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Superdrol for Health & Longevity

Evidence Review created on 10/18/2026 using AI4L / Opus 5.5

Also known as: Methasterone, Methasteron, Methyldrostanolone, 17α-Methyldrostanolone

Motivation

Superdrol (methasterone) is an oral synthetic steroid closely related to the male hormone testosterone. It draws interest from strength-focused adults because it has a reputation for building muscle and strength quickly over short courses. It works through the same cellular switch in muscle that testosterone uses.

The compound was created by a drug company in the 1950s but never approved as a medicine. It reappeared in 2005, sold to bodybuilders as a “dietary supplement” until regulators moved against it, and it is now a controlled substance in the United States. Attention since then has centered on two questions: how much muscle it actually builds, and what it does to the liver and to the body’s own hormone production.

This review examines the human evidence on Superdrol’s effects on muscle, liver and hormonal health, separating data gathered on the compound itself from data borrowed from related steroids, and sets out what that evidence means for health-focused adults weighing its use.

Benefits - Risks - Protocol - Conclusion

The items below give an in-depth, accessible starting point on Superdrol, the liver injury reports that define its clinical record, and anabolic steroid use in bodybuilding.

No content on Superdrol or methasterone itself was found from Rhonda Patrick, Peter Attia, Andrew Huberman, Chris Kresser, Life Extension or Lifespan.io, as these platforms do not cover unapproved designer steroids; Peter Attia’s podcast is listed for its in-depth discussion of anabolic steroids as a class.

Grokipedia

Superdrol

Covers chemistry, history, regulation and user-reported dosing in one place; useful for context, though several figures, such as an 8–12-hour half-life, carry no primary human source.

Examine

No Examine article on Superdrol or methasterone exists. Examine does not typically cover unapproved or controlled anabolic steroids.

ConsumerLab

No ConsumerLab article on Superdrol exists; the site’s search returns only recall and warning notices about steroid-containing bodybuilding products.

Systematic Reviews

No systematic review addresses methasterone alone; the papers below either include methasterone case reports or analyze anabolic steroids as a class.

Mechanism of Action

Methasterone is dihydrotestosterone (DHT, the potent form of testosterone made in skin and prostate) with methyl groups at carbons 2 and 17.

  • Androgen receptor activation: It binds the androgen receptor (testosterone’s muscle-building switch) about as strongly as testosterone and activated it more in assays, barely binding estrogen, progesterone or cortisol receptors (Drug Enforcement Administration (DEA) final rule, 2012).
  • Anabolic selectivity: Per the same rule, rat assays showed four times the muscle-building and one-fifth the masculinizing activity of methyltestosterone; later assays found testosterone-like prostate growth. Its commercial developer, Syntex, produced early data (Grokipedia: Superdrol). Untested in humans.
  • No estrogen conversion: As a DHT derivative it cannot become estrogen via aromatase (the enzyme converting testosterone to estradiol).
  • Oral activity and liver load: The 17α-methyl group blocks liver breakdown, allowing oral use but concentrating exposure there. Its cholestasis (blocked bile flow) may stem from inhibition of AKR1D1 (a bile-acid-making enzyme), shown in laboratory tests (Kędzierski et al., 2023), or from individual susceptibility such as bile-transport gene variants (Stolz et al., 2019).
  • Hormonal feedback: Anabolic steroids as a class suppress luteinizing hormone (LH) and follicle-stimulating hormone (FSH), the pituitary signals driving testicular testosterone and sperm production (Christou et al., 2017).
  • Pharmacokinetics: Human half-life, tissue distribution and liver enzymes are unmeasured. Liver cells convert it, chiefly by reduction and hydroxylation (chemical changes aiding excretion), into urinary metabolites (Gauthier et al., 2009); metabolites stayed detectable 10 days (Zhang et al., 2016), or 50 with newer methods (Zheng et al., 2025).

Historical Context & Evolution

  • Original development: Methasterone was synthesized in 1956; the DEA’s 2012 rule summarizes late-1950s rat studies describing it as a potent anabolic agent with weak androgenic activity and knows of no legitimate medical use or new drug application (DEA final rule, 2012). The drug company Syntex researched it for possible anti-tumor use, but it was never approved (Grokipedia: Superdrol).
  • Re-emergence as a supplement: Around 2005 it was sold as “Superdrol”, a so-called dietary supplement for bodybuilders, at 10 mg per capsule (Grokipedia: Methasterone). Its appeal rested on the 1950s rat data suggesting strong muscle-building with weak masculinizing effects.
  • Regulatory response: The U.S. Food and Drug Administration (FDA) issued a Warning Letter on Superdrol in March 2006, and the DEA classified methasterone as a Schedule III anabolic steroid effective August 29, 2012 (DEA final rule, 2012).
  • What changed: Between 2006 and 2009, hepatologists published case reports and series of cholestatic jaundice and kidney failure in users (Jasiurkowski et al., 2006; Shah et al., 2008). The shift in opinion was driven by this human harm data, not by new efficacy data: no human efficacy trial was ever run, so the favorable profile still rests on rat assays that have been neither confirmed nor refuted in people.
  • Persistence: The compound continued to appear undeclared in other products, including vitamin B capsules in 2012–2013 (Tran et al., 2023).

Expected Benefits

High 🟩 🟩 🟩

No benefit reaches High: methasterone has never been tested in a controlled human trial, so all human outcome data come from trials of other anabolic steroids.

Medium 🟩 🟩

No benefit reaches Medium: no single trial or comparison-group study of methasterone exists, and data from related compounds count as indirect evidence.

Low 🟩

Lean Mass and Muscle Strength Gains

Androgen receptor activation raises muscle protein synthesis. Evidence is indirect: trials tested injected testosterone (Bhasin et al., 1996) and oral relatives such as oxandrolone, not methasterone. In older men, oxandrolone gains vanished 12 weeks after stopping (Schroeder et al., 2004) and left walking speed unchanged (Schroeder et al., 2005).

Magnitude: Across placebo-controlled trials of various anabolic steroids, lean mass standardized mean difference (SMD, effect size in standard-deviation units) 0.62 (95% confidence interval [CI, range likely to contain the true effect] 0.35–0.89; 14 studies) and strength SMD 0.27 (95% CI 0.07–0.47; 21 studies) versus placebo (Andrews et al., 2018).

Reduced Abdominal Fat

Oral relatives of methasterone reduced trunk fat in older men. Evidence is indirect: 12-week trials tested oxymetholone and oxandrolone, not methasterone. Unlike muscle gains, oxandrolone’s fat reduction largely persisted 12 weeks after stopping (Schroeder et al., 2004).

Magnitude: Oxymetholone 50 and 100 mg/day for 12 weeks changed trunk fat by −1.7 kg and −2.2 kg versus −0.2 kg on placebo (within-group changes; not compared between groups as a reported difference) (Schroeder et al., 2003).

Speculative 🟨

Muscle Gain With Fewer Masculinizing Effects ⚠️ Conflicted

Rat assays found four times methyltestosterone’s muscle-building and one-fifth its masculinizing activity; later rat assays found testosterone-like prostate growth (DEA final rule, 2012). Animal data only. Net reading: selectivity is unconfirmed.

Benefit-Modifying Factors

  • Androgen receptor genetics: The number of CAG repeats in the androgen receptor gene (a stretch that tunes receptor sensitivity) altered some metabolic responses to testosterone in a randomized trial (Stanworth et al., 2014); its effect on response to methasterone is untested.
  • Baseline testosterone: Muscle gains in trials occurred in men with normal testosterone given doses above natural levels (Bhasin et al., 1996); no study compares response by baseline hormone level for methasterone.
  • Sex: Women gain muscle and performance from androgens, but at the cost of acne, voice deepening and menstrual disturbance (Huang & Basaria, 2018); no female data exist for methasterone.
  • Pre-existing conditions: In wasting from HIV (human immunodeficiency virus) infection, oral oxymetholone increased body weight and body cell mass versus placebo (Hengge et al., 2003); existing liver disease limits use because liver injury drives the risk profile.
  • Age: Men aged 60–87 gained lean mass and strength on oxandrolone but lost both within 12 weeks of stopping (Schroeder et al., 2004), so gains at the older end of the range are temporary.
  • Training status: Testosterone combined with resistance training increased muscle size and strength more than either alone (Bhasin et al., 1996).

Potential Risks & Side Effects

High 🟥 🟥 🟥

No risk reaches High: methasterone has never been studied in a controlled trial, and every risk rests on case reports or on studies of other anabolic steroids.

Medium 🟥 🟥

No risk reaches Medium: no comparison-group study of methasterone users exists, and controlled or observational data on other steroids count as indirect evidence.

Low 🟥

Cholestatic Liver Injury

Methasterone can block bile flow, causing deep jaundice weeks into use or after stopping. Evidence is case reports and series from several independent groups (Shah et al., 2008; Singh et al., 2009; Krishnan et al., 2009). Cases recovered without transplant. The Low grade reflects uncontrolled evidence, not mild severity.

Magnitude: In 52 pooled cases (methyldrostanolone the most common agent), median peak bilirubin was 705 μmol/L, presentation came a median 56 days after starting, and bilirubin peaked a median 28 days after stopping; none died or needed a transplant (no control group) (Abeles et al., 2020).

Acute Kidney Injury

Kidney failure can accompany severe cholestasis, probably from bile-acid damage to kidney tubules; one Superdrol user developed IgA nephropathy (kidney inflammation from antibody deposits) (Jasiurkowski et al., 2006). Further evidence is case reports of combined liver and kidney failure (Nasr & Ahmad, 2009).

Magnitude: Kidney injury occurred in 43% of 52 pooled steroid liver-injury cases, with median peak creatinine 225 μmol/L; no control group (Abeles et al., 2020).

Suppressed Natural Testosterone and Fertility

Like other androgens, methasterone signals the pituitary to stop stimulating the testes, lowering natural testosterone and sperm production (hypogonadism). Evidence is indirect: studies pooled users of various anabolic steroids. Full recovery after stopping was documented in only a minority of reported cases (Vilar Neto et al., 2021).

Magnitude: During steroid use, testosterone was 10.75 nmol/L lower than before use (weighted mean difference, a pooled average change; 95% CI −15.01 to −6.49) and remained 9.40 nmol/L lower after stopping; before–after comparison, no control group (Christou et al., 2017).

Unfavorable Cholesterol Changes

Oral 17α-methylated steroids lower high-density lipoprotein (HDL, “good”) cholesterol and raise low-density lipoprotein (LDL, “bad”) cholesterol, partly by increasing hepatic lipase (a liver enzyme that breaks down HDL). Evidence is indirect: stanozolol (Thompson et al., 1989) and oxymetholone (Schroeder et al., 2003) were tested, not methasterone.

Magnitude: Oral stanozolol lowered HDL by 33% and raised LDL by 29%, versus a 9% HDL fall and 16% LDL fall on injected testosterone, in an 11-man crossover (not compared between groups as a reported difference) (Thompson et al., 1989).

Cardiovascular Strain ⚠️ Conflicted

Evidence is indirect, from other androgens. Registry users had about triple matched controls’ heart attack and heart failure risk (Windfeld-Mathiasen et al., 2025). Another cohort found no excess neck or leg plaque, though coronary plaque rose with cumulative use (Buhl et al., 2025). Net reading: risk grows with exposure.

Magnitude: In a Danish registry of 1,189 users and 59,450 matched controls followed for about 11 years, the adjusted hazard ratio (aHR, relative risk over follow-up after accounting for other factors) was 3.00 (95% CI 1.67–5.39) for heart attack and 3.63 (95% CI 2.01–6.55) for heart failure (Windfeld-Mathiasen et al., 2025); systolic blood pressure was 12.43 mmHg higher with steroid use (pooled mean difference, 95% CI 9.59–15.26) (Mingxing & Yanfei, 2025); left ventricular ejection fraction (share of blood pumped per beat) was 52% in long-term users versus 63% in nonusers (Baggish et al., 2017); longer cumulative use carried an odds ratio (OR, relative odds) of 1.17 (95% CI 1.05–1.30) for non-calcified coronary plaque (Buhl et al., 2025).

Higher All-Cause Mortality

Anabolic steroid users died at higher rates than matched non-users, from natural causes (mostly cancer and cardiovascular disease) and unnatural ones (mostly accidents). Evidence is indirect: a Danish registry of men sanctioned for anabolic steroids, not methasterone (Windfeld-Mathiasen et al., 2024). Results were unadjusted for risk-taking or other drug use.

Magnitude: Over about 11 years, 33 of 1,189 users died versus 578 of 59,450 matched controls, hazard ratio (HR, relative risk over follow-up) 2.81 (95% CI 1.98–3.99); HR 2.24 (95% CI 1.36–3.70) for natural and 3.64 (95% CI 2.22–5.96) for unnatural deaths (Windfeld-Mathiasen et al., 2024).

Raised Red Blood Cell Count and Clotting Risk

Androgens stimulate red blood cell production (erythrocytosis), thickening the blood and, with platelet and clotting-protein changes, raising clot risk (a review by Gurumurthy & Thachil, 2025). Evidence is indirect, from other androgens: higher hematocrit (Fyksen et al., 2022) and more venous clots in registry data (Windfeld-Mathiasen et al., 2025).

Magnitude: Long-term steroid users had hemoglobin of 16.8 versus 15.0 g/dL and hematocrit of 0.50 versus 0.44 in strength-trained nonusers (cross-sectional comparison; no difference figure or CI reported) (Fyksen et al., 2022); in a Danish registry, venous thromboembolism (clots in the veins) carried an aHR of 2.42 (95% CI 1.54–3.80) versus matched controls (Windfeld-Mathiasen et al., 2025).

Acne, Hair Loss and Masculinizing Effects

Placebo-controlled trials of other steroids reported acne (Andrews et al., 2018); in women and girls, androgens cause virilization such as voice deepening, partly permanent (DEA final rule, 2012). Methasterone-contaminated vitamin capsules were associated with scalp hair loss and a child’s virilization (Tran et al., 2023).

Magnitude: About 16 residents reported symptoms, one was hospitalized for liver damage and one child showed severe virilization after using contaminated capsules; no control group (Tran et al., 2023).

Aggression and Mood Changes ⚠️ Conflicted

Androgens can raise irritability and aggression; stopping may bring low mood. Evidence is indirect, from other steroids, not methasterone (Piacentino et al., 2015). Pooled trials found self-reported aggression rose but observer-rated aggression did not (Chegeni et al., 2021). Net reading: a small, mainly self-perceived rise.

Magnitude: Self-reported aggression rose slightly versus placebo, Hedges’ g (a standardized effect size) 0.171 (95% CI 0.029–0.312; 11 trials), while observer-rated aggression did not change (Chegeni et al., 2021).

Anabolic Steroid Dependence

Repeated use can lead to dependence, with continued use despite harm and withdrawal symptoms on stopping. Evidence is indirect: pooled surveys of users of various anabolic steroids, not methasterone (Pope et al., 2014). Whether short methasterone courses carry less risk is untested.

Magnitude: Roughly 1 million of an estimated 2.9–4.0 million Americans who have used anabolic steroids may have experienced dependence (pooled estimate from 10 studies; no control group) (Pope et al., 2014).

Hepatitis-Associated Aplastic Anemia

Bone marrow failure (aplastic anemia) followed methasterone-related cholestatic hepatitis in one young man, probably through an immune attack on the marrow after liver injury. Evidence is a single case report (Khurana & Dasanu, 2014).

Magnitude: Not quantified in available studies. Only a single case report exists, so no frequency can be estimated.

Liver Tumors and Blood-Filled Liver Cysts

Prolonged anabolic steroid use is associated with peliosis hepatis (blood-filled liver cysts), hepatocellular adenomas (benign liver tumors) and hyperplasia (tissue overgrowth). Evidence is indirect: case literature on other steroids, mostly in long-term medical use (Søe et al., 1992). No methasterone case has been reported.

Magnitude: Not quantified in available studies. Only case reports exist, so no incidence figure is available.

Speculative 🟨

Risk-Modifying Factors

  • Bile-transport gene variants: Variants in ABCB11 (the gene for the bile salt export pump, which moves bile acids out of liver cells) differed significantly between bodybuilding-supplement cholestasis cases and matched controls (Stolz et al., 2019).
  • Baseline liver and lipid tests: Pre-existing raised liver enzymes, low HDL or high LDL leave less margin before steroid-related changes matter (theoretical).
  • Sex: Women face virilization, some of it permanent (DEA final rule, 2012); men face testicular suppression (Christou et al., 2017). Fifty of 52 pooled liver-injury cases were men (Abeles et al., 2020).
  • Pre-existing conditions: Kidney disease, heart disease or high blood pressure plausibly heighten the corresponding harms (theoretical); pre-existing liver disease did not raise drug-induced liver injury risk in a registry cited by Abeles et al., 2020.
  • Age: Adolescents risk premature closure of bone growth plates (DEA final rule, 2012); in men aged 65–80, oral oxymetholone 100 mg/day raised alanine aminotransferase (ALT, a liver enzyme) by 72 U/L (Schroeder et al., 2003).
  • Cumulative exposure: Longer cumulative steroid use tracked with more coronary plaque (Buhl et al., 2025); median onset of liver injury was 56 days after starting (Abeles et al., 2020).
  • Alcohol use: Regular drinking adds independent liver stress (theoretical).

Key Interactions & Contraindications

  • Vitamin K antagonist anticoagulants (blood thinners blocking vitamin K; warfarin, acenocoumarol) — Avoid (theoretical): Anabolic steroids can strengthen their effect, raising bleeding risk, as reported with stanozolol plus warfarin (Shaw & Smith, 1987). Mitigation described: frequent INR (international normalized ratio, a clotting-time test) checks.
  • Liver-toxic prescription drugs (methotrexate, isoniazid, valproate, ketoconazole) — Avoid (theoretical): Additive liver injury, with risk of combined cholestatic and drug-induced hepatitis. No mitigation is established beyond liver test monitoring.
  • Other oral 17α-methylated steroids (oxandrolone, oxymetholone, methyltestosterone) — Avoid (theoretical): Stacking adds liver load and lipid disturbance; in pooled liver-injury cases methyldrostanolone was taken alone or in combination (Abeles et al., 2020).
  • Glucose-lowering drugs (insulin, sulfonylureas such as glipizide) — Monitor (theoretical): Androgens can lower blood glucose, raising hypoglycemia (low blood sugar) risk. Mitigation described: closer glucose monitoring.
  • Over-the-counter acetaminophen (paracetamol) — Caution (theoretical): Additional liver burden during steroid exposure; mitigation described: keeping intake at the low end of labeled doses.
  • Over-the-counter NSAIDs (nonsteroidal anti-inflammatory drugs such as ibuprofen, naproxen) — Caution (theoretical): Added kidney stress where cholestasis already threatens kidney function; mitigation described: avoiding regular use during and after a course.
  • Liver-stressing supplements (high-dose green tea extract, kava, ashwagandha) — Avoid (theoretical): Additive liver injury; one pooled methyldrostanolone case had also taken ashwagandha and creatine (Abeles et al., 2020).
  • Supplements with additive androgenic effects (prohormones, “testosterone boosters”, SARMs [selective androgen receptor modulators, nonsteroidal androgen-receptor activators] such as ostarine) — Avoid (theoretical): Additive hormonal suppression and liver load; undeclared methasterone has been found even in vitamin supplements (Tran et al., 2023).
  • Alcohol — Avoid (theoretical): Additive liver injury and further HDL disturbance; mitigation described: abstinence during and for several weeks after a course.

Populations who should avoid Superdrol:

  • Women, including those pregnant or breastfeeding (virilization, some of it permanent) (DEA final rule, 2012)
  • Children and adolescents (premature growth-plate closure) (DEA final rule, 2012)
  • People with existing liver disease, prior drug-induced cholestasis or chronic viral hepatitis
  • People with kidney disease
  • People with heart disease, high blood pressure or adverse cholesterol profiles
  • Men trying to conceive (Christou et al., 2017)
  • People with prostate or breast cancer (hormone-sensitive tumors) (theoretical)
  • Athletes subject to anti-doping testing (metabolites detectable for up to 50 days) (Zheng et al., 2025)

Risk Mitigation Strategies

Doses and timings below follow common practice unless cited.

  • No exposure as the only complete mitigation: No dose or course length has been shown safe; in pooled cases, liver injury presented a median 56 days after starting (Abeles et al., 2020). Mitigates every risk listed.
  • Short courses: Courses are commonly limited to 4 weeks or less; median liver-injury onset was 56 days after starting (Abeles et al., 2020), so brevity may reduce, not remove, cholestasis risk.
  • Symptom stop rule: Stopping at the first yellowing of skin or eyes or itching, the most common presenting features in case series (Abeles et al., 2020), or at dark urine or pale stools, limits progression of cholestatic liver injury.
  • Laboratory stop threshold: Stopping at ALT ≥5× the upper limit of normal (ULN), alkaline phosphatase (ALP, a bile-duct enzyme) ≥2× ULN, or ALT ≥3× ULN plus bilirubin >2× ULN, the liver-injury definition (Aithal et al., 2011), limits damage.
  • Post-course surveillance: Jaundice appeared about 2 weeks after stopping (Shah et al., 2008); liver tests 2 and 4 weeks after the last dose catch delayed cholestasis early.
  • Kidney protection: Adequate hydration, avoiding NSAIDs and checking creatinine with each liver panel reduce the risk of unrecognized kidney injury, seen in 43% of pooled liver cases (Abeles et al., 2020).
  • Lipid and blood pressure checks: A lipid panel before and at week 4, plus home blood pressure readings, detect the HDL fall seen with oral steroids (Thompson et al., 1989) and rising pressure, limiting unrecognized cardiovascular strain.
  • Hormonal recovery check: Testosterone, LH and FSH 8–12 weeks after stopping identify persistent hypogonadism; pituitary hormones recovered over 13–24 weeks in pooled studies (Christou et al., 2017).
  • Avoiding other liver stressors: Excluding alcohol, other oral steroids and liver-stressing herbal extracts during and after a course reduces additive liver injury (theoretical).

Therapeutic Protocol

Parameters other than doses below (timing, course length, titration) reflect common practice unless cited.

  • No validated protocol: Methasterone has no tested regimen; the DEA knows of no legitimate medical use or new drug application for it (DEA final rule, 2012).
  • Dose in user practice: Original Superdrol capsules contained 10 mg (Grokipedia: Methasterone); user-reported doses range from 10 to 30 mg/day (Grokipedia: Superdrol). These are community figures, not tested doses.
  • Originator of the approach: The supplement firm Designer Supplements, associated with formulator Matt Cahill, popularized Superdrol courses for bodybuilding (Grokipedia: Methasterone).
  • Course length: Users report courses of 4–6 weeks (Grokipedia: Superdrol) or 2–4 weeks (Grokipedia: Methasterone); liver injury presented a median 56 days after starting (Abeles et al., 2020).
  • Alternative approach – supervised medicine: Trials of prescribed oral relatives used oxandrolone 20 mg/day (Schroeder et al., 2004) or oxymetholone 50–100 mg/day (Schroeder et al., 2003) for 12 weeks with monitoring; potencies differ, so these doses do not transfer.
  • Alternative approach – training alone: In the placebo-plus-exercise group, resistance training alone increased muscle size and strength (Bhasin et al., 1996).
  • Time of day: No data exist; users commonly take doses with meals to reduce gastrointestinal discomfort.
  • Half-life: Never measured in humans; the 8–12 hours often quoted is unsourced (Grokipedia: Superdrol).
  • Single or split dosing: Users commonly split the daily amount into two doses, reflecting the presumed short half-life rather than any measured profile.
  • Genetic factors: Carriers of ABCB11 variants may face greater cholestasis risk (Stolz et al., 2019); no pharmacogenetic dose guidance exists.
  • Sex differences: Female dosing has never been studied; in women, anabolic steroid use can cause permanent virilization (DEA final rule, 2012).
  • Age: In men aged 65–80, the higher oxymetholone dose raised ALT more (Schroeder et al., 2003); older adults carry more baseline cardiovascular risk.
  • Baseline biomarkers: Abnormal baseline liver tests, creatinine or lipids remove the safety margin on which any course depends (theoretical).
  • Pre-existing conditions: Liver, kidney or heart disease places a person among the populations listed to avoid it.

Discontinuation & Cycling

  • Short-term only: Methasterone is used in short courses, never lifelong (common practice); in pooled cases liver injury presented a median 56 days after starting (Abeles et al., 2020).
  • Withdrawal effects: Stopping anabolic steroids can bring depressed mood (Piacentino et al., 2015), and abrupt cessation after long-term use may trigger a withdrawal syndrome with severe depression (DEA final rule, 2012).
  • Delayed liver injury: Jaundice can first appear after the last dose and peak weeks later (Shah et al., 2008), so stopping does not end the risk window.
  • Tapering: No evidence shows that tapering prevents withdrawal or liver injury; abrupt cessation is usual practice.
  • Post-course hormone therapy: Users commonly take clomiphene or tamoxifen to restart testosterone production; a placebo-controlled trial of letrozole plus hCG (human chorionic gonadotropin, a hormone that stimulates the testes) was terminated for poor recruitment (NCT05205837).
  • Recovery timeline: Pituitary hormones returned within 13–24 weeks, while testosterone stayed lower at 16 weeks (Christou et al., 2017).
  • Cycling for efficacy: No evidence supports cycling to maintain effect; muscle gains from an oral relative disappeared within 12 weeks of stopping (Schroeder et al., 2004).

Sourcing and Quality

  • No legal pharmaceutical source: As a Schedule III substance with no known legitimate medical use, methasterone may be dispensed only by DEA registrants, and importing it for personal use counts as illegal importation in the United States (DEA final rule, 2012).
  • Counterfeit and substandard products: On the black market, an estimated 36% of anabolic steroid samples were counterfeit and a further 37% substandard (Magnolini et al., 2022).
  • Hidden in other supplements: Methasterone and related designer steroids have been found undeclared in vitamin capsules (Tran et al., 2023), so exposure is possible without intent.
  • Third-party testing: No testing program certifies methasterone products; banned-substance certification programs for sports supplements are relevant only for avoiding inadvertent exposure.
  • Reputable brands or pharmacies: None exist; the DEA knows of no legitimate medical use or new drug application, so no pharmaceutical-grade product is available (DEA final rule, 2012).

Practical Considerations

  • Time to effect: No methasterone data exist; with oxandrolone, over 90% of 12-week lean-mass gains and 74–96% of strength gains appeared within 6 weeks (Schroeder et al., 2005).
  • Common pitfalls: Stacking several oral steroids, drinking alcohol, assuming a short course is safe, ignoring symptoms that begin after stopping, and buying “Superdrol-like” products of unknown content.
  • Regulatory status: Schedule III controlled substance in the United States since August 29, 2012; manufacture, distribution and possession without lawful authority carry criminal penalties (DEA final rule, 2012).
  • Anti-doping detection: Urinary metabolites remained detectable for 10 days in one study (Zhang et al., 2016) and up to 50 days with newer methods (Zheng et al., 2025).
  • Cost and accessibility: Sale outside DEA-registered channels is illegal (DEA final rule, 2012), so it is available only through illicit markets and price, purity and legal exposure are unpredictable.

Interaction with Foundational Habits

  • Sleep: Indirect. No methasterone data exist; androgen-related irritability and low mood after stopping (Piacentino et al., 2015) can disturb sleep, and itching from cholestasis can interrupt it. Practical consideration: new insomnia or itching during or after a course is a recognized warning sign of liver injury.
  • Nutrition: Indirect. Muscle gains depend on sufficient protein and energy intake; no nutrient depletion is documented. Alcohol and liver-stressing herbal extracts add liver load (theoretical); two pooled liver-injury cases had also taken ashwagandha (Abeles et al., 2020), and diet quality matters more while HDL is suppressed.
  • Exercise: Potentiating. Testosterone plus resistance training increased muscle size and strength more than either alone (Bhasin et al., 1996). Practical consideration: intense training raises liver enzymes in blood via muscle damage (Dickerman et al., 1999), so tests are commonly drawn after a rest day.
  • Stress management: Indirect. Anabolic steroids slightly increased self-reported aggression in randomized trials (Chegeni et al., 2021); stopping can bring low mood (Piacentino et al., 2015). Practical consideration: established stress-management routines and tracking of mood help separate drug effects from life stress.

Monitoring Protocol & Defining Success

Baseline testing: Within 2 weeks before any exposure, a liver panel (bilirubin, ALT, aspartate aminotransferase [AST, a liver and muscle enzyme], ALP and gamma-glutamyl transferase [GGT, a liver enzyme not raised by exercise]), creatinine, lipids, morning testosterone with LH and FSH, a complete blood count and a blood pressure reading establish a personal reference point. Abnormal liver or kidney results at baseline leave less margin before steroid-related injury matters (theoretical).

Ongoing monitoring: Liver tests and creatinine at weeks 2 and 4 of any course, then 2, 4 and 12 weeks after the last dose, because jaundice in case series appeared after stopping and resolved over about 12 weeks (Shah et al., 2008). Lipids at week 4; testosterone, LH and FSH 8–12 weeks after stopping to track recovery (Christou et al., 2017).

Biomarker Optimal Functional Range Why Measure It? Context/Notes
Total and direct bilirubin Total 0.1–1.2 mg/dL (standard reference range) Safety check: earliest sign of cholestasis; stop trigger Rises sharply in methasterone cholestasis and can peak weeks after stopping (Abeles et al., 2020); ranges vary by laboratory
ALT and AST At or below the laboratory’s upper limit of normal (standard reference range) Safety check: liver injury; stop trigger Heavy training raises both via muscle damage; pairing with creatine kinase (CK, a muscle enzyme) and GGT separates muscle from liver sources (Dickerman et al., 1999); testing after a rest day is common practice
ALP and GGT At or below the laboratory’s upper limit of normal (standard reference range) Safety check: bile-duct markers; ALP is a stop trigger In steroid cholestasis GGT often rises only mildly (median peak 52 U/L), so bilirubin is the more sensitive marker (Abeles et al., 2020)
Creatinine Men 0.74–1.35 mg/dL; women 0.59–1.04 mg/dL (standard reference range) Safety check: kidney injury accompanying cholestasis Gained muscle mass raises creatinine slightly; cystatin C (a filtration marker unaffected by muscle mass) can clarify borderline results
HDL and LDL cholesterol No established target for this use; track change from own pre-course baseline Safety check, and expected to change (HDL falls on oral steroids) Fasting not required for HDL; falls appear within weeks of oral steroid use (Thompson et al., 1989)
Total testosterone, LH, FSH Total testosterone 264–916 ng/dL in men (standard reference range) Expected to change: suppressed during use; tracks recovery afterward Morning sample; harmonized range from Travison et al., 2017; LH and FSH ranges are laboratory-specific
Complete blood count Hemoglobin 13.2–16.6 g/dL in men; platelets 150–450 ×10⁹/L (standard reference range) Safety check: raised hematocrit (clot risk); rare marrow failure after liver injury Hematocrit runs higher in long-term steroid users (Fyksen et al., 2022); marrow failure is relevant if bruising, infections or marked fatigue appear in the months after liver injury (Khurana & Dasanu, 2014)
Lean mass by DXA scan No established target; track change from own baseline Expected to change: lean mass rises during use DXA (dual-energy X-ray absorptiometry, a low-dose body-composition scan); gains from an oral relative reversed within 12 weeks of stopping (Schroeder et al., 2004)

Qualitative markers:

  • Yellowing of skin or eyes, dark urine, pale stools or persistent itching
  • Appetite loss, nausea or upper abdominal discomfort
  • Mood, irritability and sleep quality
  • Libido and erectile function during and after a course
  • Training strength and recovery between sessions
  • Testicular size and, in women, voice, skin and menstrual changes

Emerging Research

  • No methasterone trials: ClinicalTrials.gov lists no study of methasterone, Superdrol or methyldrostanolone; current research on the compound concerns metabolism and detection (Zheng et al., 2025). Its benefit grades will stay indirect until a controlled human study exists, which its legal status makes unlikely.
  • Drug-Induced Liver Injury Network (DILIN) Prospective Study (NCT00345930): Ongoing registry of about 4,000 drug-induced liver injury cases, completion 2028, which produced the bodybuilding-supplement cholestasis series (Stolz et al., 2019). A positive genetic finding would sharpen risk-modifying factors; a null result would leave susceptibility unpredictable.
  • FIDO-DK longitudinal study (NCT05599438): Recruiting 900 Danish recreational athletes, with registry follow-up for heart attack, stroke, heart failure and death until 2040. Higher event rates in users would strengthen the cardiovascular risk item; no excess would weaken it.
  • Danish cross-sectional study (NCT05178537): Planned 1,200 current or former users; registered completion December 2025 has passed, status unknown, no results posted. Odense data from the same research group found coronary plaque rising with cumulative use (Buhl et al., 2025), cited under Cardiovascular Strain.
  • Hormone recovery trial (NCT05205837): Placebo-controlled letrozole plus hCG for steroid-induced hypogonadism; terminated in 2023 after enrolling 8 men, no results posted. A positive result would have supported a recovery protocol; its termination leaves that question open.
  • Harm-reduction trial (NCT07039539): Not yet recruiting, 32 steroid users in São Paulo, primary endpoint reduction in steroid amount used. A historically controlled trial found counseling lowered cumulative androgen dose (Verdegaal et al., 2026); a positive randomized result would confirm this, a null result would weaken it.
  • Cholestasis mechanisms: Inhibition of the bile-acid enzyme AKR1D1 (Kędzierski et al., 2023) and ABCB11 variants (Stolz et al., 2019) could explain who is injured. Confirmation could identify susceptible people; refutation would point back to dose and duration alone.
  • Evidence that could lower concern: No deaths or transplants occurred among 44 bodybuilding-supplement cholestasis cases (Stolz et al., 2019), and non-using bodybuilders show similar enzyme rises from training (Dickerman et al., 1999); larger series could refine severity estimates downward.

Conclusion

Superdrol is an oral synthetic steroid, never approved as a medicine and now a controlled substance in the United States, that works through the same pathway as testosterone. Its appeal rests on a reputation for fast gains in muscle and strength.

No controlled human study of the compound itself exists. The expected gains in muscle and the reduction in abdominal fat are borrowed from trials of related steroids, and in older men those gains faded within months of stopping. Claims of muscle gain with few masculinizing effects rest on the developer’s 1950s animal tests, not confirmed by later ones.

The harm record is more specific to the compound. Dozens of users developed severe blocked bile flow with deep yellowing of the skin, often appearing after the last dose, and some also developed kidney failure; reported cases recovered slowly, over roughly three months. Studies of related steroids add suppression of natural testosterone and fertility that can persist, worse cholesterol, heart strain that grows with total years of use, higher death rates, and masculinizing effects in women. These harms carry low grades because the evidence is uncontrolled or borrowed, not because they are mild.

The evidence base is thin on both sides. Favorable claims trace largely to old animal work by the developer, which had a commercial stake, while the harm record comes from case reports by liver specialists. Illicit products add uncertainty about contents. For health-focused adults, documented and serious downsides stand against benefits that remain unmeasured for this compound.

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