Androgenic alopecia is caused by a combination of inherited genetic sensitivity and the hormone dihydrotestosterone (DHT), which gradually shrinks hair follicles until they produce only fine, barely visible hair. It affects an estimated 50 million men and 30 million women in the United States, and more than 50 percent of men over age 50 have some degree of it.
How DHT Shrinks Hair Follicles
The central driver of androgenic alopecia is a hormone called DHT. Your body produces it when an enzyme in scalp and skin cells converts regular testosterone into this much more potent form. DHT then binds to receptors inside hair follicle cells and triggers changes in how those cells behave, essentially telling them to wind down.
The process unfolds in stages. First, the growth phase of each hair cycle gets shorter. Healthy scalp hair typically grows for two to six years before naturally shedding. In affected follicles, that window shrinks to under six months. At the same time, the daily rate of hair growth slows. Eventually the hair shaft itself gets thinner, transitioning from a thick, pigmented “terminal” hair to a fine, pale, almost invisible “vellus” hair. This is called miniaturization, and it’s the hallmark of the condition. Importantly, this process is already underway before thinning becomes visible to the naked eye. Follicle diameters drop below 60 micrometers before you or anyone else would notice reduced scalp coverage.
The Genetics Behind Follicle Sensitivity
DHT circulates through every person’s bloodstream, but only people with a specific genetic makeup lose hair because of it. The key question isn’t how much DHT you have. It’s how strongly your follicles respond to it.
The most important gene is the androgen receptor (AR) gene, located on the X chromosome. Variations in this gene can make the receptor more active, increasing sensitivity to DHT and triggering hair loss at an earlier age. Because the X chromosome is inherited from your mother, the old observation that baldness “comes from your mother’s side” has a real genetic basis, though it’s not the full picture.
A second major risk gene sits nearby on the X chromosome, called EDA2R. Together, the AR/EDA2R region and another locus on chromosome 20 are the two strongest genetic predictors of androgenic alopecia in people of European descent. But the condition is polygenic, meaning dozens of smaller genetic contributions add up. That’s why it doesn’t follow a simple “one gene, one outcome” pattern and can appear to skip generations unpredictably.
One fascinating genetic detail helps explain why the back and sides of the head resist balding even in advanced hair loss. In those occipital follicles, the AR gene’s promoter region is more heavily methylated, a chemical modification that dials down the gene’s activity. With less androgen receptor being produced, those follicles are essentially shielded from DHT. This is why hair transplant surgery takes donor hair from the back of the head: those follicles carry their DHT resistance with them.
A Chemical Signal That Stalls Growth
Beyond DHT, researchers have identified another molecule that actively inhibits hair growth in balding areas. Balding scalp contains roughly ten times more of a lipid signaling molecule called prostaglandin D2 (PGD2) compared to haired scalp: about 16.3 nanograms per gram of tissue versus 1.5 nanograms in non-balding areas. In lab studies, PGD2 applied to human hair follicles shortened hair growth by about 38 percent, and a related breakdown product of PGD2 blocked growth entirely at higher concentrations.
PGD2 appears to push follicles into their regression phase prematurely, compounding the cycle-shortening effect of DHT. It works through a specific receptor on follicle cells, and this pathway is being explored as a treatment target separate from hormone-blocking approaches.
How Female Hair Loss Differs
Women develop a different pattern of thinning, typically a widening part or diffuse thinning across the top of the scalp rather than a receding hairline. The underlying biology also differs in important ways. While androgens clearly drive hair loss in men, their role in women is less straightforward. Some women with pattern hair loss have elevated androgen levels, but many do not.
In women with normal hormone levels, the mechanism may involve follicles that are genetically hypersensitive to even ordinary amounts of circulating androgens. In other cases, the hair loss appears to operate through an entirely androgen-independent pathway that researchers still don’t fully understand. Female pattern hair loss is most common after menopause, when the protective effects of estrogen decline. The shared endpoint in both sexes is the same: follicle miniaturization and progressively finer hair. But the triggers that set it in motion are not necessarily identical.
Inflammation and Oxidative Stress
Androgenic alopecia is typically considered a non-inflammatory condition, but microscopic examination tells a more nuanced story. Biopsies of affected scalp consistently show perifollicular inflammation, clusters of immune cells gathering around the upper portion of shrinking follicles. This low-grade, subclinical inflammation appears to play an active role in the miniaturization process rather than just being a bystander.
Closely linked to this inflammation is oxidative stress, an imbalance between damaging free radicals and the body’s ability to neutralize them. The dermal papilla cells at the base of hair follicles in people with androgenic alopecia show elevated markers of oxidative damage. This creates a feedback loop: DHT-driven changes promote inflammation, inflammation generates oxidative stress, and oxidative stress further damages the follicle’s ability to sustain healthy growth cycles.
Smoking and Other Accelerators
Genetics loads the gun, but certain environmental factors pull the trigger faster. Smoking is the most studied accelerator. A systematic review found that smokers over age 30 had roughly twice the odds of developing baldness compared to nonsmokers (odds ratio of 1.93). Smoking may worsen androgen-dependent hair thinning through multiple routes: reduced blood flow to the scalp, increased oxidative damage to follicle cells, and possible effects on hormone metabolism.
How It Differs From Other Hair Loss
Not all hair loss is androgenic alopecia, and the distinction matters because the causes and treatments differ significantly. The most common lookalike is telogen effluvium, a temporary shedding triggered by stress, illness, surgery, or nutritional deficiency. Telogen effluvium typically begins suddenly, can happen at any age, and often involves hair loss beyond the scalp, including eyebrows and body hair. Crucially, the hair that sheds in telogen effluvium is normal in thickness. Under a microscope, the ratio of thick terminal hairs to fine vellus hairs stays close to the normal 7:1. In androgenic alopecia, that ratio drops below 4:1 as miniaturization takes hold.
Another key difference: telogen effluvium doesn’t follow a pattern. It causes diffuse thinning everywhere rather than the predictable receding temples and crown thinning of male androgenic alopecia or the widening central part in women. And telogen effluvium is reversible once its trigger is removed, while androgenic alopecia is progressive without treatment.