Anabolic-androgenic steroids (AAS) used at supraphysiologic doses for performance or physique purposes carry documented health risks that differ from the risks of testosterone replacement therapy in hypogonadal men. The distinction matters because they involve different doses (often 5-20 times therapeutic), different compounds (testosterone plus nandrolone, trenbolone, stanozolol, and others not used in medicine), and different populations (typically younger, healthier men without a diagnosed deficiency).
This article covers what the clinical research documents about AAS use in the context of non-medical bodybuilding and athletic performance use.
Cardiovascular Effects
The cardiovascular risk from AAS use is the most extensively documented and clinically significant concern.
Left ventricular hypertrophy (LVH): Supraphysiologic androgens directly stimulate cardiac muscle growth. Unlike athlete’s heart, the physiological LVH from endurance training, which involves both chambers and maintains normal geometry, AAS-induced LVH is typically concentric (walls thicken without commensurate chamber enlargement), reducing cardiac efficiency and increasing the risk of arrhythmia.
A 2016 study in Circulation compared cardiac function in long-term AAS users, non-using weightlifters, and sedentary controls. AAS users had left ventricular wall thickness 50% greater than non-using weightlifters at similar training volumes, with reduced diastolic function. Diastolic dysfunction reduces the heart’s ability to relax and fill between beats, an early marker of heart failure risk.
Dyslipidemia: Most AAS, particularly oral 17-alpha alkylated compounds (stanozolol, oxandrolone, oxymetholone), substantially reduce HDL cholesterol (sometimes by 40-70%) and raise LDL. Injectable testosterone produces smaller lipid changes at therapeutic doses but more pronounced changes at supraphysiologic doses.
Coronary artery disease: Case reports and case series document premature atherosclerosis and acute MI in young AAS users. A 2022 study in JAMA Internal Medicine using coronary CTA found that long-term AAS users had significantly greater coronary artery plaque burden than age-matched non-users, even after controlling for other cardiovascular risk factors.
Cardiomyopathy and sudden death: AAS use is associated with dilated cardiomyopathy following cessation, particularly after years of use. Some sudden cardiac death cases in young male athletes have been attributed to AAS-related cardiomyopathy. The exact prevalence is unknown because AAS use is often not disclosed at autopsy or during clinical evaluation.
Hormonal Effects After Cessation
The HPG axis suppression from AAS is more severe than from therapeutic TRT because the doses are higher and the duration often longer.
After stopping AAS, testosterone recovery can take 6-18 months. Some men do not fully recover natural production. This is particularly true for men who used high-dose multiple-compound cycles for years, who may be left with permanent secondary hypogonadism requiring TRT.
The post-cycle syndrome in heavy AAS users, low testosterone, low libido, fatigue, depression, is severe enough that many users return to AAS to escape it rather than waiting for natural recovery. Post-cycle therapy protocols (clomiphene, tamoxifen, sometimes HCG) reduce recovery time but do not guarantee full recovery.
Hepatotoxicity
Oral 17-alpha alkylated steroids are hepatotoxic. The 17-AA modification that allows oral bioavailability also impairs hepatic metabolism. Elevated liver enzymes, peliosis hepatis (blood-filled cysts in the liver), hepatic adenoma, and in rare cases hepatocellular carcinoma have been documented in oral AAS users.
Injectable testosterone and most injectable AAS are not 17-AA modified and do not carry the same hepatotoxic risk.
Psychological Effects
Aggression: The relationship between AAS and aggression is real but variable. Not all AAS users experience increased aggression, and the effect depends on compound, dose, individual susceptibility, and context. Controlled trials that administer testosterone at supraphysiologic levels show increased irritability and aggression-related behaviors in a subset of participants.
Dependence: AAS produce psychological dependence in a substantial proportion of long-term users. The dependence is maintained by multiple mechanisms: performance improvements, body image concerns about loss of muscle, avoidance of the hormonal crash after stopping, and, for some users, direct mood effects from the drugs.
Hypomania and depression: The period of active AAS use can produce hypomania in some users, elevated mood, increased energy, reduced need for sleep. Post-cycle periods or after cessation are characterized by depression driven by hypogonadal state and withdrawal from the direct neurological effects.
What This Means for Men Considering AAS
The risks documented here are not primarily from therapeutic doses of testosterone for diagnosed hypogonadism, they are from the doses and compounds used in non-medical athletic and bodybuilding contexts. The clinical distinction between medical TRT and non-medical AAS use should inform any conversation about testosterone.
For therapeutic testosterone use in diagnosed hypogonadism, see TRT Side Effects: What the Research Actually Shows.
