I suppose that would certainly be one major benefit, ey? 
Khera said he is not to find a treatment but the
'cause" only…Thats his job is to find the cause…But the problem I had as moonchild said he just Started comparing them?! uhhhh
Thanks for the comprehensive reply @axolotl. It’s great to see all the pieces finally coming together with this condition.
It’s interesting that you mentioned antiandrogenic substances being a potential aid for wound healing, but for PFS patients that just causes us to crash further right?
It can be tested i guess. And cyp11a1 might be one of the key issues.
And one thing sodium bicarbonate does…Increases cAMP signaling…
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https://academic.oup.com/jcem/article/90/8/4858/2838533
Treatment with atRA significantly augmented CYP17, CYP11A1, and StAR mRNA accumulation with maximal induction occurring within 16–24 h after treatment (Fig. 3).
Other study shows different results ? or i dont undestand something
We also investigated the effects of atRA on the expression levels of StAR, Cyp11a1, and 3β-hydroxysteroid dehydrogenase (3β-HSD) mRNAs. GCs were cultured for 3–12 h with or without atRA (30 μM; Fig. 2B–D). Treatment with atRA resulted in significant augmentation of StAR
and Cyp11a1 mRNA levels at all times. In contrast, 3β-HSD mRNA was unaltered
Yep, different effects of RA on 3b-HSD in glial cells and granulosa cells from the looks of it. The study I was referencing:
-“ATRA also strongly induced the expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) (an increase of 5- and 50-fold, respectively).”
I have read the study, very nice one! so if we inhibitthe methilation we can have normal neurosteriods and feel better?
I think its very strong correlation specially after the one i the control group that had it had some specific health issue (I dont know if its related with that gene). And also open the possibility to study the cause of the alteration using animal models and also give us the opportunity of a new protocol.
Epigenetic Modifications Do Occur in PFS Patients, New Research Demonstrates
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Hello I have check what natural sources inhibit DNMT1 and SURPRISE all of the are 5ar inhibitors… What is going on?
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Gettin closer. Gosh what a relief if we could get to the bottom of this shit
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I am re-reading the 2016 Harvard study (which indirectly hinted that PFS sufferers were just depressed guys) and we can suspect that those researchers knew that epigenetics played a role, but they deliberately chose not to follow that path of research:
“Although we did not find evidence of sequence variation in AR , SRD5A1 , or SRD5A2 genes, or of significant alterations in expression of AR-dependent genes in the skin, we cannot exclude the possibility of variations in other genes or in the gene expression levels in other tissues or specific brain regions involved in regulation of mood and sexual function. It is also possible that finasteride may exert epigenetic effects which may account for persistent symptoms.”
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155688/)
Why didn’t they conduct any research on this? That Harvard study was instrumental to the pharmaceutical industry, because it simply placed the responsibility on the patients.
Unbelievable.
I hope the Baylor study doesn’t make the same “mistake”.
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There was a Satanic cult on Harvard so I can image what you say is true, they are together with merck for the NWOshit
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(first paragraph)
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As far as I know, they tested skin not from the penis but from the back, which was a deliberate sabotage of the study and against the pre-agreed research protocol. Why they did that is anyone’s guess.
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What’s important for Merck is that the Baylor study was late enough not to come out before the conclusion of the class action law suit, which saved them a couple of billion of dollars.
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So basically there was conflict of interest this entire time as everyone suspected? I’m brain fogged at the moment could someone break this down to me?
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Its illogical to think that any Doctor that is on Merck’s payroll is going to bite the hand that feeds them.
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