Benign prostatic hyperplasia is a non-cancerous enlargement of the prostate that compresses the urethra, causing frequency, nocturia and a weak stream.Benign prostatic hyperplasia (BPH) is non-cancerous enlargement of the prostate transition zone. ~50% by age 50, ~90% by 80 have histological BPH. The enlarged gland compresses the urethra, causing frequency, urgency, nocturia, weak stream — not cancer, but QoL-impacting.
2 · DHT · fuel for the prostate
In the prostate, 5α-reductase converts testosterone into dihydrotestosterone (DHT), which binds the androgen receptor more tightly and strongly drives prostate growth.Testosterone is converted in the prostate by 5α-reductase (mainly type 2 isoenzyme) to dihydrotestosterone (DHT). DHT binds the androgen receptor with 3-10x the affinity of T and dissociates much slower — a potent driver of prostate growth. This is the target of finasteride/dutasteride: inhibit 5α-reductase, DHT drops 70-90%, prostate shrinks 20-30%.
3 · Saw palmetto · what the evidence says
Saw palmetto is the most used botanical for BPH, but high-quality show no difference from placebo.Saw palmetto (Serenoa repens) berry extract is the most used botanical for BPH. Proposed mechanisms: weak 5α-reductase inhibition, anti-estrogenic, anti-inflammatory. But high-quality (CAMUS 2011, n=369; Tacklind 2012 Cochrane) show no difference from placebo. Early positive results came from low-quality trials.
4 · What actually works
α-blockers relax prostate and bladder-neck smooth muscle for relief within days, while 5α-reductase inhibitors shrink the prostate over 3-6 months.α-blockers (tamsulosin, terazosin): relax prostate/bladder neck smooth muscle, rapid relief (days). 5α-reductase inhibitors (finasteride, dutasteride): shrink prostate, 3-6 months, good long-term. PDE5 inhibitors (tadalafil): also improve BPH symptoms. Surgery (TURP, HoLEP): moderate-severe refractory cases.