Post Finasteride Syndrome

William Clearfield, D.O., FAAMA, DABMA, FAARFM

Medical Director, Clearfield Family Medicine, Reno, NV; Executive Director, American Osteopathic Society of Rheumatic Diseases

Approved in 1992 to reduce benign prostatic hypertrophy, finasteride competitively inhibits type II and type III isozymes of 5a-reductase, resulting in reduced dihydrotestosterone (DHT). Elevated DHT is the primary driver of testosterone-related issues in men and women. DHT causes benign prostatic hypertrophy and androgenic alopecia. A not so funny thing happened on the way to a bushy head of hair and better urinary flow, however. Termed Post Finasteride Syndrome (PFS), an estimated to be 3-5% of all finasteride users, repre-senting nearly 400,000 patients in 2018 alone, began reporting a constellation of severe adverse effects persisting long after discontinuing finasteride use. Symptoms included sexual and neurologic disorders, including decreased or complete loss of sex drive, erectile dysfunction, impotence, chronic anxiety, depression, and an altered gut microbiome. Many patients claim these symptoms are perma-nent. Etiologies of PFS include changes in penile vascular architecture, interference, and reduction of the neurosteroid that influences GABA, the calming neurotransmitter production, allopregnanolone. We discuss finasteride in detail, the symptoms of PFS, along with recommended laboratory studies and a remedial program. Finasteride is frequently cited in AMMG’s TBI program as a drug to avoid due to long-lasting behavioral and mood changes. Our goal is to explore the growing problem of PFS in depth.