Clomid belongs to a class of compound known as Selective Estrogen Receptor Modulators, or SERMS. These compounds bind to certain estrogen receptors in our research subjects. There are several compounds in this class such as Tamoxifen , Toremifene, Raloxifene and finally Clomiphene(Clomid). While they all have similar characteristics and effects, they also have distinct differences in their chemical structure and the affinity or strength by which they bind to various estrogen receptors. This is what dictates the differences in these compounds and their appropriate applicability in our research. Some bind very strongly to the estrogen receptor in breast tissue – making them good choices for gyno treatment or prevention. Some act strongly on the hypothalamus inducing testosterone production. Some do both, in fact all do both in varying degrees.
Clomid’s strongest attribute for our research purposes would be its effect on testosterone production. This effect is exerted first via the hypothalamus. It essentially “tricks” the body into the production of testosterone by inhibiting negative feedback on the hypothalamus. Negative feedback is the effect estrogen has in regulating testosterone production. As levels of estrogen increase they inhibit the production of testosterone. This is signaled by the estrogen receptor in the hypothalamus. Clomid selectively and effectively blocks this receptor. The research subjects’ body does not perceive this elevated level of estrogen and testosterone production does not cease. This allows for much higher levels of testosterone. There is a secondary effect that Clomid exerts which is on the pituitary. It triggers a series on endocrine reactions that result in a surge of gonadotropins. Gonadtropins signal the production of luteinizing hormone and follicle stimulating hormone which in turn triggers the production of testosterone.
It is this dual effect on the hypothalamus and pituitary that separates Clomid from other SERMS. While all SERMS exhibit these effects in varying degrees it would appear Clomid utilizes these combined effects most efficiently to trigger the strongest response as far as the production of testosterone.
This is well documented in research showing the reversal of testicular shutdown of research subjects using Clomid therapy. It is also clearly evidenced in research subjects where Clomid has effectively been used as a safe form of testosterone replacement therapy.
It should also be mentioned that some of the foremost researchers in this area have documented a synergy with tamoxifen in their research in reversing the shutdown of testosterone production in research subjects exposed to anabolic or androgenic substances.
All in all, alone or in combination, Clomid is a powerful research compound that should be a staple in everyone’s research inventory.
Refs:
*Int Braz J Urol. 2012 Jul;38(4):512-8
*West J Med. 1995 February; 162(2): 158–160
*BJU Int. 2011 Nov 1. doi: 10.1111/j.1464-410X.2011.10702.x. [Epub ahead of print]
* Int J Impot Res. 2003 Jun;15(3):156-65.Clomiphene increases free testosterone levels in men with both secondary hypogonadism and erectile dysfunction: who does and does not benefit? Guay AT, Jacobson J, Perez JB, Hodge MB, Velasquez E.SourceCenter for Sexual Function (Endocrinology), Peabody, Massachusetts 01960, USA. [email protected]
*Anabolic Steroids – A Question of Muscle: Human Subject Abuses in Anabolic Steroid Research” Dr Michael Scally
Clomid’s strongest attribute for our research purposes would be its effect on testosterone production. This effect is exerted first via the hypothalamus. It essentially “tricks” the body into the production of testosterone by inhibiting negative feedback on the hypothalamus. Negative feedback is the effect estrogen has in regulating testosterone production. As levels of estrogen increase they inhibit the production of testosterone. This is signaled by the estrogen receptor in the hypothalamus. Clomid selectively and effectively blocks this receptor. The research subjects’ body does not perceive this elevated level of estrogen and testosterone production does not cease. This allows for much higher levels of testosterone. There is a secondary effect that Clomid exerts which is on the pituitary. It triggers a series on endocrine reactions that result in a surge of gonadotropins. Gonadtropins signal the production of luteinizing hormone and follicle stimulating hormone which in turn triggers the production of testosterone.
It is this dual effect on the hypothalamus and pituitary that separates Clomid from other SERMS. While all SERMS exhibit these effects in varying degrees it would appear Clomid utilizes these combined effects most efficiently to trigger the strongest response as far as the production of testosterone.
This is well documented in research showing the reversal of testicular shutdown of research subjects using Clomid therapy. It is also clearly evidenced in research subjects where Clomid has effectively been used as a safe form of testosterone replacement therapy.
It should also be mentioned that some of the foremost researchers in this area have documented a synergy with tamoxifen in their research in reversing the shutdown of testosterone production in research subjects exposed to anabolic or androgenic substances.
All in all, alone or in combination, Clomid is a powerful research compound that should be a staple in everyone’s research inventory.
Refs:
*Int Braz J Urol. 2012 Jul;38(4):512-8
*West J Med. 1995 February; 162(2): 158–160
*BJU Int. 2011 Nov 1. doi: 10.1111/j.1464-410X.2011.10702.x. [Epub ahead of print]
* Int J Impot Res. 2003 Jun;15(3):156-65.Clomiphene increases free testosterone levels in men with both secondary hypogonadism and erectile dysfunction: who does and does not benefit? Guay AT, Jacobson J, Perez JB, Hodge MB, Velasquez E.SourceCenter for Sexual Function (Endocrinology), Peabody, Massachusetts 01960, USA. [email protected]
*Anabolic Steroids – A Question of Muscle: Human Subject Abuses in Anabolic Steroid Research” Dr Michael Scally
