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It is the myth and misunderstanding that that SERMs, such as Nolvadex and Clomid, act to lower estrogen levels. This myth most likely stems from the fact that SERMs too are referred to as ‘Estrogen blockers’, and so various individuals may have misunderstood ‘blocking Estrongen’ to mean ‘Estrogen elimination’, which could not be further from the truth. SERMs instead only block the activity of Estrogen in select tissues in the body by way of blocking the action of Estrogen at the receptor sites in breast tissue by occupying the receptor sites in place of Estrogen so that Estrogen itself cannot exert its effects there through receptor site binding. SERMs will also act as Estrogens at receptor sites at other cells in other areas of the body (the liver, for example in Nolvadex’s case). This is where the ‘selective’ part of ‘selective Estrogen receptor modulator’ comes into play. However, SERMs do no reduce circulating levels of Estrogen in blood plasma. Aromatase inhibitors are the compounds that instead serve to do this by eliminating the production of Estrogen through binding to and disabling the aromatase enzyme, which is the enzyme responsible for the conversion (or aromatization) of androgens into Estrogen. Aromasin is a very strong and very potent steroidal aromatase inhibitor of the suicidal type, and information within the packaging in prescription Aromasin describes the ability for Aromasin to reduce Estrogen levels by 85%, as evidenced by studies on breast cancer patients. Suicidal aromatase inhibitors such as Aromasin (Exemestane) serve to permanently inhibit and disable the aromatase enzyme to which it is bound to. This renders the enzyme inactive forever. The body will eventually manufacture more aromatase enzymes, but the currently bound enzymes are bound indefinitely, eliminating any risk for Estrogen rebound. This is unseen with the other two major aromatase inhibitors (Arimidex and Letrozole), which are non-suicidal aromatase inhibitors that are only bound to the aromatase enzyme for limited time periods before the aromatase inhibitors unbind and become metabolized. If a non-suicidal aromatase inhibitor is halted too abruptly, the circulating inhibited aromatase enzymes that have not been metabolized out of the body will then become free again, and begin aromatizing androgens into Estrogens at an often rapid rate. This is not the case with Aromasin. Exemestane was initially designed by Pharmacia & Upjohn for the treatment of female breast cancer patients, specifically post-menopausal patients, and it is used as an adjunct therapy when other first-line treatments for breast cancer (such as Nolvadex) have failed. 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