What Does Winstrol Do? Effects, Uses, and Risks

Winstrol, the brand name for the synthetic anabolic steroid stanozolol, promotes muscle growth, increases strength, and reduces body fat by mimicking the tissue-building effects of testosterone while carrying a comparatively lower androgenic (masculinizing) profile. Developed in the late 1950s, it has legitimate but narrow medical uses and a much larger underground following among bodybuilders and athletes. The drug also carries serious health risks, particularly to the liver, cardiovascular system, and hormonal balance, that make its non-medical use a genuine gamble.

How Winstrol Works in the Body

Stanozolol belongs to a class of drugs known as anabolic-androgenic steroids. It binds to the same receptors that testosterone does, but its chemical structure has been modified to favor the anabolic (tissue-building) side of the equation over the androgenic (sex-characteristic) side. Early clinical characterization described it as having roughly a 30-to-1 anabolic-to-androgenic ratio, which is why it was historically attractive for patients who needed muscle-sparing therapy without heavy masculinizing side effects.¹

One of the drug’s more distinctive actions is a sharp suppression of sex hormone-binding globulin, or SHBG, a protein in the blood that latches onto sex hormones and keeps them inactive. In healthy subjects given stanozolol for just three days, SHBG levels dropped to roughly half their starting value.² The practical result is that more free testosterone and other androgens circulate in the blood, amplifying the hormonal environment for muscle growth even beyond stanozolol’s own direct receptor activity. This SHBG-lowering effect is one reason bodybuilders sometimes stack Winstrol with other steroids, believing it frees up those compounds to work harder.

What It Does to Muscle

At the cellular level, stanozolol promotes muscle protein synthesis primarily by increasing the concentration of RNA in muscle tissue. Animal research found that the drug’s anabolic effect on muscle involved higher RNA levels without changing the efficiency of each RNA unit, and that stanozolol also had an anticatabolic action, blunting the muscle-wasting effects of stress hormones like corticosterone.³ In plain terms, the drug both accelerates muscle building and slows muscle breakdown, a two-pronged effect that explains why users report visible changes in muscle hardness and lean mass within weeks.

Clinical data in malnourished patients with chronic obstructive pulmonary disease showed that oral anabolic steroid treatment over several months led to meaningful weight gain (averaging close to two kilograms), increases in lean body mass, and measurable growth in arm and thigh muscle circumference compared to controls who actually lost weight over the same period.⁴ These gains are modest compared to what a healthy young athlete would experience at supraphysiological doses, but they confirm the direction of the drug’s effect in real human tissue.

Approved Medical Uses

Winstrol’s clearest legitimate medical role is in the management of hereditary angioedema, a rare genetic condition that causes sudden, severe swelling in the face, throat, limbs, and gut. The swelling episodes are caused by a deficiency or dysfunction of a protein in the complement system, and stanozolol helps by stimulating the liver to produce more of that protein. Most patients in long-term studies achieved control of their attacks at doses between 0.5 and 2 milligrams daily, far below the doses athletes use.⁵ All 27 patients in one systematic assessment reached a minimum effective dose within that range and maintained symptom control with minimal side effects over a two-year period.¹

Research into why stanozolol works for hereditary angioedema while some other anabolic steroids do not points to its specific chemical structure. When investigators compared 17-alpha-alkylated steroids like stanozolol and danazol against non-alkylated alternatives, only the alkylated compounds prevented attacks, suggesting the drug’s ability to survive first-pass liver metabolism is part of what makes it effective for this condition.⁶ That same structural feature, unfortunately, is also what makes stanozolol particularly hard on the liver.

Historically, stanozolol was also prescribed for postmenopausal osteoporosis, anemia, and muscle-wasting conditions. Most of these indications have been replaced by newer, more targeted therapies. In the United States, Winstrol is no longer widely marketed for human use, though generic stanozolol remains available in some countries, and the drug circulates widely on the black market.

Liver Damage

The 17-alpha-alkylation that lets stanozolol survive passage through the liver is also the source of its most dangerous short-term risk. The drug can cause cholestasis, a condition where bile flow within the liver stalls, leading to jaundice, severe itching, and in worst cases, liver failure requiring transplantation. Case reports describe patients developing severe intrahepatic cholestasis and liver failure after stanozolol use.⁴

The exact mechanism is still being worked out. One line of research has identified a stanozolol-specific binding protein in liver membranes that appears to alter how the liver handles glucocorticoid signaling, which may explain why stanozolol seems to cause cholestasis more readily than some other steroids.⁴ Earlier hypotheses centered on the drug interfering with bile acid transport across liver cell membranes. Either way, the clinical picture is clear: liver enzyme elevations are common even at therapeutic doses, and at the higher doses athletes favor, frank liver injury is a real possibility. Peliosis hepatis, a condition where blood-filled cysts form in the liver, has also been reported with long-term use of 17-alpha-alkylated steroids including stanozolol.

Cardiovascular Effects

If liver toxicity is Winstrol’s acute danger, the cardiovascular changes it triggers are its slow-burning one. Stanozolol hammers blood lipid profiles in a pattern that pushes hard toward atherosclerosis. In one well-known head-to-head comparison, stanozolol cut HDL (“good”) cholesterol by about a third and slashed the HDL2 subfraction, the most cardioprotective component, by roughly 70 percent. At the same time, LDL (“bad”) cholesterol climbed nearly 30 percent. Parenteral testosterone, by contrast, had milder and in some cases opposite effects on these markers.⁷

A study in postmenopausal women being treated with stanozolol for osteoporosis found a 53 percent drop in HDL cholesterol and a 21 percent increase in LDL, causing the LDL-to-HDL ratio to spike from 2.5 to 6.8, a shift the researchers flagged as reason for caution in long-term use.⁸ Another study specifically examining the mechanism found that stanozolol increased hepatic lipase activity by about 277 percent in controls, which drives HDL levels down by accelerating the breakdown of HDL particles. HDL cholesterol fell roughly 49 percent and apolipoprotein A-I, the main structural protein in HDL, dropped 41 percent.⁹

These are not subtle shifts. An LDL-to-HDL ratio above 5 is generally considered high risk for cardiovascular disease, and Winstrol can push it well past that threshold in weeks. The lipid disturbance reverses after the drug is stopped, but repeated or prolonged cycles could contribute to plaque buildup in coronary arteries over time. Beyond lipids, animal research has shown that stanozolol can cause structural heart damage. A study in rats found that stanozolol increased fibrotic markers in heart tissue, lowered the heart’s antioxidant defenses, and elevated markers of oxidative stress and DNA damage in cardiac cells.¹⁰ Those effects were worse when stanozolol was combined with cannabis, a pairing that is not uncommon in recreational polydrug use.

Hormonal Shutdown and Reproductive Harm

Winstrol, like every exogenous anabolic steroid, sends a signal to the brain that the body already has plenty of androgens. The hypothalamus and pituitary gland respond by dialing down production of the hormones that tell the testes to make testosterone and sperm. The result is suppressed testosterone production, shrunken testes, and reduced sperm counts. Anabolic steroid intake can lead to suppressed gonadotropins, reduced sperm concentration, testicular dysfunction, and hypogonadism, which in turn can cause decreased libido and erectile dysfunction.¹¹

Recovery after stopping is possible but slow. Review data suggest that while serum testosterone levels typically normalize within about three months after cessation, full sperm production takes an average of 12 months to come back. And recovery is not guaranteed: up to 27 percent of former users show persistent hypogonadism and psychiatric withdrawal symptoms years later.¹¹ Those numbers apply to anabolic steroids broadly, not stanozolol exclusively, but the mechanism of hormonal suppression is the same regardless of which steroid triggers it. Someone running a Winstrol-only cycle should not assume the drug is gentle on the endocrine system just because it is often marketed as a “mild” steroid.

Effects on Women

Winstrol’s relatively low androgenic ratio made it one of the steroids sometimes considered “female-friendly” in bodybuilding circles. That reputation is misleading. Women are far more sensitive to androgenic effects because their baseline testosterone levels are a fraction of men’s, so even a steroid with a lower androgenic profile can cause virilization: deepening of the voice, growth of facial and body hair, clitoral enlargement, menstrual irregularity, and male-pattern hair loss.

Voice changes deserve special attention because they are often irreversible. Research tracking the long-term effects of anabolic steroids on the female voice over a 20-year period found that anabolic and androgenic steroids can produce lasting vocal changes that are clinically significant and difficult to treat.¹² The vocal cords thicken under androgenic stimulation, and unlike most other virilizing effects, that thickening does not reverse when the drug is stopped. A woman who uses Winstrol even briefly risks permanent voice deepening if she is susceptible.

Brain and Mood Changes

The “roid rage” stereotype oversimplifies the picture, but anabolic steroids do alter brain chemistry in ways that affect mood, anxiety, and emotional regulation. Depression in particular appears to be a common adverse reaction in people who misuse anabolic steroids. Animal research using stanozolol specifically found that chronic administration significantly altered brain monoamine systems, the same neurotransmitter pathways involved in major depressive disorder. The drug produced neurochemical modifications in brain areas tied to depression and stress-related states.¹³

Anxiety is another concern. In an elevated-plus-maze experiment, a standard test for anxious behavior in rodents, animals given stanozolol showed reduced exploration of open spaces, a hallmark of increased anxiety. The study also found something more alarming: significant reduction of neuronal density in the amygdala, the brain region central to fear and emotional processing. Male animals treated with stanozolol lost roughly 18 percent of neurons in one amygdala subregion, and the losses were comparable in females. The researchers concluded that the indiscriminate use of these substances causes death of brain amygdala neurons.¹⁴ These are animal studies at supraphysiological doses, so they do not translate directly to every human user at every dose, but they offer a biological mechanism for the mood instability that steroid users and their partners frequently report.

Tendons and Injury Risk

One underappreciated risk of Winstrol use is its potential impact on tendons. Among bodybuilders, there is a widespread belief that Winstrol “dries out” joints and tendons, making them stiffer and more prone to tearing. The scientific picture is frustratingly incomplete. A systematic review examining the mechanical, structural, and biologic effects of anabolic steroids on tendons found 18 studies, almost all in small animal models, and reported that results were contradictory.¹⁵ Some studies suggested that anabolic steroids made tendons stiffer or weaker, others found no change, and the heterogeneity of designs made firm conclusions impossible.

What is agreed upon is that Winstrol does not increase joint fluid the way some other steroids (like nandrolone) do, and it reduces subcutaneous water retention. Combined with rapid strength gains, this means the muscles may become capable of generating forces that the tendons, which adapt much more slowly, are not yet strong enough to handle. Whether the drug directly weakens tendons or simply creates a mismatch between muscle and tendon capacity, the clinical result is the same: tendon injuries appear overrepresented among Winstrol users compared to users of other anabolic steroids. Anyone using the drug while training heavy should be aware that their tendons are not keeping pace with their muscles.

Effects on Blood Cell Production

Stanozolol, like many anabolic steroids, stimulates the production of red blood cells. This is one reason it was historically prescribed for certain anemias. Research in a mouse model of immune-mediated bone marrow failure found that stanozolol, combined with immunosuppressive therapy, improved red blood cell production by upregulating the erythropoietin receptor on bone marrow cells. Treated mice showed higher serum erythropoietin levels and greater erythropoietin receptor expression than controls.¹⁶

For a healthy person abusing the drug, increased red cell production sounds benign but carries its own risks. Elevated red blood cell counts thicken the blood, raising the risk of clots, stroke, and heart attack. Athletes who combine Winstrol with other erythropoietic agents or who are already dehydrated from cutting weight for competition are in particularly dangerous territory. Polycythemia, an abnormally high red cell count, is one of the more common lab abnormalities found in steroid users and one of the easiest to miss without routine blood work.

How Long Winstrol Shows Up on Drug Tests

For athletes in tested sports, detection is a major consideration, and Winstrol has become progressively harder to get away with. Anti-doping laboratories have identified specific metabolites that persist in urine long after the drug’s active effects have faded. Recent advances in detection now target stanozolol’s glucuronide conjugates, particularly a metabolite called 17-epistanozolol-N-glucuronide, which has been detected in urine up to 28 days after a single administration.¹⁷ Earlier methods relying on conventional metabolites had much shorter detection windows. Newer techniques using high-resolution mass spectrometry have made it possible to confirm stanozolol use with high confidence almost a month after the last dose.¹⁸

This matters beyond the world of elite sport. Many amateur athletic federations, military branches, and law enforcement agencies now conduct steroid testing, and stanozolol is among the most commonly flagged substances. The drug’s notoriety in high-profile doping scandals, from Olympic sprinting to professional baseball, has made it a particular priority for anti-doping authorities. Anyone considering Winstrol for performance enhancement in any tested context should assume the detection window is at least a month with current technology, and that testing methods continue to improve.

Winstrol in Veterinary Medicine

A detail that sometimes surprises people is that a large share of the stanozolol circulating on the black market was originally manufactured for animals, not humans. Veterinary stanozolol (often sold under the brand name Winstrol-V) is used in horses and dogs to stimulate appetite, promote weight gain, and increase red blood cell production after illness or surgery. The injectable veterinary formulation is a water-based suspension rather than an oil-based solution, which is part of why Winstrol injections have a reputation for being painful. The water-based suspension does not stay at the injection site the way oil-based preparations do, leading to more local irritation. Underground users often resort to frequent injections at rotating sites to manage the discomfort, which introduces its own infection risks. The diversion of veterinary products into human use also means that dosing, sterility standards, and quality control are all unpredictable.