By Anabolic steroids are among the most widely used performance-enhancing drugs in the world – and among the most misunderstood. Estimates suggest that 3-4 million Americans have used anabolic steroids at some point, the vast majority outside of any medical context. They’re used in professional sports, amateur bodybuilding, recreational gyms, and increasingly by men in their 20s and 30s who simply want to look better.
The public conversation about anabolic steroids tends toward two unhelpful extremes: the “they’ll kill you immediately” messaging that loses credibility with anyone who knows a healthy-looking steroid user, and the bodybuilding community’s normalization of them as a routine tool with manageable risks. Neither is accurate. The truth is that anabolic steroids produce real, dramatic physiological effects – and carry real, serious long-term health consequences that are substantially underappreciated by most people using them.
This article covers what anabolic steroids actually are, how they work, what they do to the body, and what the evidence shows about their risks – including the ones most users don’t find out about until the damage is done.
What Anabolic Steroids Are
Anabolic-androgenic steroids (AAS) are synthetic derivatives of testosterone. “Anabolic” refers to their muscle-building properties; “androgenic” refers to their masculinizing effects. Both properties are inseparable to varying degrees – attempts to create purely anabolic steroids without androgenic effects have not fully succeeded.
Testosterone itself is the original anabolic steroid – it’s produced naturally in the testes (in men) and in smaller amounts by the ovaries and adrenal glands (in women). Synthetic AAS were developed starting in the 1930s-50s, initially for legitimate medical purposes: treating muscle wasting diseases, hypogonadism, delayed puberty, anemia, and osteoporosis.
Clinically used anabolic steroids include:
- Testosterone (various esters: cypionate, enanthate, propionate) – used in TRT
- Nandrolone (Deca-Durabolin) – used for anemia, muscle wasting
- Oxandrolone (Anavar) – used for weight restoration after illness, burns
- Stanozolol (Winstrol) – used for hereditary angioedema
- Oxymetholone (Anadrol) – used for anemia
Common black-market compounds used in bodybuilding also include:
- Trenbolone – veterinary drug not approved for human use; among the most potent and highest-risk AAS
- Boldenone (Equipoise) – veterinary drug
- Methandrostenolone (Dianabol) – oral, highly liver-toxic
- Various designer steroids created specifically to evade drug testing
How Anabolic Steroids Work
The primary mechanism: AAS bind to androgen receptors in muscle cells (and throughout the body). This androgen receptor activation triggers changes in gene expression that:
- Increase muscle protein synthesis – accelerating the rate at which muscle tissue is built from amino acids
- Decrease muscle protein breakdown – reducing catabolism (muscle breakdown), particularly important during caloric restriction
- Increase nitrogen retention – creating a positive nitrogen balance that reflects net anabolic (building) state
- Increase satellite cell activity – the muscle stem cells involved in repair and growth
- Increase red blood cell production – through stimulation of erythropoietin in the kidneys; increases oxygen-carrying capacity
The result: dramatically accelerated muscle growth beyond what’s achievable through training and nutrition alone. A landmark study by Bhasin and colleagues at Boston University (NEJM, 1996) demonstrated that men given supraphysiological testosterone doses gained significantly more muscle than placebo – even without exercise. Those who combined testosterone with exercise gained the most. The study directly established that the muscle-building effect is pharmacological, not merely potentiating the effects of training.
What supraphysiological means: Normal male testosterone levels are approximately 300-1000 ng/dL. Therapeutic TRT targets the mid-normal physiological range. Bodybuilding doses typically run 5-20x the normal physiological level, and “stacks” (combinations of multiple compounds) can push effective androgen exposure dramatically higher.
The Hypothalamic-Pituitary-Testicular Axis: The Shutdown Problem
This is the most immediately significant and most underappreciated consequence of anabolic steroid use – and the one that most directly affects younger users.
The body regulates testosterone production through a feedback loop: the hypothalamus releases GnRH → pituitary releases LH and FSH → testes produce testosterone and sperm. When exogenous (external) testosterone or AAS is introduced, the hypothalamus detects elevated androgens and shuts down GnRH production → LH and FSH drop to near zero → the testes stop producing testosterone and sperm → testicular atrophy occurs.
During a steroid cycle: The user’s own testosterone production is essentially zero. The exogenous steroids provide androgen, so the user doesn’t feel this – but their testes have stopped functioning.
After stopping a steroid cycle: The hypothalamic-pituitary-testicular (HPT) axis must recover – the brain must restart GnRH production, then LH/FSH, then testicular testosterone production. This recovery:
- Takes weeks to months in first-time users after short cycles
- May take 6-18 months after prolonged or heavy use
- May be permanently incomplete after years of heavy use, particularly if started young
Post-cycle therapy (PCT): Bodybuilding culture uses SERMs (selective estrogen receptor modulators like clomiphene and tamoxifen) and hCG to try to restart the HPT axis. PCT can accelerate recovery but doesn’t guarantee it and doesn’t eliminate the risk of incomplete recovery.
The permanent hypogonadism risk: A significant subset of long-term AAS users develop hypogonadism that doesn’t fully recover. Studies have found that 20-30% of former AAS users have persistently suppressed testosterone years after stopping. These individuals may require lifelong TRT to maintain normal testosterone function – a consequence many young users don’t anticipate when they start their first cycle.
The HPT axis shutdown is not a temporary side effect that resolves cleanly when you stop. In heavy or prolonged users – particularly those who start young – it can produce permanent hypogonadism requiring lifelong testosterone replacement. This is one of the most important facts about anabolic steroid use that most users discover only after the damage is done.
Cardiovascular Effects: The Most Serious Long-Term Risk
The cardiovascular consequences of anabolic steroid use are the most medically serious and the most likely to cause premature death. The evidence is clear and consistent across multiple study designs.
Left Ventricular Hypertrophy
AAS cause hypertrophy (enlargement) of the left ventricle of the heart – the chamber that pumps oxygenated blood to the body. Unlike the physiological cardiac hypertrophy of trained endurance athletes (which is adaptive and benign), AAS-induced LVH is pathological – it impairs diastolic function (the heart’s ability to relax and fill between beats) and is associated with arrhythmias and sudden cardiac death.
Multiple echocardiography studies comparing AAS users to non-using athletes find significantly greater LV wall thickness, impaired diastolic function, and reduced ejection fraction in current and former AAS users.
Dyslipidemia
AAS dramatically worsen the lipid profile:
- HDL (good cholesterol) drops dramatically – often by 40-70% from baseline. Oral anabolic steroids are particularly devastating to HDL.
- LDL increases – particularly with oral 17-alpha alkylated steroids
- Triglycerides rise
The resulting lipid profile (very low HDL, elevated LDL) accelerates atherosclerosis. Studies using coronary CT angiography find significantly greater coronary artery plaque burden in AAS users compared to non-using athletes of similar age, training history, and cardiovascular risk factors.
Thrombosis Risk
AAS increase red blood cell production (elevated hematocrit), platelet aggregability, and various clotting factors – creating a prothrombotic state that increases risk of deep vein thrombosis, pulmonary embolism, stroke, and MI.
Premature Cardiovascular Disease
The cumulative evidence: AAS users have substantially higher rates of MI, stroke, and sudden cardiac death compared to non-using athletes of similar demographics. A 2017 study in Circulation found that long-term AAS users had significantly reduced LV function and significantly higher prevalence of coronary artery disease compared to non-using weightlifters. Former users showed partial but incomplete recovery.
Several studies find that competitive bodybuilders have dramatically higher all-cause mortality than the general population – with cardiovascular disease being the primary driver.
Liver Toxicity
Oral 17-alpha alkylated steroids (Dianabol/methandrostenolone, Anavar/oxandrolone, Winstrol/stanozolol, Anadrol/oxymetholone) are modified at the 17-alpha position to survive first-pass hepatic metabolism – which is what makes them orally active. This modification is also what makes them hepatotoxic.
Effects of oral AAS on the liver:
- Elevated liver enzymes (ALT, AST) – almost universal with oral AAS use
- Peliosis hepatis – blood-filled cysts in the liver; can rupture causing life-threatening hemorrhage
- Cholestasis – impaired bile flow
- Hepatocellular carcinoma – liver cancer; associated with prolonged oral AAS use (case series and case reports; rare but documented)
Injectable testosterone and most injectable AAS (not 17-alpha alkylated) have significantly lower liver toxicity – which is part of why injectable forms are often preferred by long-term users. However, oral AAS remain widely used for their convenience and rapid action.
Psychiatric and Behavioral Effects
Aggression (“roid rage”): AAS increase aggressive behavior – this is documented in controlled research, though the dramatic “roid rage” of popular imagination is an exaggeration for most users. The effect is real but highly variable, influenced by dose, specific compounds, and individual predisposition. High-dose trenbolone is particularly associated with significant psychiatric effects.
Dependence: AAS produce psychological dependence. Users describe continued use despite knowing the risks, inability to stop or reduce use, and distress when not using (“muscle dysmorphia” – a body image disorder where people perceive themselves as insufficiently muscular regardless of actual size). Withdrawal symptoms include fatigue, depression, reduced libido, and mood instability during HPT axis suppression.
Depression during and after use: The HPT axis suppression during and after cycles produces a period of near-zero endogenous testosterone and elevated estrogen (from aromatization of exogenous androgens) – a hormonal environment associated with significant depression, particularly in the weeks to months after stopping. This is a meaningful suicide risk factor in AAS users.
Cognitive effects: Some research suggests prolonged AAS use is associated with impaired verbal memory and visuospatial cognition – possibly related to androgen receptor effects in the brain.
Other Effects
Acne: AAS dramatically worsen acne through increased sebum production. Severe cystic acne – including on the back, chest, and shoulders – is characteristic of AAS use and can leave permanent scarring.
Hair loss: AAS accelerate androgenetic alopecia (male pattern baldness) in genetically predisposed individuals. DHT-derived compounds (trenbolone, Winstrol) are particularly aggressive for hair loss.
Gynecomastia: Excess androgens aromatize (convert) to estrogens. In men, this can cause development of breast tissue (gynecomastia). Users often take aromatase inhibitors (anastrozole, letrozole) to prevent this – which creates its own problems including bone density loss and cardiovascular effects.
Injection site infections: Black-market AAS are not manufactured under pharmaceutical standards. Contaminated products and non-sterile injection technique cause abscesses and infections, including life-threatening cases of bacterial endocarditis (heart valve infection).
Stunted growth in adolescents: AAS cause premature closure of the epiphyseal growth plates – adolescent users may have permanently reduced adult height.
In women: Virilization (masculinization) – deepening of the voice (irreversible), clitoral enlargement (largely irreversible), facial hair growth, menstrual disruption, breast tissue reduction. Women are significantly more sensitive to androgen effects than men.
The “Natural” Bodybuilding Deception
A meaningful proportion of people claiming natural (drug-free) physiques are using anabolic steroids. This creates unrealistic expectations about what is achievable naturally – leading people to believe they’re failing when they simply haven’t achieved a chemically enhanced physique through natural means.
The physiological ceiling of natural muscle gain is real and well-documented. Most research suggests natural men can gain approximately 1-2 lbs of muscle per month under optimal conditions, with total lifetime natural muscle gain potential of approximately 40-50 lbs above an untrained baseline. Physiques significantly beyond this in terms of muscularity combined with low body fat almost certainly involve AAS.
Frequently Asked Questions
Are anabolic steroids illegal in the US? Yes – anabolic steroids are Schedule III controlled substances under the Anabolic Steroid Control Act. Possession without a valid prescription is a federal crime. Sale or distribution carries more serious penalties. However, enforcement against individual users is limited, and black-market availability is widespread.
Is testosterone different from anabolic steroids? Testosterone is an anabolic steroid – it is the prototypical one. Medically prescribed testosterone for hypogonadism (TRT) uses physiological replacement doses targeting normal testosterone levels. Anabolic steroid abuse uses supraphysiological doses – often 5-20x normal levels. The compound is the same; the dose, context, and medical oversight are different.
Can you use anabolic steroids and be healthy long-term? The evidence doesn’t support this for supraphysiological doses. Some argue that TRT-range doses with medical oversight carry manageable risk – this is debatable. The doses used in bodybuilding contexts have consistent, documented associations with cardiovascular damage, HPT axis disruption, and other serious consequences. The long-term cardiovascular mortality data from competitive bodybuilding populations is particularly sobering.
Do anabolic steroids permanently affect the brain? Research is ongoing. Some studies find persistent changes in mood regulation, impulse control, and verbal memory in long-term former users. Animal studies find structural brain changes with high-dose androgen exposure. Whether these are fully reversible is not established.
Why do some doctors prescribe these for medical conditions if they’re so dangerous? The risk-benefit calculation changes dramatically in clinical contexts. For a cancer patient losing muscle mass, a child with delayed puberty, or a person with severe anemia, the benefits of short-term clinical AAS use under medical supervision may outweigh the risks. These are very different from years of supraphysiological self-administration without monitoring.
Disclaimer
This article is for educational purposes only and does not constitute medical advice. This article describes the pharmacology and documented health effects of anabolic steroids – it is not a guide to their use. Anabolic steroid use outside of prescribed medical contexts is illegal in the United States and carries serious health risks documented in this article.
References
- Bhasin S, Storer TW, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. New England Journal of Medicine. 1996;335(1):1-7. https://doi.org/10.1056/NEJM199607043350101
- Baggish AL, Weiner RB, Kanayama G, et al. Long-term anabolic-androgenic steroid use is associated with left ventricular dysfunction. Circulation: Heart Failure. 2010;3(4):472-476. https://doi.org/10.1161/CIRCHEARTFAILURE.109.931063
- Rasmussen JJ, Schou M, Madsen PL, et al. Increased LV mass and reduced cardiac function in long-term anabolic androgenic steroid users. Circulation. 2017;135(21):1991-2001. https://doi.org/10.1161/CIRCULATIONAHA.116.026903
- Kanayama G, Hudson JI, Pope HG Jr. Long-term psychiatric and medical consequences of anabolic-androgenic steroid abuse. Drug and Alcohol Dependence. 2008;98(1-2):1-12. https://doi.org/10.1016/j.drugalcdep.2008.05.004
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- National Institute on Drug Abuse (NIDA). Anabolic steroids DrugFacts. https://nida.nih.gov/publications/drugfacts/anabolic-steroids
- US Drug Enforcement Administration (DEA). Anabolic steroids. https://www.dea.gov/factsheets/anabolic-steroids
- Achar S, Rostamian A, Narayan SM. Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm. American Journal of Cardiology. 2010;106(6):893-901. https://doi.org/10.1016/j.amjcard.2010.05.013
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