Male pattern baldness — androgenetic alopecia — is the most common form of hair loss in men, affecting approximately 50% of men by the age of 50. Despite its prevalence, the underlying biology is not always well understood by patients, who often attribute it to stress, diet, or lifestyle when the root cause is primarily genetic and hormonal.
The primary driver is dihydrotestosterone (DHT), a metabolite of testosterone produced by the enzyme 5-alpha reductase. In men with genetic susceptibility — specifically, follicles that express a high density of androgen receptors — DHT binds to these receptors and triggers a signalling cascade that progressively shortens the anagen growth phase of the follicle. Each successive hair produced is slightly shorter, finer, and less pigmented than the last. This is the miniaturisation process.
The genetic component is polygenic — influenced by variants across multiple genes, inherited from both parents. The precise combination of variants determines both susceptibility and pattern. Family history on both sides is relevant, though no simple Mendelian inheritance pattern applies.
Not all follicles are equally sensitive to DHT. The follicles at the back and sides of the scalp — the donor zone — have low androgen receptor expression and are DHT-resistant. This is why the horseshoe pattern of preserved hair at the sides persists even in advanced baldness, and why these follicles make ideal donor material for transplant surgery.
DHT levels in the bloodstream are not directly correlated with the severity of pattern hair loss. Two men with identical serum DHT can have very different baldness patterns — the difference lies in follicle sensitivity, not hormone levels.
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