I think this looks very interesting for us.
It was designed as an anti estrogen but is also an anabolic. It supposedly binds to the ER but is not estrogenic. It is used widely to reduce gyno. You will find many have had success using it in this manner. It was designed as a breast cancer drug like all anti estrogens. Obviously was not very sutable as it is anabolic.
Anyway I am pretty sure my PFS is caused though the Estrogen receptor at this stage. I beleive there is some metabolite which is binding to it and estrogenic gene expression. I am pretty sure this is not an estrogen created by aromotase as if that was the case an AI would work well to fix us up. It does not.
I am thinking something along the lines of : en.wikipedia.org/wiki/5%CE%B1-An … CE%B2-diol
"5α-Androstane-3β,17β-diol, also called 3β-androstanediol, and often shortened to 3β-diol, is an endogenous steroid hormone. It is a 5α-reduced and 17β-hydroxylated metabolite of dehydroepiandrosterone (DHEA) as well as a 3β-hydroxylated metabolite of dihydrotestosterone (DHT). Similarly to DHEA, 3β-diol is a high-affinity full agonist of the ERβ, and hence, an estrogen. In contrast, it does not bind to the androgen receptor.[1]
Where I am at the moment I am going to find it hard to get this stuff. Is there anyone else out there willing to give it a try? Blocking the ER with a SERM is not going to be a good idea as they act as estrogens in some tissues and agonists in others.
It would be really good to rule out the ER.
We can then look at blocking the progesterone receptor with mifepristone.
In my case I do not think the androgen receptor is blocked as when I inject fair sums of T my body hair grows, my hair on my head falls out and I have to shave more often. Despite this I am unable to gain muscles like old days and still have fat around my hips etc.