Why Finasteride Causes Decreased Libido
Finasteride causes decreased libido by inhibiting 5-alpha-reductase enzyme, which blocks the conversion of testosterone to dihydrotestosterone (DHT), and while DHT's primary role is in prostate and hair follicle tissue, the reduction in DHT levels appears to affect sexual function through mechanisms that remain incompletely understood. 1, 2
Mechanism of Action and Hormonal Effects
Finasteride selectively inhibits the type II isoenzyme of 5-alpha-reductase, reducing serum DHT levels by approximately 70% and prostatic tissue DHT by approximately 80%. 1, 3
This DHT suppression occurs rapidly after a single dose and persists for up to 4 days, longer than expected from the drug's elimination half-life, due to finasteride's high affinity for the 5-alpha-reductase enzyme. 3
Serum testosterone levels actually increase in patients receiving finasteride as a compensatory response, but these levels typically remain within the normal range. 3, 4
The paradox is that testosterone—not DHT—is considered the primary androgen responsible for central and peripheral modulation of sexual function through humoral endocrine and paracrine effects, yet decreased libido still occurs. 4
Clinical Incidence and Pattern
Decreased libido affects 2-4% more patients than placebo, with absolute rates of 3.4-10% in treatment groups depending on study duration and population. 2
In the first year of therapy, decreased libido occurs in 6.4% of patients, but this rate decreases to 2.6% in years 2-4 of continued treatment. 5
Sexual side effects, including decreased libido, typically diminish over time even while continuing the medication and generally resolve after discontinuation in most patients. 2
The magnitude of sexual dysfunction is clinically modest: finasteride causes a mean difference of only 3.21 points on a 0-100 scale compared to 1.26 points for each year of aging—roughly equivalent to 2.5 years of natural aging. 2, 6
Unresolved Mechanistic Questions
The exact mechanism by which DHT reduction leads to decreased libido remains unclear, particularly given that testosterone (which increases with finasteride) is the primary androgen for sexual function. 4
DHT does potentiate the effect of testosterone on erectile function, suggesting that even though DHT is not the primary driver, it plays a modulatory role in sexual function that extends beyond its local tissue effects. 7
The fact that sexual side effects persist in a small subset of patients even after discontinuation (post-finasteride syndrome) suggests potential neurosteroid effects or other mechanisms beyond simple DHT suppression, though this remains controversial and poorly defined. 1, 2
Important Clinical Context
Discontinuation rates due to adverse events are 6-7% in both finasteride and placebo groups, indicating that many reported sexual side effects may not be directly drug-related and could reflect the natural prevalence of sexual dysfunction in the population. 2, 6
The nocebo effect likely contributes to reported sexual dysfunction, as awareness of potential side effects can influence their occurrence. 4
Age and comorbidities are major confounders—baseline sexual dysfunction is common in BPH populations, with 46% of men in the PLESS study having pre-existing sexual dysfunction at screening. 2
FDA-Recognized Persistent Effects
The FDA amended finasteride labels to warn about sexual dysfunction that continued after discontinuation of treatment, including decreased libido, though this is based on postmarketing reports rather than prospective trials. 2, 8
These persistent symptoms were reported rarely and occurred in men taking concomitant medications and/or with comorbidities, making the independent role of finasteride uncertain. 8