Finasteride
| Finasteride | |
|---|---|
 | |
| Formula | C23H36N2O2 |
| Class | |
| Administration | Oral |
| Solubility | |
| Legal status | Prescription only |
| Brand names | Propecia (1 mg, hair loss), Proscar (5 mg, BPH) |
| Bioavailability | ~65% |
| Recommended dose | |
| Upper limit | |
| LD50 | |
| Ray's verdict | Not commented on directly by Peat; Danny Roddy (Peat-adjacent author) argues it works by mimicking progesterone, not by simple "anti-male-hormone" action, and documents serious persistent side effects |
Finasteride is a type-II 5-alpha-reductase inhibitor that lowers DHT (dihydrotestosterone) by roughly 70% within 24 hours of a standard 1 mg dose.[1] It is FDA-approved for male-pattern baldness (Propecia) and benign prostatic hyperplasia (Proscar).
Effectiveness and the androgen theory's problem
[edit]Finasteride regrows or preserves hair in only about 40% of users, despite reliably lowering DHT in nearly all of them, a mismatch Roddy argues undercuts the simple story that DHT alone causes pattern baldness.[1] He also notes younger men respond better than older men, and that finasteride can arrest hair loss in some women with normal androgen levels, both of which fit poorly with a pure anti-androgen mechanism.[1]
Roddy's alternative reading is that finasteride is chemically similar to progesterone and may work partly through progesterone-like effects rather than DHT suppression alone — consistent with finasteride's feminizing side effects (see below) and with pregnancy's high progesterone state often producing thicker hair.[1]
Side effects
[edit]Finasteride's side effects are well documented and can persist after stopping the drug:
- Gynecomastia[2]
- Depression[3]
- Persistent sexual dysfunction and, in a subset of former users, suicidal ideation[4]
An independent study of 72 users found 94% developed low libido, 92% erectile dysfunction, 92% decreased arousal, and 69% orgasm problems.[5] Merck's own updated label now warns that sexual dysfunction "continued after discontinuation of treatment."[1]
In rats, dosing finasteride from late gestation through the first days after birth (blocking the 5-alpha-reductase-2 enzyme during the developmental window that normally masculinizes the brain) left adult males' ordinary mating behavior intact, but when those males were subsequently given estradiol, 53% displayed same-sex mounting behavior versus controls, evidence of incomplete brain defeminization from disrupting perinatal androgen signaling.[6]
See also
[edit]References
[edit]- ↑ 1.0 1.1 1.2 1.3 1.4 Danny Roddy, Hair Like a Fox (2013), citing Vermeulen A, et al., "Hormonal effects of a 5 alpha-reductase inhibitor (finasteride) on hormonal levels in normal men and in patients with benign prostatic hyperplasia," Eur Urol. 1991;20 Suppl 1:82-6.
- ↑ Ramot Y, et al. "Finasteride induced Gynecomastia: Case report and Review of the Literature," Int J Trichol. 2009;1(1):27-29.
- ↑ Rahimi-Ardabili B, et al. "Finasteride induced depression: a prospective study," BMC Clin Pharmacol. 2006;6:7.
- ↑ Irwig MS. "Depressive symptoms and suicidal thoughts among former users of finasteride with persistent sexual side effects," J Clin Psychiatry. 2012;73(9):1220-3.
- ↑ Irwig MS, Kolukula S. "Persistent sexual side effects of finasteride for male pattern hair loss," J Sex Med. 2011;8(6):1747-53.
- ↑ Ribeiro CM, Pereira OC. "5alpha-reductase 2 inhibition impairs brain defeminization of male rats: reproductive aspects," Pharmacol Biochem Behav. 2005;82(1):90-97. doi:10.1016/j.pbb.2005.08.015. PMID 16168471.