Testosterone Replacement Therapy (TRT) is a medical treatment used to address low testosterone levels, a condition known as hypogonadism. This therapy aims to restore hormone concentrations to a normal physiological range, often resulting in improved energy, mood, and muscle mass. The influence of increased androgens on hair follicles can lead to various effects across the body, causing changes in hair growth patterns, which is a common concern for TRT patients.
The Expected Outcome: Increased Body Hair Growth
Elevated androgen levels from TRT generally stimulate hair growth in many areas of the body. This effect results from hormonal action on androgen-sensitive hair follicles. The degree of change is highly individual and depends significantly on genetics and the administered testosterone dose.
The noticeable change is the transformation of fine, light vellus hair into terminal hair. Terminal hair is thicker, longer, and more pigmented. Androgenic stimulation causes vellus follicles to mature into terminal hair follicles, mimicking the changes seen during male puberty. Patients commonly observe increased hair density on the chest, back, arms, legs, and face, and existing body hair may become coarser, darker, and grow faster.
Understanding the Androgenic Mechanism
The mechanism driving hair change involves androgens, specifically Dihydrotestosterone (DHT), which is the primary driver of body hair maturation. DHT is synthesized from testosterone through the action of the enzyme 5-alpha reductase (5α-R).
This 5-alpha reductase enzyme is present in various tissues, including the skin and hair follicles. When TRT raises circulating testosterone levels, it provides more substrate for 5α-R to convert into DHT. DHT is significantly more potent than testosterone, exhibiting a much higher affinity for androgen receptors on the hair follicles.
The binding of DHT initiates a signal cascade that stimulates the hair follicle. This stimulation lengthens the anagen (active growth phase) of the hair cycle, leading to the production of longer, thicker, and darker terminal hair. The extent of the hair growth response is dictated by the local concentration of 5α-R and the sensitivity of the androgen receptors in that specific area.
The Paradox: Body Hair Growth Versus Scalp Thinning
Despite stimulating body hair growth, the same androgenic mechanism can have the opposite effect on genetically predisposed scalp hair follicles. While DHT promotes terminal hair growth on the body, it accelerates the process of miniaturization in sensitive scalp follicles.
The difference lies in the genetic sensitivity of the hair follicles themselves, which varies depending on their location. In the presence of elevated DHT, genetically sensitive scalp follicles begin to shrink. This process shortens the active growth phase and prolongs the resting phase of the hair cycle.
Over time, affected follicles produce progressively finer, shorter, and lighter hair until they cease producing visible hair altogether, a condition known as androgenetic alopecia (male pattern baldness). TRT does not cause baldness but rather accelerates a pre-existing genetic tendency by increasing the amount of circulating testosterone available for conversion to DHT. Individuals without this genetic predisposition may not experience noticeable scalp thinning even with elevated hormone levels.