Androgenetic Alopecia (AGA), the common form of progressive hair thinning, affects a large percentage of the population. A persistent misconception suggests that high levels of the male sex hormone testosterone are the direct cause of this condition. While hormones are involved, the direct link between circulating testosterone levels and the onset of baldness is not supported by scientific evidence. Individuals with a full head of hair often have similar or even higher testosterone levels than those experiencing significant hair loss. AGA is not caused by too much testosterone, but rather by a complex biological interaction involving a different hormone and genetic predisposition.
The Real Culprit: Dihydrotestosterone
The actual molecule responsible for pattern hair loss is dihydrotestosterone (DHT), a derivative of testosterone. Testosterone acts as a precursor, and a small percentage is converted into the significantly more potent DHT within the body’s tissues. This conversion process is facilitated by the 5-alpha reductase enzyme.
This enzyme is present in various parts of the body, including the liver, prostate, skin, and hair follicles. 5-alpha reductase catalyzes the transformation of testosterone into DHT, which is estimated to be three to ten times more powerful. This localized conversion explains why DHT’s impact is primarily felt in specific tissues, such as the prostate gland and susceptible scalp follicles.
Only a small fraction of total circulating testosterone, typically four to eight percent, is converted into DHT. High levels of this potent molecule are found in the scalps of individuals with pattern baldness, even if their overall blood testosterone levels are normal. While DHT plays a necessary role in the development of male secondary sexual characteristics, it becomes problematic in genetically sensitive hair follicles later in life.
How Hormones Affect Hair Follicle Growth
DHT affects the hair growth cycle by targeting androgen receptors present in the dermal papilla cells. Hair follicles normally cycle through three main phases: anagen (growth), catagen (transition), and telogen (resting). The typical anagen phase can last for several years, allowing for long, healthy hair growth.
When DHT binds to receptors in susceptible follicles, it initiates follicular miniaturization. This action dramatically shortens the duration of the anagen phase, causing the hair to spend less time actively growing. Consequently, the affected hair follicle shrinks in size with each successive growth cycle.
Over time, the terminal hairs become progressively thinner, shorter, and finer. Eventually, the follicle may produce only colorless, barely visible vellus hairs or cease production entirely. This disruption leads to the visible signs of thinning and pattern baldness, as the follicles can no longer sustain healthy hair production.
Why Only Some People Experience Hair Loss
The difference between individuals with comparable hormone levels is due to genetic sensitivity. Androgenetic Alopecia requires a hereditary predisposition, largely influenced by the Androgen Receptor (AR) gene. This gene dictates the structure and density of androgen receptors located on the hair follicles.
Individuals who experience pattern hair loss have follicles genetically programmed to be highly sensitive to DHT. Their follicles possess a greater number of, or more reactive, androgen receptors, which enhances the hormone’s miniaturizing effect. Hair loss is not correlated with the absolute quantity of circulating hormones, but rather the intensity of the follicular reaction to normal hormone levels.
This genetic sensitivity explains why hair loss follows a distinct pattern, typically affecting the crown, temples, and vertex of the scalp. Follicles on the back and sides of the head are generally resistant to DHT’s effects, maintaining hair growth even in advanced cases. This inherited instruction set makes follicles in specific scalp regions vulnerable to DHT.