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In males as well as females, its Estrogen antagonistic effect on the hypothalamus will trigger a release of LH (Luteinizing Hormone) and FSH (Follicle Stimulating Hormone). These two hormones in men are the signal hormones that signal the testes to begin or increase its production of Testosterone, and this total process is known as the HPTA (Hypothalamic Pituitary Testicular Axis). In females, this same action occurs, except LH and FSH will trigger the release of eggs from from the ovaries (known as follicular rupture), which would lead to increased chances of contraception. This total process in females is known as the HPOA (Hypothalamic Pituitary Ovarian Axis). Much like Nolvadex, Clomid is what would be considered an Estrogen that acts as a 'fake' Estrogen in areas of the body, such as breast tissue (so as to block the effects of 'real' Estrogen, while it also works as an actual Estrogen in other areas of the body, is anavar worth it. This is another manner of describing the agonistic/antagonistic nature of Clomid in regards to Estrogen. For anabolic steroid using athletes and bodybuilders that are for the most part males, Clomid can serve as an effective anti-Estrogen for the purpose of mitigating one particular unwanted side effect of Estrogen as a result of the use of aromatizable anabolic steroids (such as Testosterone, Dianabol, Boldenone, etc. This particular unwanted side effect is that of gynecomastia, which refers to the development of breast tissue resulting from excess Estrogen levels in body. Because of Clomid's Estrogen antagonistic effects on the hypothalamus resulting in the increased production of gonadotropins LH and FSH, Clomid can effectively be utilized to increase endogenous Testosterone production in males. This is especially important for anabolic steroid using individuals that wish to restore proper hormonal function during the weeks following the conclusion of an anabolic steroid cycle, a period known as PCT (Post Cycle Therpay). The traditional protocol for such a use is that of a combination of Nolvadex, Clomid, and HCG (Human Chorionic Gonadotropin) for the duration of several weeks, and although much better more modern protocols have been developed, this long-standing traditional PCT protocol is still effective. The use of Clomid for this purpose will be covered in further detail under the Clomid doses section of this profile. All of the tripohenylethylene compounds under the SERM family (Nolvadex, Clomid, and Toremifene) also exhibit Estrogen agonistic effects in the liver, meaning the liver is one such area of the body where SERMs such as Clomid (Clomiphene Citrate) will act as an Estrogen rather than block Estrogenic activity there. In studies, this has shown to be a beneficial aspect of SERMs, as Estrogens as well as Estrogen agonists (such as Clomid and Nolvadex) impart a positive effect on cholesterol values through actions in the liver. This is the reason as to why the reduction of Estrogen levels through the use of an aromatase inhibitor (AI) is not always the best decision, as the reduction in Estrogen often results in negatively impacted cholesterol profiles as demonstrated anecdotally as well as in clinical studies. Chemical Characteristics of Clomid. Clomid (Clomiphene Citrate) is a non-steroidal selective Estrogen receptor modulator (SERM) that possesses both mixed agonistic as well as antagonistic properties in relation to Estrogen in different areas of the body. Clomid belongs to a family of compounds known as triphenylethylene compounds, of which Nolvadex (Tamoxifen Citrate) is also a member of, and a very closely related compound to Clomid. Clomid's primary use within the medical field is that of a fertility drug in females but also among males as well. It has already been established that Clomid, being a SERM, does not reduce circulating Estrogen levels in the body, but instead serves to occupy the receptor sites in breast tissue so that Estrogen itself cannot bind to these receptors due to Clomid's stronger binding strength to it. In layman's terms, Clomid essentially acts as a 'fake' Estrogen that acts as a placeholder at the receptor sites in breast tissue. As a result, Estrogen cannot activate gene transcription in the cells there in order to formulate gynecomastia, and any existing Estrogen that has already bound to receptor sites will essentially be 'forced' out of the receptor sites by Clomid which then occupies the receptor site instead. However, it must be noted that Clomid's action in this area is far weaker and less efficient than its close relative compound Nolvadex, which serves as a better choice for this purpose. Although Clomid could indeed be utilized by anabolic steroid using individuals that wish to prevent or eliminate and reverse formulating gynecomastia in its early stages, its more effective and promising role is that of an endogenous Testosterone production stimulating compound. This is the primary purpose and function of Clomid among anabolic steroid using athletes and bodybuilders, and is the primary desired effect in this sense.
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