Anabolic Androgenic Steroids (AAS) are synthetic derivatives of the male hormone testosterone, misused primarily for rapid increases in muscle mass and strength. While the term “steroids” is often used broadly, the discussion surrounding premature death centers almost entirely on AAS. The physiological changes induced by the non-medical use of these substances are profound and systemic, often leading to irreversible damage in major organ systems. This article clarifies the specific mechanisms and presents the clinical evidence that links AAS use directly to an increased risk of premature mortality.
Clarifying the Terminology
The word “steroid” describes a large class of organic compounds, which can cause confusion regarding health risks. Anabolic Androgenic Steroids (AAS) are distinct from corticosteroids, which include medications like prednisone or hydrocortisone. Corticosteroids mimic the body’s natural cortisol, reducing inflammation and suppressing the immune system, and are widely prescribed for conditions such as asthma and autoimmune disorders. AAS, however, are synthetic analogs of testosterone that bind primarily to androgen receptors. The “anabolic” effect promotes tissue growth, while the “androgenic” effect enhances male characteristics. This article focuses exclusively on the non-medical use of AAS in supraphysiological doses.
Cardiovascular System Damage
Damage to the heart and circulatory system represents the most significant threat to the lifespan of an AAS user. These substances cause adverse cardiac remodeling, leading to the thickening of the heart muscle, known as left ventricular hypertrophy (LVH). This thickening reduces the volume of the heart’s pumping chambers, making the muscle less efficient and leading to an anabolic steroid-induced cardiomyopathy.
AAS use also profoundly alters the body’s lipid profile, causing dyslipidemia. This involves a dramatic decrease in high-density lipoprotein (HDL) and an increase in low-density lipoprotein (LDL). This adverse shift contributes to accelerated atherosclerosis, the hardening and narrowing of arteries due to plaque buildup. Atherosclerosis increases the risk of coronary artery disease and myocardial infarction (heart attack).
AAS also contribute to systemic hypertension (elevated blood pressure) by affecting fluid balance and vascular tone. High blood pressure places chronic strain on the arterial walls, accelerating plaque formation and increasing the risk of stroke. Furthermore, AAS can increase red blood cell production (polycythemia), which thickens the blood and raises the risk of dangerous clotting events like thrombosis. These combined effects set the stage for premature cardiac failure or sudden cardiac death.
Secondary Organ Toxicity and Systemic Failure
Beyond the heart, AAS misuse places severe strain on other major organ systems, contributing to long-term systemic failure. The liver is particularly vulnerable, especially with the use of oral AAS formulations. These are linked to cholestasis, which impairs bile flow. More serious consequences include the formation of blood-filled cysts known as peliosis hepatis and an increased risk of hepatic tumors.
The kidneys also suffer damage, often indirectly through severe hypertension and direct toxicological effects. High blood pressure damages the delicate filtering units within the kidney, while AAS use can directly induce glomerular cell injury. This damage can progress to conditions like focal segmental glomerulosclerosis, leading to protein leakage and ultimately chronic kidney failure.
Systemic fragility is compounded by the suppression of the body’s natural hormone production, known as the hypothalamic-pituitary-testicular axis (HPTA). Introducing high doses of external testosterone signals the body to stop producing its own, leading to testicular atrophy and hypogonadism. The long-term disruption of this axis destabilizes the entire endocrine system, impacting bone density, mood regulation, and overall metabolic health.
Evidence of Increased Mortality Risk
Epidemiological studies have directly addressed the relationship between AAS use and premature death, confirming a statistically significant increase in mortality risk. One large Danish observational study tracked a cohort of young male AAS users over a mean follow-up period of 11 years. The study found that AAS users had a hazard ratio (HR) of 2.8 for all-cause mortality compared to matched non-users in the general population.
The increased death rate was categorized into both natural and unnatural causes. Mortality from natural causes, primarily driven by cardiovascular events and cancer, was found to have an HR of 2.2. However, the risk of unnatural death, which includes accidents, violent crimes, and suicide, was even higher, with an HR of 3.6.
This suggests that the behavioral side effects of AAS, such as severe mood swings, aggression, and psychological distress, significantly contribute to the overall premature death toll alongside physical organ damage. These findings underscore a quantifiable and substantially elevated risk of premature mortality from multiple pathways.