Finasteride
Finasteride is a medication for pattern hair loss. It is technically an antiandrogen, but it is not a testosterone blocker.
Pattern hair loss is caused mainly by dihydrotestosterone (DHT): a hormone that is produced in the body from testosterone, and is more masculinizing than testosterone itself. Where other antiandrogens block both DHT and testosterone, finasteride only selectively blocks the production of DHT, without blocking testosterone. (Steiner, 1993).
In transfeminine people, finasteride is widely inappropriately prescribed as a testosterone blocker, with several large trans healthcare providers incorrectly claiming that the drug lowers testosterone (example; example). In reality, finasteride slightly increases testosterone levels. (Steiner, 1993; Rittmaster, 1994; Libecco & Bergfeld, 2004; Leinung, Feustel, & Joseph, 2018).
While finasteride could nonetheless be beneficial in some cases (for example, as hair loss prevention before beginning hormone therapy), in general, its effects on DHT can be achieved by simply lowering testosterone levels instead, and for this reason researchers have questioned the drug’s usefulness in feminizing hormone therapy. (Irwig, 2021).
In transmasculine people, finasteride is sometimes used to prevent pattern hair loss while taking testosterone (Moreno-Arrones, Becerra, & Vano-Galvan, 2017).
Key points
- Like other antiandrogens, blocks DHT to prevent male pattern baldness
- Unlike other antiandrogens, does not block testosterone
- Often inappropriately used in transfeminine people with the intention of blocking testosterone
- Maximally effective at a dose of 1 mg
Dosing
Finasteride is a pill that is swallowed. Trans people most commonly take it at a dose of 1 mg or 5 mg once daily. Dosages above 1 mg daily are not any more effective for pattern hair loss, and may increase the risk of side effects with no benefit. (Libecco & Bergfeld, 2004; Shapiro & Kaufman, 2003).
Risks & management
Finasteride may have a very small risk of causing negative sexual, psychological, and neurological effects that persist even after stopping the drug. These are sometimes referred to as post-finasteride syndrome.
Interactions
Finasteride has minimal interactions with other drugs. (Sudduth & Koronkowski, 1993)
Other information
Finasteride is also called "F-Pecia", "Finalo", "Finast", "Finax", "Fincar", "Finpecia", "Finstide", "Harifin", "Healpecia", "Penester", "Propecia", "Proscalpin", "Proscar", "Prosteride", "Ricit", or simply "fin".
See also
References
- Irwig M. S. (2021). Is there a role for 5α-reductase inhibitors in transgender individuals?. Andrology, 9(6), 1729–1731. [DOI:10.1111/andr.12881]
- Leinung, M. C., Feustel, P. J., & Joseph, J. (2018). Hormonal Treatment of Transgender Women with Oral Estradiol. Transgender health, 3(1), 74–81. [DOI:10.1089/trgh.2017.0035]
- Libecco, J. F., & Bergfeld, W. F. (2004). Finasteride in the treatment of alopecia. Expert opinion on pharmacotherapy, 5(4), 933–940. [DOI:10.1517/14656566.5.4.933]
- Moreno-Arrones, O. M., Becerra, A., & Vano-Galvan, S. (2017). Therapeutic experience with oral finasteride for androgenetic alopecia in female-to-male transgender patients. Clinical and experimental dermatology, 42(7), 743–748. [DOI:10.1111/ced.13184]
- Rittmaster R. S. (1994). Finasteride. The New England journal of medicine, 330(2), 120–125. [DOI:10.1056/NEJM199401133300208]
- Shapiro, J., & Kaufman, K. D. (2003). Use of finasteride in the treatment of men with androgenetic alopecia (male pattern hair loss). The journal of investigative dermatology. Symposium proceedings, 8(1), 20–23. [DOI:10.1046/j.1523-1747.2003.12167.x]
- Steiner J. F. (1996). Clinical pharmacokinetics and pharmacodynamics of finasteride. Clinical pharmacokinetics, 30(1), 16–27. [DOI:10.2165/00003088-199630010-00002]
- Sudduth, S. L., & Koronkowski, M. J. (1993). Finasteride: the first 5 alpha-reductase inhibitor. Pharmacotherapy, 13(4), 309–329. [DOI:10.1002/j.1875-9114.1993.tb02739.x]