Cytadren (aminoglutethimide)

Aminoglutethimide is mainly identified as an inhibitor of adrenocortical steroid synthesis. Its primary function is to block the conversion of cholesterol to pregnenolone, which is required for the biosynthesis of adrenal glucocorticoids, mineral corticoids, estrogens, and androgens. Aminoglutethimide is a nonspecific inhibitor, and also blocks several other steps in steroid synthesis including hydroxylation at C-11, C-18, and C-21, and the aromatization of androgen to estrogens, The drug may be used clinically to treat estrogen dependent breast cancer, and to treat Cushing’s syndrome, which is a condition where the body overproduces the hormone cortical. The effect that Aminoglutethimide can have on cortical and estrogen production is what makes this a drug of interest to athletes and bodybuilders. The drug also works by inhibiting cortical production. While cortical is an essential hormone for life, its  levels may also vary greatly within “normal” ranges depending on the individual, their training and dietary status. Aminoglutethimide was FDA approved as an anticonvulsant drug in 1960 under the main trade name of Cytadren. Side effects were common with treatment, however, including drowsiness, dizziness, and partial loss of motor control. In 1966 reports of adrenal insufficiency subsequent to Aminoglutethimide use were reported. The drug was withdrawn from the U.S market as an anticonvulsant that same year due to its recently understood effects on the adrenal gland. The drug is most commonly supplied in tablets of 250mg.

In terms of research conducted in athletes or those looking to use the drug for athletic or cosmetic purposes, there is of course very little as is the case with many drugs used by bodybuilders and strength athletes. For this reason we are left to extrapolate the best methods to use aminoglutethimide from anecdotal information as well as trying to form the available research to fit into our needs. A significant aspect of aminoglutethimide is that along with its ability to inhibit both cortisol and aromatization, it also suppresses the production of adrenal androgens. Obviously this would be a negative for someone that was not using exogenous hormones, but since it is unlikely that athletes or other steroid users would be administering aminoglutethimide without also using anabolic steroids this is likely not to be a concern for most. The cortisol inhibiting effect of aminoglutethimide is short lived in the body due to the body’s ability to adapt to the action of the drug. By lowering the natural production of cortisol the body will begin to produce adrenocorticotropic hormone. The hormone sparks an increase in cortisol production in the body to help normalize its levels causing the action of the drug to become basically moot. It is believed by some that if one staggers their use of the drug to a schedule similar to two days on and then two days off that this may be enough to ward off the body’s response to the lowered cortisol levels while still reaping the benefit of partial suppression. There is little research to indicate that this is true however. It appears that there is a significant risk of hepatoxicity with aminoglutethimide when used over extended periods of time even at relatively moderate dosages. For this reason lengthy use of the drug would not be recommended for most users and even short cycles of it are likely to increase liver values.

Athletes and bodybuilders looking to take Cytadren for the suppression of cortisol usually take the drug in a dosage of 1000mg per day for a period of 2-3 weeks or less. A schedule of 2 days on and 2 days off may be used in an effort to extend the effectiveness of the drug for extended periods of time.