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Mta3.4
Methandrostenolone (Dianabol) Research
Mostly mechanism / observationalLimited safety
7 peer-reviewed studies
What the evidence says
Mostly mechanism / observational
Most Methandrostenolone (Dianabol) 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 1976–1990 with a typical study size of 11 participants.
Based on 7 studies · 4 RCTs · 30 total participants
Confidence
Moderate
By outcome
Lean mass & nitrogen balance
Mostly mechanism / observational4 studies
Strength & performance
Mostly mechanism / observational4 studies
Safety profile
Mostly mechanism / observational3 studies
Liver & hepatotoxicity
Too few graded studies2 studies
Hormones & virilization
Too few graded studies2 studies
Cholesterol & lipids
Too few graded studies1 study
Older research base
Newest study from 1990
197619831990
1RCTn=7 · very small study1981
Body weight, potassium and nitrogen, muscle size, and leg performance and strength increased significantly during training on the drug, but not during the placebo period ... The finding of increased body nitrogen suggested that the muscles had gained normal tissue.
Hervey GR, Knibbs AV, Burkinshaw L, Morgan DB, Jones PR, Chettle DR, et al. · Clinical science (London, England : 1979) (1981)
The pivotal positive trial: a double-blind, placebo-controlled crossover experiment in seven male weight-lifters in regular training — 100 mg/day methandienone for 6 weeks alternating with placebo, separated by a 6-week washout
Body weight, total body potassium AND total body nitrogen, muscle size, and leg performance and strength all increased significantly on the drug but not on placebo
The increase in total body nitrogen indicated the muscles had gained real lean tissue, not merely intracellular fluid — resolving the open question from the 1976 trial
On methandienone the subjects gained weight (mean 3.3 kg) and accumulated a disproportionately large amount of potassium (420 mmol); the increase in weight was confined to the lean part of the body, and the muscles increased in size.
Hervey GR, Hutchinson I, Knibbs AV, Burkinshaw L, Jones PR, Norgan NG, et al. · Lancet (London, England) (1976)
The foundational controlled trial: 11 athletic men given methandienone 100 mg/day for 6 weeks in a double-blind crossover during weight-training
On the drug the men gained a mean ~3.3 kg of body weight that was confined to the lean compartment, with a disproportionately large accumulation of total body potassium and increased muscle size
Strength and performance improved over each training period but not significantly more on drug than placebo — an honest caveat the 1981 follow-up was designed to resolve
A significant increase in TBK occurred in the treated group, primarily in the first 6 mo ... If methandrostenolone is capable of producing an increment in bone mass in osteoporosis, it was not readily observable.
Aloia JF, Kapoor A, Vaswani A, Cohn SH · Metabolism: clinical and experimental (1981)
A two-compartment, double-blind, randomized, parallel trial comparing methandrostenolone with placebo in osteoporosis over 24 months
Total body potassium (a lean-tissue marker) rose significantly in the treated group, mostly in the first 6 months — consistent with an anabolic, lean-mass effect
Honest negative on the bone endpoint: no sustained increase in bone mass was demonstrable, and anabolic steroids may not durably uncouple bone formation from resorption
The HDL2 cholesterol concentration decreased by about 80% and HDL3 cholesterol by about 55% ... the study group had significantly lower HDL cholesterol concentrations than the control group.
Alén M, Rahkila P, Marniemi J · International journal of sports medicine (1985)
Counter-evidence on the adverse lipid harm: a controlled clinical trial of power athletes self-administering testosterone and anabolic steroids (including methandrostenolone) versus training controls over 9 months
HDL and HDL2 cholesterol fell dramatically on androgens — HDL2 by ~80% and HDL3 by ~55% — to extremely low concentrations, with the difference from controls significant from 8 to 32 weeks
Quantifies the severe, atherogenic lipid shift that accompanies anabolic-steroid use in real-world dosing, with no offsetting cardiovascular benefit
In all cases where an effect was achieved, the drug used was methandrostenolone or stanozolol ... The use of AAS as ergogenic drugs must be deprecated because of their marginal effects, the risks of side effects and the unsporting, unethical aspects.
Søe M, Jensen KL, Gluud C · Ugeskrift for laeger (1989)
A review of placebo-controlled studies of anabolic-androgenic steroids on muscle strength, body weight and lean body mass in body-building men
In about half the placebo-controlled studies a significant effect was found — and in every case where an effect was achieved, the drug was methandrostenolone or stanozolol, placing methandrostenolone among the AAS most likely to actually work
Honest counterweight in the same review: the effects were judged marginal and the authors deprecate AAS use given side-effect risk and the unethical/unsporting nature
6Observational1981
The long-term effects of an anabolic steroid (Dianabol) on the liver of motor-active mice was investigated. The pathologic changes occurring are due to cholestasis, peliosis hepatis, and diffuse hepatitis.
Stang-Voss C, Appell HJ · International journal of sports medicine (1981)
Compound-specific hepatotoxicity evidence: a long-term study of Dianabol (methandrostenolone) in motor-active mice examining liver parenchyma
Produced cholestasis, peliosis hepatis and diffuse hepatitis, with a suggested pathogenic chain from cholestasis and peliosis toward cirrhosis
Animal evidence, but directly on Dianabol itself rather than the class — the structural liver injury that 17α-alkylation produces
A 30 year old bodybuilder who had been taking anabolic steroids for 18 months presented with bleeding oesophageal varices. Serious liver disease secondary to anabolic steroids including peliosis hepatis, nodular hyperplasia and malignant change is well recognized.
Winwood PJ, Robertson DA, Wright R · Postgraduate medical journal (1990)
Severe-harm counter-evidence in a human: a case report of a 30-year-old bodybuilder on anabolic steroids for 18 months who presented with bleeding oesophageal varices
Frames the worst-case end of AAS hepatotoxicity — serious liver disease including peliosis hepatis, nodular hyperplasia and malignant change, here progressing to portal hypertension and variceal haemorrhage
Documents that the liver injury is not merely reversible enzyme elevation but can produce life-threatening structural and vascular complications in long-term users