The Science of Anabolic Steroid Abuse (Auchus)

The Science of Anabolic Steroid Abuse (Auchus)

Academic endocrinology lecture by Dr. Richard J. Auchus (UT Southwestern, Division of Endocrinology & Metabolism) on the science of anabolic-androgenic steroids (AAS). An external clinical/scientific reference — not Justin's protocol. ^[1]

Myths vs Reality

Common medical myths: AAS are used mostly by pro athletes, users die of cancer/liver failure/strokes, it's "not germane to my practice," and they have no place in good medicine. Reality: use is common in the general population (children to businessmen — an entire subculture), AAS are very addicting in specific users, clinicians will encounter users, and androgens play a prominent legitimate role in medicine (HIV, cancer, critical illness, the elderly). ^[1]

Anabolic vs Androgenic

• Anabolic: ability to aid assimilation of nutrients (nitrogen) into tissue.
• Androgenic: masculinizing properties.
• "Weak androgens" are precursors of strong (DHEA, androstenedione); strong = testosterone, dihydrotestosterone.
• The two properties have thus far been inseparable — presumed same mechanism of action. ^[1]

Androgen Metabolism (Enzymes)

Key enzymatic transformations on the steroid nucleus: aromatization (aromatase → estrogens), 5α/5β-reduction (5α/5β-reductases → e.g., DHT), 3α-reduction (3α-HSDs), 17β-dehydrogenation (17β-HSD type II), and 6α/6β-hydroxylation (P450 3A4, etc.). Synthetic derivatives are built by modifying testosterone: 17β-esterification and 17α-alkylation (oral bioavailability), 19-nor modification, A-ring modifications, and 5α-reduction. ^[1]

Target-Organ Physiological Effects

Testosterone and metabolites act on: CNS (↑libido, well-being, aggression, spatial cognition), hypothalamus/pituitary (↓GnRH/LH/FSH; ↑GH), larynx (lowers voice), breast (E₂ ↑size), liver (↓SHBG, HDL), kidney (↑erythropoietin), genitals (↑development, spermatogenesis, erections), prostate (↑size/secretions), skin (↑facial/body hair, sebum), bone (↑BMD), muscle (↑lean mass, strength), adipose (↑lipolysis, ↓abdominal fat), blood (↑hematocrit), immune system (↓autoantibody production). ^[1]

Prevalence & User Dichotomies

Prevalence: high school 3–12% M / 0–4% F (30% nonathletes); college athletes 2–30% M / 2–10% F (football, track & field); professional/elite estimated 30–100%, highest in powerlifters and bodybuilders. Two major dichotomies: professional vs recreational (different goals/drug-testing fear; escalation greater in non-professionals) and male vs female (men across all sports, greater in power sports; women more restricted — bodybuilders, track & field, sprint swimmers — but usage gaining in other sports and youth). ^[1]

Source Note

External academic reference (Auchus, UT Southwestern). Distilled from the lecture's science slides (myths/reality, anabolic-vs-androgenic, metabolism enzymes, target-organ effects, prevalence). Later slides cover side-effect severity, detection technology, and precursor metabolism. Use as neutral endocrinology grounding; for applied protocols see Justin's own pages.

Cross-References

• ped-protocols-overview
• testosterone-foundation-protocols
• growth-hormone-science