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Introduction to Winstrol (Stanozolol)


Winstrol (aka Stanozolol) is one of the more common and more popular anabolic steroids out there, and it has a few notable reasons for being so. This is the anabolic steroid that had made its claim to fame for being the anabolic steroid that the Canadian Olympic sprinter Ben Johnson was supposedly tested positive for. It is quite structurally different from most other anabolic steroids, as it has a 3-2 Pyrazol group that is attached to the whole structure of the typical steroid structure. Even one without chemistry knowledge would immediately be able to tell the difference between the Winstrol and a common anabolic steroid such as Testosterone, just by comparing a picture of the two side by side. It is known that this additional functional group contributes to stronger androgen receptor binding. Winstrol is a DHT-derived anabolic steroid, but this modification of its chemical structure allows it to be far more active and effective in muscle tissue, where in comparison, Dihydrotestosterone (DHT) is not. DHT is not a very anabolic hormone, and has very little to no anabolic effects in muscle tissue. DHT-derived anabolic steroids such as Winstrol, Anavar, Primobolan, Masteron, and so on and so forth, are all DHT-based but they possess chemical modifications that alter their anabolic effects to be at least somewhat anabolic in muscle tissue.


The primary advantages to having DHT-based anabolic steroids are the advantages that are associated with DHT itself: for one thing, it does not interact with the aromatase enzyme, thereby negating any potential estrogen conversion. Along with this comes the diminished risk of water retention (and the associated high blood pressure risk), and other estrogen-related side effects. Naturally, people would gravitate towards anabolic steroids such as Winstrol for its ability to avoid these potential side effects.


Winstrol For SaleWinstrol’s androgenic rating is 30, and its anabolic rating is 320. To understand what these numbers mean, one must understand that the base reference for these numbers is the #1 basic anabolic steroid: Testosterone. Testosterone is the ‘measurement bar’ by which all other anabolic steroids are referenced by. So, in comparison, Testosterone’s anabolic and androgenic rating are both 100. What this means to the user is that upon first glance, Winstrol is 320% more anabolic than Testosterone, and it is 30% less androgenic than Testosterone. This, however, is not the full truth as sometimes these numbers can be quite confusing. First, one must understand that because Winstrol is a DHT-based anabolic steroid, the androgenic rating is very much related to DHT rather than Testosterone. Therefore, we must first recognize that DHT is 3-5 times more androgenic than Testosterone, and this places DHT’s androgenic rating in the 300-500 range (remember that Testosterone’s androgenic rating is 100). With this in mind, the androgenic effects of Winstrol would actually be a little greater in practice than theory would have you believe. It is important to remember this. Due to these chemical modifications and properties, Winstrol displays a much longer half-life than Testosterone or dihydrotestosterone. Winstrol’s half-life is approximately 24-48 hours. Many of these modifications also owe to the fact that Winstrol has a very high binding affinity for SHBG (Sex Hormone Binding Globulin), which will allow for far more of this anabolic steroid, as well as others simultaneously used (perhaps testosterone, for example), to be free to do its job in binding to receptor sites and signalling growth. As well, not only will it avoid binding to SHBG, it has also been shown in studies to actually suppress levels of SHBG in the human body. In one study, 25 test subjects were administered Winstrol orally for three days and blood tests following this 3 day period displayed a 48.8% reduction in SHBG [1].


One important characteristic of Winstrol to be made note of, is that both the injectable as well as oral variants are the exact same chemically. We know that in order for an anabolic steroid to be bioavailable orally, it must be modified at the 17th carbon with an alkyl group addition. This places more stress on the liver, as now the anabolic steroid is far more resistant to hepatic breakdown. Unfortunately, because the oral preparations as well as the injectable preparations are both the exact same chemical structure, they will both place a fairly equal amount of toxicity on the liver, even though injectable preparations will avoid the first pass.


Now we raise the question: where does Winstrol fit into an anabolic steroid cycle and when? I will expand further upon this in the next section, but first let’s compound what we have discussed so far, and perhaps discuss a few more characteristics that would narrow down its purpose. I have already discussed its non-aromatizing properties due to it being a DHT-derivative, therefore negating potential water retention, and associated blood pressure increases, and so on and so forth. It also has the ability to lower the levels of SHBG in the body. Where this places Winstrol as a favourable compound would be in the range of ‘cutting compounds’ due to its nature to completely avoid water and fat retention. All of Winstrol’s characteristics make it a great adjunct to a solid base compound, such as Testosterone. Although most people would not be too fond of using Winstrol for bulking and mass cycles, I believe that it could possibly have its uses there as well, and I would not negate the fact that it would be effective in this regard. However, what sets Winstrol short on its use in bulking cycles is the sheer fact that there are far better and more effective compounds out there for bulking cycles, and that would make one more apt to save Winstrol for a cutting cycle, maintenance cycle, or lean mass cycle with minimal to moderate mass gains.


 [1] Sex hormone-binding globulin response to the anabolic steroid stanozolol: evidence for its suitability as a biological androgen sensitivity test. Sinnecker G, Köhler S. Department of Pediatrics, University of Hamburg, West Germany. J Clin Endocrinol Metab. 1989 Jun;68(6):1195-200.

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