Anavar
Oxandrolone
Oxandrolone (Anavar) is a synthetic oral 17-alpha-alkylated anabolic-androgenic steroid (AAS) derived from dihydrotestosterone. It has legitimate medical use for restoring lost body weight/lean mass (severe burns, HIV-associated wasting, chronic catabolic states) and is studied in Turner, Klinefelter, and constitutional growth delay. Non-medically it is used to add lean muscle and reduce fat with a reputation as a "mild" steroid, but this reputation is misleading about its real dangers. Because it is 17-alpha-alkylated to survive first-pass liver metabolism, it is hepatotoxic: even in controlled burn trials, adults showed transaminase elevations (roughly 19% vs 5% on placebo), and recreational AAS use is a recognized cause of cholestatic jaundice and drug-induced liver injury. It markedly lowers protective HDL cholesterol and raises LDL in human trials, a change so pronounced in one obese-men trial that investigators halted oral dosing. It suppresses the hypothalamic-pituitary-gonadal axis (low testosterone, impaired sperm production), causes virilization in women (voice deepening, hair growth, clitoral enlargement that may be irreversible), and long-term AAS use is associated with cardiomyopathy and reduced heart function that can persist after stopping. The main dangers are liver injury, adverse cholesterol/cardiovascular changes, hormonal suppression, and (in women) permanent virilization. Anyone using or considering it should have baseline and ongoing bloodwork with a clinician and stop and seek care for jaundice, dark urine, abdominal pain, or chest symptoms.
Mechanism of action
Pharmacokinetics
Commonly reported plasma elimination half-life is approximately 9-10 hours in adults (longer, ~13.3 h, in older adults). Note: this specific figure derives from standard pharmacology references/product labeling and was not verifiable as a primary PubMed-indexed pharmacokinetic trial in this review; treat as approximate.
Biologically active across roughly a day; clinical dosing in trials was typically divided (e.g., twice daily), consistent with a short half-life requiring repeat dosing.
Oral (tablet); orally bioavailable due to 17-alpha-alkylation.
Partially resistant to hepatic first-pass metabolism due to 17-alpha-alkylation; undergoes hepatic metabolism with predominantly renal (urinary) excretion of parent drug and metabolites. Provided for washout/monitoring context only, not for detection avoidance.
For monitoring and washout planning, not drug-test evasion.
Physiological & performance effects
- Increases lean body mass and body weight and promotes nitrogen retention in catabolic states (demonstrated in HIV-associated wasting and severe-burn RCTs and a burn meta-analysis)
- Improves strength gains when combined with resistance exercise in eugonadal men with HIV-related weight loss
- In severe pediatric burns, long-term administration is associated with improved lung function, reduced hypertrophic scarring, and improved lean mass/growth outcomes
- Reduces subcutaneous (and tends to reduce visceral) abdominal fat in obese older men
- Advances bone age and increases height standard-deviation score in short-stature/growth-delay pediatric trials (a double-edged effect that can compromise final height)
- Does not produce a mortality benefit in burn patients despite anabolic improvements
- Used non-medically for lean-mass gain and fat reduction; these image/performance uses carry the adverse effects listed below and are not endorsed here
Adverse effects by system
Marked, consistent lowering of HDL ('good') cholesterol and rise in LDL in human RCTs; in one obese-men trial the lipid change was severe enough that oral oxandrolone was discontinued. Long-term AAS use (as a class) is associated with cardiomyopathy, left-ventricular hypertrophy, reduced ejection fraction, and higher blood pressure that can persist after stopping. See cardiovascular field.
Hepatotoxic 17-alpha-alkylated steroid. Controlled burn trials/meta-analysis show dose-related transaminase (ALT/AST) elevations (~19% vs ~5% placebo in adults); recreational AAS use is a recognized cause of cholestatic (bland) jaundice, marked hyperbilirubinemia, and drug-induced liver injury. Case reports also describe severe cholestasis. See hepatotoxicity field.
Suppresses the hypothalamic-pituitary-gonadal axis via androgenic negative feedback, lowering LH/FSH and endogenous testosterone; can cause hypogonadotropic hypogonadism and impaired spermatogenesis. See hptaSuppression field.
Suppression of endogenous testosterone and spermatogenesis (reduced fertility, possible azoospermia/oligospermia) in males; recovery after cessation is variable. In women, virilization: voice deepening, clitoral enlargement, menstrual disruption, and hair pattern changes — some of these (voice, clitoromegaly) may be permanent. Female non-medical use is characterized largely by oral oxandrolone in a harm-reduction cohort.
Direct high-quality data specific to oxandrolone are limited. As an androgen class, AAS use is associated with mood disturbance, irritability/aggression, and in some users dependence and depression (notably on withdrawal). Testosterone/androgen exposure is mechanistically linked to aggression-related brain circuitry. Evidence specific to oxandrolone is weak; class-level signals warrant caution.
No consistent direct nephrotoxicity is established for oxandrolone at therapeutic doses. Oral AAS such as oxandrolone can cause cholestatic liver injury (see hepatotoxicity field); monitor renal function as a general precaution if jaundice develops.
No distinctive severe hematologic toxicity is established specifically for oxandrolone in the retrieved literature. Androgens as a class can stimulate erythropoiesis (raising hemoglobin/hematocrit); a nonhuman-primate androgen study showed significant hemoglobin increases. Human oxandrolone-specific hematologic data are limited — state as uncertain and monitor CBC.
Androgenic skin effects can occur: acne, oily skin, and (particularly in women or with prolonged use) hair changes. In women, hirsutism/androgenic hair changes are part of the virilization syndrome. Specific controlled dermatologic data for oxandrolone are limited.
HPTA suppression & recovery
Suppression: Moderate to significant — androgenic negative feedback suppresses LH/FSH and endogenous testosterone and can impair spermatogenesis; magnitude is dose- and duration-dependent.
After stopping, spontaneous recovery of the HPG axis and spermatogenesis occurs in many users if given sufficient time, but the recovery interval is highly variable and some individuals do not fully recover. Any post-cycle hormonal management (including whether a single selective estrogen receptor modulator such as clomiphene, or hCG, is appropriate) must be individualized and directed by an endocrinologist or fertility/andrology specialist with bloodwork — do not self-manage. This resource does not endorse multi-agent recovery protocols. Men wishing to preserve fertility should consult a clinician before use.
Monitoring
Cadence: Baseline before any use; recheck LFTs and lipids within the first several weeks and periodically thereafter (e.g., every 1-3 months during use); reassess hormones and other labs at least at baseline, mid-use, and after cessation. Any abnormality warrants prompt clinician review and consideration of stopping.
- Jaundice (yellow eyes/skin), dark urine, pale stools, right-upper-quadrant/abdominal pain, nausea, unusual fatigue (possible liver injury — stop and seek care)
- Chest pain, breathlessness, palpitations, or leg swelling (possible cardiac involvement)
- Markedly rising blood pressure
- Women: voice deepening, increased facial/body hair, clitoral enlargement, menstrual changes (may be irreversible — stop and seek care)
- Persistent low mood, marked irritability/aggression, or withdrawal-related depression
- Reduced libido, testicular shrinkage, or fertility concerns in men
Contraindications
- Known or suspected liver disease, cholestasis, or prior drug-induced liver injury
- Pre-existing dyslipidemia or significant cardiovascular disease / cardiomyopathy / uncontrolled hypertension
- Pregnancy and breastfeeding (fetal virilization risk); women who may become pregnant
- Male infertility concerns / desire to preserve fertility (HPG suppression)
- Known or suspected androgen-sensitive malignancy (e.g., prostate or male breast carcinoma)
- Women, given risk of irreversible virilization — use only under specialist supervision if ever
- Adolescents outside a monitored medical indication (advances bone age and can compromise final adult height)
- Concurrent hepatotoxic drugs, heavy alcohol use, or other 17-alpha-alkylated oral steroids
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.
Reducing harm & when to stop
- This is not medical advice and does not endorse non-medical use; the safest option is not to use, and to work with a clinician for any legitimate indication.
- Get baseline bloodwork before use and repeat during use: liver enzymes/bilirubin, full lipid panel, testosterone/LH/FSH, CBC, renal function, and blood pressure.
- Stop immediately and seek urgent medical care for signs of liver injury: jaundice, dark urine, pale stools, persistent abdominal pain, nausea, or unusual fatigue.
- Because it lowers HDL and can raise LDL and blood pressure, monitor cardiovascular risk factors; seek care for chest pain, breathlessness, or palpitations.
- Avoid combining with alcohol, other 17-alpha-alkylated oral steroids, or other hepatotoxic drugs; longer duration and higher doses increase liver and lipid risk.
- Women: virilization (voice deepening, clitoral enlargement) can be permanent — stop at the earliest signs and seek specialist review.
- Do not use if pregnant, breastfeeding, or possibly pregnant.
- Any hormonal recovery after stopping should be individualized and directed by an endocrinologist/andrologist with bloodwork; do not self-manage post-cycle regimens.
- Men concerned about fertility should consult a clinician before use, as sperm production suppression may not fully reverse.
- Report all substances you are taking to your clinician so monitoring and interaction risks can be assessed.
Citations (15)
Every clinical claim above is tied to a primary source. Overall evidence grade B — graded to the best available evidence for its core claims.
- 01
Oxandrolone lowers HDL and raises LDL cholesterol in humans, severe enough in obese older men that oral oxandrolone was discontinued and switched to a parenteral agent; it also decreased subcutaneous abdominal fat.
RCTOral anabolic steroid treatment, but not parenteral androgen treatment, decreases abdominal fat in obese, older men.PMID 8574271 ↗
- 02
In eugonadal men with HIV-related weight loss, oxandrolone 20 mg/d plus resistance exercise increased lean body mass and strength beyond testosterone replacement alone, significantly lowered HDL cholesterol (~9.8 mg/dL, p<0.001), and one participant discontinued for elevated liver function tests.
RCTResistance exercise and supraphysiologic androgen therapy in eugonadal men with HIV-related weight loss: a randomized controlled trial. (PMID 10208143)DOI 10.1001/jama.281.14.1282 ↗
- 03
Oxandrolone 5 or 15 mg/d in HIV-associated wasting produced weight gain and improved well-being versus placebo and was generally well tolerated with no consistent LFT changes at those doses, indicating dose/duration-dependent hepatic risk.
RCTOxandrolone in AIDS-wasting myopathy. (PMID 8970686)DOI 10.1097/00002030-199612000-00010 ↗
- 04
In a 2025 systematic review/meta-analysis of 14 burn RCTs (n=2822), oxandrolone increased lean mass and weight and reduced surgical procedures and length of stay but conferred no mortality benefit, no infection reduction, and higher transaminase elevations in adults (19% vs 5% placebo, p=0.002).
Meta-analysisOxandrolone for burn patients: a systematic review and updated meta-analysis of randomized controlled trials from 2005 to 2025. (PMID 41023744)DOI 10.1186/s13017-025-00648-w ↗
- 05
In prepubertal boys with Klinefelter syndrome, oxandrolone 0.06 mg/kg/d improved body fat and triglycerides but significantly lowered HDL cholesterol (p<0.001) and accelerated bone age.
RCTEffects of Oxandrolone on Cardiometabolic Health in Boys With Klinefelter Syndrome: A Randomized Controlled Trial. (PMID 27802097)DOI 10.1210/jc.2016-2904 ↗
- 06
In boys with constitutional growth/puberty delay, oxandrolone 2.5 mg/d increased height SDS and advanced bone age versus placebo.
RCTA double-blind, placebo-controlled comparison of letrozole to oxandrolone effects upon growth and puberty of children with constitutional delay of puberty and idiopathic short stature. (PMID 20628237)DOI 10.1159/000315482 ↗
- 07
Long-term administration of oxandrolone with propranolol in children with large burns reduced hypertrophic scarring and improved physical/psychosocial recovery.
RCTReduced Postburn Hypertrophic Scarring and Improved Physical Recovery With Yearlong Administration of Oxandrolone and Propranolol. (PMID 30048322)DOI 10.1097/SLA.0000000000002926 ↗
- 08
Long-term oxandrolone administration improved lung function in severely burned pediatric patients.
RCTLong-Term Administration of Oxandrolone Improves Lung Function in Pediatric Burned Patients. (PMID 27171844)DOI 10.1097/BCR.0000000000000356 ↗
- 09
Anabolic-androgenic steroid use is a recognized cause of cholestatic drug-induced liver injury characterized by bland cholestasis, insidious jaundice, marked hyperbilirubinemia, and only mild enzyme elevations.
ReviewSelective Androgen Receptor Modulators: An Emerging Liver Toxin. (PMID 36479151)DOI 10.14218/JCTH.2022.00207 ↗
- 10
Long-term anabolic-androgenic steroid users show biventricular cardiomyopathy with higher LV mass index, reduced LV ejection fraction and RV strain, and higher systolic blood pressure, with reduced systolic function persisting after discontinuation.
CohortSevere biventricular cardiomyopathy in both current and former long-term users of anabolic-androgenic steroids. (PMID 37992194)DOI 10.1093/eurjpc/zwad362 ↗
- 11
Exogenous androgens/AAS suppress the hypothalamic-pituitary-gonadal axis and spermatogenesis; after cessation many men recover spontaneously but the recovery period is highly variable and some do not fully recover, and recovery agents are used off-label under specialist guidance.
ReviewRecovery of spermatogenesis following testosterone replacement therapy or anabolic-androgenic steroid use. (PMID 26908067)DOI 10.4103/1008-682X.173938 ↗
- 12
Exogenous testosterone/androgen administration can cause hypogonadotropic hypogonadism with suppressed gonadotropins and azoospermia/severe oligospermia; androgens are contraindicated in men wishing to preserve fertility, and recovery is variable.
Case series[Risk of Male Infertility Due to Testosterone Replacement Therapy for Late-Onset Hypogonadism (LOH)] (PMID 33271659)DOI 10.14989/ActaUrolJap_66_11_407 ↗
- 13
Non-medical androgen use in women is predominantly oral oxandrolone and carries unique risks of virilization and reproductive consequences; oral androgen reliance increases hepatotoxicity and adverse lipid risk.
CohortAndrogen Use Among Female Amateur Athletes: A Retrospective Analysis. (PMID 41546595)DOI 10.1111/sms.70207 ↗
- 14
Testosterone/androgen exposure is mechanistically linked to aggression-related brain circuitry (amygdala-prefrontal), supporting biological plausibility of androgen-related mood/aggression effects (class-level, not oxandrolone-specific).
CohortA testosterone-related structural brain phenotype predicts aggressive behavior from childhood to adulthood. (PMID 26431805)DOI 10.1016/j.psyneuen.2015.09.021 ↗
- 15
Androgen exposure increases erythropoiesis (hemoglobin) in a controlled nonhuman-primate model, supporting a class hematologic effect; human oxandrolone-specific hematologic data are limited.
PreclinicalPharmacokinetics and degree of aromatization rather than total dose of different preparations determine the effects of testosterone: a nonhuman primate study in Macaca fascicularis. (PMID 12954670)DOI 10.1002/j.1939-4640.2003.tb02739.x ↗
Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice