Stanozolol (Winstrol)

Stanozolol, sold under the brand name Winstrol, is a synthetic anabolic-androgenic steroid (AAS) derived from dihydrotestosterone. It is best known in doping history as the steroid that cost Ben Johnson his 1988 Seoul Olympic 100 m gold medal. Despite a strong reputation in fitness circles for producing a lean, “dry” look, the rigorous human evidence for its physique benefits is thin, while its adverse effects on cholesterol and the liver are well documented. It is not a peptide and not a SARM.

What it is

Stanozolol is a synthetic anabolic-androgenic steroid derived from dihydrotestosterone (DHT). Its distinctive structural feature is a pyrazole ring fused to the A-ring of the steroid nucleus, making it a “heterocyclic” steroid. Like other orally active steroids, it is 17α-alkylated (17α-methyl); that methyl group lets it resist hepatic first-pass metabolism — the basis for its oral bioavailability — but it is also the structural reason for the hepatotoxicity shared by all 17α-alkylated orals.

Mechanistically, stanozolol is an agonist at the androgen receptor (AR), with relatively low AR binding affinity but a comparatively favorable anabolic-to-androgenic balance. It is non-aromatizable (it cannot be converted to estradiol), so on its own it does not directly cause estrogenic effects, though it can still suppress endogenous testosterone. It also lowers sex-hormone-binding globulin (SHBG). It was historically marketed both as oral tablets and as an injectable aqueous (microcrystalline) suspension — note that, unlike many oil-based esterified injectables, the injectable form is a water suspension, so “ester-timing” concepts do not apply to it.

The claims

Medically, stanozolol was used for prophylaxis of hereditary angioedema (HAE) — reducing the frequency and severity of attacks — and for some anemias, with historical or investigational use in catabolic/debilitating states, osteoporosis, and venous insufficiency/lipodermatosclerosis. In HAE, attenuated androgens (danazol, stanozolol, oxandrolone) were for decades a mainstay of oral long-term prophylaxis, acting by raising hepatic synthesis of C1-esterase inhibitor and C4 levels; they have largely been superseded by modern targeted therapies (C1-INH concentrates, lanadelumab, berotralstat, and others).

In athletics and bodybuilding, stanozolol is sought for lean-mass retention, strength, and a “dry/hard” physique during fat-loss phases — partly because it does not aromatize, so it causes little water retention.

What the evidence actually shows

The performance and physique reputation rests largely on uncontrolled and anecdotal use; rigorous controlled human efficacy data for stanozolol on muscle or strength in healthy athletes are limited.

• HIV/AIDS wasting: the cited human data are weak. Berger et al. (1993) reported 3 AIDS patients with HIV-1 wasting myopathy who responded favorably (strength, muscle bulk, body weight, well-being) to anabolic steroids — but this is an uncontrolled case series, not a randomized trial. It is hypothesis-level evidence, not proof of efficacy.
• Lipid and metabolic effects (well documented): controlled human studies consistently show stanozolol markedly lowers HDL cholesterol. Thompson et al. (JAMA 1989) found oral stanozolol cut HDL-C by about 33% and the HDL2 subfraction by about 71%, with apolipoprotein A-I down roughly 40% and LDL-C raised about 29% — far worse on lipids than intramuscular testosterone. Other controlled work shows it lowers lecithin-cholesterol acyltransferase, apolipoprotein D, and Lp(a) (Albers et al., 1984), and studies of hepatic-lipase-deficient subjects implicate raised hepatic lipase in its HDL-lowering effect (Bausserman et al., 1997).
• Hereditary angioedema: systematic-review-level evidence (Bork et al. critical appraisal, 2015) supports attenuated androgens — including stanozolol — as effective at reducing attacks, but at the cost of a substantial burden of adverse effects on long-term use.

The bottom line on physique claims: the lean-mass and strength benefits in healthy people are largely supported by low-quality and anecdotal evidence, while the adverse metabolic effects are robustly demonstrated.

Legal and regulatory status

In the United States, anabolic steroids — including stanozolol — are Schedule III controlled substances under the Controlled Substances Act. They were placed there by the Anabolic Steroids Control Act of 1990 (signed November 1990, effective February 1991) and the category was expanded by the Anabolic Steroid Control Act of 2004. Non-medical possession or distribution is a federal crime. Stanozolol is no longer marketed in the US, so products sold online as “Winstrol” sit entirely outside the prescription and regulatory system.

For comparison: clenbuterol is not FDA-approved for humans and is not a scheduled controlled substance (it can be legally used in veterinary contexts); HGH is governed by its own statute, 21 U.S.C. § 333(e), and is not a controlled substance.

In sport, stanozolol is prohibited at all times (in and out of competition) as an anabolic androgenic steroid under WADA class S1 (Anabolic Agents), subsection S1.1 (Anabolic Androgenic Steroids). The 2026 List clarifies that prohibited anabolic agents include “other substances with a similar chemical structure or similar biological effect(s), including their esters.” (For comparison: clenbuterol is also S1, listed under S1.2 — “other anabolic agents”; HGH and hCG fall under S2, Peptide Hormones, Growth Factors, and Related Substances.) Stanozolol is infamous in doping history: Ben Johnson was stripped of his 1988 Seoul Olympic 100 m gold after testing positive for it.

Safety

• Hepatotoxicity (the signature risk of 17α-alkylated orals): LiverTox groups stanozolol with the alkylated androgens that cause “bland cholestasis” (jaundice and pruritus, often with only a modest enzyme rise), peliosis hepatis (blood-filled hepatic cysts that can rupture), hepatic adenomas and hepatocellular carcinoma (with long-term use, typically over years), and nodular regenerative hyperplasia. A documented case (Stępień et al., 2015) describes a 19-year-old amateur bodybuilder who, after injecting stanozolol for about 2 months, developed severe intrahepatic cholestasis and acute liver failure (bilirubin peaking around 56 mg/dL) and recovered over months. Injury is often reversible on discontinuation but can be severe.
• Cardiovascular and lipids: strong, reproducible HDL-cholesterol suppression (with HDL2 hit hardest) produces an atherogenic lipid shift, raising concern for accelerated atherosclerosis, alongside reported effects on left-ventricular structure/function and the thrombotic risk associated with AAS use generally.
• HPTA suppression and fertility: exogenous androgen suppresses the hypothalamic-pituitary-testicular axis, reducing LH and FSH and leading to suppressed endogenous testosterone, impaired spermatogenesis, testicular atrophy, and potential infertility that may persist after stopping. This is a class effect of exogenous androgens.
• Estrogenic effects / gynecomastia: stanozolol itself does not aromatize, so it is not a direct cause of gynecomastia; however, HPTA suppression and any concomitant aromatizable steroids can still alter the androgen-to-estrogen balance.
• Virilization (especially in women): deepening voice, hirsutism, clitoral enlargement, and menstrual disruption — some of these changes are irreversible.
• Hematologic: androgens can raise hematocrit and cause erythrocytosis (polycythemia), increasing thrombotic risk.
• Other: tendon and connective-tissue concerns, acne and oily skin, hair loss in predisposed individuals, fluid and electrolyte effects, mood and aggression changes, and — in children — premature epiphyseal closure. The injectable aqueous suspension is associated with painful injection-site reactions.

Bottom line

Stanozolol is a 17α-alkylated anabolic-androgenic steroid with a real but largely historical medical role (hereditary angioedema, some anemias) and a notorious doping history. The human evidence for its physique and performance benefits is weak and largely anecdotal, while its harms — particularly HDL suppression and liver injury — are well documented. It is a Schedule III controlled substance in the US, no longer marketed there, and prohibited at all times in sport. The popular image of Winstrol as a clean way to get “lean and hard” understates serious metabolic and hepatic risks.

Evidence grade: Preliminary human.

Sources

• LiverTox: Androgenic Steroids (NCBI Bookshelf, NBK548931)
• Stanozolol — Wikipedia
• Thompson PD et al. 1989 — contrasting effects of testosterone and stanozolol on serum lipoprotein levels (JAMA; PMID 2915439)
• Albers JJ et al. 1984 — reduction of LCAT, apolipoprotein D and Lp(a) with stanozolol (Biochim Biophys Acta; PMID 6236850)
• Bausserman LL et al. 1997 — short-term stanozolol on serum lipoproteins in hepatic lipase deficiency (Metabolism; PMID 9284885)
• Berger JR, Pall L, Winfield D 1993 — anabolic steroids in HIV-related wasting myopathy, case series (South Med J; PMID 8351543)
• Stępień PM et al. 2015 — severe intrahepatic cholestasis and liver failure after stanozolol usage (Clin Exp Hepatol; PMID 28856252)
• Critical appraisal of androgen use in hereditary angioedema: a systematic review (Ann Allergy Asthma Immunol 2015)
• DEA Diversion — Anabolic Steroids (Schedule III; ASCA 1990/2004)
• Anabolic Steroids Control Act of 1990 — Congress.gov H.R.4658
• WADA 2026 Prohibited List
• USADA 2026 WADA Prohibited List summary
• 21 U.S. Code § 333 (HGH penalty, subsection (e))