if it’s not the cause but effect of PFS as it seems to be
in theory:
a drug to downregulate 5ar
a DNMT-inhibitor
or something like this maybe
why’d you fund this industry rather than supplement straight DHT or methyl DHT?
more important, why treat the symptom with more drugs which may turn you dependent instead of trying to revert the condition
there’s no magical neuro-steroid/transmitter when your hormone system is broken, the latter is in a higher hierarchy
WTF!? What good would this do? Whether enzyme inhibition, or downregulation of transcription, how would this help when this is what got many of us into this mess in the first place.
Also, nandrolone is highly anabolic with very little androgenic activity and that is why it is a popular treatment when anabolic effects are sought after in women and children. This is also a likely explanation for “Deca Dick.” Why on Earth are you pushing ideas like this? To make people worse? I mean, I truly don’t believe you have malicious intent, but I don’t understand what type of beneficial outcome you would expect from anti-androgenic effects.
this is your affirmation, what i think is that AR silencing caused the condition, 5ar methylation being like i said the effect…if you read the post and the papers carefully i believe you can piece it together, i tend to think about the body as an emergent structure trying to achieve homeostasis, if the methylated gene is overexpressed how you expect to reactivate it?
i dont believe in instant symptomatic healing by drugs, if the cause is epigenetic the cure must also be
@VinnyG , My affirmation is confirmed by the number of people with this condition that took 5-ar inhibitors. This isn’t a guess or conjecture. This also goes in hand with an anti-androgenic effect leading to eventual silencing of the AR signal.
Hypermethylated genes don’t get overexpressed; quite the opposite. DNA methylation recruits DNA binding proteins and promotes a condensed chromatin structure, leading to steric hindrance of polymerase binding.
Trying not to be rude when I say this, but should you be making treatment recommendations based on something you have a misceonseption of?
the good’ol correlation / causation, but the body is not a bidimensional entity, it´s the AR silencing that induced the low 5-aR and led to all of this not the opposite, according to the theory
right, but you´re being reductionist when you look only at one enzyme
no, it makes sense that only some need the gene to be methylated since people are born with low / high expression naturally, and the enzyme is not the causation
According to the theory and plenty of evidence, lowered androgenic signalling leads to AR overexpression. Low 5-ar activity is but one way to achieve lowered androgenic signalling.
See the 5-ari Withdrawal Syndrome theory paper and Di Loreto study.
Methylation of the 5-ar II gene also appears to be one regulatory mechanism that may occur due to a perceived excess of DHT (increase of DHT in combination with AR overexpression) in some cell types. @axolotl discovered evidence of this. It’s good stuff:
-“However, the DNA methylation of srd5α2 increased following 5α-DHT treatment suggesting that androgens can modulate epigenetic mechanisms in amphibians”
.
Wha??? …RNA polymerase binding is essential for gene expression. I don’t understand.
[quote=“Dubya_B, post:102, topic:37018”]Low 5-ar activity is but one way to achieve lowered androgenic signalling.
See the 5-ari Withdrawal Syndrome theory paper and Di Loreto study.
Methylation of the 5-ar II gene also appears to be one regulatory mechanism that may occur due to a perceived excess of DHT (increase of DHT in combination with AR overexpression) in some cell types. axolotl discovered evidence of this. It’s good stuff:
[/quote]
that is exactly what im saying, dont confuse it for the cause tho
yes, in a phasic manner, nobody is debating that
These posts have been moved from Altered methylation pattern of the SRD5A2 gene in cerebrospinal fluid of post-finasteride patients: a pilot study since they add nothing useful to the conversation.
The cause being 5-ar enzymatic inhibition in the case of finasteride, dutasteride, and possibly Accutane to some extent.
This can lead to AR overexpression when DHT is lowered to a significant degree by 5-ar inhibition. This must also be where our misommunication lies.
This is different than decreased mRNA expression resulting from a methylated promoter, which I agree is a plausible result of overexpression combined with a return of normal levels of DHT.