That's reasonable bro, especially because of the widespread confusion about estrogens & their attenuated link or association to IGF-I.
I've written elsewhere about the phenomenon of aromatization per se being what increases IGF-I, whereas estrogens (e.g., E2) actually negatively feed back. That is to say, while the process of aromatization – (3 steps, completed by cleavage of the bond between C10 and C19 to yield formic acid and the aromatized A-ring product with loss of the hydrogen atoms at the 1β and 2β positions) – increases IGF-I, its aromatic products (estrogens) reduce IGF-I. What this results in is a sort of parabolic shape to the aromatizing androgen (e.g., Test, Deca, MENT, Dbol, Methyltest, etc.) dose/IGF-I curve with an inflection point where blood concentrations of the aromatic product (e.g., E2) start to become high.
Here are some links where I discuss this:
https://www.professionalmuscle.com/...-dosages-effects-of-estradiol-igfbp-1.169919/ (the title post of this thread), specifically, the concepts demonstrating that estrogens increase IGFBP-1, reducing IGF-I bioavailability and unleashing GH secretion by feedback withdrawal. Hence, women have higher GH levels than men by body surface area and are less sensitive per-mg to rhGH.
is this how exemestane increases IGF-1? Excessive estrogen levels suppress IGF-1, therefore taking exemestane will bring it back up?