I’m not a science man so I’m not going to pretend that I know what I’m talking about here so that’s why I’m just juggling this idea. What if everything is stemming from the 5alpha-steroid reductase type 2 gene (SRD5A2) which is having a down stream effect on other genes like a domino effect? In theory wouldn’t this be the first gene to be methylated if indeed DHT flooding into the receptors caused a silencing.
Didn’t only like 53% of people with PFS in the Melcangi study have a methylated SRD5A2 gene though
Did they? Was this against the control studies
Technically, all of the controls were unmethylated because one of the controls had a brain inflammatory condition so it should be ruled out. So if 100% of controls are unmethylated and less than half of pfs are unmethylated, that is a strong indicator of a unique trait pfs people have. If this is repeated in another study it would make this theory stronger.
Also there are many other studies showing that inflammation directly methylates SRD5A2 and silences it.
I cannot comment on the science but if you are interested, read this:
… a group of scientists have identified a genetic switch which is thought to be unique to sexual function. They believe that this switch plays a crucial role in controlling the brain signals which initiate an erection, and new genome editing technologies such as Crispr-Cas9 could one day allow scientists to reactivate this switch in patients.
Interesting Pete.
Can you please link these studies. I want to read.