It really is.
Also I am still not understanding how the symptoms are actually caused. Epigentic change, androgen receptor overexpression, site specific alterations etc. At the end it seems very vague still.
If most PFS patients had an overexpression of the androgen receptor shouldnt it be easy to test and prove? If this is an important cause, shouldnt we be able to explain how it causes physical changes for example?? If it were so significant, shouldnt this debate be over already?
Can anyone present an exact causal, step by step, explanation of symptoms like penile shrinkage, jaw wastage, fatique, etc etc? Or is this all correlation in correlation out mental gymnastics?
I know it seems like an absurd question, but at times I have the feeling that you moderators already believe that you know whats causing this. Then present an Input (finasteride) to OUTPUT (symptoms) explanation (i.e. a causal explanation not a correlation theory). What do you actually know and what dont you know? At what part of INPUT (finasteride) OUTPUT (symptom) do you still have a stumbling stone? What is the problem? If you had a very compelling causal theory, shouldnt you be able to prove it in a study conclusively?
If Baylor, a study co-designed by awor, does not push us forward in a significant way, will it mean that your understanding is much more limited than you thought?
I am not trying to be confrontational. I am just seeking some clarity here.