Dihydrotestosterone (DHT) is a potent androgen formed when testosterone is converted by the enzyme 5α-reductase. It binds more strongly to androgen receptors than testosterone, which gives it greater biological activity at lower concentrations. DHT is essential for male development, deep voice, genital growth, and muscle mass, but in adulthood it can drive hair loss and acne.
Despite long-standing concern, clinical studies show that high DHT does not increase the risk of prostate cancer or benign prostatic hyperplasia. It also does not significantly affect cholesterol or cardiovascular risk (Swerdloff et al., 2017; Anawalt, 2017; Page et al., 2011; Kunelius et al., 2002). In men receiving testosterone therapy, DHT often rises but has not been shown to increase prostate disease incidence.
Elevated DHT can, however, increase red blood cell production, known as erythrocytosis. This raises hematocrit, which may increase clot risk if not monitored, particularly during testosterone therapy (Aghazadeh et al., 2013; Swerdloff et al., 2017). DHT also drives androgenic alopecia (male pattern baldness) and acne by stimulating sebaceous gland activity (Anawalt, 2017; Chen et al., 2020). Laboratory studies suggest high DHT may affect tendon cell growth and repair, but this remains experimental (Denaro et al., 2010).
In women, the effects of high DHT are more clinically significant. Elevated DHT disrupts ovulation and contributes to polycystic ovary syndrome (PCOS) by promoting granulosa cell death and hormonal imbalance (Li et al., 2024; Chen et al., 2015). Animal studies show DHT can increase visceral fat, body weight, and insulin resistance, reproducing metabolic features of PCOS (Chen et al., 2015). At the cellular level, excess DHT increases oxidative stress and mitochondrial injury in ovarian cells, impairing fertility (Li et al., 2024).
DHT also affects inflammation and blood vessels. It can either suppress or promote inflammation depending on the tissue and receptor environment (Osterlund et al., 2010; Gornstein et al., 1999; Yang et al., 2020; Liang et al., 2023; Lee et al., 2019). It may increase immune cell adhesion to vessel walls, which is theoretically pro-atherogenic, but human studies have not shown an increased cardiovascular event rate (McCrohon et al., 1999; Goglia et al., 2010).
In men, high DHT is usually a cosmetic or hematologic issue rather than a systemic threat. It does not raise prostate or cardiovascular risk. In women, elevated DHT is often a sign of hormonal imbalance that can affect fertility and metabolism. Suppressing DHT pharmacologically should be considered carefully, as it may blunt some of testosterone’s beneficial effects on muscle, cognition, and libido.