMT1) and the cytokines, TNF-alpha, NF-κB and IL-6, regulated DNMT1protein expression and thereby indirectly affected SRD5A2 promoter methylation and gene expression.
Induction of inflammation with lipopolysaccharide (LPS) stimulated the TNFR1/NF-κB/IL-6/DNMT1 pathway, leading to hypermethylation of the SRD5A2 promoter and silencing of SRD5A2, while treatment with both LPS and TNF-alpha inhibitor reversed this pathway and reactivated SRD5A2.