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 which takes place in a variety of tissues, such as mammary gland, adipose tissue, liver and brain;induced by aromatase enzyme, testosterone is converted to 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 (Equipose) and Nandrolone (Decadurabolin). Both of them have a moderate estrogenic activity.As known 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 estrogens’ 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 receptors surface.
Insulin like growth factor (IGF1) 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 IGF1 peptide.
Therefore, fewer estrogens result in less production of the anabolic hormone.Τhe use of tamoxifen citrate/Nolvadex (Selective Estrogen Receptors Modulators-SERMs) has a negative impact on IGF1 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 estrogens 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 anti-oxidant effect on the oxidation of those fractures. As a result, LDL is decreased, while HDL is elevated. This is why Selective Estrogen Receptors Modulators (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 of estrogens are 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 Ω3 (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 (Dianabol) 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 estrogen in men, is essential for modulating libido, erectile function, and spermatogenesis.  AI’s such as Exemestane/Aromasin, Letrozol /Femara and Anastrozol /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 on 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 used 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 estrogens to get lower, when we stop using SERM’s. 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 (Hypothalamus-Pituitary-Testicular Axis/HPTA, Leydig, Sertoli, germ cells,epididymis, mature sperm) by estrogen. 
Estrogen levels that are in imbalance with testosterone levels (increased ratio of estrogens/androgens) are responsible for the development of gynecomastia (bitch titts).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. Gynecomastia is the benign enlargement of male breast glandular tissue and is the most common breast condition in males. This term is often used by bodybuilders, due to accumulated estrogens under the nipple (areola), leading to breast tenderness. Medications which can cause gynecomastia include:
– AAS converted to estrogens (beta estradiol) by the enzyme aromatase. Estrogenic AAS are: Oxymetholone depending on aromatization environment, Nandrolone, Equipose, Testosterone, Methandienone /Methyltestosterone and Methyltestosterone.
– Finasteride, an anti-androgen used in the treatment of benign prostate hyperplasia (5a reductase inhibitor).
– Spironolactone (Aldosterone’s inhibitor),a diuretic with anti-androgenic property, can produce dose-dependent gynecomastia. The fact that the adrenal cortex produces a fair amount of dehydroepiandrosterone (DHEA), it is understandable, that abuse of spironolactone will lead to gynecomastia,by distorting androgen/estrogens balance.
– Ranitidine/Cimetidine: used in the treatment of duodenal ulcer (androgen receptor blocker)
– Opioids pain killers: codeine
– Marijuana (androgen receptor blocker): weed,pot
– Barbiturates: Diazepam (valium)
Initially, the problem is addressed by reducing weight and lowering body fat percentage, accompanied by resistance training. If there is no improvement, the athlete should undergo a hormonal blood panel (beta estradiol, estrone, prolactine), which could reveal any supraphysiological serum levels of these hormones. Accordingly, he should use an anti-estrogen (Tamoxifen/Nolvadex along with Mesterolone/Proviron, or aromatase inhibitors, such as Anastrozole/Arimidex,, Letrozole/Femara and Exemestane/Aromasin). In case the problem persists, then the gland should be removed surgically (mastectomy).Liposuction is a surgical procedure, which removes breast fat, but not the breast gland tissue itself.
In order to prevent the side effects of aromatization (water retention and fat storage), we commonly use either Selective Estrogen Receptors Modulators (SERMs) or the more potent aromatase inhibitors(AIs).SERMs (Tamoxifen, Clomiphene) occupy locally the estrogenic receptors, thus making the circulating estrogens unable to attach to the receptors. AI’s suppress estrogen production by inhibiting the action of the enzyme aromatase, which converts androgens into estrogens. The two types of AI’s include suicidal steroidal inhibitors, such as Exemestane/Aromasin and non-steroidal inhibitors, such as Anastrozole/Arimidex and Letrozole/Femara. Exemestane prevents the rise of estradiol (E2) for quite a while, after its being used,thus preventing any rebound effect. The drug almost suppresses plasma and tissue estrogen level (estradiol-E2) by 85% in vivo of total estrogen. Occasionally, synthetic forms of Dihydroxytestosterone/DHT (Mesterolone/Proviron and Drostanolone/Masteron) are also used in order to enhance anti-estrogenic effect.
Usually bodybuilders prefer AI’s during pre contest preparation. The reason is that they are extremely effective. However, each coin has two sides; cutting down dramatically the levels of estrogens has a cost to the athlete. First of all, estrogens play a significant role in muscle growth.Insulin like groth factor/ IGF1 is a peptide responsible for anabolism and cartilage growth. Somatomedin C levels decrease as potent anti-estrogens are used. IGF1 is synthesized in liver parenchyma. Estrogens cause water retention and fat storage. Water retention in muscle tissue is very important, since a molecule of glycogen requires the presence of water molecule in order to be synthesized. As a result, the stronger anti-estrogenic agents we use, the lesser glycogen storage we will have. This of course has a tremendous cost on muscle endurance and strength as well. ATP/CP for anaerobic oxidation of glucose requires the existence of muscle glycogen as well.
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