Hi moonchild, your searches are very interesting. I have pssd. I wanted to think about some issues: We are hypothesizing that epigenetic modifications have taken place after taking drugs. This hypothesis that I also share has only been partially confirmed, for example, in the last study by Melcangi (in which the 5ar promoter was essentially hypermetilated), although in reality we have noticed a correlation, which is not necessarily a contributing factor. So I wanted to ask you, in your opinion, given that we do not yet have definitive proofs of these epigenetic alterations, given that we do not know with certainty the genes involved, the use of these HDACi could not be dangerous? Let me explain, if we were to modify the genetic expression of oncogenes or tumor suppressors would it not be a risk? Can we think that they act mainly on the genes that have been hypermetilated, so they should work? And if for example the gene that has been silenced and is the cause of our problems (we as regards the pssd we are oriented on the various genes, but in particular on some protein that includes the complexp of the receptor 5ht1a or the proteins responsible for its signaling) even if hypermetilated by drugs, was it still less methylated than other oncogenes? They would still be demethylated a lot more in their relationship, am I wrong?
