Masteron Side Effects


Masteron itself is an anabolic steroid that is considered fairly mild in terms of the majority of Masteron side effects. However, there can be areas in which Masteron may have barely any effect at all while other aspects of it may present more pronounced or ‘harsher’ side effects in individuals who are especially sensitive to them.

Estrogenic Side Effects

Masteron is a DHT-derivative, and as such, it does not possess any ability what so ever at any dose to be aromatized by the aromatase enzyme. Therefore, no Estrogenic side effects as a result of Masteron itself should occur or be of any concern to the user. In fact, due to Masteron’s properties as an anti-estrogen and an aromatase inhibitor, it should serve to act as a moderate aromatase inhibitor and reduce Estrogen levels as a result. This is why it is advised to utilize Masteron with other aromatizable androgens, such as Testosterone or Dianabol.


Androgenic Side Effects

Although Masteron possesses a weaker androgenic strength rating than Testosterone, it is still considered an anabolic androgenic steroid and the risk of androgenic side effects still does exist with Masteron. Masteron in particular was designed for use in female breast cancer patients, which serves as an explanation for the lower androgenic strength rating of it (25 – 40 versus Testosterone’s androgenic rating of 100). Androgenic side effects can still manifest themselves with this anabolic steroid, especially in individuals who are far more sensitive to androgenic side effects than the average anabolic steroid user. Androgenic side effects include the following: increased sebum secretion (oily skin), increased bouts of acne (linked to increased sebum secretion), bodily and facial hair growth, and the increased risk of triggering Male Pattern Baldness (MPB) in individuals that possess the genetic trait required for the condition to manifest itself. Masteron side effects where androgenicity is concerned also includes virilization effects in female users as evidenced by the medical and clinical data involving female breast cancer patients who have been treated with Masteron. Virilization effects can include the development of male secondary sex characteristics (deepening of the voice, growth of body and facial hair), clitoral enlargement, and menstrual irregularities. A positive note here on Masteron side effects is that Masteron does not interact with the 5-Alpha Reductase enzyme (the enzyme responsible for the conversion of Testosterone to the much more androgenic Dihydrotestosterone), and so therefore there is no risk involved in Masteron converting to any metabolite that is stronger in androgenic effects. Therefore, the androgenic strength associated with Masteron should be the androgenic strength that one should experience fairly consistently throughout use.

HPTA and Endogenous Testosterone Production Side Effects

All anabolic steroids when utilized at doses necessary for physique and performance enhancement can and will cause suppression of the HPTA (Hypothalamic Pituitary Testicular Axis) and natural endogenous Testosterone production. Possible total shut-down of these endocrine systems can result as well. Masteron side effects are no exception to this rule for all anabolic steroids. Following the end of any cycle, a thorough and proper Post Cycle Therapy (PCT) program is always necessary, where Testosterone-stimulating ancillary compounds such as Nolvadex and/or HCG are utilized in order to facilitate the normalization of the HPTA and endogenous Testosterone production as quickly as possible. Failure to do so can result in permanent damage to the HPTA, whereby the individual produces insufficient levels of Testosterone, and medical treatment in the form of TRT (Testosterone Replacement Therapy) for life will be required.

Hepatotoxic Side Effects

Masteron is not a C17-alpha alkylated anabolic steroid, and presents no hepatotoxic effects on the body. Liver problems are not known to be an associated with Masteron side effects.

Cariovascular Side Effects

It is an established fact that all anabolic steroids express negative impacts on cholesterol levels in the human body. This involves the reduction of HDL (the good cholesterol) and increases of LDL (the bad cholesterol). The result of such changes involves an increased risk of arteriosclerosis, and the degree to which these changes occur for the worse are usually dose-dependent (with higher doses increasing the negative changes and the risks). Other factors that affect these negative cholesterol changes are: duration of use, and route of administration. This is where oral anabolic steroids hold a negative reputation for exhibiting a far worse negative impact on cholesterol in comparison to injectable anabolic steroids. This is because the liver serves to function as the cholesterol processing center for the human body, and the increased hepatotoxicity associated with anabolic steroids will result in even worse negative cholesterol changes.

Masteron in particular may possibly exhibit even worse effects on the negative cholesterol changes it imparts on the human body. This is due to Masteron’s aromatase inhibiting and anti-estrogenic properties, as the reduction of Estrogen levels below normal physiological levels has been demonstrated in studies to impart an even worse impact on cholesterol profiles than when anabolic steroids are administered alone without an aromatase inhibitor. Testosterone in particular has demonstrated in one clinical study to have only a mild impact on HDL cholesterol after a 12 week period where 280mg of Testosterone Enanthate was administered weekly. The cholesterol profiles had later changed for the worse when an aromatase inhibitor was included, which resulted in a significant 25% drop in HDL cholesterol[1]. This must be remembered by any potential user of Masteron, and Estrogen levels must be closely monitored so as to ensure Masteron does not reduce Estrogen to the point whereby cholesterol profiles are impacted negatively.



Masteron References:


[1] High-density lipoprotein choilesterol is not decreased if an aromatizable androgen is administered. Friedl K, Hannan C et al. Metabolism 39(1) 1990;