Androgens and Anabolic Steroids
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Direct answer
Replacement testosterone aims to reproduce physiological levels: injectable enanthate or cypionate 200 mg intramuscularly every two weeks, transdermal gel 5 g (50 mg) daily, or oral testosterone undecanoate 40 mg two to three times daily with a fatty meal (extensive first-pass lymphatic absorption). Aromatisation to oestradiol explains gynaecomastia, and 5-alpha reduction to dihydrotestosterone drives prostate and skin effects — the two pathways organising most adverse reactions: erythrocytosis, HDL-cholesterol fall, acne, lipid worsening, and hypothalamic-pituitary suppression with testicular atrophy and azoospermia. Anabolic steroids — 17-alpha-alkylated derivatives like stanozolol — add hepatotoxicity and are misused for bodybuilding. The therapeutic mirror-image is the antiandrogen group: receptor blockers (flutamide, bicalutamide, enzalutamide), synthesis inhibitors, 5-alpha-reductase inhibitors (finasteride, dutasteride), and steroidogenic antagonists (spironolactone, cyproterone).
What you must remember
- Preparation logic: esters lengthen the injection interval (undecanoate in castor oil can go 10-14 weeks); transdermal gel mimics diurnal physiology but risks partner transfer; oral undecanoate needs fat co-ingestion.
- Two activation pathways: aromatase yields oestradiol (gynaecomastia, bone benefit in men), 5-alpha reductase yields DHT (prostatic growth, androgenetic alopecia) — DHT itself cannot aromatise.
- Dose anchors: testosterone enanthate 200 mg IM every 2 weeks (or 100 mg weekly for smoother levels); gel 50 mg applied to shoulders; undecanoate 40 mg BD-TDS orally.
- Adverse-effect cascade: HPG axis suppression (LH/FSH fall, testicular atrophy, infertility), erythrocytosis (check haematocrit), HDL reduction, oedema, sleep apnoea worsening, and stimulation of androgen-dependent carcinoma.
- 17-alpha-alkylated steroids: stanozolol, methyltestosterone — cholestatic jaundice, peliosis hepatis, hepatocellular adenoma; the alkyl group that survives first-pass metabolism is the culprit.
- Antiandrogens by site: receptor blockers bicalutamide/flutamide (prostate cancer, combined with castration), finasteride 1 mg for alopecia and 5 mg for benign prostatic hyperplasia, spironolactone (receptor blocker plus synthesis inhibitor) for hirsutism, cyproterone for precocious puberty and hypersexuality.
- Flutamide monotherapy paradox: giving an androgen blocker alone can raise testosterone via LH surge — combine with a GnRH analogue or surgical castration for prostate cancer.
- WADA relevance: all anabolic steroids are prohibited at all times in sport; testicular atrophy plus a high haematocrit in a gym-going young man is the clinical tell.
A clinic conversation that carries the whole topic
A 55-year-old with fatigue, low libido and morning testosterone of 180 ng/dL (confirmed twice) opts for gel. At review, symptoms have lifted but haematocrit has crossed 54 percent — dose reduction, not discontinuation, is the first move, and venesection if it exceeds 56. His brother, on the other hand, is a 26-year-old bodybuilder using an injectable "cycle" bought in a gym: shrunken testes, tender gynaecomastia and jaundiced sclerae summarise both pathways plus the alkylated oral in his stack; sperm count will take six to twelve months to recover after cessation. Their father, 78, takes finasteride 5 mg for prostatism and asks why his PSA fell by half — 5-alpha-reductase inhibition shrinks the gland and halves PSA independent of cancer, so the threshold for biopsy doubles. Three generations, one receptor family: replacement physiology, abuse toxicology, and therapeutic antagonism.
Where students slip
The classic slip is treating testosterone as the direct androgen at every tissue; in the prostate, skin and hair follicle it is a prohormone, converted by 5-alpha-reductase to the more potent DHT — which is exactly why finasteride shrinks prostates without abolishing libido. Second, candidates forget that DHT and the 5-alpha-reduced androgens cannot aromatise, so pure DHT-like anabolics cause less gynaecomastia but full androgenic skin effects. Third, the infertility point deserves emphasis in the Indian context where parenthood expectations are high: exogenous testosterone suppresses spermatogenesis and is contraindicated in men seeking fertility, for whom the correct drug is human chorionic gonadotropin or clomiphene.
Frequently asked questions
Why does testosterone cause gynaecomastia?
Peripheral aromatase converts a fraction of the dose to oestradiol, which stimulates breast tissue — dose-related and more obvious with high injectable peaks.
Which testosterone preparations spare the liver, and which damage it?
Esters given intramuscularly and transdermal gels bypass first-pass metabolism and are not hepatotoxic; 17-alpha-alkylated oral steroids cause cholestatic injury and hepatic tumours.
How does finasteride differ from bicalutamide pharmacologically?
Finasteride inhibits 5-alpha-reductase, reducing DHT formation inside the prostate, while bicalutamide blocks the androgen receptor itself and is reserved for prostate cancer therapy.
Why is exogenous testosterone a poor choice in a man desiring fertility?
It suppresses LH and FSH, shutting down intratesticular testosterone and spermatogenesis, producing azoospermia that may take months to reverse.
What pattern suggests anabolic steroid misuse in a young man?
Rapid muscle gain with testicular atrophy, gynaecomastia, severe acne, raised haematocrit and low HDL cholesterol, plus striae and injection-site marks.