While this isn’t related directly to PFS, it is interesting to see a demethylating agent like 5-aza-deoxycitidine used to reverse erectile dysfunction caused by induced hypermethylation of a gene involved in the synthetic pathway of nitric oxide:
This looks very important. I will try to read and understand it later. If someone more knowledgeable about genetics and biology can comment that would be nice.
At this point anything is possible could be related or no.
This isn’t likely to be related to PFS in any way, shape, or form, except that DNA methylation is probably a component of PFS. Too presumptuous to say that it is related at least.
The type of ED described in the study is strictly vascular in nature due to loss of production of nitric oxide. The gene discussed in the study that is underexpressed due to promoter methylation (DDAH-2) gets rid of a molecule called ADMA that inhibits a nitric-oxide producing enzyme.
Testosterone deficiency was found to increase ADMA. I can’t find access to the full article through the paywall, but in the google scholar search results it appears to state this effect isn’t a result of decreased expression of DDAH-2:
no significant differences in expression were observed for DDAH-1 and DDAH - 2 (Figure 5
They fed the rats excessive amounts of an amino acid that acts as a methyl-donor precursor (methionine) to achieve this hypermethylation effect.
Methionine gets converted into SAMe (S-Adenosyl Methionine), which acts as a methyl donor. I wonder if I accidentally replicated this study in myself (n=me) by supplementing excessive amounts of SAMe.
btw- nice new avatar @MOONCHILD, but you are only allowed one account per member here. Would you like your older account to be deleted, or would you like the newer account deleted?
Haha. Just realized the opening post reads like “blah blah blah.”
Basically, these scientists were playing around with blunt epigenetic instruments to cause ED, and then reverse it.
We can only hope and pray that the Baylor Study stay true to the Occam’s Razor principle and we learn that the root cause of PFS boils down to a singular issue. The probability of this happening is very low. The more heterogeneous the epigenetic variations are, the harder it will be to concoct a treatment.
That being said, perhaps there are some hormonal or neurosteroidal variations which are common among sufferers, even though the epigenetic variations themselves might differ. In this case, they could be treated directly, such as SAGE 217, a synthetic version of allopregnanolone treating a deficiency in allopregnanolone.