Skip to content
StackItSmart
CCase reports / series
HepatotoxicHigh riskCardiotoxicNeuropsychiatric

Dianabol

Methandrostenolone · Dbol · Metandienone

Dianabol (methandrostenolone / methandienone / Dbol) is a synthetic, orally active anabolic-androgenic steroid (AAS) — a 17-alpha-alkylated derivative of testosterone. It was historically marketed for a handful of medical wasting conditions but is now used almost entirely non-medically by weightlifters and bodybuilders to add muscle mass and strength rapidly. It is not currently a first-line prescription drug in most countries and its use in this context is unsupervised. The main dangers are serious and well-documented at a class and, in several cases, compound-specific level: liver injury with a cholestatic (bile-flow-obstructing) pattern that can progress to jaundice and, rarely, liver failure; a sharp fall in protective HDL cholesterol that accelerates atherosclerosis; reduced heart pumping (systolic) and relaxation (diastolic) function with long-term use; suppression of the body's own testosterone production that can persist for years after stopping; fluid retention and raised blood pressure; and mood/aggression changes. Because it is taken by mouth and 17-alpha-alkylated (a chemical modification that lets it survive first-pass liver metabolism), it places a distinctive strain on the liver. This monograph leads with those risks. It is educational only and not medical advice; anyone using or considering AAS should be under the care of a physician and obtain regular bloodwork.

Clinical readoutAAS · oral-17aa
Hepatic strainHigh
CardiovascularModerate
HPTA suppressionVery high
Half-life
19 d
Route
Oral
Evidence
C
Active
Short — androgenic/anab…
19 d5.4 wk8.1 wk10.9 wk13.6 wk
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ The parent drug has a short plasma half-life (on the order of several hours), consistent with the need for daily or divided oral dosing described in the literature; however, precise human plasma half-life values are not well characterized in modern clinical pharmacology studies. Long-term urinary metabolites are detectable far longer — a single 5 mg oral dose has been detected up to ~19 days later via a long-term metabolite in doping-control excretion studies.
Pharmacology

Mechanism of action

Methandrostenolone is a structural analogue of testosterone (17-beta-hydroxy-17-alpha-methyl-androsta-1,4-dien-3-one). It binds the androgen receptor and drives androgen-receptor-mediated gene transcription in skeletal muscle, promoting a positive nitrogen balance and increased protein synthesis, which underlies its muscle-building effect. The added 1,2 double bond reduces its affinity for aromatase relative to testosterone but it still undergoes some conversion to estrogenic metabolites, contributing to fluid retention and gynecomastia. The 17-alpha-methyl group makes it orally bioavailable by slowing hepatic first-pass degradation, and this same modification is central to the hepatotoxicity shared by oral 17-alpha-alkylated AAS. Like other exogenous androgens, it suppresses the hypothalamic-pituitary-testicular (HPT) axis via negative feedback, lowering luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and thereby endogenous testosterone and spermatogenesis. Much of the detailed characterization of its metabolism comes from doping-control (urinary metabolite) research rather than dedicated clinical pharmacology.
Kinetics

Pharmacokinetics

Half-life

The parent drug has a short plasma half-life (on the order of several hours), consistent with the need for daily or divided oral dosing described in the literature; however, precise human plasma half-life values are not well characterized in modern clinical pharmacology studies. Long-term urinary metabolites are detectable far longer — a single 5 mg oral dose has been detected up to ~19 days later via a long-term metabolite in doping-control excretion studies.

Active duration

Short — androgenic/anabolic activity of the parent compound spans roughly a day, hence the historically reported daily oral use; metabolite detectability greatly outlasts pharmacologic effect.

Route

Oral (tablet). 17-alpha-alkylation confers oral bioavailability by resisting hepatic first-pass metabolism.

Metabolism & clearance

Extensively metabolized in the liver to numerous hydroxylated and reduced metabolites; metabolites are excreted predominantly in the urine (characterized in human urinary excretion and preclinical distribution studies). Note: pharmacokinetic and washout information here is for monitoring and clinician discussion only, not for evading drug testing.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Increases skeletal muscle mass and strength via androgen-receptor-mediated increases in protein synthesis and nitrogen retention (class effect of AAS used non-medically for muscle building).
  • Produces rapid apparent weight gain, partly from intracellular and extracellular fluid retention rather than lean tissue alone.
  • Historically produced positive nitrogen balance in clinical settings; modern use is non-medical and unsupervised.
  • Effects are dose-related and accompanied by the adverse effects listed below; there is no established 'safe' non-medical dose.
Safety

Adverse effects by system

Cardiovascular

Marked reduction in HDL ('good') cholesterol and adverse lipid shifts documented in power athletes self-administering AAS (including methandrostenolone), promoting atherosclerosis. Long-term AAS use is associated with reduced left-ventricular systolic and diastolic function and accelerated, dose-dependent coronary atherosclerosis, plus hypertension, prothrombotic changes, cardiomyopathy, and reports of sudden cardiac death.

Hepatic

As an oral 17-alpha-alkylated AAS, it is hepatotoxic. Case reports specifically attribute cholestatic jaundice (with markedly elevated bilirubin) to methandrostenolone; oral 17-alpha-alkylated AAS as a class can cause cholestatic hepatitis and, rarely, submassive hepatic necrosis and fatal liver failure. Peliosis hepatis and hepatic tumors are described with long-term 17-alkylated androgen use at a class level.

Endocrine / HPTA

Suppresses the HPT axis: exogenous androgen lowers LH/FSH and endogenous testosterone. Current AAS users show suppressed gonadotropins and reduced inhibin B and anti-Müllerian hormone (impaired spermatogenesis); former users can show reduced testosterone and reduced Leydig-cell capacity years after cessation.

Reproductive

Suppressed spermatogenesis and reduced fertility (decreased inhibin B/AMH in current users), decreased libido and erectile dysfunction reported in former users; gynecomastia can occur due to estrogenic metabolites. Testicular atrophy is an expected consequence of HPT suppression.

Neuropsychiatric

AAS use is associated with mood and behavioral changes including increased aggression/hostility (supraphysiologic androgen levels), and hypomania/mania, irritability, and depressive symptoms (including during withdrawal). Personality factors may confound some observed aggression.

Renal

Acute kidney injury (acute tubular necrosis) has been reported in association with methandrostenolone use, sometimes accompanying severe cholestasis; also a fatal-outcome/multi-organ context in case reports. Renal effects are less common than hepatic/cardiovascular but documented.

Hematologic

Androgens as a class stimulate erythropoiesis and can raise hemoglobin/hematocrit (potential erythrocytosis), and AAS use is associated with prothrombotic changes and thrombosis in case reports. Methandrostenolone-specific hematologic trial data are limited; hematocrit should still be monitored.

Dermatologic

Androgenic skin effects are expected as a class: acne and oily skin; male-pattern hair loss in predisposed individuals. Compound-specific dermatologic data for methandrostenolone are limited; these are class/androgenic effects rather than methandrostenolone-specific trial findings.

Recovery

HPTA suppression & recovery

Suppression: Marked — exogenous androgen suppresses LH/FSH and endogenous testosterone; suppression can outlast use.

Recovery of the HPT axis is variable and individual. Case-control and cross-sectional human data show former AAS users can have lower testosterone, hypogonadal symptoms, and reduced Leydig-cell capacity years after stopping. Any recovery approach must be directed by an endocrinologist and guided by serial bloodwork. Where medication-assisted recovery is considered, only a single-SERM approach is within scope of this educational resource; dual-SERM protocols are explicitly out of scope. Do not self-manage recovery.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Liver function tests (ALT, AST, ALP, GGT, total and direct bilirubin)Fasting lipid panel (total cholesterol, LDL, HDL, triglycerides)Complete blood count including hematocrit/hemoglobinBlood pressureReproductive hormones (total/free testosterone, LH, FSH; consider estradiol)Renal function (creatinine, eGFR)Consider cardiac evaluation (echocardiography) with long-term use

Cadence: Baseline before any use; early re-check (e.g., within the first few weeks) given rapid-onset hepatic and lipid effects; then periodically during use and after cessation until values normalize. Cadence should be set by a treating clinician.

Warning signs — seek care
  • Yellowing of skin or eyes (jaundice), dark urine, pale stools, right-upper-quadrant abdominal pain, itching — possible cholestatic liver injury; stop and seek care urgently.
  • Severe abdominal pain, nausea/vomiting (possible pancreatitis) or reduced urine output/swelling (possible kidney injury).
  • Chest pain, breathlessness, palpitations, or syncope — possible cardiac involvement; seek emergency care.
  • New or worsening high blood pressure.
  • Severe mood change, aggression, mania, or depressive/suicidal thoughts.
  • Headache, visual changes, or signs of thrombosis (limb swelling, one-sided weakness).
Do not use if

Contraindications

  • Pre-existing liver disease or abnormal liver function (oral 17-alpha-alkylated hepatotoxicity).
  • Cardiovascular disease, dyslipidemia, hypertension, or elevated cardiovascular risk (adverse lipids, myocardial and atherosclerotic effects).
  • Known or suspected prostate or breast carcinoma (androgen-sensitive malignancy — class contraindication for androgens).
  • Pregnancy and breastfeeding (virilization/fetal harm — class contraindication for androgens).
  • History of polycythemia/erythrocytosis or thrombotic disease.
  • Personal or family history of significant mood disorder given psychiatric/aggression effects.
  • Adolescents (risk of premature epiphyseal closure and endocrine disruption).
  • Any use without medical supervision and regular bloodwork is strongly discouraged.
Combinations

Interaction profile

  • MajorWith another anabolic steroid: Additive cardiovascular strain
  • MajorWith a thermogenic stimulant: Additive cardiovascular strain
  • ModerateWith thyroid hormone: Additive cardiovascular strain
  • ModerateWith growth hormone: Additive cardiovascular strain
  • MajorWith another 17α-alkylated oral: Additive liver strain
  • MajorWith a liver-signal SARM: Additive liver strain
  • MajorWith another anabolic steroid: Blood / clotting
  • MajorWith a clot-promoting SERM: Blood / clotting
  • ModerateWith an aromatase inhibitor: Hormonal
  • ModerateWith an anabolic steroid: Hormonal
  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • This is educational information only, not medical advice, and does not endorse use. These substances carry serious risks; anyone using or considering them should consult a qualified physician and obtain regular bloodwork. 21+ only.
  • Because it is an oral 17-alpha-alkylated steroid, the liver is a primary risk organ. Stop and seek urgent medical care for jaundice (yellow skin/eyes), dark urine, pale stools, severe abdominal pain, or persistent itching.
  • Get baseline bloodwork before any use and periodic monitoring during and after — at minimum liver enzymes and bilirubin, a full lipid panel, hematocrit, blood pressure, and reproductive hormones.
  • Seek emergency care for chest pain, breathlessness, palpitations, fainting, one-sided weakness, or limb swelling (possible cardiac or thrombotic events).
  • HDL cholesterol can fall sharply and quickly; discuss cardiovascular risk with a clinician and do not ignore rising blood pressure.
  • Suppression of your own testosterone can persist for years after stopping. Do not attempt to self-manage hormonal recovery; recovery should be directed by an endocrinologist with serial bloodwork. Only single-SERM approaches are within scope here.
  • Combining AAS with other AAS or drugs of abuse increases risk; absence of interaction data is not evidence of safety.
  • If you experience severe mood change, aggression, mania, or depressive or suicidal thoughts, seek help promptly.
  • There is no established safe non-medical dose; higher doses and longer duration increase liver, cardiovascular, and endocrine harm.
Evidence

Citations (15)

Every clinical claim above is tied to a primary source. Overall evidence grade C — graded to the best available evidence for its core claims.

  1. 01

    Methandrostenolone/methandienone is an oral 17-alpha-alkylated AAS derivative of testosterone used non-medically for muscle building, with drug-induced liver injury (commonly cholestatic) as a major risk.

    Case reportAnabolic Steroid-Induced Cholestatic Jaundice in a Young Adult: An Emerging Clinical Challenge Underscoring the Importance of a Thorough Drug History.PMID 42299185 ↗

  2. 02

    Methandrostenolone use can cause cholestatic jaundice with markedly elevated bilirubin, and in reported cases concurrent acute kidney injury (acute tubular necrosis) and acute pancreatitis.

    Case reportCholestatic jaundice, acute kidney injury and acute pancreatitis secondary to the recreational use of methandrostenolone: a case report.PMID 21470406 ↗

  3. 03

    Metandienone (10-50 mg/day orally) combined with another AAS produced severe cholestasis with very high bilirubin and acute renal failure in a bodybuilder.

    Case report[Severe cholestasis with kidney failure from anabolic steroids in a body builder].PMID 10506840 ↗

  4. 04

    Oral 17-alpha-alkylated AAS can cause cholestatic liver injury and, rarely, submassive hepatic necrosis and fatal liver failure.

    Case reportFatal anabolic androgenic steroid overdose in an amateur bodybuilder: a clinical and autopsy reportPMID 37948000 ↗

  5. 05

    AAS use (including methandrostenolone) in power athletes markedly reduces HDL and HDL2 cholesterol, an atherogenic change.

    CohortSerum lipids in power athletes self-administering testosterone and anabolic steroids.PMID 4030188 ↗

  6. 06

    Self-administered androgenic steroids reduce serum HDL cholesterol substantially (about 54%) in power athletes, raising coronary heart disease risk.

    CohortReduced high-density lipoprotein-cholesterol in power athletes: use of male sex hormone derivates, an atherogenic factor.PMID 6511154 ↗

  7. 07

    Long-term AAS use is associated with reduced left-ventricular systolic and diastolic function and dose-dependent accelerated coronary atherosclerosis.

    CohortCardiovascular Toxicity of Illicit Anabolic-Androgenic Steroid UsePMID 28533317 ↗

  8. 08

    AAS cause a range of cardiovascular effects including left-ventricular hypertrophy, hypertension, HDL reduction, prothrombotic changes, cardiomyopathy, and sudden cardiac death.

    Review[Cardiovascular side effects of anabolic-androgenic steroids].PMID 17036188 ↗

  9. 09

    Current AAS users show suppressed gonadotropins and reduced inhibin B and AMH (impaired spermatogenesis); former users can show lower testosterone and hypogonadal symptoms years after cessation.

    CohortFormer Abusers of Anabolic Androgenic Steroids Exhibit Decreased Testosterone Levels and Hypogonadal Symptoms Years after Cessation: A Case-Control Study.PMID 27532478 ↗

  10. 10

    Former illicit androgen users exhibit decreased Leydig-cell capacity approximately two years after cessation, associated with erectile function.

    CohortCharacterization of Leydig Cell Dysfunction in Previous Illicit Androgen Users.PMID 40052766 ↗

  11. 11

    Supraphysiologic androgen levels in weightlifters are associated with increased aggression, though findings may be confounded by personality factors.

    CohortMeasures of aggression and mood changes in male weightlifters with and without androgenic anabolic steroid use.PMID 12762541 ↗

  12. 12

    Performance-enhancing drug (including AAS) use is linked to increased risk of death and cardiovascular, psychiatric, metabolic, endocrine, hepatic, and renal disorders, and an AAS withdrawal syndrome; adverse effects are widely underappreciated.

    GuidelineAdverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement.PMID 24423981 ↗

  13. 13

    Methandienone pharmacokinetics/metabolism are characterized largely through doping-control urinary metabolite studies; a single 5 mg oral dose is detectable via a long-term metabolite up to ~19 days later.

    CohortMass spectrometric identification and characterization of a new long-term metabolite of metandienone in human urine.PMID 16804957 ↗

  14. 14

    Methandrostenolone is extensively metabolized with metabolites excreted mainly in the urine.

    Preclinical[Dynamic distribution of methandrostenolone in the body of white rats].PMID 3691778 ↗

  15. 15

    AAS hepatotoxicity as a class, including with 17-alpha-alkylated agents, includes cholestasis, hepatocellular adenoma, hepatocellular carcinoma, and peliosis hepatis.

    ReviewHepatotoxicity associated with illicit use of anabolic androgenic steroids in doping.PMID 28379599 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice