May be of interest. See plot linked therein.
Big difference between endogenous T production with an intact HPTGA vs using exogenous T where one uncouples negative feedback loop between T/E2 and hypothalamus/pituitary.
With endogenous T production there is typically strong correlation between TT and SHBG. With exogenous T use you see SHBG decrease over time with TRT/AAS usage [usually dose dependent].
Also usually misunderstood…your T dose sets your free T level and then SHBG sets your Total T. That is fT level set by mass action (how much T you inject) then SHBG binds some fT to TT by dynamic equilibrium (storage). At steady state for same injection amount per unit time, the amount of fT leaving body is proportional to amount entering body. At steady state there is no accumulation hence SHBG can’t change fT level for a constant T dosage per unit time (only the storage amount). Also ignoring downstream conversion, E2, etc.
You can try this experiment yourself by keeping your TRT dose constant and drop SHBG with another medication like oxandrolone/etc. Now compare your pre and post TT/ fT levels using accurate TT/fT methods.
I’d argue (if SHBG does play a role) that more realistically the honeymoon period fades for many due to T/AAS abuse which erodes SHBG over time (there’s probably a bunch of factors in the erosion of that honeymoon phase). You don’t see SHBG increase over time with with exogenous T use. We still don’t understand the full roles of fT/TT and relative impacts which are coupled with SHBG.