Quote:
Originally Posted by Millard Baker \Clomid acts as an estrogen, rather than an antiestrogen, by sensitizing pituitary cells to the action of GnRH. Although tamoxifen is almost as effective as Clomid in binding to pituitary estrogen receptors, tamoxifen has little or no estrogenic activity in terms of its ability to enhance the GnRH-stimulated release of LH. The estrogenic action of Clomid at the pituitary represents a unique feature of this compound and that tamoxifen may be devoid of estrogenic activity at the pituitary level. |
Wow. I've known that this is Dr. Scally's position, but I never knew that this was his reasoning behind the use of clomid. Based on the research, his statements are incorrect. What he is describing is estrogen priming. it's when estrogen makes the pituitary more sensitive to GnRH, so that more LH is released for a given GnRH stimulus. This is well known to occur in females. Unlike females, however, men don't have a preovulatory period or spikes in LH. Estrogen priming does NOT occur in males. For starters, take a look at an authoritative reference work like Grossman's
Clinical Endocrinology, which states that "In males, the situation is more straightforward...
Oestrogens in the male reduce pituitary responsiveness to GnRH." You can't get much clearer than that. There is a stark contrast to the positive feedback that estrogen has in the pituitary of females.
Grossman's statement is corroborated by
the most recent research on the specific effects of testosterone and estrogen on the pituitary and hypothalamus of healthy men. It was clearly shown estrogenic action at the pituitary has an inhibitory effect on LH output. In other words, estrogen decreases pituitary sensitivity to GnRH. Estrogen does not produce positive feedback as seen in estrogen priming in females. The paper stated in its conclusion that "These data confirm previous work from our group which ... showed [estrogen] has both hypothalamic
and pituitary sites of negative feedback in the male." In fact, "negative feedback at the pituitary requires aromatization," as testosterone itself doesn't produce negative feedback at the pituitary.
Finally, if all that were not enough, there's
a research study that directly examined the effects of nolva and clomid on the pituitary of human males. They infused the men with 100 mcg of GnRH and then measured LH output from the pituitary. The men taking nolvadex at 20mg/day had a significantly increased LH response to GnRH. In contrast, the men taking clomid had reduced LH output, a decreased sensitivity to GnRH. The researchers stated that "a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation."
All in all, I don't see how Dr. Scally could argue that he uses clomid for a beneficial effect of estrogen priming in males when both research and experts in endocrinology squarely contradict the notion. Clomid has an estrogenic effect at the pituitary, yes, but the evidence shows that it will serve to inhibit LH output (and thus inhibit HPTA recovery) in contrast to nolva. All else being equal, that would make nolva superior to clomid for PCT.
If anyone is able to contact Dr. Scally and ask him about this, I'd love to hear his response.
-Conciliator