Anabolic-androgenic steroids (AAS) are synthetic compounds that mimic the effects of the male sex hormone testosterone. They are primarily used to increase muscle mass and strength (anabolic effects). For young men in their late teens or early twenties, introducing supraphysiological (above-normal) doses of these potent hormones severely disrupts multiple biological systems. This interference leads to immediate, visible changes and serious, long-term internal damage affecting endocrine, cardiovascular, and psychological health.
Immediate Physical and Developmental Manifestations
A developing body is uniquely vulnerable to excess hormones, leading to rapid and often irreversible physical changes. One serious effect in teenagers is the premature cessation of height increase. Anabolic steroids accelerate the closure of the epiphyseal plates, or growth plates, which are responsible for linear growth. Once these growth plates fuse, no further height can be gained, resulting in permanently stunted stature.
The influx of synthetic hormones quickly triggers noticeable changes in the skin and hair. Severe acne often develops across the face, back, and shoulders due to overstimulation of the sebaceous glands. AAS use can also accelerate male pattern baldness (androgenetic alopecia) in genetically predisposed men. This hair loss occurs because steroids increase the production of dihydrotestosterone (DHT), a potent testosterone metabolite that shrinks hair follicles.
A common side effect is gynecomastia, the development of non-fatty breast tissue. This occurs because the body attempts to manage excessive synthetic testosterone by converting some of it into estrogen through aromatization. The elevated estrogen level stimulates the growth of glandular tissue in the chest. Once formed, this glandular tissue is often permanent and may require surgical removal, even after steroid use has stopped.
Disruptions to the Endocrine System
The most profound internal effect of anabolic steroid use is the suppression of the Hypothalamic-Pituitary-Testicular Axis (HPTA), which controls natural hormone production. The HPTA uses a negative feedback loop to maintain stable testosterone levels. When external steroids are introduced, the hypothalamus and pituitary gland detect the abnormally high levels of circulating androgens.
In response, the brain signals the pituitary to drastically reduce or stop the release of Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH). These gonadotropins signal the testes to produce natural testosterone and sperm. When the pituitary signal is suppressed, the testes become functionally dormant.
The direct consequences of this shutdown lead to hypogonadism. The testes, no longer stimulated to produce hormones, physically shrink (testicular atrophy). Furthermore, the cessation of FSH signaling impairs spermatogenesis, severely reducing the sperm count, often to zero (azoospermia). This dramatically impacts fertility.
While some users initially experience a boosted libido due to high androgen levels, long-term suppression of natural testosterone can lead to erectile dysfunction and decreased sexual interest. Recovery of the HPTA is highly variable, depending on the duration and dosage of steroid use. Recovery can take months to over a year, and some individuals experience persistent hypogonadism requiring ongoing medical intervention.
Systemic Cardiovascular and Hepatic Risks
Anabolic steroid use presents serious, life-threatening risks to major organs, particularly the heart and liver. Cardiovascular damage begins with an adverse alteration of the lipid profile. Steroids profoundly suppress High-Density Lipoprotein (HDL) cholesterol (the “good” cholesterol), often reducing it by 30 to 70%. Simultaneously, many steroids, especially oral compounds, increase Low-Density Lipoprotein (LDL) cholesterol (the “bad” cholesterol) that deposits in vessel walls.
This combination creates a highly atherogenic state, dramatically accelerating atherosclerosis (hardening of the arteries). Anabolic steroids are also strongly associated with hypertension (high blood pressure). Studies show current users have significantly higher average systolic blood pressure compared to non-users, increasing the risk of strokes and heart attacks.
The heart muscle itself is affected, leading to Left Ventricular Hypertrophy (LVH), an abnormal enlargement of the heart’s main pumping chamber. Unlike the healthy enlargement seen in athletes, this steroid-induced remodeling impairs the heart’s ability to relax and fill with blood. This leads to diastolic dysfunction and increases the risk of heart failure and sudden cardiac death. AAS also increase the risk of blood clots (thrombosis) by altering coagulation factors.
The liver is also susceptible to damage, particularly from oral steroid formulations modified to survive initial breakdown. This hepatotoxicity can be severe, with some individuals experiencing Grade III and IV liver toxicity within weeks. Long-term use is associated with hepatic tumors, ranging from benign adenomas to malignant hepatocellular carcinoma. A rarer complication is peliosis hepatis, characterized by blood-filled cysts in the liver parenchyma that can rupture and cause life-threatening internal bleeding.
Psychological and Behavioral Alterations
Supraphysiological doses of androgens flooding the brain trigger significant and unpredictable changes in mood and behavior. During use, many young men report mood disturbances including heightened irritability, hostility, and anxiety. These emotional extremes can swing toward hypomania or mania, characterized by increased energy, grandiosity, and poor judgment.
The most widely recognized behavioral effect is increased aggression and hostility, colloquially termed “Roid Rage.” This can lead to poor impulse control and violent behavior. Although these episodes are often idiosyncratic, elevated androgen levels contribute to an inability to manage stressful situations or perceive social cues accurately.
Many users are driven by an underlying body image disorder, such as muscle dysmorphia, where they perceive themselves as perpetually too small. This distorted self-image fuels the continued use of the drug despite negative consequences, creating a cycle of psychological dependence.
The most dangerous psychological effects occur during the withdrawal phase, or the “post-cycle crash.” This happens when the external steroid source is removed and natural testosterone production remains suppressed. This hormonal crash can lead to severe depressive episodes, intense fatigue, anxiety, and loss of libido. The risk of severe depression and suicidal ideation is elevated during this withdrawal period.