Male baldness is primarily caused by a hormone called DHT (dihydrotestosterone) shrinking hair follicles in genetically susceptible men. By age 50, roughly 30% to 50% of men show noticeable hair loss, and by 70, fewer than 15% still have a full head of hair. While genetics and hormones drive the vast majority of cases, inflammation, nutrient deficiencies, and stress can also play a role.
How DHT Shrinks Hair Follicles
Your body converts testosterone into DHT using an enzyme found in hair follicles, the prostate, and skin. DHT is more potent than regular testosterone, and it’s essential during puberty for developing male characteristics. But in adulthood, it becomes the primary driver of hair loss.
Here’s what happens: DHT binds to receptors on hair follicles across the top and front of your scalp. Once attached, it activates genes that cause the follicle to gradually miniaturize. Each hair growth cycle becomes shorter, so the follicle produces thinner, finer hairs until eventually it stops producing visible hair altogether. The growth phase of a healthy scalp hair normally lasts two to six years. In affected follicles, DHT compresses that phase, speeding up the cycle while shrinking the follicle with each round.
This process explains why balding hair doesn’t disappear overnight. It’s a slow transition from thick terminal hairs to wispy, nearly invisible ones. The follicles on the sides and back of your head have receptors that are far less sensitive to DHT, which is why those areas typically keep their hair even in advanced baldness.
The Role of Genetics
Hair loss runs in families, but the inheritance pattern is more complicated than the old “blame your mother’s father” rule. While the most well-established gene linked to male baldness, the AR gene, does sit on the X chromosome (which you inherit from your mother), it’s not the whole picture. Researchers suspect that variants in several other genes also contribute, meaning baldness can come from either side of the family.
The AR gene controls how your body builds androgen receptors, the proteins that DHT latches onto. Men with certain variations of this gene produce receptors that are more easily activated by DHT than normal. So two men can have identical DHT levels, but the one with more sensitive receptors will lose more hair. This is why some men with high testosterone keep full heads of hair while others start thinning in their twenties. It’s not how much DHT you produce that matters most; it’s how strongly your follicles respond to it.
The Typical Pattern of Loss
Male baldness follows a recognizable sequence, classified on a seven-point scale developed by researchers Hamilton and Norwood. It generally starts with recession at the temples, creating an M-shaped hairline. In the early stages, the hairline hasn’t pulled back more than a couple of centimeters. As it progresses, the recession deepens past the middle of the scalp, and thinning begins at the crown. In later stages, the two areas of loss merge, leaving hair only around the sides and back.
Not every man progresses through all stages. Some stabilize at a receding hairline and never lose crown hair. Others thin diffusely across the top without much temple recession. The speed and extent of progression depend largely on your genetic sensitivity to DHT.
Inflammation as a Contributing Factor
Beyond hormones, low-grade inflammation around hair follicles appears to accelerate the miniaturization process. Scalp biopsies from balding areas consistently show clusters of immune cells, elevated inflammatory signaling molecules, and activated immune responses that aren’t present in non-balding skin.
Researchers have found that a common skin bacterium, Cutibacterium acnes (the same species involved in acne), is more abundant in miniaturized follicles. Its increased presence corresponds with heightened immune activity in those follicles. UV exposure, hormonal signaling, and microbial colonization can all trigger this micro-inflammation. Whether the inflammation causes the miniaturization or simply makes existing DHT-driven damage worse is still being worked out, but the two processes clearly feed each other.
Nutrient Deficiencies That Worsen Thinning
While nutritional problems rarely cause the classic horseshoe pattern of male baldness, they can accelerate thinning or trigger a different type of hair loss called telogen effluvium, where hair sheds diffusely across the entire scalp.
Iron and vitamin D are the two nutrients most consistently linked to hair loss. In one study comparing people with diffuse hair loss to healthy controls, those losing hair had significantly lower iron stores (average ferritin of about 15 ng/ml versus 25 ng/ml in controls) and lower vitamin D levels (14 ng/ml versus 17 ng/ml, with the normal range starting at 20). Interestingly, zinc, B12, folate, and thyroid hormone levels showed no meaningful difference between the two groups, suggesting their role in hair loss may be overstated.
If you’re losing hair in a pattern that doesn’t match the typical temple-and-crown recession, or if it came on suddenly, a blood test checking iron and vitamin D levels is worth considering.
Stress-Related Shedding vs. Pattern Baldness
Sudden hair loss after a stressful event, a serious illness, surgery, or rapid weight loss is usually telogen effluvium, not true male pattern baldness. The distinction matters because telogen effluvium is temporary. It can begin at any age, causes diffuse shedding (often more than 100 hairs a day), and doesn’t change the frontal hairline shape. Microscopically, the shed hairs are all of uniform thickness, meaning the follicles haven’t miniaturized.
Pattern baldness, by contrast, produces hairs of varying thickness because follicles are at different stages of shrinking. Dermatologists can distinguish the two by examining hair diameter variation: in telogen effluvium, fewer than 20% of hairs differ in diameter, while in pattern baldness, the variation is much greater, with many follicles producing thin, wispy hairs alongside thicker ones. The ratio of full-thickness hairs to miniaturized ones drops below 4:1 in pattern baldness, compared to a healthy 7:1.
How Treatments Target the Cause
Because DHT is the central driver, the most effective medical treatments work by reducing DHT levels or blocking its effects. The standard oral medication for male hair loss works by inhibiting the enzyme that converts testosterone to DHT. At a typical dose, it reduces DHT in the scalp by about 64% and in the bloodstream by roughly 71%. Even doses as low as 0.2 mg per day achieve near-maximum DHT suppression, which is why clinical results across different dosages tend to be similar.
Topical treatments that increase blood flow to the scalp work through a different mechanism, essentially prolonging the growth phase of the hair cycle. They don’t address DHT directly but can slow miniaturization and, in some men, partially reverse it. These two approaches are often used together.
The earlier treatment starts, the more effective it tends to be. Once a follicle has fully miniaturized and scarred over, no medication can revive it. This is why men who begin treatment while they still have thinning hair rather than bare scalp generally see better outcomes.