The vast majority of individuals investigating and educating themselves on anabolic steroids in general or on a particular anabolic steroid such as Winstrol will often be concerned with many of the associated side effects. Winstrol does possess various potential side effects, most of which are side effects that are very common with all anabolic steroids.
It is of extreme importance that every reader must understand that not all side effects are bound to occur just because they have been listed, hence why they are known as potential side effects. The fear that many individuals develop about particular side effects (or anything in general) is usually always due to ignorance of the topic, and general lack of education. Proper informed unbiased education is the key to removing that fear of the unknown and replacing that fear with confidence. What must be understood are the potential side effects, what they are, how they are caused, under what conditions they occur, and the frequency and intensity of these potential side effects. Winstrol side effects are no exception to this rule – increased understanding and knowledge is the key to overcoming the fear of the unknown.
Estrogenic Side Effects of Stanozolol
Winstrol side effects do not include any measurable Estrogenic or Estrogen-related side effects. Winstrol, being a DHT-derivative, does not interact with the aromatase enzyme (the enzyme responsible for the conversion of androgens into Estrogen) and itself is not Estrogenic in nature. Therefore, no anti-Estrogens or aromatase inhibitors are necessary with Winstrol use, and none of the typical Estrogen-related side effects should be experienced from Winstrol. Estrogenic side effects include: water retention and bloating, blood pressure elevations (as a result of the water retention), increased possible fat retention/gain, and gynecomastia.
Androgenic Side Effects of Winstrol
Winstrol possesses a far weaker androgenic strength rating than Testosterone, but the possibility of androgenic side effects resulting from Winstrol cannot be dismissed. Winstrol’s androgenic effects may still be experienced by many users, especially in those that possess a greater sensitivity to androgenic side effects than the general average population. Recall that Winstrol does not interact with the 5-alpha reductase enzyme, which is the enzyme responsible for the reduction of Testosterone into the far stronger androgen Dihydrotestosterone (DHT). Because of Winstrol’s inability to interact with this enzyme, it cannot be converted into any stronger androgens due to the fact that it is already a DHT in nature (although modified). Therefore, any measurable androgenic side effects resulting from Winstrol in general is what should be expected throughout any Winstrol cycle, due to the fact that it does not convert into any stronger androgens. What also results from its inability to interact with the 5-alpha reductase enzyme is the inability for 5-alpha reductase inhibitors such as Finasteride to reduce the androgenic effects from Winstrol. This is because 5-alpha reductase inhibitors such as Finasteride only prevent the conversion of Testosterone into DHT, which Winstrol is incapable of doing. Androgenic side effects include: 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.
HPTA and Endogenous Testosterone Production Side Effects
All anabolic steroids possess the capability to suppress and/or shut down the body’s natural endogenous Testosterone production, and Winstrol side effects are no exception to this well-established rule. Winstrol in particular has demonstrated very strong suppression of the Hypothalamic Pituitary Testicular Axis (HPTA). Various clinical studies have demonstrated that when healthy male test subjects were administered 10mg daily for a period of 14 days, blood plasma Testosterone levels plummeted by 55%. Therefore, it is pretty evident that any claims made about Winstrol being a ‘mild’ compound on the HPTA (a frequent occurrence among individuals involved in the anabolic steroid culture) should be dismissed as misinformation. It is highly advised that any Winstrol user engage in a proper PCT (Post Cycle Therapy) protocol, which should always include the use of Testosterone production stimulating ancillary compounds, such as Nolvadex and/or HCG (Human Chorionic Gonadotropin) for an average PCT period of 4 – 6 weeks following the end of a cycle of any anabolic steroid regardless of how ‘mild’ it is claimed to be in terms of its impacts on the HPTA. Failure to do so can result in permanent damage to the HPTA, whereby the individual will insufficiently produce proper levels of Testosterone for the remainder of his life, which if left untreated will ultimately medical intervention in the form of TRT (Testosterone Replacement Therapy).
Hepatotoxic Side Effects
Hepatotoxicity is a concern with Winstrol, and is certainly in the list of Winstrol side effects. This particular attribute and Winstrol side effect has been covered several times throughout this profile. It is well-known that Winstrol is a C17-alpha alkylated compound, which places varying degrees of measurable hepatotoxicity on the body. Both the injectable and oral preparations possess this chemical modification, as both formats are of the exact same identical chemical configuration. Winstrol in particular is known for placing measurably less hepatic strain on its users than other C17-alpha alkylated anabolic steroids, such as Dianabol or Anadrol, for example. Studies have administered 12mg daily of Winstrol for a total 27 week period to test subjects, which resulted in no noticeable changes in liver enzyme values in each test subject’s blood samples (serum aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, bilirubin, and alkaline phosphatase were all monitored). This does provide a very good indication and a large amount of insight as to the effects of Winstrol administration on the liver, but what must be observed here is that the doses utilized in the mentioned studies are far lower doses than individuals use for the purpose of performance and physique enhancement, which are often in the range of two to seven times the amount administered in the study (and sometimes more than that). Therefore, it is important to remember that hepatotoxicity increases in relation to increased doses, so hepatotoxicity is still a considerable concern if an individual engages in high doses or lengthy prolonged use.
The hepatotoxicity of the injectable format of Winstrol has also been investigated in studies, where severe hepatotoxicity has been demonstrated in what would be considered healthy individuals. Therefore, potential hepatotoxicity from the injectable Winstrol preparation is equally a concern as well, once again, due to the fact that there is no difference between the chemical structures of both preparations even though the injectable format does avoid the first pass through the liver. The difference between the two in terms of hepatotoxicity should be such that the oral format presents a greater degree of hepatotoxicity than the injectable. However, the injectable preparation still exhibits notable amounts as well. In general, it has been determined that on a mg for mg basis, Winstrol presents less hepatotoxicity than other oral anabolic steroids administered at the same doses.
It is therefore recommended that it is recommended to limit oral Winstrol use to periods of no longer than 6 – 8 weeks, and the injectable preparation for periods no greater than 10 weeks. It is also highly recommended that users supplement with a proven liver support and health supplement, such as TUDCA/UDCA while using oral anabolic steroids.
Cardiovascular Side Effects
Negative cardiovascular risks, side effects, and cholesterol changes are a known side effect shared by all anabolic steroids, and this side effect does apply to side effects. Negative cardiovascular side effects resultant from anabolic steroid use 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. In terms of the route of administration, oral anabolic steroids are known for having a reputation as being much worse for their negative impacts 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.
Winstrol in particular is known for exhibiting some profound negative cholesterol changes in humans as evidenced by some clinical studies. Winstrol administered orally at just 6mg daily for a 6 week period resulted in a reduction of HDL by 33%, alongside an LDL increase of 29% (all test subjects were healthy males engaged in regular physical exercise). Even the injectable Winstrol preparation has demonstrated to produce negative cholesterol profile changes. Only a single 50mg dose of injectable Winstrol was administered to 12 healthy test subjects, and resulted in significant HDL reduction with an increase in LDL (these negative cholesterol changes remained for a 4 week period following administration before returning to normal values).
 The influence of 6 months of oral anabolic steroids on body mass and respiratory muscles in undernourished COPD patients. Ivone Martins Ferreira, leda Verreschi et al. CHEST 114 (1) July 1998 19-28.
 Contrasting effects of testosterone and stanozolol on serum lipoprotein levels. Thompson TD, Cullinane EM, Sady SP, Chenevert C, Saritelli AL, Sady MA, Herbert PN. JAMA. 1989 Feb 24;261(8):1165-8.