Testosterone is an androgen, or male sex hormone, that plays a broad role in the human body. However, it is not the direct cause of pattern hair loss. The condition known as Androgenetic Alopecia (AGA), which affects both men and women, is driven by a highly potent derivative of testosterone: Dihydrotestosterone (DHT). The interaction of DHT with genetically predisposed hair follicles dictates whether hair loss will occur.
The Conversion Process: From Testosterone to DHT
The transformation of testosterone into DHT is a specific chemical reaction catalyzed by an enzyme called 5-alpha reductase (5AR). This enzyme is present in various tissues throughout the body, including the prostate, skin, liver, and the hair follicles of the scalp. 5AR converts approximately 5% to 7% of circulating testosterone into DHT, a process that happens locally within the target tissues.
Dihydrotestosterone is a stronger androgen than testosterone, binding to androgen receptors with an affinity estimated to be up to five times greater. The 5AR enzyme is primarily found in two main types, with Type II being the dominant isoform present in the outer root sheath of the hair follicle. The localized presence of the 5AR Type II enzyme means that DHT is synthesized right where it affects susceptible hair follicles. This mechanism explains why hair loss is a highly localized phenomenon on the scalp, even when systemic testosterone levels remain normal.
The Genetic Blueprint: Receptor Sensitivity
The difference in hair loss severity among individuals with similar hormone levels lies in the genetic sensitivity of the hair follicles themselves. This sensitivity is determined by the Androgen Receptors (AR) located primarily within the dermal papilla, a cluster of cells at the base of the hair follicle. These receptors allow androgens like DHT to bind and initiate a biological signal.
Genetic predisposition, which is largely inherited, controls the quantity and responsiveness of these androgen receptors on the scalp. A person with highly sensitive ARs will find that even normal levels of DHT are sufficient to trigger the hair loss process. The gene for the Androgen Receptor is located on the X chromosome, which explains the strong hereditary link to the condition.
The genetic makeup dictates which areas of the scalp are affected, leading to the characteristic patterns of AGA. Follicles at the crown and temples often possess a higher concentration of these sensitive receptors, making them prime targets for DHT’s effects. Conversely, hair follicles on the back and sides of the head are typically genetically resistant, which is why they usually remain intact.
The Result: Follicle Miniaturization and Hair Thinning
When DHT binds to sensitive androgen receptors in the dermal papilla, it initiates a cascade of events that ultimately leads to follicular miniaturization. This process is the physical manifestation of Androgenetic Alopecia and causes the hair follicle to shrink progressively in size with each subsequent growth cycle.
Hair growth occurs in three main phases: the Anagen (growth) phase, the Catagen (transition) phase, and the Telogen (resting/shedding) phase. DHT disrupts this cycle by shortening the Anagen phase, which is when the hair fiber is actively being produced. A shorter growth phase means the hair cannot achieve its full length or thickness before the cycle prematurely ends.
As the Anagen phase shortens and the Telogen phase lengthens, the thick terminal hairs are gradually replaced by shorter, finer, and less pigmented vellus hairs. This progressive reduction in hair shaft diameter and length creates the visible appearance of thinning hair. Eventually, the follicle may shrink to the point where it becomes dormant and can no longer produce a visible hair fiber.
Targeting the Pathway: Medications that Block DHT
Since the conversion of testosterone to DHT is the central mechanism of pattern hair loss, therapeutic interventions often focus on blocking this specific pathway. The most common class of medications used are 5-alpha reductase inhibitors (5-ARIs), which directly interfere with the enzyme responsible for the conversion.
Finasteride is a widely used 5-ARI that works by inhibiting the Type II isoform of the 5AR enzyme. By inhibiting the enzyme, Finasteride effectively reduces the amount of DHT available to bind to the sensitive hair follicle receptors. This reduction in the hormonal signal can slow or stop the progressive miniaturization of the hair follicles.
Dutasteride is another 5-ARI that is considered more potent because it inhibits all three types of the 5AR enzyme, leading to an even greater overall reduction in DHT levels. These treatments aim to mitigate the hormonal cause of AGA by reducing the concentration of the triggering molecule, DHT. Other interventions, such as certain topical treatments, are sometimes used to locally reduce the effects of the hormone on the scalp.