Androgenetic alopecia (AGA), commonly known as male pattern baldness, is a highly prevalent condition marked by a characteristic pattern of hair loss in men. This phenomenon can begin as early as the late teens or early twenties. The difference in hair loss patterns between sexes is rooted in the interplay between inherited genetic sensitivity and the varying levels of specific sex hormones. The expression of hair loss is profoundly influenced by the hormonal environment created by these differences.
Dihydrotestosterone (DHT) and Follicle Miniaturization
The primary biological agent responsible for pattern hair loss is a potent androgen hormone called Dihydrotestosterone (DHT). DHT is synthesized from the more common male hormone, testosterone, through the action of an enzyme called 5-alpha reductase. This enzyme is present in various tissues, including the scalp’s hair follicles, where it converts testosterone into its more biologically active form.
Once formed, DHT acts on the hair follicles of individuals who are genetically predisposed to its effects. DHT molecules bind to specialized androgen receptors located within the dermal papilla, the base of the hair follicle. This binding initiates a degenerative process known as follicular miniaturization, the defining characteristic of AGA.
Miniaturization causes a progressive change to the hair growth cycle. The anagen (growth phase) of the cycle becomes gradually shorter with each successive cycle, while the telogen (resting phase) becomes disproportionately longer. Consequently, the hairs produced by the affected follicles become progressively thinner, shorter, and less pigmented.
Over time, the once-robust terminal hairs are replaced by fine, nearly invisible vellus hairs, and eventually, the follicle may cease producing hair altogether. The areas most affected are typically the crown and the frontal hairline. Hair on the sides and back of the scalp remains largely unaffected due to its inherent genetic resistance to DHT, explaining the characteristic horseshoe pattern of male baldness.
The Genetic Predisposition
The susceptibility of a hair follicle to the miniaturizing effects of DHT is determined by an individual’s genetic makeup. Androgenetic alopecia is a polygenic condition, meaning its development and severity are influenced by multiple genes working in combination. This complexity makes it difficult to predict the exact pattern or onset of hair loss based on family history alone.
One of the most significant genes associated with pattern hair loss is the Androgen Receptor (AR) gene. This gene provides instructions for making the androgen receptor protein, which DHT binds to in the hair follicle. The AR gene is located on the X chromosome, which men inherit exclusively from their mothers.
The location of the AR gene on the X chromosome led to the belief that baldness is inherited solely from the maternal grandfather. While the AR gene has a strong association, it is not the only gene involved. Many other genetic variants contributing to baldness are located on autosomal chromosomes, which are inherited from both parents.
Research has identified over 63 genetic variants linked to male pattern baldness, with only a small fraction found on the X chromosome. Therefore, a man’s genetic predisposition is a blend of contributions from both parental lines. The ultimate severity is determined by the combined impact of these inherited traits and the individual’s hormonal environment.
Hormonal Differences and Protection in Women
The difference in the prevalence and presentation of pattern hair loss between men and women is largely due to systemic hormonal variations. Men have significantly higher levels of circulating testosterone, which translates into greater production of DHT by the 5-alpha reductase enzyme. Women, by contrast, have much lower baseline levels of these androgens.
Women possess another hormonal element that offers a degree of protection: estrogen. Estrogen is thought to counteract the effects of androgens by promoting hair health and prolonging the anagen phase of the hair growth cycle. It may also inhibit the activity of the 5-alpha reductase enzyme, reducing the local conversion of testosterone into DHT within the scalp.
When women experience androgenetic alopecia, medically termed Female Pattern Hair Loss (FPHL), it typically presents differently than in men. Instead of a defined receding hairline or a bald spot on the crown, FPHL usually involves diffuse thinning over the top and central parts of the scalp. The frontal hairline is often spared, preserving the appearance of the hair’s edge.
The protective hormonal environment in women is evident in the timing of FPHL, which often becomes more noticeable after menopause. The natural decline in estrogen levels following this life stage removes some of the hormonal buffering. This allows the effects of androgens to become more pronounced in genetically susceptible women.