This is one of the more sweeping articles I’ve seen when it comes to looking at a possible type of hierarchy beyond the Androgen Receptor.
The conclusion is pretty wild.
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An interesting read, but they skipped-over AR and only a brief mention of androgens 
The altered microbiome is only a consequence and not the cause. Trying to fix the microbiome is useless. Poor Douglasmich did at least seven faecal transplants before he died. He said that unfortunately they had only changed the consistency and smell of his stool, but that hormonal receptors prevail over everything.
Rest in peace, Mich. I love you.
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The thought here would be specific missing microbes. If so, no amount of hormone or diet manipulation would bring them back.
That being said, as far as a fecal transplant I think that could be a dangerous proposition that could present with more problems down the line. Even though I have some belief in possible microbiome alterations or deficiency even before taking said drug(s), this is something I would never pursue or even recommend.
Were all of Douglasmich posts on propeciahelp or was he also posting on other websites?
He was a member on propeciahelp, solve, and chimed-in on on the “repairing long-term Accutane damage” page (his name was “BlackFox” there) to warn people against 5-ARIs for Accutane-induced hair loss.
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Saving this for later.
Retinoic acid-related Orphan Receptor γ (RORγ): connecting sterol metabolism to regulation of the immune system and autoimmune disease
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ROR-γ drives androgen receptor expression and represents a therapeutic target in castration-resistant prostate cancer
The androgen receptor (AR) is overexpressed and hyperactivated in human castration-resistant prostate cancer (CRPC). However, the determinants of AR overexpression in CRPC are poorly defined. Here we show that retinoid acid receptor-related orphan receptor γ (ROR-γ) is overexpressed and amplified in metastatic CRPC tumors, and that ROR-γ drives AR expression in the tumors. ROR-γ recruits coactivators SRC-1 and -3 to an AR-RORE to stimulate AR gene transcription. ROR-γ antagonists suppress the expression of AR and its variant AR-V7 in prostate cancer (PCa) cell lines and tumors. ROR-γ antagonists also markedly diminish genome-wide AR binding, H3K27ac abundance and expression of the AR gene network. Lastly, ROR-γ antagonists suppressed tumor growth in multiple AR-expressing but not AR-negative xenograft PCa models, and effectively sensitized CRPC tumors to enzalutamide, without overt toxicity in mice. Together, these results establish ROR-γ as a key player in CRPC by acting upstream of AR and a potential therapeutic target for advanced PCa.