Is androgen receptor overexpresssion pushing this syndrome?

What’s everyone’s thoughts?

1 Like

Personally I have no technical skills or knowledge to make my own assessment but I believe what awor and axo in terms of the theory.

1 Like

If it is, I don’t understand why everyone is using Tribulus. It upregulates the receptors more

1 Like

It can give improvement because it also has an antiandrogenic effect.

Tribulus killed me.

I am not sure what you mean by “pushing” it. AR overexpression is most definitely not the cause of the syndrome but a consequence of it. There are multiple theories why it happens.

One theory is that that AR is overexpressed simply because there is DHT shortage in the tissues as 5ar type II is impaired due to methylation of the gene encoding for it. There is a lot of evidence for that theory in my opinion. Read my post here: Tribulus stopped working. What else works?

There is an alternative theory as well.

1 Like

Why do you think AR overexpression isn’t the cause?

Sibelio, I’m still eagerly waiting for somebody to try to disprove this line of reasoning with the evidence which we have to date. Surely this theory stands up to ‘Occam’s razor’ than the AR over expression being the root cause line of thinking…

1 Like

We know the gene encoding for 5ar type 2 is methylated from Melcangi’s recent paper. That must translate into lower concentrations of 5ar type 2 and also DHT - in relevant tissues. Those can in theory be measured. Tissue concentrations of DHT can for sure be measured.

Is there a theory that postulates that AR overexpression is the root cause of PFS? I don’t think the dominant theory argues for that, does it? I think it argues that AR stay overexpressed because the signal is shut down downstream from the receptor.

Now, why the signal would be shut down downstream from the receptor when androgen levels go down after a single pill of finasteride and when AR is not yet overexpressed - that I want to get an answer for.