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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
Most Stanozolol (Winstrol) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality randomised trials published 1989–2017 with a typical study size of 44 participants.
Based on 7 studies · 2 RCTs · 55 total participants
Confidence
LowBy outcome
Stanozolol (Winstrol) has an evidence score of 4.2/10 — emerging evidence based on 7 indexed studies, including 1 meta-analysis. 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 illegal without a prescription and unmonitored. Informational, harm-reduction entry only — not a recommendation. Representative study: PMID 25707325.
Oxandrolone (Anavar)
Mostly mechanism / observationalA prescription oral anabolic-androgenic steroid (AAS) — brand Anavar/Oxandrin — and a DEA Schedule III CONTROLLED SUBSTANCE. It has genuine randomized-trial evidence in FDA-approved, 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 illegal without a prescription and carries real liver, lipid, and endocrine harm. Informational, harm-reduction entry only — not a recommendation.
Last reviewed June 2026 · evidence from 7 studies · how we score
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.
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 illegal without a prescription and unmonitored. Informational, harm-reduction entry only — not a recommendation.
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 illegal, 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).
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 both illegal without a prescription and 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.
Tap node to isolate • Pinch to zoom • Tap edge for research
There is no legitimate non-medical dose. 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.
Can be taken without food
| Form | Type |
|---|---|
| 💊Prescription oral tablet (Winstrol) — clinician-directed, hereditary-angioedema prophylaxis only | Recommended |
There is no legitimate over-the-counter or supplement form. It is a Schedule III controlled substance; non-prescription material is illegal to possess without an Rx and frequently counterfeit. Modern HAE care increasingly favours C1-inhibitor and kallikrein-targeted therapies over attenuated androgens.
Minimum: 4 weeks
Optimal: 24 weeks
Cycling: Not required
Note: No non-medical timing is endorsed. It is a controlled-substance prescription drug with documented hepatotoxicity, a severe adverse lipid shift and HPTA suppression; approved use is physician-directed at the lowest effective dose with monitoring. This library does not schedule its use.
Dose-response data unavailable. The current published research for Stanozolol (Winstrol) does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
The strongest evidence point and its approved use: in hereditary angioedema, stanozolol raises C1-inhibitor/C4 and reduces attack frequency, with durable control documented over 20–40 years of cohort follow-up at low maintenance doses.
As an androgen-receptor agonist it adds lean mass and strength, the basis for its illegal bodybuilding 'cutting' use — but there is no controlled-trial body-composition indication, and any such use is unsupervised and unlawful without a prescription.
Among the most dramatic lipid effects of any studied drug: a crossover trial measured a 33% fall in HDL, a 71% fall in the cardioprotective HDL2 subfraction, a 40% fall in apoA-I and a 29% rise in LDL in just six weeks of oral use.
17α-alkylated and hepatotoxic — transaminase rises and cholestasis on treatment, and for anabolic steroids as a class, peliosis hepatis, hepatic adenoma and hepatocellular carcinoma. Liver-function monitoring is required even in approved use.
Suppresses the hypothalamic-pituitary-testicular axis and virilizes — deepened voice, hirsutism, menstrual disruption that can be irreversible in women; animal data also show anabolic steroids stiffen tendon and alter collagen, the basis for the tendon-rupture concern in users.
Avoid — a controlled-substance prescription drug, not a supplement; a severe HDL crash, hepatotoxicity, HPTA suppression and virilization, and illegal to use without a prescription.
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.
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.
The commonly studied dose of Stanozolol (Winstrol) is There is no legitimate non-medical dose. 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.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
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.
Stanozolol (Winstrol) should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are severe HDL crash / adverse lipid shift, hepatic transaminitis / cholestatic liver injury, peliosis hepatis / hepatic tumour (AAS class). 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; possession/use without an Rx is illegal, and it is not a dietary supplement; Pre-existing liver disease or elevated liver enzymes — 17α-alkylated and hepatotoxic (cholestasis, peliosis); Known or suspected prostate or male breast carcinoma; hypercalcemia.
Nandrolone (Deca-Durabolin)
Mostly mechanism / observationalAn 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 illegal without a prescription and carries real cardiovascular, endocrine and sexual harm. Informational, harm-reduction entry only — not a recommendation.
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.