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What is it gynecomastia and how is it treated?

The problem I’m about to explain may have been encountered by many steroid users, who may have already treated it or are still suffering from it.

Gynecomastia is a condition that is characterised by the enlargement of the male breast gland due to a hormonal imbalance. There are different types of gyno (gynecomastia), but of course I’m going to focus on the one that is generated by iatrogenic causes, in particularly by the use of anabolic steroids. The mammary gland is made up by a tissue hosting numerous receptors for estrogens, both on men and women, and therefore high amounts of these hormones stimulate the growth of this tissue, causing gyno on men. With the use of steroids, there is an elevated amount of exogenous androgens in the bloodstream that causes a hormonal imbalance altering that homeostasis the body constantly tries to keep, so to counterbalance the excess of androgens the body resorts to an enzyme called aromatase, which purpose is to convert testosterone and other androgens to estradiol and estrogens. Aromatase is synthesised and stored in various tissues, such as gonads, and mainly adipose tissue. That’s one reason for the low levels of testosterone and high levels estrogens in obese individuals, who usually also present problems with their fertility and gynecomastia or lipomastia.

It’s important to specify that aromatisation, the process that involves the conversion of androgens to estrogens through aromatase, can only occur on those steroids that are derived from testosterone, but it cannot occur on those that are derived from dihydrotestosterone (DHT), as the substrate of the aromatase is not compatible with DHT. DHT derivatives include stanozolol (winstrol), drostanolone (masteron), methenolone (primobolan), those are all molecules used on cutting and pre-competition cycles, as not being able to convert to estrogens they do not cause any water retention. Another molecule that cannot aromatise is trenbolone, although due to its nature, being a 19-nor-testosterone (like deca), it may cause gyno through a different mechanism that does not involve estrogens.

The use of 19-nor-testosterones has been often associated to an increse in prolactin levels, another hormone, not a steroidal one, mediated by other mechanisms but with similar effects on the mammary gland, so gyno often paired to galactorrhea, a milky secretion from mammary glands in men.

Now that I’ve presented the causes for gynecomastia, I will categorise them and list the available treatments depending on the cause.

Gynecomastia from estrogens

Treatments for this type of gyno involve the the use of drugs called aromatase inhibitors. There are two kinds of inhibitors for this enzyme: steroidal and non-steroidal.

Exemestane (also known as Aromasin) is a steroidal aromatase inhibitor. Its structure, similar to the substrate of the hormone 4-androstenedione, allows it to bind it to the enzyme irreversibly causing the inhibition, this process is also known as “suicidal inhibition”. Because it is irreversible it will ensure there will be no rebound after its interruption. Formestane (Lentaron) is another steroidal inhibitor with a similar way of action. Their half-life is around 24 hours, therefore daily administrations are the most suitable.

Letrozole (Femara) and anastrozole (Arimidex) are two non-steroidal aromatase inhibitors and its inhibition is reversible. Despite having a similar mechanism of action to steroidal inhibitors, which involves the compatibility with the substrate of the aromatase in order to bind to it, their action is reversible. Such detail means that there might be a rebound, usually stronger with anastrozole than letrozole, as letrozole has also a direct impact on estrogen levels in the blood, rather than just temporarily binding to aromatase like anastrozole. The studies reported dosages of 2.5mg of letrozole and 1mg of anastrozole daily until the complete regression of gynecomastia.

The use of SERMs (Selective Estrogen Receptor Modulators) like tamoxifen (Nolvadex) is recommended to immediately treat the symptoms of gynecomastia. On its own, it’s usually not enough to treat the problem, as its action as a SERM is limited to temporarily “block” the estrogen receptor to avoid those from binding with them and therefore operate their effect on the mammary glands, whilst having no effect on estrogen levels in the blood stream which still remain high and will be ready to bind to the receptors as soon as the SERM has come off them. Because of this it’s recommended to use tamoxifen along with an aromatase inhibitor in order to prevent gynecomastia from occurring again once tamoxifen has been interrupted. Studies report effective dosages at 20mg daily of tamoxifen.

Gynecomastia from prolactin

Prolactin is a hormone released by lactotroph cells in the hypophysis and its main role is to promote lactation. Logically, in mammary glands, where lactogenesis takes place, is also where you find prolactin receptors. Despite being mainly a female hormone, it still finds some place in men as well, where it can cause gynecomastia and/or galactorrhea. Its mechanism is completely different from estrogen, as it’s not one, chemically talking it’s a peptide and it’s produced by the hypophysis stimulated by TRH. The main cause for hyperprolactinemia in bodybuilding, with gynecomastia, is often correlated to the use of 19-nor-testosterones such as nandrolone and trenbolone. An aromatase inhibitor and tamoxifen may in fact have no effect on prolactin levels, as its production is not mediated by aromatase. In such cases, D2 dopaminergic receptor agonists are required, cabergoline (Cabaser or Dostinex) is the most suitable in this case. Vitamin B6 has shown to be an effective control for prolactin of dosages superior to 300mg daily. Thyroid hormones such as T3 and T4 can have a suppressive effect on prolactin as well, due to their suppression of TSH by negative feedback, which is also regulated by TRH, therefore a suppression of TSH may induce a suppression on TRH as well, therefore inhibiting the production of prolactin. That is of course, a method to be considered only in certain cases, like cutting cycles and it’s definitely not recommended to newbies or as a prolactin inhibitor method only, as thyroid hormones require a certain degree of knowledge to be run appropriately.

 

References

Cohen  PG. The hypogonadal-obesity cycle: role of aromatase in modulating the testosterone-estradiol shunt–a major factor in the genesis of morbid obesity. Med Hypothesis, 1999

Shiau AK, Barstad D, Loria PM et al. The structural basis of estrogen receptor/coactivator recognition and the antagonism of this interaction by tamoxifen. Cell, 1998

Willem de Ronde e Frank H de Jong. Aromatase inhibitors in men: effects and therapeutic options. Reprod Biol Endocrinol. 2011

Khan HN1, Rampaul R, Blamey RW. Management of physiological gynaecomastia with tamoxifen. Breast. 2004

Santosh KS. Aromatase inhibitors in male sex Indian J Endocrinol Metab. 2013

Neslihan C et al. Gynecomastia: Clinical evaluation and management. Indian J Endocrinol Metab. 2014

Folkerd EJ et al. Suppression of plasma estrogen levels by letrozole and anastrozole is related to body mass index in patients with breast cancer. J Clin Oncol. 2012

Khan HN et al. Management of physiological gynaecomastia with tamoxifen. Breast. 2004

Daria La Torre and Alberto Falomi. Pharmacological causes of hyperprolactinemia. Ther Clin Risk Manag. 2007

Cataldo NA et al. The effect of thyroid hormones on prolactin secretion by cultured bovine pituitary cells. Metabolism 1982

Barni S et al. Clinical efficacy of the aromatase inhibitor anastrozole in relation to prolactin secretion in heavily pretreated metastatic breast cancer. Tumori 1998

Mike Costantini

Enhanced athlete since I was 17, my aim is to write on a safer use of steroids and performance enhanced drugs through this website sharing my knowledge and to offer consultations on training and advices on how to improve your physique and reach your goals. You can contact me privately at bulktodominate@protonmail.com or using the red widget at the bottom right.

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Mike Costantini
Enhanced athlete since I was 17, my aim is to write on a safer use of steroids and performance enhanced drugs through this website sharing my knowledge and to offer consultations on training and advices on how to improve your physique and reach your goals. You can contact me privately at bulktodominate@protonmail.com or using the red widget at the bottom right.