So after posing a thread about 19 nors and prolactin in the steroid section (which sparked a great amount of knowledge going back and forth) I decided to look more into the different anti estrogens and came across this article.

This article was written by L. Rea from MesoRX and talks about the effects of different anti estrogens.

Nothing in this article is intended to take the place of advice from a licensed health professional. Consult a physician before taking any medication.

: Thank you for reading CME and I hope that you enjoy Beast. It is always great to know people benefit from my efforts!

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 (female dog 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.

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.

                           Residual  Aromatase (%)
/
4-Androstenoldione                       91.9                                                              8.1
------------------------0---------------------------------------0--------------------------------------0
/
Exemestane                                 97.9                                                              2.1
------------------------0---------------------------------------0--------------------------------------0
/
Aminoglutethimide                         90.6                                                              9.4
------------------------0---------------------------------------0--------------------------------------0
/
Anastrozole                                  96.7                                                              3.1
------------------------0---------------------------------------0--------------------------------------0
/
Letrozole                                      98.7                                                             1.3

 -----------------------0---------------------------------------0---------------------------------------0

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.

/
4-Androstenoldione              Increases IGF-1                                        26%
-------------------------0----------------------------------0-----------------------0
/
Letrozol                             Increases IGF-1                                        24%
-------------------------0----------------------------------0-----------------------0
/
Anastrozole                        Decreases IGF-1                                        18%
-------------------------0----------------------------------0-----------------------0
/
Tamoxifen                          Decreases IGF-1                                      23.5%
-------------------------0----------------------------------0-----------------------0
/
Fulvestrant                        Decreases IGF-1                                        70%
-------------------------0----------------------------------0-----------------------0
/
Aminoglutethimide                Increases IGF-1                                         27%
-------------------------0----------------------------------0-----------------------0
/
Exemestane                        Increases IGF-1                                         28%
-------------------------0----------------------------------0-----------------------0

Other things to consider pre-contest or simply as a matter of achieving desired results at any point in the pursuit of freak status include…
When attempting to evaluate "the best" choice for any item, the question of specific-intent should come into play first. If you asked for solely my opinion, then I would choose the product that covered the greatest number of needs for specific-intent or goal(s). Personally I prefer Formestane (under whatever name the product is provided, in the purest most active form).

Formestane increases IGF-1 secretion and activity.
Formestane decreases the number of progesterone receptors (inhibits the trenbolone and "deca-dick" type side effects and increases fat loss)
Formestane inhibits 91.9% of aromatase enzyme production
Formestane increases HPTA activity similar to HCG and Clomid together
Formestane is anabolic and androgenic (At 500mg weekly the product is similar in effects to 250mg of Primobolan Enanthate)
Formestane is a "suicide inhibitor" of aromatase. Specifically this means that it will irreversibly bind to the aromatase enzyme and permanently deactivate it
Formestane (The sterile injectable form) possesses a 4-day half-life
Formestane decreases SHBG 34% thus increasing androgen activity.
Formestane inhibits DHT (dehydrotestosterone) formation and activity.
Formestane possesses 1% of the binding affinity of DHT to DHT receptors
Formestane has been shown to decrease prostate concerns such as BPH.
Formestane has been shown to continue to increase HPTA function above natural levels even after 22 weeks of continuous administration

(Formestane is the 4-andro on the charts)