Glossary

5

• 5α-Reductase The enzyme that converts testosterone to DHT. Two isoforms, three target tissues, and the pharmacological target of finasteride and dutasteride.

A

• Anabolic:Androgenic Ratio A 1950s–60s classification derived from the Hershberger rat bioassay. Abandoned by modern pharmacology for good reasons.
• Anastrozole A competitive reversible aromatase inhibitor. The first-line AI for on-cycle E2 management. Steep dose-response — over-dosing crashes E2 reliably.
• Aromatization CYP19A1-catalysed conversion of androgens to estrogens. The single biggest driver of on-cycle side-effect management.

B

• Bioavailability The fraction of administered compound reaching systemic circulation in active form. A pharmacokinetic variable, not a dose-conversion factor.

C

• Cabergoline A long-acting D2 dopamine receptor agonist. The standard pharmacological intervention for hyperprolactinaemia on 19-nor cycles.
• Clomiphene A SERM with antagonist activity at hypothalamic estrogen receptors. Effective for HPTA recovery but carries the zuclomifene isomer issue producing "clomid fog."

D

• DHT Dihydrotestosterone. The 5α-reduced metabolite of testosterone — more potent than the parent at the androgen receptor, dominant at scalp and prostate.
• Dutasteride A dual Type I and Type II 5α-reductase inhibitor. Reduces serum DHT by ~95% versus finasteride's ~70%. More complete protection at proportional side-effect risk.

E

• Erythrocytosis Pathological elevation of red blood cell mass producing hyperviscosity. The dominant cardiovascular biomarker on TRT and AAS protocols.
• Ester A fatty-acid chain esterified to the 17β-hydroxyl of a steroid. Controls depot-release kinetics, half-life, and detection window.
• Estradiol The dominant estrogen in human physiology. Aromatised from testosterone via CYP19A1. Essential for male bone, joint, libido, and cardiovascular function.
• Exemestane A steroidal suicide aromatase inhibitor. Irreversible enzyme inactivation eliminates the rebound elevation pattern characteristic of anastrozole and letrozole.

F

• Finasteride A Type II selective 5α-reductase inhibitor. Reduces serum DHT by ~70% via blockade of testosterone-to-DHT conversion. The standard pharmacological intervention for androgenic alopecia.
• FSH Follicle-Stimulating Hormone. The pituitary gonadotropin driving Sertoli-cell function and spermatogenesis. Recovers slower than LH post-cycle.

G

• GnRH Gonadotropin-Releasing Hormone. The hypothalamic peptide that drives pulsatile pituitary secretion of LH and FSH. Pulse frequency, not amplitude, encodes the signal.

H

• Half-life The interval over which serum concentration of a compound falls by 50%. Drives injection frequency, cycle-tail kinetics, and PCT timing.
• HCG Human Chorionic Gonadotropin. A placental glycoprotein hormone structurally homologous to LH. Used as on-cycle Leydig preservation, pre-PCT bridge, or post-cycle salvage.
• Hepatotoxicity Hepatocyte injury or cholestatic dysfunction from a xenobiotic. In AAS the concern concentrates on 17α-alkylated orals.
• HPTA Hypothalamic–Pituitary–Testicular Axis. The negative-feedback loop that runs endogenous testosterone. Shut down by every AAS cycle.

I

• Iatrogenic Hypoestrogenaemia The clinical syndrome of crashed estradiol from over-aggressive AI dosing. Arthralgia, libido loss, lipid degradation, mood depression, accelerated bone resorption.

L

• Letrozole A high-potency competitive aromatase inhibitor. Reserved for established gynaecomastia regression rather than routine on-cycle E2 management.
• LH Luteinizing Hormone. The pituitary gonadotropin that drives Leydig-cell testosterone synthesis. Suppressed within 14 days of any AAS protocol.

N

• NAC N-acetylcysteine. Synthetic L-cysteine precursor that replenishes hepatic glutathione consumed by alkylated-oral metabolism. The standard antidote in acetaminophen overdose.

P

• PCT Post-Cycle Therapy — a pharmacological protocol targeting HPTA restart. SERM, hCG, or both, timed to ester clearance.
• Prolactin Anterior pituitary hormone regulated by dopamine. Elevated by 19-nor compounds and GH/peptide protocols. Threshold for cabergoline intervention.

R

• Receptor Binding Affinity The Ki or IC50 measuring how tightly a ligand occupies its target receptor. For AAS the target is AR. Binding is necessary but not sufficient.

S

• SHBG Sex Hormone Binding Globulin. A liver-synthesised β-globulin that binds circulating testosterone and regulates its bioavailable fraction.

T

• Tamoxifen A SERM with antagonist activity at hypothalamic and breast-tissue estrogen receptors. The first-line PCT compound and gynaecomastia treatment without isomer issues.
• TUDCA Tauroursodeoxycholic acid. Taurine conjugate of UDCA prescribed for cholestatic liver disease; the evidence-based hepatoprotectant during oral AAS use.