Finasteride

Finasteride (Propecia, Proscar) is a synthetic 4-azasteroid that selectively inhibits the Type II isoform of 5α-reductase (SRD5A2). The enzyme blockade reduces conversion of testosterone to dihydrotestosterone (DHT) in scalp follicles, prostate, and other Type II-expressing tissues. The compound is the standard pharmacological intervention for androgenic alopecia and benign prostatic hyperplasia.

Mechanism — selective Type II 5α-reductase inhibition:

5α-reductase exists in two isoforms with distinct tissue distributions. Type I (SRD5A1) is expressed in skin, liver, and brain. Type II (SRD5A2) is expressed in prostate, scalp follicles, seminal vesicles, and reproductive tract — the dominant isoform driving scalp DHT conversion.

Finasteride binds Type II 5α-reductase with high affinity and minimal Type I activity. At standard 1 mg/day dose: serum DHT reduction approximately 70%, scalp DHT reduction 60–70%. At 5 mg/day (the BPH indication dose): serum DHT reduction approximately 90%, with marginal additional scalp benefit.

Clinical evidence base for androgenic alopecia:

The foundational efficacy trials are Kaufman et al. 1998, J Am Acad Dermatol — finasteride 1 mg/day demonstrated statistically significant hair retention and modest regrowth versus placebo across 2-year follow-up in men with vertex hair loss. Effect maintained as long as dosing continues; discontinuation produces loss of accumulated benefit within 6–12 months as DHT exposure resumes.

Dosing protocol:

– Standard hair loss: 1 mg/day, oral, with or without food
– Lower-dose alternative: 0.5 mg/day produces approximately 75% of the efficacy with proportionally lower side-effect incidence (Drake et al. 1999, J Am Acad Dermatol)
– BPH indication: 5 mg/day (oncology dose, not used for hair loss alone)
– Cycle harm-reduction: start 2 weeks before AAS cycle initiation through PCT completion to saturate the inhibitor before androgen exposure begins

The mechanism limitation on AAS protocols:

Finasteride does not protect against compounds that ARE DHT-derivatives or that bypass 5α-reductase. The inhibitor acts on the conversion step; if no conversion is required for scalp AR binding, the inhibitor is irrelevant.

Compounds where finasteride is pharmacologically irrelevant:

– Trenbolone: 19-nor 5α-reduced compound that binds AR directly with ~5× testosterone affinity. Finasteride does not affect trenbolone scalp action.
– Drostanolone (Masteron): DHT derivative; binds scalp AR directly.
– Stanozolol (Winstrol): DHT derivative; binds scalp AR directly.
– Oxandrolone (Anavar): DHT derivative; same mechanism limitation.
– Methenolone (Primobolan): DHT derivative; same.

For cycles dominated by these compounds, finasteride does not reduce scalp risk and pharmacological hair-protection options narrow to topical interventions (minoxidil, ketoconazole shampoo) and acceptance of the genetic risk.

The nandrolone exception — finasteride is contraindicated:

Nandrolone is reduced by 5α-reductase to dihydronandrolone (DHN) — a weaker androgen than DHT. Blocking the conversion with finasteride leaves the parent nandrolone available for AR binding at scalp tissue, paradoxically worsening rather than improving scalp risk. Toorians et al. 1996, J Clin Endocrinol Metab documented the mechanism. Avoid finasteride during nandrolone protocols.

Side-effect profile:

– Sexual side effects: libido reduction, erectile dysfunction, ejaculate volume reduction documented in 2–8% of users in RCT data; higher in user-reported surveys. Mechanism includes both DHT-deficiency effects and disruption of the 5α-reductase pathway producing allopregnanolone (a positive GABA-A modulator with anxiolytic effects).
– Mood effects: depression, anxiety reported in some users via central neurosteroid pathway disruption.
– Post-finasteride syndrome (PFS): persistent symptoms after cessation documented in the medical literature but uncommon. Most side effects resolve within weeks of discontinuation.
– Gynaecomastia: rare but documented; mechanism involves slight estrogen-DHT ratio shift.
– PSA suppression: finasteride reduces serum PSA by approximately 50%; bloodwork interpretation requires correction (multiply measured PSA by 2 for prostate cancer screening assessment).

Practical recommendation:

Start at 0.5 mg/day for 2–4 weeks to establish tolerance, escalate to 1 mg/day if no significant side effects. Discontinue immediately if persistent libido or mood effects develop. Topical formulations (compounded 0.25% finasteride in alcohol/propylene glycol) are an alternative for users who experience oral side effects but want continued protection — research evidence is improving but inconsistent versus oral.