So if SFN attenuates AR signaling, as discussed, that means it blocks AR signaling to a degree. Right?
So, if SFN treatment increases the amount of 3α-HSDs in the liver which accelerates the degradation of blood DHT aiding in MBP, then there is a reduction of DHT in the body. Would this not indicate it was acting outside of cancerous prostate cells?
Examining the effects of SFN (Blocking AR signaling, Reducing Serum DHT), one could then look at the effects of say, Spironolactone, which blocks AR signaling and in turn reduced serum DHT.
And for my phone, which isn't fancy, it's just a pain to respond to forum posts. The form which you would write in is tiny and it's just a mess lol.
We don't know for sure, that is why I asked you for another study to clarify.
No, it doesn't mean that. SFN can potentially lower DHT by increasing its conversion to DHT metabolites (which are also androgens). It is not blocking the entire cascade of DHT and DHT metabolites (look at all the metabolites finasteride lowers besides DHT including androsterone) like say finasteride does by inhibiting 5AR. All SFN does it speed up conversion from DHT to DHT's metabolites, which are also androgens and have androgenic properties.
Check out this hormone chart and pathways and look at DHT's metabolites.
https://hackstasis.com/threads/hormonal-charts-pathways.73/
Spiro does a million things, its hair growth properties are more related to minoxidi IMO. They both severely influence electrolytes very similarly so no one knows the exact MoA. What do you mean that spiro blocks AR "signaling"? All spiro does is bind to the AR so androgens can't bind to it and exert their actions (i.e. applying topically to the scalp for hair loss).
I'll give you another example though. RU58841 for hair loss blocks the AR but does not influence DHT or T serum levels. According to your theory, if the AR was blocked or signal was inhibited it would reduce DHT, but it does not do that meaning blocking the AR or interfering the with AR signalling does not necessarily correlate with reduced DHT in serum.
RU-58841 - Wikipedia
Nicotine works similarly but just in reverse that is how nicotine can increase DHT. It simply works the other way around by reducing DHT's metabolites by getting converted further into DHT.
Nicotine inhibits the breakdown of DHT from the androgen 3 alpha hydroxysteroid
Nicotine and cotinine effects on 3 alpha hydroxysteroid dehydrogenase in canine prostate. - PubMed - NCBI
Now, for instance lets say you argue that the cancer benefits of HDAC inhibition being lowered is from the reduction of DHT. Well, there are many things that are considered HDAC inhibitors niacin/niacinamide being one of them.
Niacinamide does the exact opposite. It is androgenic and increases DHT signalling yet is a HDAC inhibitor.
Multiple roles of HDAC inhibition in neurodegenerative conditions
Inhibition of SIRT1 deacetylase suppresses estrogen receptor signaling. - PubMed - NCBI
Hormonal Control of Androgen Receptor Function through SIRT1
The NAD-dependent histone deacetylase Sir2 plays a key role in connecting cellular metabolism with gene silencing and aging. The androgen receptor (AR) is a ligand-regulated modular nuclear receptor governing prostate cancer cellular proliferation, differentiation, and apoptosis in response to androgens, including dihydrotestosterone (DHT). Here, SIRT1 antagonists induce endogenous AR expression and enhance DHT-mediated AR expression
