Prolonged androgen deprivation leads to downregulation of androgen receptor

So the majority on here are of the mindset that trying to achieve a type of downregulation of the AR is the right thing to do? I’ve done some browsing. Ok. Hypothetically what if the problem was increased or aberrant AR signaling that becomes pathological?
Everything is showing downregulation as a consequence though.
The thought of this flood of hormones returning after cessation of the drug, isnt that a normal process thats to be expected?
Why is it being made to seem abnormal or sensationalized?
It would seem hormones return, receptor activity stays diminished, or
Receptor activity increases, AR signaling increases, and something needs to pump the brakes.

Prolonged androgen deprivation leads to downregulation of androgen receptor and prostate-specific membrane antigen in prostate cancer cells

Pulled this from an old thread.

Finasteride downregulates the Androgen Receptor (AR)

The biological basis for the use of an anti-androgen and a 5a-reductase inhibitor in the treatment of recurrent prostate cancer: Case report and review

laboratory experiments showing that finasteride, separate from its ability to reduce DHT, can modulate factors influencing cancer proliferation and evolution to the androgen independent state through its direct action on the androgen receptor (AR).

Moreover, Wang et al, have shown that AR phosphorylation determined whether AR ligands act as agonists or antagonists. For instance, [b]DHT, a natural ligand of AR, significantly stimulated expression and phosphorylation of AR and, as a result, acts as a strong AR agonist /b. [b]The authors also showed, in another experiment, that finasteride markedly inhibited PSA secretion and expression while the level of AR was dramatically decreased

the levels of AR proteins were decreased either by bicalutamide or by finasteride alone, and this decrease was enhanced by the two-drug combination. As an AR regulated down-stream gene, the expression of PSA paralleled the decrease of AR expression/phosphorylation.

^and isnt there a recent thread still going on here looking at Bicalutamide as a solution?
Why?

How many studies have shown overexpression of AR vs downregulation?
Im not just talking about Fin, but include Accutane and everything else anti-androgen.

Hey man, could you help me out, in what kind of timespan does ADT run its coarse, and at what time will the androgen receptor be downregulated? Do you have an idea? Because that might mean a swift exogenous supply of androgens must be warranted to prevent this outcome from occurring.