I'm just trying to clarify a few things in regard to PCT, etc. (Please correct me if in all the area I'm wrong, or partially incorrect).
So, in my limited understanding (and please forgive me because I'm speaking in very basic terms): Estradiol is a type of Estrogen, listed as E2 on blood tests. Basically Estradiol binds to androgen receptors, blocking testosterone from binding to it, causing the testosterone to be useless. Estradiol can even cause your body to create fewer androgen receptors. Estradiol production is caused by conversion of testosterone by aromatase.
AI's like adex bind to aromatase enzymes and prevent them from converting testosterone into estradiol. They don't work on directly on Estrogen receptors. That is done by SERM's such as Clomid and Nolva.
So...a standard PCT cycle of 4 weeks: Running a SERM for all 4 weeks (lets say Clomid: 100 mg, 50 mg, 50 mg, 25 mg) while running an AI for the first 3 weeks (lets say Adex: 0.5 mg 3 x per week, then stopping on the 4th week). I guess I'm trying to understand the science behind doing it that way. Is it because the SERM is working on all kinds of Estrogen and directly on the Estrogen receptors, yet the AI is working specifically on aromatase and we can assume that by week 4 the AI has done it's "job"...and the last week of the SERM is to "kill off", for lack of a better term, any Estrogen receptors that are left over...keeping in mind that we still need some estrogen in our body.
I guess that's a good starting point...any thoughts or clarification would be greatly appreciated.
So, in my limited understanding (and please forgive me because I'm speaking in very basic terms): Estradiol is a type of Estrogen, listed as E2 on blood tests. Basically Estradiol binds to androgen receptors, blocking testosterone from binding to it, causing the testosterone to be useless. Estradiol can even cause your body to create fewer androgen receptors. Estradiol production is caused by conversion of testosterone by aromatase.
AI's like adex bind to aromatase enzymes and prevent them from converting testosterone into estradiol. They don't work on directly on Estrogen receptors. That is done by SERM's such as Clomid and Nolva.
So...a standard PCT cycle of 4 weeks: Running a SERM for all 4 weeks (lets say Clomid: 100 mg, 50 mg, 50 mg, 25 mg) while running an AI for the first 3 weeks (lets say Adex: 0.5 mg 3 x per week, then stopping on the 4th week). I guess I'm trying to understand the science behind doing it that way. Is it because the SERM is working on all kinds of Estrogen and directly on the Estrogen receptors, yet the AI is working specifically on aromatase and we can assume that by week 4 the AI has done it's "job"...and the last week of the SERM is to "kill off", for lack of a better term, any Estrogen receptors that are left over...keeping in mind that we still need some estrogen in our body.
I guess that's a good starting point...any thoughts or clarification would be greatly appreciated.