Ment / test cycle and how much AI?

[Type-IIx]

In the recent bloodwork where test-primo was 1.67:1, my E2 was 21.8 but when test-primo was a ratio of 0.87:1 by E2 was 22. Shouldn’t it have been even less?

Makes me think the dose-response is non-linear and that Primo may modulate estradiol at a low threshold honestly. I think perhaps the "ratio" concept is just bad bro-science.

 

[Jbagel132]

Makes me think the dose-response is non-linear and that Primo may modulate estradiol at a low threshold honestly. I think perhaps the "ratio" concept is just bad bro-science.

So basically this means that while increasing testosterone dosage might increase the aromatization effect, increasing the primobolan dosage won’t increase its INHIBITION effect? In other words, merely the presence of primobolan has a static aromatase inhibition effect in the body, and increasing its dose won’t increase this effect?

 

[TRENdy07]

Is the conversion of estrogen from ment, detectable on blood labs?

 

[Type-IIx]

So basically this means that while increasing testosterone dosage might increase the aromatization effect, increasing the primobolan dosage won’t increase its INHIBITION effect? In other words, merely the presence of primobolan has a static aromatase inhibition effect in the body, and increasing its dose won’t increase this effect?

Within certain reasonable doses, I think this is quite possible. This is a steroid forum hypothesis, but perhaps yes.

My sort of wild hypothesis is that some individuals like yourself may possess predominantly a 17β-HSD isozyme that with AAS that possess a secondary 17β-hydroxy group, such as EQ, Primo, Mast, and which yield predominantly 17-keto metabolites, may have this effect. It would sort of tie together the anecdotes of these compounds acting as anti-estrogens for so many. Harmful mutations (which you do NOT have) of this enzyme can cause effects like development of secondary sex characteristics, gynecomastia, infertility.

 

[Jbagel132]

Within certain reasonable doses, I think this is quite possible. This is a steroid forum hypothesis, but perhaps yes.

My sort of wild hypothesis is that some individuals like yourself may possess predominantly a 17β-HSD isozyme that with AAS that possess a secondary 17β-hydroxy group, such as EQ, Primo, Mast, and which yield predominantly 17-keto metabolites, may have this effect. It would sort of tie together the anecdotes of these compounds acting as anti-estrogens for so many. Harmful mutations (which you do NOT have) of this enzyme can cause effects like development of secondary sex characteristics, gynecomastia, infertility.

We seen that 350mg/400mg test cyp/primo e had me at 22 pg/mL for E2. You would think at 350mg test my E2 would be higher than 300mg but primobolan was also over twice as much. Does that mean that increasing the test dose won’t necessarily offset the AI effects?

 

[Type-IIx]

We seen that 350mg/400mg test cyp/primo e had me at 22 pg/mL for E2. You would think at 350mg test my E2 would be higher than 300mg but primobolan was also over twice as much. Does that mean that increasing the test dose won’t necessarily offset the AI effects?

I think increasing the test is going to increase your E2. Simply put, T aromatizes.

Now if you increase Primo dose as well, within a reasonable limit (say up to 600mg), if my forum hypothesis ends up correct, T will increase aromatization and the Primo won't linearly/dose-dependently lower or "crash" your E2 (it will lower E2 reasonably in line with the E2 concentrations at 400mg Primo). Unless (and it is possible) Primo TRULY acts as an aromatase inhibitor, which is possible since exemestane derives some of its AI action via the AR. But even if it does act as a sort of quasi-AI via the AR, this would suggest that (like AIs) it's unable to completely abolish E2 in men.