Dr. Testosterone
By George Touliatos, MD

ESTROGEN FACTS

The hormonal status of a steroid user is very important and the correct balance between androgens and estrogens plays a significant role. Aromatization is a biochemical process that takes place in a variety of tissues, such as mammary gland, adipose tissue, liver and brain; induced by aromatase enzyme, testosterone is converted to beta-estradiol (E2).

The more estrogenic a steroid is, the more profound anabolic effect will have. Oxymetholone/Anadrol and methandrostenolone/Dianabol are two examples of 17-alkalized anabolic pills with a high estrogenic capacity.

Other anabolic-androgenic steroids (AAS) used during bulking (off-season) are boldenone (Equipoise) and nandrolone (Deca-Durabolin). Both of them have a moderate estrogenic activity.

The androgen fluoxymesterone/Halotestin, a drug used for advanced breast cancer in women, does not aromatize and has no effect on the aromatase enzyme.

Estrogens do play an important role in muscle development. Estrogens make androgen receptors more receptive to the anabolic molecule. This was shown in a study where scientists castrated male guinea pigs and then granted them the powerful anabolic steroid 17-alkylated pill methyltrienolone (M3). With their castration, the mice dramatically increased estrogen levels and eliminated their androgens. It was observed that the link between M3 and receptors was 500% more powerful than before their castration. This explains how important estrogens are for the effect of the steroid molecule attachment into their receptor’s surface.

Insulin-like growth factor (IGF-1) is a peptide responsible for muscle development and regeneration of the cartilage.

It is known, that among the factors for GH release, is the presence of estradiol (E2).

The concentration of somatomedin C decreases as estrogens are reduced. Aromatization is a process that promotes the presence of the IGF-1 peptide. Therefore, fewer estrogens result in less production of the anabolic hormone. Τhe use of tamoxifen citrate/Nolvadex (selective estrogen receptors modulators or SERMs) has a negative impact on IGF-1 production in the liver. Proof that estrogens promote anabolism and contribute to weight gain plus muscularity through water retention and glycogen, is the fact that one of the strongest 17-alkalized oral AAS, fluoxymesterone/Halotestin, with an anabolic ratio (18) times greater than testosterone and (8) times more anabolic than oxymetholone/Anadrol, yet is not used for weight gain itself, but to increase muscle strength, hardness and muscle density.

The presence of estrogens is beneficial for the atherosclerotic profile. This is the reason why women have lower mortality in heart attacks. Therefore, the lower estrogen one has, the worse the ratio of high-density lipoprotein (HDL) cholesterol/low-density lipoprotein (LDL) cholesterolis.

The correlation between estrogens and atherogenesis is linked with oxidation of lipoproteins HDL and LDL. It seems that estrogens do have an antioxidant effect on the oxidation of those fractures. As a result, LDL is decreased, while HDL is elevated. This is why SERMs, Tamoxifen/Nolvadex in particular, has the unique ability to improve HDL/LDL ratio, since it acts selectively in certain tissues (liver), occupying the estrogenic receptors, thus making circulating estrogens unable to attach to the receptors.

On the other hand, too much estrogen is linked to increased risk of thrombosis. Furthermore, estrogens are a negative feedback for hypothalamic pituitary testicular axis (HPTA) and GnRH.

It is well known that women who use contraceptive pills have a higher risk for thrombotic episodes and should use salicylic acid/aspirin, or fish oil omega-3 (EPA/DHA).

Estrogens have the ability to increase bone mineral density (BMD) and act against osteropenia/osteoporosis. Furthermore, aromatization and water retention aid joints and synovial space, by adding more fluid within (lubrication). Therefore, it is preferable to use estrogenic compounds during the off-season time, when heavy loads are lifted in training.

Estrogens and serotonin (the joy hormone) also are directly related. It has been estimated that aromatase inhibitor users suffer from mood disorders, mood swings, being emotionally unstable and occasionally have symptoms of melancholy, or even depression.

It is also known that methandrostenolone/methandienone users can become addicted to the euphoric effect it has upon the user’s psychology. This is due to the fact that estrogens are linked to the feeling of well-being, due to their relation to serotonin, the neurotransmitter of happiness.

Menopausal women seem to have mood swings and be rather unstable to their emotional status. As a result, similar brain chemistry would affect a male bodybuilder.

Estradiol (E2), the main representative of estrogens, is essential for modulating libido, erectile function and spermatogenesis.

Aromatase inhibitors such as exemestane/Aromasin, Letrozole/Femara and anastrozole/Arimidex have a negative impact on sexual drive during a steroid cycle.

While it seems that testosterone is the main reason for an enhanced libido, the truth is far from it. Estrogens play a significant role in a male’s libido too. This was experimentally demonstrated by two groups of men who were under testosterone treatment, while another group took testosterone and an anti-estrogenic agent. The final conclusion was that men who did not use the anti-estrogenic treatment had an improved sexual drive.

Crushing on beta-estradiol will cost in erectile dysfunction (ED).
 

Of course, after a typical post-cycle therapy (PCT), the use of both is critical in order for estrogens to get lower, when we stop using SERMs.
 

Lower estrogens will then give a signal to hypothalamus for GnRH release. Estrogen receptors (ER), as well as aromatase, are abundant in brain, penis and testis, organs important for sexual function. In the brain, estradiol synthesis is increased in areas related to sexual arousal.

In the testes, spermatogenesis is modulated at every level (HPTA, Leydig, Sertoli, germ cells, epididymis, mature sperm) by estrogen.

Estrogen levels that are in imbalance with testosterone (increased ratio of estrogens/androgens) are responsible for the development of gynecomastia (bitch tits).

Furthermore, estrogens can increase serum levels of sex hormone-binding globulin (SHBG), which binds free testosterone (the active form-FT), leading to decreased levels of FT and testosterone’s action in male mammary gland.
 
George Touliatos, MD is an author, lecturer, champion competitive bodybuilder and expert in medical prevention regarding PED use in sports. Dr. Touliatos specializes in medical biopathology and is the medical associate of Orthobiotiki.gr and Medihall.gr, Age Management and Preventive Clinics in Athens, Greece. He is the author of four Greek books on bodybuilding, has extensively developed articles for www.anabolic.org and is the medical associate for the book Anabolics, 11th Edition (2017). Dr. Touliatos has been a columnist for the Greek editions of MuscleMag and Muscular Development magazines, and has participated in several seminars across Greece and Cyprus, making numerous TV and radio appearances, doing interviews in print and online. His personal website is https://gtoul.com

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