Finasteride
Competitive inhibitor of type II 5-alpha reductase, the enzyme that converts testosterone to dihydrotestosterone (DHT) in prostate, scalp, and liver tissue. Reduces serum DHT by approximately 70% without affecting testosterone levels directly. Does not inhibit type I 5-alpha reductase at clinical doses.
Three tiers ordered by aggressiveness. Tier chips on every OPTIMIZE intervention let you filter the catalog by your evidence tolerance.
- total-testosterone
- free-testosterone
- dhea-s
- estradiol
- psa
- alt
- ast
- pregnancy-exposure
- hepatic-impairment
- pediatric-use
- PMID:9951956The effects of finasteride on scalp skin and serum androgen levels in men with androgenetic alopecia — J Am Acad Dermatol, 1999
- PMID:12639651The influence of finasteride on the development of prostate cancer — N Engl J Med, 2003
- PMID:22789024Adverse effects of 5-alpha reductase inhibitors: a systematic review — J Sex Med, 2012
Finasteride is the compound that forces you to make a trade. 70% DHT reduction preserves hair follicles. DHT is also the androgen driving libido, neurosteroid synthesis, and spatial cognition. The pharmacology is clean. The decision is not. Most men on TRT who add finasteride are managing a side effect of elevated testosterone conversion. The 1mg dose was originally a marketing decision. Merck needed a different dose from the 5mg BPH tablet to justify a separate patent. The 0.25mg dose achieves roughly 60% of the DHT suppression at a fraction of the side effect risk. Dose-response curves matter more than label doses.
This is not medical advice
Discuss with a licensed clinician before starting, stopping, or changing any compound. This page documents what the research literature describes — it is not a prescription.
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