Quote:
Originally Posted by thesinner
Ok, I'm going to explain how ephedrine works, to better illustrate how SERMs and AI's work:
Very simply ephedrine blocks up specific andregenic receptors, thus freeing up more of your body's adrenaline to perform its other functions in the body.
A SERM works in a similar manner. It blocks certain estrogenic receptors to free up estrogen to perform other functions in the body.
An AI works in pretty much the opposite manner of a SERM. AI's take up the aromatase enzyme, which frees up more testosterone to perform other functions in the body.
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Actually, ephedrine is a b-adreneric
agonist, not
antagonist, meaning it opens these receptors to accepting adrenal hormones like adrenaline.
The HPTA stimulating effect of most SERMs in men comes from blocking estrogen receptors at the hypothalamus or pituitary. Estrogens in men come from aromatization of androgens. If the receptors are tricked into thinking the body is low on estrogens, it upregulates the production of androgens in hopes of creating more estrogens downstream.
It's actually a very similar concept with AIs, as you are tricking the body into upregulating testosterone production because of lack of estrogens. One difference is, the AIs will actually lower the serum estrogens vs. just blocking their effects... of course the debate goes on and on about estrogen-receptor upregulation from this, but the limited data I have seen suggests this is not a problem with
steriodal AIs.