Free dihydrotestosterone, or free DHT, is the unbound and biologically active portion of dihydrotestosterone circulating in the blood. Dihydrotestosterone is a powerful androgen, meaning a hormone that drives male pattern physical traits and supports reproductive tissue function. Only a small fraction of DHT circulates freely. Most of it is attached to carrier proteins, primarily sex hormone binding globulin, or SHBG, and albumin. When DHT is not bound, it can diffuse into cells and activate the androgen receptor, a protein inside cells that turns specific genes on or off in response to hormone signals.
DHT is produced mainly from testosterone through the action of an enzyme called 5 alpha reductase. An enzyme is a protein that speeds up chemical reactions in the body. This conversion happens especially in androgen sensitive tissues such as the prostate, skin, and hair follicles. In many of these tissues, testosterone acts as a prohormone, meaning it serves as a precursor that is converted into the more potent DHT. DHT binds the androgen receptor more strongly than testosterone and produces a more intense signal inside the cell.
Once formed, DHT can be further broken down into metabolites such as 3 alpha androstanediol glucuronide. A metabolite is a breakdown product of a hormone. This particular metabolite reflects androgen activity in tissues like skin more accurately than blood DHT itself. That distinction matters because circulating free DHT does not always mirror what is happening inside target tissues.
In men, DHT is essential for normal prostate development and contributes to benign prostatic hyperplasia, or BPH, which is noncancerous enlargement of the prostate that can cause urinary symptoms. However, intraprostatic DHT production within the gland is more important than blood levels. Medications called 5 alpha reductase inhibitors reduce tissue DHT and improve BPH symptoms. That said, modest increases in circulating DHT during testosterone therapy have not consistently been linked to higher prostate cancer risk in clinical reviews.
In hair follicles, DHT plays a central role in androgenetic alopecia, commonly called male pattern hair loss. Inside scalp hair follicles, DHT shortens the growth phase of hair and gradually miniaturizes the follicle. Yet this process depends more on local enzyme activity and androgen receptor density than on serum free DHT alone. This is why blood levels do not perfectly predict hair loss severity.
In women, DHT measurement has limited clinical value in most cases of excess androgen symptoms such as acne or hirsutism, which refers to male pattern hair growth. Total and free testosterone are generally better first line markers. DHT metabolites can sometimes better reflect skin level androgen activity than circulating DHT itself. In polycystic ovary syndrome, or PCOS, current evidence supports testosterone based measurements rather than DHT for diagnosis.
For patients focused on lifespan and healthspan, free DHT is best understood as part of the broader androgen signaling network. It is not usually a primary screening test, but in the right context it can add nuance, particularly when evaluating androgen therapy, prostate health, or unexplained symptoms related to androgen excess or deficiency.