Winstrol (aka stanozolol)
Winstrol (AKA Stanozolol)
Chemical Name: 17β-Hydroxy-17-methyl-5alpha-androstano[3,2-c]pyrazole
Molecular Weight: 328.49 g/mol
Formula: C21H32N2O
Original Manufacturer: Winthrop Laboratories
Half Life: 9 hours (oral), 24 hours (injectable)
Detection Time: 2 months
Anabolic Rating: 320
Androgenic Rating: 30
History and Overview of Winstrol
Winstrol is the trade name and brand name of an anabolic steroid more formally and properly known as stanozolol.
It exists in both oral and injectable forms and is ranked third among the top three most widely used and most popular anabolic steroids among bodybuilders and athletes.
The second place is held by Deca Durabolin (nandrolone decanoate) and the first place is held by Dianabol (methandrostenolone).
Winstrol is most famous and well-known because of Canadian Olympic sprinter Ben Johnson's positive test for (winstrol) at the 1988 Seoul Olympics.
However, Winstrol's origins date back to 1959, when details were first published in the medical and scientific community [1].
It was the Winthrop Laboratories in the UK that marketed stanozolol to the prescription drug market, and in 1961, Sterling in the US bought the patent and introduced it to the US market under the brand name Winstrol [2].
Since its introduction to the prescription drug market, Winstrol has been approved for a wide range of treatments, from tissue and muscle wasting diseases to osteoporosis to treating burn victims and stunted children.
However, Winstrol has not been very effective as a treatment for anemia [3].
The mechanism of action of Winstrol is quite remarkable in many ways. Winstrol's primary action is through binding to the androgen receptor rather than non-receptor mediated action[4], which is common to other anabolic steroids such as Dianabol and Anadrol.
Winstrol also has a low affinity for binding to the glucocorticoid binding site, in addition to some androgen receptor-independent activity[5][6][7][8].
Winstrol also has very low levels of progestogenic activity in the body[8].
An impressive and somewhat unique feature of Winstrol is its ability to significantly lower SHBG (sex hormone binding globulin) levels in the body, allowing testosterone and other anabolic hormones to more freely exert their anabolic actions in muscle tissue[10].
Winstrol has the ability to stimulate and promote excellent and high levels of protein synthesis[11][12].
Winstrol has also been observed to have the ability to promote collagen synthesis in the body[13].
Chemical Properties of Winstrol (Stanozolol)
The chemical structure of Winstrol is very different from all other anabolic steroids.
However, it is a derivative of dihydrotestosterone (DHT), with a 3-2 pyrazole group attached to the first cycloalkane ring (called the A ring) of the anabolic steroid structure.
Even for someone unfamiliar with chemistry, this becomes very noticeable when you place a picture of Winstrol's chemical structure side-by-side with its precursor hormone, DHT.
The pyrazole group attached to the A-ring actually replaces the 3-keto group in the same position.
Notably, this key modification causes Winstrol to be classified as a heterocyclic steroid.
This functional group, the pyrazole group, is actually responsible for Winstrol's stronger binding affinity to the androgen receptors in muscle tissue.
Winstrol is a DHT derivative with a modification that distinguishes it from DHT, and is actually much more active in muscle tissue than DHT itself.
Unfortunately, DHT itself is almost immediately rendered inactive by two enzymes once it enters muscle tissue. Winstrol has been modified to effectively avoid this problem.
All anabolic steroids in the DHT derivative family, including Winstrol, Anavar, Primobolan, Masteron, and others, have modified chemical structures to confer significant activity and effectiveness within muscle tissue; unmodified DHT itself does not survive metabolism in muscle tissue.
The pyrazole structure also significantly alters the strength of Winstrol's anabolic and catabolic effects, making it more anabolic and significantly less catabolic.
This is why Winstrol has a very strong separation of anabolic and androgenic activity.
Winstrol also has a methyl group attached to the 17th carbon (called C17 alpha alkylation), which is a chemical structure modification that allows the anabolic steroid to survive the first pass through the liver when taken orally, making it more resistant to liver metabolism.
Characteristics of Winstrol (stanozolol)
Studies have shown that the primary mechanism of action of Winstrol is through binding to cellular androgen receptors, as opposed to non-receptor mediated actions (such as Dianabol or Anadrol).
Winstrol is also believed to have a very small form of measurable anti-progestogenic properties with respect to the progesterone receptor, although this is not fully understood.
In addition to its slight antagonistic effect on the progesterone receptor, winstrol has been found to have a low affinity for glucocorticoid binding site interactions and activity independent of androgen receptors, progesterone receptors, and glucocorticoid receptors.
Winstrol has also been found to have no notable progestogenic activity in vivo.
Winstrol has a very high binding affinity for sex hormone binding globulin (SHBG), which means that much more Winstrol (and other anabolic steroids that can stack with it, such as testosterone) is freely available in the bloodstream to signal muscle growth.
SHBG is a protein that sticks to and binds to other sex hormones (testosterone, estrogen, or synthetic anabolic steroids), rendering them useless as long as SHBG is bound to them.
In effect, SHBG “handcuffs” the hormone it binds to, preventing it from doing its job.
In addition to preventing SHBG from binding to other anabolic steroids, Winstrol has also been shown to be a potent inhibitor of SHBG production in the body.
For example, in one study involving 25 male subjects, oral administration of Winstrol resulted in a 48.4% reduction in SHBG levels in just three days.
Because Winstrol is a DHT derivative, it has the advantage of not being able to bind to the aromatase enzyme, which is a benefit typically associated with DHT and all other DHT derivatives, and therefore has no potential for estrogen conversion.
As a result, water retention (and the associated risk of increased blood pressure) and other estrogen-related side effects are avoided.
Also, because it is a DHT derivative, it cannot interact with 5-alpha reductase, the enzyme that converts testosterone to dihydrotestosterone.
Since Winstrol is already a modified form of DHT, there is no chance of this happening.
Due to its structural modifications, Winstrol has a longer half-life, with the injectable form of Winstrol having a half-life of approximately 24 hours and the oral form of Winstrol having a half-life of 9 hours.
In relation to testosterone, Winstrol has an androgenic strength rating of 30 and an anabolic strength rating of 320, which is quite significant considering that Winstrol has slightly more than three times the anabolic strength of testosterone.
For an individual to understand the meaning of these numbers and ratings, they must understand that the primary reference measure for these strength ratings is the top anabolic steroid testosterone.
Testosterone is used as the measuring stick or yardstick against which all other anabolic steroids are referenced and compared (similar to the Celsius scale, which uses the freezing and boiling points of water as a reference point for temperature measurement).
Understanding this, anyone can easily see that Winstrol has three times the anabolic strength of testosterone (testosterone has an anabolic and androgenic rating of 100, respectively).
In terms of percentages, we can describe Winstrol as 320% more anabolic than testosterone and 30% less androgenic than testosterone.
An important fact to remind the reader is that both the injectable and oral formulations of Winstrol have the exact same chemical structure.
This is unlike almost all other anabolic steroids where the oral formulation is always C17-alpha alkylated and the injectable lacks this methylation (often the injectable compound is also esterified to control the rate of release and half-life).
This is not the case with Winstrol, where the oral and injectable formulations are exactly 100% identical to each other.
This presents some concerns that readers should be aware of:
That the result is more hepatotoxicity (liver toxicity), and that both the injectable and oral formulations have the hepatotoxic variant of the C17-alpha alkylation, which means that both formulations can impose roughly the same level of hepatotoxic burden on the liver.
However, the injectable formulation is slightly less hepatotoxic than the oral Winstrol formulation because it avoids the first pass through the liver, but it is nonetheless hepatotoxic and should have a limited duration of use.
Winstrol Side Effects
The main areas of concern when it comes to Winstrol side effects are, in a nutshell, hepatic (liver) issues related to hepatotoxicity, hypothalamic-pituitary-testicular axis (HPTA) disorders, and negative cardiovascular effects.
Because Winstrol is a DHT-derived anabolic steroid, it does not convert to estrogen at any dose.
This means that you should not experience estrogenic side effects from using Winstrol alone.
Therefore, side effects such as gynecomastia, water retention and bloating, or any other side effects as a result of estrogen buildup are completely absent.
Although Winstrol is less androgenic than testosterone, androgenic side effects are still a potential risk, but at a much lower level and may only significantly affect users who are particularly sensitive to androgens.
Androgenic side effects include oily skin and increased acne, body hair growth, male pattern baldness (MPB), and benign prostatic hyperplasia (BPH).
The use of 5-alpha reductase (5AR) inhibitors such as finasteride, dutasteride, Proscar, or Propecia is completely ineffective because Winstrol is not converted to DHT.
One notable concern is the issue of HPTA suppression that occurs when using anabolic steroids.
Studies have shown that as little as 10 mg of Winstrol per day leads to a 55% decrease in endogenous testosterone production in 14 days [14].
Hepatotoxicity is one effect to watch out for, especially when using oral Winstrol [15].
The injectable formulation of Winstrol has also raised concerns in studies, with even healthy individuals eventually experiencing severe hepatotoxicity [16].
For this reason, it is recommended that Winstrol, especially the oral formulation, be used for no more than six to eight weeks at a time.
Cardiovascular health issues are particularly important when it comes to Winstrol side effects.
First and foremost, Winstrol is notorious for causing very serious and dangerous negative changes in blood cholesterol levels, even at low oral doses (6 mg/day) [17].
Even (Winstrol) stanozolol injections have been shown to have a very negative effect on blood cholesterol [18].
To add to the concerns about the cardiovascular effects of Winstrol, there is evidence that even small doses can stimulate cardiac hypertrophy [19].
Winstrol Cycles and Uses
Winstrol cycles are generally intended for cutting, body fat reduction and pre-contest preparation, with the end goal being to achieve very low body fat levels and increased physique definition.
There are some who claim that it can also be used for bulking, mass and strength gains, but there are other anabolic steroids that are generally cheaper than Winstrol and better suited for these purposes.
The general consensus is that Winstrol cycles should be reserved for body fat loss.
Therefore, a Winstrol cycle will typically include a base compound with similar uses, such as Testosterone Propionate, in an 8-10 week cycle.
Intermediate and advanced Winstrol cycles may also include a stack of three compounds, typically testosterone propionate, trenbolone acetate, and Winstrol (oral or injectable).
Additionally, due to the differences in hepatotoxicity between oral and injectable Winstrol formulations, the injectable may be administered for longer than the oral (8-10 weeks for the injectable versus 6-8 weeks for the oral).
Winstrol Dosage and Administration
Winstrol is a very versatile anabolic steroid, and its dosage varies greatly (especially between oral and injectable forms).
In the medical field, Winstrol doses are typically 6mg per day, ideally split up over the course of the day (e.g. 2mg tablets taken three times a day).
As an injectable, Winstrol was typically prescribed at a dose of 50 mg every two to three weeks.
However, this medical dosage and frequency of Winstrol for athletic and performance enhancement purposes is not helpful at all.
A typical Winstrol dosage for athletics, physique, and strength is around 50 to 100 mg every other day (for injectables), which equates to around 200 to 400 mg per week.
Oral Winstrol averages around 60mg per day, and lower doses of Winstrol (e.g. 25-50mg per day) are said to be effective for all users and athlete groups.
Since Winstrol is not an incredibly powerful anabolic steroid for bulking and weight gain, there is no need to increase doses to extreme or dangerous levels, and the aforementioned doses are in the appropriate range for the purpose of aiding in body shape and fat loss.
For women, a dosage of 5 to 10 mg per day of the oral formulation is common among female bodybuilders and athletes who want to avoid the risk of virilization or other side effects.
The injectable Winstrol is less common among female athletes and bodybuilders, but it is recommended to inject 15 mg every other day (roughly 60 mg total per week).
Winstrol reference
[1].Clinton RO et al. J.Amerchem. Soc. 81 (1959):1513.
[2].S. Patent No. 3,030,358.
[3]. July 2004;34(3):149-52.
[4].Anabolic-androgenic steroid interactions with rat androgen receptors in vivo and in vitro: a comparative study. Feldkoren Bl, Andersson S. J Steroid Biochem Mol Biol 2005 Apr;94(5):481-7. Epub March 17, 2005.
[5].Differential effects of stanozolol on human skin and synovial membrane fibroblasts in vitro: DNA synthesis and receptor binding. Ellis AJ, Cawston TE, Mackey EJ. Agent Action. March 1994;41(1-2):37-43.
[6].Identification of specific binding sites for the anabolic steroid stanozolol in liver microsomes of male rats. Boada LD, Fernandez L, et al. J Pharmacol Exp Ther 1996 Dec;279(3):1123-9.
[7].Stanozolol and danazol, unlike natural androgens, interact with low-affinity glucocorticoid binding sites from liver microsomes of male rats. Fernandez L, Chirino R, Boada LD, Navarro D, Cabrera N, del Rio L, Diaz-Chico BN. Endocrinology. 1994 Mar;134(3):1401-8.
[8].Di Yi Jun Yi Da Xue Xue Bao. 2003 Nov 23(11):1117-20.
[9].Desaulles PA et al. Helb. Med Acta 27(1960), 479.
[10].Sex hormone binding globulin response to the anabolic steroid stanozolol: evidence for its suitability as a biological androgen sensitivity test. G Sinnecker, S Kohler. Journal of Clin Endo Metab. 68:1195, 1989.
[11].J Vet Res. 64(4):246-8, October 2000.
[12].J Am Vet Med Assoc. 1997 Sep 15;211(6):719-22.
[13].JInvest Dermatol. December 1998;111(6):1193-7.
[14].Changes in hormone levels in normal men treated with the anabolic steroid stanozolol. Small M, Beastall GH, Semple CG, Cowan RA, Forbes CD, Clin Endocrinol (Ocf). 1984 July 21(1):49-55.
[15].Effects of 6 months of oral anabolic steroids on body mass and respiratory muscle in malnourished COPD patients. Ivone Martins Ferreira, leda Verreschi et al. CHEST 114 (1) July 19-28, 1998.
[16].Androgenic/anabolic steroid-induced toxic hepatitis. Stimac D, Milic, S Dintijana RD, Kovac D, Ristic S. J Clin Gastroenterol. 2002 Oct 35(4):350-2.
[17].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. JAMA. 1989 Feb 24;261(8):1165-8.
[18].Effects of intramuscular stanozolol on fibrinolysis and blood lipids. Small M, McArdie BM, Lowe GD, Forbes CD, Prentice CR, Thromb Res. 1982 Oct 1;28(1):27-36.
[19].J Steroid Biochem Mol Biol. 2005 Jan;93(1):43-8. Epub January 25, 2005.
