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Studies
Stz4.2
Stanozolol (Winstrol) Research
Mostly mechanism / observational
19 peer-reviewed studies
What the evidence says
Mostly mechanism / observational
Most Stanozolol (Winstrol) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from high-quality randomised trials published 1972–2017 with a typical study size of 11 participants.
Based on 19 studies · 14 RCTs · 11 total participants
Confidence
Moderate confidence
By outcome
Hereditary angioedema
Mostly mechanism / observational3 studies
Liver & hepatotoxicity
Mostly mechanism / observational3 studies
Lean mass & anabolic effectAn anabolic-androgenic steroid (Winstrol) that builds lean mass/strength in non-medical use, but causes a severe HDL crash, hepatotoxicity, HPTA suppression, and tendon risk. A controlled substance (medically approved only for hereditary angioedema). · Not established for physique use
Belch JJ, Madhok R, McArdle B, McLaughlin K, Kluft C, Forbes CD · Q J Med (1986)
15Crossovern=11 · very small study1989
In plain English: Stanozolol reduced HDL-cholesterol and the HDL2 subfraction by 33% and 71%, respectively. ... Apolipoprotein A-I level decreased 40% during stanozolol ... The low-density lipoprotein cholesterol concentration increased 29% with stanozolol.
The headline counter-evidence on lipids: a randomized crossover trial in 11 male weight-lifters comparing oral stanozolol 6 mg/day with supraphysiological intramuscular testosterone enanthate over six weeks
Oral stanozolol cut HDL cholesterol by 33%, the cardioprotective HDL2 subfraction by 71% and apolipoprotein A-I by 40%, while raising LDL cholesterol by 29% — one of the most dramatic lipid derangements documented for any drug
The effect dwarfed that of supraphysiological IM testosterone in the same men, isolating the harm to the oral 17α-alkylated route rather than androgenicity per se
16Review2017
In plain English: Relevant concern has been raised by the AAS hepatotoxicity including adenoma, hepatocellular carcinoma, cholestasis, and peliosis hepatis.
Solimini R, Rotolo MC, Mastrobattista L, Mortali C, Minutillo A, Pichini S, Pacifici R, Palmi I · European review for medical and pharmacological sciences (2017)
Mandatory class-level counter-evidence on non-medical use: a review of the hepatotoxic effects of anabolic-androgenic steroids in doping and general-population misuse
AAS hepatotoxicity spans hepatic adenoma, hepatocellular carcinoma, cholestasis and peliosis hepatis — the severe end of the liver-injury spectrum
Notes AAS are frequently present in over-the-counter 'dietary supplements' without label declaration, leaving consumers unaware of the risk
17Observational2007
In plain English: The minimal initial effective dosage of stanozolol was 0.5 to 2.0 mg daily, although most patients achieved symptomatic control and decreased the dose and frequency as the frequency of attacks decreased.
Sloane DE, Lee CW, Sheffer AL · The Journal of allergy and clinical immunology (2007)
Outcome anchor for the approved indication: a cohort of hereditary-angioedema patients treated with stanozolol for 20 to 40 years at a single institution
Documents durable attack control at low maintenance doses (initial 0.5–2.0 mg/day, often reduced further over time)
Long follow-up also surfaces the long-term harms — patients were monitored with hepatic-function assays, serum lipids, PSA and liver ultrasound, with treatment-related symptoms reported
In plain English: Attenuated androgens have been successful in the short- and long-term treatment of HAE ... Scheduled monitoring of liver function tests and lipid profiles in patients treated with these medications is critical.
Banerji A, Sloane DE, Sheffer AL · Annals of allergy, asthma & immunology (2008)
State-of-the-art review of 40–50 years of attenuated-androgen use (including stanozolol) for hereditary angioedema
Confirms successful short- and long-term treatment of HAE — the clinical consensus underpinning the approved indication
States that scheduled monitoring of liver-function tests and lipid profiles is critical, and that use in children and pregnant women must be undertaken with great caution
In plain English: The results of the biomechanical tests suggested that anabolic steroids produce a stiffer tendon, which fails with less elongation. ... Alterations of the sizes of the collagen fibrils were noted on electron microscopy.
Miles JW, Grana WA, Egle D, Min KW, Chitwood J · The Journal of bone and joint surgery. American volume (1992)
Mechanistic animal evidence for the connective-tissue concern: 24 rats randomized across anabolic-steroid and exercise variables, with biomechanical and histological tendon testing
Anabolic steroids produced a stiffer tendon that failed with less elongation, with altered collagen-fibril sizes on electron microscopy
Offers a biological basis for the tendon- and ligament-rupture reports in athletes who use anabolic steroids