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Stanozolol (Winstrol) — oral 17α-alkylated anabolic-androgenic steroid; FDA-approved for hereditary angioedema prophylaxis; DEA Schedule III controlled substance
A prescription oral anabolic-androgenic steroid (AAS) — brand Winstrol — and a DEA Schedule III CONTROLLED SUBSTANCE. Its one approved indication is prophylaxis of hereditary angioedema (HAE), where decades of cohort and systematic-review evidence confirm it reduces attack frequency. But it is 17α-alkylated and hepatotoxic (cholestasis, and — for AAS as a class — peliosis and liver tumours), and it causes one of the most DRAMATIC HDL crashes of any drug studied — a classic crossover trial measured a 33% fall in HDL, a 71% fall in HDL2, and a 29% rise in LDL. It also suppresses the HPTA and virilizes. It is NOT a dietary supplement and NOT a longevity drug; non-medical bodybuilding ('cutting') use is unmonitored. Described for harm-reduction information only — not a recommendation.
Prescription medication — not a dietary supplement
Stanozolol (Winstrol) is a prescription (or investigational) drug, not a supplement. It is included here for reference because people research and discuss it (often used off-label) — not as a recommendation. Take it only under a qualified clinician's supervision and only as prescribed; do not source it from grey-market vendors, where identity, purity, and dosing are unverified. The evidence below reflects its clinical trials.
What the evidence says
Stanozolol (Winstrol) doesn't have enough studies with structured effect-size data yet to pool a verdict. Browse the studies below for individual findings.
Most evidence is from high-quality randomised trials published 1972–2021 with a typical study size of 11 participants.
Based on 21 studies · 14 RCTs · 11 total participants
Confidence
Moderate confidenceBy outcome
Stanozolol has genuine, decades-long evidence in its one approved indication — long-term prophylaxis of hereditary angioedema — where a systematic review (Riedl 2015) confirms high prophylactic efficacy and a 20–40-year cohort (Sloane 2007) shows durable attack control. But it is a 17α-alkylated, hepatotoxic, DEA Schedule III controlled substance, and it produces one of the most dramatic HDL crashes of any studied drug — a crossover trial (Thompson 1989) measured a 33% HDL fall, a 71% HDL2 fall and a 29% LDL rise in six weeks. Add cholestasis/peliosis/liver-tumour risk for AAS as a class, HPTA suppression and virilization, and the fact that it is a prescription drug — not a dietary supplement or longevity drug — with unmonitored bodybuilding use, and it sits in the low-mid range: lifted by real approved-indication evidence, weighed down hard by the lipid harm, hepatotoxicity and legal status.
Stanozolol (brand name Winstrol) is an oral 17α-alkylated anabolic-androgenic steroid (AAS) — a synthetic derivative of dihydrotestosterone, modified at the 17-alpha position so it survives first-pass hepatic metabolism and can be taken by mouth (an injectable aqueous-suspension 'depot' form also exists).
In the US it is a prescription drug and a Schedule III controlled substance under the Controlled Substances Act; possession or distribution without a valid prescription is a federal crime.
Its established medical indication is long-term prophylaxis of hereditary angioedema (HAE) — a C1-esterase-inhibitor-deficiency disorder of recurrent, potentially life-threatening swelling — where 'attenuated androgens' (stanozolol, danazol, oxandrolone) raise C1-inhibitor and C4 levels and reduce attack frequency.
The evidence here is genuine, if mostly observational: a systematic review of androgen use in HAE (Riedl 2015) graded fifteen level-2 studies plus many case series and confirmed a high level of prophylactic efficacy, and a Brigham cohort followed patients on stanozolol for 20–40 years (Sloane 2007), documenting durable attack control at low maintenance doses (often 0.5–2 mg/day) — alongside the long-term harms.
The honest counterweight defines the compound, and it is unusually stark on lipids.
In a landmark crossover trial in male weight-lifters (Thompson 1989, JAMA), six weeks of oral stanozolol 6 mg/day cut HDL cholesterol by 33% and the cardioprotective HDL2 subfraction by 71%, dropped apolipoprotein A-I by 40%, and raised LDL cholesterol by 29% — a far more severe lipid derangement than supraphysiological intramuscular testosterone produced in the same men, pinning the effect on the oral 17α-alkylated route, not androgenicity per se.
A double-blind, placebo-controlled RCT in older patients with lipodermatosclerosis and venous ulcers (Carson 2015) likewise tracked liver-enzyme and lipid changes on stanozolol 2 mg twice daily.
Because it is 17α-alkylated, stanozolol is hepatotoxic: cholestasis and transaminase rises on treatment, and — for the AAS class broadly — peliosis hepatis, hepatic adenoma and hepatocellular carcinoma (Solimini 2017).
It suppresses the hypothalamic-pituitary-testicular axis and virilizes (deepened voice, hirsutism, menstrual changes) — effects that can be irreversible in women.
Animal work also flags connective-tissue effects: anabolic steroids made rat tendon stiffer and failure-prone with altered collagen-fibril architecture (Miles 1992), the mechanistic basis for the tendon-rupture concern in athletes who use AAS.
The score reflects real, decades-long prophylactic efficacy in HAE — its approved use — set against a 17α-alkyl hepatotoxicity profile, one of the most severe HDL crashes documented for any drug, HPTA suppression and virilization, and the reality that this is a controlled substance, not a supplement, with non-medical 'cutting' use carrying those same harms without medical monitoring.
Stanozolol is a synthetic dihydrotestosterone derivative that binds and activates the androgen receptor in skeletal muscle and other tissues, driving the anabolic and androgenic signalling that underlies both its lean-mass effect and its virilizing, HPTA-suppressing harms.
In hereditary angioedema — its approved use — attenuated androgens raise hepatic synthesis of C1-esterase inhibitor and C4, correcting the complement-pathway deficiency that drives bradykinin-mediated swelling and thereby reducing attack frequency.
The 17α-alkyl group that makes stanozolol orally active also makes it hepatotoxic (cholestasis and, for AAS broadly, peliosis and liver tumours) and drives a severe first-pass hepatic effect on lipoproteins — a dramatic HDL/HDL2 and apoA-I fall with a rise in LDL. The same androgenic activity suppresses the hypothalamic-pituitary-testicular axis and virilizes.
How Stanozolol (Winstrol) works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Avoid — a controlled-substance prescription drug, not a supplement; a severe HDL crash, hepatotoxicity, HPTA suppression and virilization, and not for self-experimentation.
High caution even when prescribed — virilizing effects (voice deepening, hirsutism, menstrual changes) can be permanent; discontinue at the first androgenic sign.
Major interaction — requires clinician-managed anticoagulant dose reduction and frequent INR checks.
Avoid entirely — androgenic; causes fetal virilization.
Like other 17α-alkylated androgens, stanozolol potentiates warfarin, raising INR and bleeding risk; anticoagulant doses often need reduction with close INR monitoring under a clinician.
Stanozolol is itself hepatotoxic; combining it with other hepatotoxic agents or alcohol compounds the risk of cholestatic injury and transaminitis.
Anabolic steroids can alter insulin sensitivity and glucose handling, potentially requiring antidiabetic-dose adjustment.
Stacking androgenic agents compounds hepatic burden, HPTA suppression and the severe adverse lipid shift; the combined risk is additive and uncharacterised in non-medical use.
Tip: Oral stanozolol produces one of the largest documented HDL/HDL2 falls (e.g. −33% HDL, −71% HDL2) with a rise in LDL — an adverse cardiovascular-risk shift. Lipid monitoring is required; reversibility depends on discontinuation.
Tip: 17α-alkylated and hepatotoxic — periodic transaminase monitoring is required even in approved use; stop and seek care for jaundice, dark urine or right-upper-quadrant pain.
Tip: Anabolic-androgenic steroids as a class are linked to peliosis hepatis, hepatic adenoma and hepatocellular carcinoma; risk rises with prolonged or high-dose use. There is no safe self-monitoring framework for non-medical use.
Tip: Suppresses endogenous testosterone, LH and FSH, and virilizes — deepened voice, hirsutism, menstrual disruption in women may be irreversible. Stop at the first sign of voice change in women.
Stanozolol (Winstrol) has an evidence score of 4.2/10 — emerging evidence based on 21 indexed studies. A prescription oral anabolic-androgenic steroid (AAS) — brand Winstrol — and a DEA Schedule III CONTROLLED SUBSTANCE. Its one approved indication is prophylaxis of hereditary angioedema (HAE), where decades of cohort and systematic-review evidence confirm it reduces attack frequency. But it is 17α-alkylated and hepatotoxic (cholestasis, and — for AAS as a class — peliosis and liver tumours), and it causes one of the most DRAMATIC HDL crashes of any drug studied — a classic crossover trial measured a 33% fall in HDL, a 71% fall in HDL2, and a 29% rise in LDL. It also suppresses the HPTA and virilizes. It is NOT a dietary supplement and NOT a longevity drug; non-medical bodybuilding ('cutting') use is unmonitored. Described for harm-reduction information only — not a recommendation. Representative study: PMID 25707325.
Dosing for Stanozolol (Winstrol): No self-directed dose is recommended by SupStack. Stanozolol is a prescription-only, DEA Schedule III controlled substance; this library does NOT provide a body-composition dosing protocol. For context only: in hereditary-angioedema prophylaxis, clinicians titrate to the lowest effective dose — cohort data describe initial dosing around 0.5–2 mg/day with most patients later reducing further — and a lipodermatosclerosis trial used 2 mg twice daily, all under medical supervision with liver-enzyme and lipid monitoring. That is not an endorsement of self-administration.
Timing is flexible for Stanozolol (Winstrol) — consistent daily use matters more than the time of day. Approved use is the lowest effective maintenance dose under medical supervision with periodic liver-enzyme and lipid monitoring.
No consumer dose of Stanozolol (Winstrol) is endorsed, so there is no dose at which it can be called safe. Talk to a healthcare provider before taking it. Reported side effects include peliosis hepatis / hepatic tumour (AAS class), severe HDL crash / adverse lipid shift, hepatic transaminitis / cholestatic liver injury, HPTA suppression & virilization. How often they occur is not established for all of them. Use caution if any of these apply to you: Anyone seeking it for body composition or athletic performance without a prescription — a DEA Schedule III controlled substance; it is not a dietary supplement, and laws on supply, possession, import and use depend on the country and circumstances; Pre-existing liver disease or elevated liver enzymes — 17α-alkylated and hepatotoxic (cholestasis, peliosis); Known or suspected prostate or male breast carcinoma; hypercalcemia.
Epicatechin
Mixed evidenceDark chocolate flavanol with consistent human evidence for improved endothelial function and modest blood pressure reduction. Muscle-building claims are not supported in humans.
Oxandrolone (Anavar)
Too few graded studiesA prescription oral anabolic-androgenic steroid (AAS) — brand Anavar/Oxandrin — and a DEA Schedule III CONTROLLED SUBSTANCE. It has genuine randomized-trial evidence in formerly FDA-approved (withdrawn June 2023), supervised muscle-wasting settings: it adds lean body mass, speeds wound healing and shortens hospital stay in severe burns, raises body weight in HIV-associated wasting, and modestly increases adult height in Turner syndrome. But it is 17α-alkylated and hepatotoxic (dose-related transaminase rises, cholestasis, and — with anabolic steroids generally — peliosis and liver tumours), it sharply lowers HDL and raises LDL cholesterol, and it suppresses the hypothalamic-pituitary-testicular axis and virilizes. It is NOT a dietary supplement and NOT a longevity drug; non-medical bodybuilding use is unsupervised and carries real liver, lipid, and endocrine harm. Described for harm-reduction information only — not a recommendation.
Nandrolone (Deca-Durabolin)
Too few graded studiesAn injectable anabolic-androgenic steroid (AAS) — brand Deca-Durabolin, the long-acting decanoate ester of 19-nortestosterone — and a DEA Schedule III CONTROLLED SUBSTANCE. It has genuine randomized-trial evidence in supervised, catabolic-illness settings: it adds lean body mass and weight in HIV-associated wasting, adds muscle mass and physical function in dialysis patients, and raises hemoglobin in dialysis anemia (a historic FDA-approved indication, since largely replaced by erythropoietin). But it suppresses the hypothalamic-pituitary-gonadal axis — and because it is a long-ester 19-nortestosterone with progestogenic activity, that suppression and the resulting sexual dysfunction ('deca dick') can be prolonged. It worsens the lipid profile (lowers HDL), is associated with cardiac remodelling/cardiomyopathy and premature atherosclerosis in long-term high-dose users, and virilizes. It is NOT a dietary supplement and NOT a longevity drug; non-medical bodybuilding/performance use is unsupervised and carries real cardiovascular, endocrine and sexual harm. Described for harm-reduction information only — not a recommendation.
Oxymetholone (Anadrol)
Too few graded studiesA potent prescription ORAL anabolic-androgenic steroid (AAS) — brand Anadrol/Anapolon — and a DEA Schedule III CONTROLLED SUBSTANCE. Oxymetholone has a US FDA approval record for ANADROL-50 under NDA 016848. The 2026 Orange Book lists this product as discontinued. This record does not establish current availability or authorisation of another product or use. It has real randomized-trial evidence in supervised muscle-wasting settings: it adds body weight and lean/body cell mass in HIV-associated wasting, raises lean mass and strength in older men, and increases haemoglobin and muscle mass in dialysis patients; a Cochrane review found limited evidence, from one 24-person study, that it raises haemoglobin in the anaemia of chronic kidney disease, and judged the evidence insufficient. But it is 17α-alkylated and markedly HEPATOTOXIC — anabolic steroids as a class have been associated with cholestasis, peliosis hepatis with life-threatening liver failure or bleeding into the abdomen, and liver tumours, including reported fatal malignancies (historical Anadrol-50 US boxed warning, 2004). It also sharply lowers HDL and raises LDL cholesterol, suppresses the hypothalamic-pituitary-testicular axis, and virilizes. It is NOT a dietary supplement and NOT a longevity drug; non-medical bodybuilding use is unsupervised and carries those liver, lipid, and endocrine harms unmonitored. Described for harm-reduction information only — not a recommendation.
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Reviewed by Dr. Baher Al Hakim · Last reviewed June 2026 · evidence from 21 studies · how we score · editorial policy
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
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