Aromatase Inhibition

Aromatase Inhibition in Male Athletes Using Anabolic-Androgenic Steroids


Most of the available studies on anti-estrogens (aromatase inhibitors and estrogen receptor antagonist) are performed upon breast cancer patients. As such, to some extent, the results may vary in regard to healthy male athletes. Personally I have always found this boarder-line idiocy due to the fact that there are millions of males with gynecomastia (bitch tits) and corresponding inhibition of HPTA function (the body’s androgen producing system) that would crawl over glass to participate in medical studies of this nature.

A Very Quick Physiology Lesson

The male body uses an enzyme called aromatase to convert a percentage of susceptible androgens into estrogens. Naturally this includes both those the body produces and those introduced from outside the body such as AAS (Anabolic Androgenic Steroids). In most cases the result is predominantly a very powerful estrogen called estradiol.
Aromatase is present in most body tissues and the circulatory system. Unfortunately fat cells produce a scary amount of this man-altering enzyme…which of course explains why fat guys get boobs. (Yikes!)
When we think of aromatase inhibitors we often assume that they are all the same with various levels of results…depending upon dosages. While the latter may be true, the prior statement certainly is not.
Aromatase Inhibitor "Types"?

Let’s do a quick review of the types of aromatase inhibitors that are available. These include type 1, or steroidal inactivators, and type 2, or nonsteroidal inhibitors. The type 1 aromatase inhibitors include exemestane and formestane and are actually androgen analogues (cool stuff if applied right!). The type 2 inhibitors include aminoglutethimide, anastrozole, letrozole, and vorozole.

There are both similarities and differences between the type 1 and 2 aromatase inhibitors. Their similarities include the fact that both inhibit aromatase in a very specific fashion and reduce endogenous or circulating estrogens. On the other hand, the steroidal inhibitors are rather better classified as inactivators, in that they bind to the aromatase molecule in an irreversible fashion (they hold on and do not let go). Because aromatase is rapidly replaced within the body, however, the significance of this property in terms of clinical benefit is unclear in some ways. In addition, the "inactivators" have a structure quite similar to that of androgens and may, in higher doses, have anabolic steroid or androgen-type properties.

Of the type 2 agents, letrozole tends to be more potent than anastrozole and both are more potent than aminoglutethimide in regard to estrogen production. Of the type 1 agents, exemestane is considerably more potent than formestane. But again in each case this may be dose dependant more so than a question of effectiveness of the drug itself. In vivo (tested in live subjects rather than a test tube), the aromatase inhibitors can be graded as shown in the basic table below.

Relative Potency of Type 1 and Type 2 Aromatase Inhibitors

Product Aromatase
Inhibition (%) Residual Aromatase (%)
Formestane/
4-Androstenoldione 91.9 / 8.1
Aromasin/Exemestane 97.9 / 2.1
Cytadren/
Aminoglutethimide 90.6 / 9.4
Arimidex/Anastrozole 96.7 / 3.1
Femara/Letrozole 98.7 / 1.3

So far it would appear that Letrozole is the leader, huh?
Anti-Estrogens And IGF-1 Production
GH (Growth Hormone) is like a master hormone for tissue growth and fat regulation due to its own intrinsic qualities and its propensity to be converted into or trigger the production and release of Growth Factors. Of these Growth Factors, one of the best known in regard to muscle growth is IGF-1 (Insulin-Like Growth Factor-1).

As most are aware by now, IGF-1 is a powerful anabolic and anti-catabolic hormone. Whether in pre-contest mode or packing on the mass, the amount of circulating and stored IGF-1 an athlete maintains plays a powerful role in the results achieved. Obviously as IGF-1 levels decrease so does the potential for packing on the beef, and the amount of lean tissue lost during calorie-restricted periods increases as well. (Not good)
Estrogen, and more so estradiol, can trigger GH release from the pituitary gland. Aromatase inhibitors decrease the amount of circulating estrogen/estradiol and estrogen receptor antagonist keep estrogen out of the specific pituitary receptors. So in many regards the use of anti-estrogens can effect IGF-1 production and in some cases affect the number of IGF-1 receptors our tissues posses.

Product Effect Percentage

Formestane/
4-Androstenoldione Increases IGF-1 26%
Femara/Letrozol Increases IGF-1 24%
Arimidex/Anastrozole Decreases IGF-1 18%
Nolvadex/Tamoxifen Decreases IGF-1 23.5%
Faslodex/Fulvestrant Decreases IGF-1 70%
Cytadren/
Aminoglutethimide Increases IGF-1 27%
Aromasin/Exemestane Increases IGF-1 28%

Yet all the more reason to use Aromasin and Letrozole...