Foro de culturismo, musculación, pesas, fitness y esteroides anabólicos

Originally posted by Black Baccara
Clomid is a SERM and it exerts both antiestrogenic and estrogenlike effects. Bodybuilders always focus on the first but sometimes estrogenic effects could me more useful. On this board there are lot of discussions to determine the best choice between nolvadex and Clomid for PCT purpose.

Because when we think about these compounds, we think mostly about their antiestrogenic natures and because tamoxifen is a more potent anti-estrogen, it can be thought to be the best choice. I have often read this sort of reasoning : SERM can induce gonadotropins by counteracting the negative feedback. It is true and easy to understand when we speak about normal men with normal HPT axis. But in the case of PCT this reasoning is irrelevant because androgens are the sole way of synthesis of estrogens. So if androgens are low, estrogens are low too and they cannot exert any feedback and the use of SERM in PCT appears questionable.

From a reported case of a male bodybuilder with prolonged HPTA suppression and impotence disorder : despite a treatment with HCG. LH, FSH and T were low 9 months after that drugs had been discontinuated. A month treatment with clomiphene 100mg ED restored HPT axis to normal men levels.

http://www.pubmedcentral.gov/picrender.fcgi?artid=1022657&blobtype=pdf

How Clomid can be helpful in PCT despite very low androgens and estrogens levels ?
Maybe because an estrogenic effect, estradiol is known to be both a positive and negative signal for the pituary. So, if LH doesn't raise after the discontinuation of AAS administration, as it is generally the case, the reason can be a pituary desensitization to GnRH signal. In this case the lack of estrogen can explain why the HPT axis can't be restored and the use of an estrogenic compound like Clomid can be helpful and a better choice than an anti-E :

[B]Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro

The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enClomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its EnClomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin. [/B]