The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
It will increase testosterone in a dose dependent manner, but it has many other pharmacodynamic effects, which is the effect of the drug on the body other than its effect on the hypothalamus and the pituitary. So in the hypothalamus and the pituitary, it does what's called negative feedback inhibition or it blocks the action of estrogen. So it crowds out estrogen from the estrogen receptor on the hypothalamus and the pituitary.
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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
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so you could say okay if the response to HCG is favorable then you know directly stimulating the L EG cell produces testosterone assuming you had enough testosterone to aromatize to estrad that was a meaningful impact from inhibiting its negative feedback to begin with so it's like at least with a G&R Agonist I know I'm maximally stimulating pituitary output to whatever capacity it is with Clomid I'm just inhibiting negative feedback to whatever suboptimal capacity my ER is agonized yep although you'd want to think if you gave a high enough dose yeah you're right in my case maybe that wouldn't work cuz my estral is so low to begin with you're not inhibiting that much that's a very interesting point so you're um if estral is really low Clomid could fail just on the basis of that
although what you could do is then you could use Clomid sure right so then you could say okay if the response to HCG is favorable then you know directly stimulating the L EG cell produces testosterone assuming you had enough testosterone to aromatize the estrad that was a meaningful impact from inhibiting its negative feedback to begin with so it's like at least with a G&R Agonist I know I'm maximally stimulating pituitary output to whatever capacity it is with Clomid I'm just inhibiting negative feedback to whatever suboptimal capacity my ER is agonized
so you're um if estral is really low Clomid could fail just on the basis of that like if you really wanted to test pit pituitary output potential you would use a uh G&R Agonist and see what happens