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Aromatase Inhibitors(AI) like Arimidex, Aromasin, and Letrozole are used to block the aromatase enzyme from converting Testosterone to Estrogen. Bodybuilders are advised to take an AI because abusing Testosterone leads to excessive estradiol levels. High estrogen levels can cause fluid retention, loss of sex drive, prostate enlargement and gynecomastia.
Do aromatase inhibitors reduce the estrogenic effects of other steroids besides Testosterone?
Well for certain aromatase inhibitors do not block nandrolone from converting to estradiol. Nandrolone probably converts to estrogen, not through the action of aromatase, but through the action of organic acids or alkalines in the body that act on nandrolone after it is converted to its 1-beta hydroxylated derivative. This means that estrogen inhibitors like Arimidex, which decrease the activity of aromatase, may not stop nandrolone from aromatizing to estrogen.
Aromatization of steroids is a complex process of consecutive oxidation reactions which are catalyzed by cytochrome P450 enzymes. The conversion of the natural C19 steroids, testosterone and androstenedione, into estradiol-17beta and estrone is dependent on the oxidative elimination of the angular C19-methyl group. This complex key reaction is catalyzed by the cytochrome P450 aromatase, which is expressed in many tissues of the adult human (e.g. ovary, fat tissue), but not in the liver. However, 19-nortestosterone derivatives are characterized by the lack of the C19-methyl group. Therefore, for the aromatization of these synthetic steroids, the action of the cytochrome P450 aromatase is not necessary and the oxidative introduction of double bonds into the A-ring can be catalyzed by other hepatic cytochrome P450 enzymes. The final key process in the formation of a phenolic A-ring, both in natural androgens and 19-nortestosterone derivatives, is the enolization of a 3-keto group to the C2-C3-enol or the C3-C4-enol moiety, which occurs without the action of enzymes.
19-nortestosterone derivatives (norethisterone, norethynodrel, tibolone) can readily be aromatized in the adult human liver. This leads to the formation of the potent estrogens ethinylestradiol from norethisterone or norethynodrel and 7 alpha-methyl-ethinylestradiol from tibolone. This may have clinical consequences, e.g. the elevated risk of venous thromboembolic disease in premenopausal women treated with high doses of norethisterone for bleeding disorders, or the elevated risk of stroke or endometrial disease in postmenopausal women treated with tibolone.
Testosterone derived oral anabolic steroids like Dianabol and MethylTestosterone(MT) convert to metabolism resistant 17a-methyl-estradiol. Normethandrone also converts to 17a-methyl-estradiol. Normethandrone is an oral nandrolone derived steroid, but converts to the same estrogenic metabolite as Dianabol and MT. Based on this it is highly likely that Aromatase inhibitors do not work for Dianabol and MT like once thought. Synthetic estrogens do not show up on a standard blood test, so it is difficult to access if aromatase inhibitors reduce estrogen levels on Dianabol and MethylTestosterone.
Do aromatase inhibitors reduce the estrogenic effects of other steroids besides Testosterone?
Well for certain aromatase inhibitors do not block nandrolone from converting to estradiol. Nandrolone probably converts to estrogen, not through the action of aromatase, but through the action of organic acids or alkalines in the body that act on nandrolone after it is converted to its 1-beta hydroxylated derivative. This means that estrogen inhibitors like Arimidex, which decrease the activity of aromatase, may not stop nandrolone from aromatizing to estrogen.
Aromatization of steroids is a complex process of consecutive oxidation reactions which are catalyzed by cytochrome P450 enzymes. The conversion of the natural C19 steroids, testosterone and androstenedione, into estradiol-17beta and estrone is dependent on the oxidative elimination of the angular C19-methyl group. This complex key reaction is catalyzed by the cytochrome P450 aromatase, which is expressed in many tissues of the adult human (e.g. ovary, fat tissue), but not in the liver. However, 19-nortestosterone derivatives are characterized by the lack of the C19-methyl group. Therefore, for the aromatization of these synthetic steroids, the action of the cytochrome P450 aromatase is not necessary and the oxidative introduction of double bonds into the A-ring can be catalyzed by other hepatic cytochrome P450 enzymes. The final key process in the formation of a phenolic A-ring, both in natural androgens and 19-nortestosterone derivatives, is the enolization of a 3-keto group to the C2-C3-enol or the C3-C4-enol moiety, which occurs without the action of enzymes.
19-nortestosterone derivatives (norethisterone, norethynodrel, tibolone) can readily be aromatized in the adult human liver. This leads to the formation of the potent estrogens ethinylestradiol from norethisterone or norethynodrel and 7 alpha-methyl-ethinylestradiol from tibolone. This may have clinical consequences, e.g. the elevated risk of venous thromboembolic disease in premenopausal women treated with high doses of norethisterone for bleeding disorders, or the elevated risk of stroke or endometrial disease in postmenopausal women treated with tibolone.
Testosterone derived oral anabolic steroids like Dianabol and MethylTestosterone(MT) convert to metabolism resistant 17a-methyl-estradiol. Normethandrone also converts to 17a-methyl-estradiol. Normethandrone is an oral nandrolone derived steroid, but converts to the same estrogenic metabolite as Dianabol and MT. Based on this it is highly likely that Aromatase inhibitors do not work for Dianabol and MT like once thought. Synthetic estrogens do not show up on a standard blood test, so it is difficult to access if aromatase inhibitors reduce estrogen levels on Dianabol and MethylTestosterone.
