FML, I empathise but you’re asking for information we simply don’t - and can’t - have. There isn’t even any anecdotes, let alone “more than just an anecdote of an individual”. You’ll thus be finding contradiction because, if people are suggesting anything you should do regarding this, it is 100% their personal guesswork with no possible basis. Taking into account the absence of any information on predisposition to PFS, if x size sample of men stop the drug and none get PFS, with half “tapering off”, what can we learn? The same as if any number got it. Precisely nothing. There is no way to learn because until you know that that person would get PFS before they stop, what they do around stopping is totally irrelevant because the vast majority of people can stop - and do - and their sides resolve. There is literally no way to deduce anything regarding this until the point where we understand the mechanism of PFS. Even if it is something that puts your mind at ease, finasteride presents significant practical difficulty tapering as @Saro49 has been recently posting regarding.
With the symptoms and situation of PFS, we have thousands of anecdotes that have allowed us to construct a picture of what’s happening that ultimately led to the ongoing major study. It allows us to predict likely reactions to some substances, for instance. From my involvement in the scientific side, I am personally optimistic we are beginning to form a picture of “what”. However, we do not know “why” PFS happens and what the (genetic, epigenetic or both) predisposition to it is. All we know in terms of acquisition is described on the site. We also know due to studies, data from global agencies, membership of our forum, and the vast use of the medication that this problem is extremely rare.
Regarding testosterone, PFS is not hypogonadism. I have hormonal profiles from before and my testosterone doubled in the presence of bottom of the range lutenizing hormone over the months following my crash, over which time I had the onset of ongoing pain and deterioration of androgenic tissues. And regarding triptorelin, considering many of us believe gnrh analogues cause a condition which is the same as “PFS” and are in touch with patient groups about said commonalities, that’s about the daftest thing you could do.
I know it’s not what you want to hear but this is the stupid situation in 2018 because this garbage is still pushed freely with woefully inadequate understanding or warning from the practitioners responsible, and the disease you’re worried about apparently doesn’t exist, which sadly doesn’t stop my perineum burning and brain frying.
I really wish I could tell you something else but you need to bear in mind there is simply no way anyone can have any information on this considering what I’ve just outlined.
