Androgenetic alopecia (AGA) is primarily caused by the hormone dihydrotestosterone (DHT), which leads hair follicles to shrink and produce thinner, shorter hairs until they eventually stop producing hair. Finasteride, a common AGA treatment, blocks the conversion of testosterone to DHT by inhibiting the enzyme 5-alpha-reductase type 2. At a 1 mg/day dose, finasteride reduces serum and scalp DHT by 60-70%.

Originally approved by the US Food and Drug Administration (FDA) in 1992 for treating benign prostatic hyperplasia (BPH), finasteride was later found to be effective in treating AGA in men and now has an FDA indication for this purpose.

Several clinical trials have evaluated finasteride’s efficacy in treating AGA. In one randomized, placebo-controlled trial, 1553 men aged 18-41 with mild-to-moderate AGA were treated with either 1 mg/day of finasteride or a placebo for one to two years. Finasteride significantly increased hair growth and improved hair quality on the vertex scalp compared to the placebo. By month 24, two-thirds of finasteride patients were rated as improved (30% slightly improved, 36% moderately or greatly improved), while only 1% lost hair (compared to a third of placebo patients). However, despite over 80% of patients reporting slowed hair loss, only 50% of finasteride patients reported satisfaction with their hair overall (versus 25% in the placebo group), indicating that it is effective, but not often sufficient alone as a treatment for most men.

Studies have also demonstrated finasteride’s efficacy for frontal/anterior hair loss, although it seems less effective than in the vertex scalp. In another randomized, double-blind, placebo-controlled trial, 326 men with frontal male pattern hair loss were assigned to receive either finasteride 1 mg/day or a placebo for 24 weeks. Finasteride-treated patients (37%) showed a significant increase in frontal scalp hair count and significant improvements in patient, investigator, and global photographic assessments. Efficacy was maintained or improved throughout the second year of the study.

Finasteride also contributes to hair weight (determined by hair length and thickness), as shown in a randomized, placebo-controlled trial over four years. Patients treated with finasteride showed a 21.6% mean increase in hair weight from baseline, compared to a 24.5% mean decrease in placebo-treated men. Over the same period, the finasteride group experienced a 7.2% mean increase in hair count from baseline, compared to a 13% mean decrease in the placebo group.

Additionally, several meta-analyses have evaluated the overall efficacy of finasteride in treating AGA. One such analysis of 12 randomized controlled trials involving 3927 male patients found finasteride significantly increased hair growth and improved hair quality compared to the placebo.

Dutasteride is a potent medication that inhibits DHT production by blocking both types of the enzyme responsible for DHT production (5-alpha-reductase type 1 and type 2). This results in a mean serum reduction in DHT of 93-94%, with a half-life approximately ten times that of finasteride. While fewer clinical trials have evaluated dutasteride’s efficacy in treating AGA, the available evidence suggests it may be more effective than finasteride. Dutasteride is used off-label for AGA treatment.

In a randomized, controlled trial involving 153 men aged 18-49 with AGA, participants were given either 0.5 mg/day of dutasteride or a placebo for six months. After six months, 61.6% of dutasteride-treated men were rated by investigators as having improved vertex scalp hair growth, compared to 20% in the placebo group. Patient self-assessments also favored dutasteride, with 71% reporting improvement versus 36% in the placebo group. The most common adverse effect was sexual dysfunction, experienced by 4% of dutasteride participants and 3% of the control group.

Another study involving 917 men aged 20 to 50 with AGA randomized participants to receive dutasteride (0.02, 0.1, or 0.5 mg/day), finasteride (1 mg/day), or a placebo for 24 weeks. Hair count and width increased dose-dependently with dutasteride, and 0.5 mg/day dutasteride proved superior to both 1 mg/day finasteride and the placebo. Side effects were similar across all groups.

Higher doses of dutasteride (up to 2.5 mg/day) are even more effective, but they come with a significant increase in reported side effects. Consequently, 0.5 mg/day is typically used due to the higher side effect profile at larger doses.