Anabolic Steroids: What They Are, Uses, Side Effects & Risks
An In‑Depth Guide to Anabolic Steroids
(Prepared for healthcare professionals, coaches, students, and anyone looking to understand the science, risks, and legal aspects of anabolic steroids)
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1. What Are Anabolic (Anabolic–Androgenic) Steroids?
Term Definition
Anabolic Promotes cell growth & protein synthesis → muscle building, bone density, etc.
Androgenic Mimics the effects of natural male sex hormone testosterone (e.g., libido, body hair).
Steroid Lipid‑based molecules derived from cholesterol that act as hormones.
Key Points
They are synthetic derivatives of testosterone or other endogenous steroids.
Commonly used medically for: delayed puberty, muscle wasting, anemia, certain immunodeficiencies, and hormone replacement therapy.
Popular in sports/bodybuilding for performance enhancement & physique improvement.
2. Primary Hormones Involved
Hormone Source Role Effect of Exogenous Administration
Testosterone Leydig cells (testes), adrenal cortex, ovaries (small amounts) Main male sex hormone; regulates libido, spermatogenesis, muscle mass, bone density ↑ Muscle growth, strength, red blood cell production. Can suppress natural LH/FSH → ↓ endogenous testosterone
LH (Luteinizing Hormone) Anterior pituitary Stimulates Leydig cells to produce testosterone Inhibited by high exogenous testosterone; leads to decreased LH levels
FSH (Follicle-stimulating hormone) Anterior pituitary Stimulates Sertoli cells for spermatogenesis Suppressed when endogenous testosterone low
Testosterone (Esterified forms: Testosterone enanthate, cypionate, etc.) Anabolic steroid Increases protein synthesis, nitrogen retention → muscle growth High doses can lead to gynecomastia due to aromatization into estrogen
Aromatase Enzyme converting testosterone to estradiol Overexpression leads to increased estrogen, causing breast tissue growth Aromatase inhibitors (ex: anastrozole) used to reduce estrogen production
Key Takeaways
Suppression of the HPG axis: Administering external testosterone reduces endogenous LH and FSH due to negative feedback, leading to decreased testicular function.
Gynecomastia mechanism: Aromatase converts excess testosterone into estradiol. If aromatase activity is high or if testosterone dose is very high, estrogen can dominate causing breast tissue proliferation.
Therapeutic interventions: Use of anti-estrogens (tamoxifen) or aromatase inhibitors can help manage gynecomastia in patients requiring testosterone therapy.
References
Baker et al., "Testosterone Therapy and Gynecomastia." J Clin Endocrinol Metab 2022; 107(3): 987–993.
Smith & Jones, "Mechanisms of Testosterone-Induced Breast Development." Horm Res Paediatr 2019; 92: 1‑8.
World Health Organization (WHO), International Classification of Diseases (ICD‑11), Chapter 10 – Endocrine disorders, 2022 update.
(Note: The above references are illustrative; actual literature should be consulted for clinical decision-making.)
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