Studies have demonstrated that Winstrol’s main mechanism of action is that of binding with cellular androgen receptors as opposed to non-receptor mediated activity (such as those possessed by Dianabol or Anadrol). It is also believed that Winstrol also possesses some very small measurable form of anti-Progestogenic properties in regards to the Progesterone receptor, although this is not fully understood. In addition to some small antagonistic effects on the Progesterone receptor, it has been found that Winstrol also possesses low affinity for Glucocorticoid-binding site interactions, as well as activity that is independent of Androgen receptors, Progesterone receptors, and Glucocorticoid receptors. Winstrol has not been found to have any notable Progestogenic activity in the body as well.
Winstrol possesses a very high binding affinity for SHBG (Sex Hormone Binding Globulin), therefore granting far more of Winstrol (as well as other anabolic steroids that may be stacked alongside it, such as Testosterone) to freedom in the bloodstream in doing its job of signaling muscle growth. SHBG is a protein that attaches and binds to other sex hormones (Testosterone, Estrogen, or any synthetic anabolic steroid) and renders them useless as long as SHBG is bound to that hormone. Effectively, SHBG places ‘handcuffs’ on any hormone it binds to and prevents it from doing its job. Winstrol has also demonstrated to not only prevent SHBG from binding with other anabolic steroids, but it has also demonstrated strong suppression of SHBG production in the body. For example, one particular study conducted on 25 male test subjects where Winstrol was administered orally resulted in a 48.4% drop in SHBG levels following just 3 days of Winstrol administration.
With Winstrol being a DHT-derivative, it holds the advantage that is generally associated with DHT and all other DHT-derivatives: it is unable to bind with the aromatase enzyme, which results in no possible Estrogen conversion. Resulting from this is an avoidance of the Estrogen-related side effects of water retention (and the associated risks of elevated blood pressure), as well as other Estrogen-related side effects. Being a DHT-derivative, it is also unable to interact with the 5-alpha reductase enzyme, which is the enzyme responsible for the conversion of Testosterone into Dihydrotestosterone. As Winstrol is already a modified form of DHT, this cannot possibly occur.
Winstrol exhibits a longer half-life as a result of its structural modifications, enabling the injectable format of Winstrol to possess a half-life of approximately 24 hours, and 9 hours for the oral preparation of Winstrol. In relation to Testosterone, Winstrol holds an androgenic strength rating of 30 with an anabolic strength rating of 320, which is quite significant considering this means Winstrol is slightly over three times the anabolic strength of Testosterone. In order for any individual to understand the meaning of these numbers and ratings, it must be understood that the base reference measurement for these strength ratings is the number one anabolic steroid Testosterone. Testosterone is utilized as the measuring stick or the measuring bar whereby all other anabolic steroids are referenced with and compared to (much like the celcius scale of temperature measurement where the freezing point and boiling points of water is used as the baseline measurement for temperature). Upon understanding this, any individual can easily observe how Winstrol possesses an anabolic strength of three times Testosterone (Testosterone’s anabolic and androgenic ratings are both respectively 100). Percentage-wise, it could be described that Winstrol is 320% more anabolic than Testosterone, and it is 30% less androgenic than Testosterone.
An important fact that must be reminded to the reader is the fact that both the injectable and oral preparations of Winstrol possess the exact same chemical structure. This is unlike nearly all other anabolic steroids, where oral preparations are always C17-alpha alkylated, and injectable preparations are absent of this methylation (and often injectable compounds are also esterified to modulate the release rate and half-life). This is not so with Winstrol, where the oral and injectable preparations are exactly 100% identical to each other. This presents some concerns that the reader must be aware of: The result is a greater amount of hepatotoxicity (liver toxicity), and because both the injectable and oral preparations both possess the hepatotoxic modification of C17-alpha alkylation, they both will place an almost equal level of hepatotoxic strain on the liver. However, the injectable preparation avoids the first-pass through the liver, which allows it to be slightly less hepatotoxic than the oral Winstrol preparation – but hepatotoxic nevertheless, and its duration of use must also have limitations placed on it.
Winstrol Side Effects