Reported Characteristics

Active-Life: 8-12 hours

Drug Class: Steroid Biosynthesis Inhibitor (oral)

Average Reported Dosage: 500mg-2000mg Daily

Acne: None

Water Retention: None

High Blood Pressure: Unknown

Noted Comments: Powerful endogenous hormone inhibitor Aromatization: None Liver Toxic: High potential

Aminoglutethimide is normally prescribed for patients with breast cancer or Cushings Syndrome. In both cases patients suffer from catastrophic physiological decline. To a profound degree this is notably due to severe over production of endogenous glucocorticoids. The one glucocorticoid most readers would be familiar with is cortisol.

Bodybuilders and strength athletes have often utilized this drug as a means of inhibiting the P-450 and aromatase enzymes. This obviously refers to inhibition of the two potential pathways in which susceptible AAS are converted into estrogens. The result of administration of aminoglutethimide is partial or complete inhibition of endogenous hormone biosynthesis. When this drug is introduced into the body it blocks the conversion of cholesterol into pregnenolone. Since this is the first step in all hormone biosynthesis: By blocking the conversion of C-19 androgens into C-15 estrogens it functions as an anti-estrogen. This is one of the obvious intents reported users had in mind. But by inhibiting the conversion of cholesterol into pregnenolone it also proportionately inhibits the endogenous biosynthesis of all hormones including androgens, estrogens, aldosterone, and cortisol. This brings the discussion to the second reason this drug use was commonly reported. Cortisol is a catabolic hormone that just loves to eat muscle tissue. In fact it is a significant part of the equation that induces genetic limitations to muscular augmentation. Many authorities and athletes alike have realized on a few facts: (1) Less cortisol = less muscle catabolism (destruction) (2) Less estrogen = less fat accumulation and less gyno resulting in a leaner physique (3) Less aldosterone = less water retention and a harder appearance. But less conversion of cholesterol into pregnenolone = less endogenous testosterone. Most noted these effects were highly desirable since the absence of natural testosterone production was abundantly replace through AAS use. And it was generally acknowledged that the absence of competing hormones had a profound synergistic effect upon those the self-administered.

According to the available returns the average reported dosages were 500-750mg daily to inhibit excessive estrogen formation from AAS aromatization and 1000-2000mg daily for the purpose of cortisol inhibition. Most reported a scaled weekly dosage increase was most effective: Week #1 250mg 2xd, week #2 250mg 3xd, week #3 & 4 500mg 2xd.

*My personal experience with this drug was that a 2 day on - 2 day off protocol worked best with fewer negative side effects.

Of the many side effects is that the drug inhibits the body's ability to react to inflammatory responses. This means it can prevent the body from inhibiting hemorrhaging (I do hope that no one cut themselves shaving!) and fight disease among other things. It can also make a bodybuilder a victim of CUSSING SYNDROME. Other side effects include: Sore joints from a reduction in glucocorticoids, reduced white/red blood cell counts, reduced platelet counts, and liver disease.

The package insert states 2-7 250-mg tabs daily for treatment of CUSHINGS SYNDROME. CUSHINGS victims have a "much" higher cortisol/cortisone production than even the most over trained athlete. For this reason 500 mg-1000 mg daily total was considered more than enough for a chemically enhanced bodybuilder for cortisol/cortisone suppression, and 250 mg -500 mg sufficient for use as an anti-estrogen and aldosterone control drug during cycles. It was also noted that Aminoglutethmide was not be utilized for more than 4-6 weeks. At that point, the body responded by increasing production of ACTH and a whole new series of catabolic effects resulted.



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