Pattern hair loss
Based on Wikipedia: Pattern hair loss
Here's a biological paradox that has puzzled scientists for decades: the same hormones that cause a teenage boy to sprout a beard will, in that same body, cause the hair on top of his head to fall out. The androgens—male sex hormones—grow hair everywhere except where most people want it. This cruel joke of evolution is called androgenetic alopecia, or pattern hair loss, and by age fifty, it affects roughly half of all men and a quarter of all women.
But this isn't just a cosmetic nuisance. Recent research suggests that the receding hairline you notice in your thirties might be an early warning sign of something far more serious happening inside your body.
The Hippocratic Wreath
Pattern hair loss earned its more poetic name from a distinctive feature: as baldness progresses in men, it spares a horseshoe-shaped ring of hair around the sides and back of the head. Ancient physicians noticed this pattern and called it the "Hippocratic wreath," after the father of medicine himself. Hippocrates, incidentally, was bald.
The pattern differs between men and women. In men, hair loss typically begins at the temples—that slow creep of the hairline backward—and at the crown, that circular patch on top of the head that catches the sun. These two regions gradually expand until they meet, leaving only the wreath behind. Complete baldness is rare.
Women experience something different. Rather than receding temples, women with pattern hair loss see diffuse thinning across the entire scalp, as if someone gradually turned down the density setting on their hair. The hairline usually stays put, but the hair behind it becomes progressively thinner, eventually revealing the scalp beneath. Complete baldness in women is extremely rare.
What Castrated Men Taught Us
The connection between male hormones and baldness was established through a rather unusual line of evidence: eunuchs—men who were castrated before puberty—never go bald.
This observation, documented across cultures and centuries, pointed researchers toward testosterone and its derivatives. But testosterone itself isn't the direct culprit. The real actor is dihydrotestosterone, or DHT, a more potent version of testosterone created when an enzyme called five-alpha reductase converts testosterone in various tissues throughout the body. The scalp happens to have particularly high levels of this enzyme.
DHT binds to receptors in hair follicles on the scalp and, through mechanisms not fully understood, causes those follicles to gradually shrink—a process called miniaturization. Each hair growth cycle produces thinner, shorter, lighter hairs until eventually the follicle produces only tiny, nearly invisible vellus hairs, the kind of fine fuzz you see on a child's cheek.
The fascinating twist: those same hair follicles aren't dead. They're dormant. Recent research has found that the stem cells needed to regenerate hair follicles are still present in bald scalps. The follicles haven't been destroyed; they've been silenced.
The Androgen Paradox
Why would the same hormone grow a thick beard on a man's chin while killing the hair on his head? Scientists call this the "androgen paradox," and it turns out the answer lies in our evolutionary past.
A protein called KRT37—a type of keratin, the structural building block of hair—behaves differently in humans than in our closest relatives. In chimpanzees, KRT37 is expressed in hair follicles all over the body, including the head. But modern humans lost KRT37 expression specifically in scalp hair follicles. This keratin is the only one regulated by androgens, which means when DHT shows up, it affects human scalp follicles in ways it doesn't affect the scalp of other great apes.
This wasn't always the case. Homo sapiens acquired this sensitivity through genetic changes that our great ape cousins don't share. We evolved to go bald. The evolutionary reason, if there is one, remains unclear. Some researchers have speculated that visible baldness served as a social signal in early human societies—perhaps indicating age and therefore wisdom, or simply genetic identity within a group.
The Inheritance Question
Folk wisdom says to look at your mother's father to predict your own hair fate. Like most folk wisdom, this is partially right and mostly wrong.
For years, scientists described pattern hair loss as an autosomal dominant trait—meaning you needed only one copy of the gene, from either parent, to potentially develop the condition. But this model doesn't quite fit the data. Studies have found that about eighty percent of bald men have bald fathers, which is far higher than you'd expect from a straightforward autosomal pattern. This suggests the genetics are more complicated, possibly involving genes on the Y chromosome—which can only be inherited from fathers—or something called genomic imprinting, where certain genes behave differently depending on which parent they came from.
The bottom line: your mother's father matters, but so does your father's hairline, and so do a host of other genetic factors we're still working to identify.
A Window Into Metabolic Health
Here's where pattern hair loss becomes more than skin deep.
Multiple studies have found that men who develop androgenetic alopecia early—before age thirty-five—have significantly higher rates of metabolic syndrome, a cluster of conditions that dramatically increases the risk of heart disease, stroke, and type 2 diabetes. We're not talking about small differences. Young men with early hair loss show approximately four times the rate of metabolic syndrome compared to their full-haired peers.
The specific components of metabolic syndrome associated with early hair loss include abdominal obesity, high blood pressure, and low levels of high-density lipoprotein (HDL)—the so-called "good cholesterol." Low HDL shows the strongest association of all.
This connection runs deep enough that researchers have proposed early male pattern baldness as a male equivalent of polycystic ovary syndrome, or PCOS, in women. PCOS involves insulin resistance, elevated androgens, and metabolic dysfunction. Interestingly, women with pattern hair loss also show increased rates of PCOS, and family members of women with PCOS have higher rates of insulin resistance.
The mechanism linking hair loss to metabolic disease appears to involve insulin. Men with premature hair loss tend to have lower levels of sex hormone-binding globulin, or SHBG, a protein that binds to testosterone and keeps it from being converted to DHT. Lower SHBG means more free testosterone available for conversion to DHT, and it also correlates strongly with insulin resistance.
This relationship is bidirectional and self-reinforcing. Obesity leads to higher insulin production and lower SHBG. Lower SHBG contributes to insulin resistance. Insulin, in turn, suppresses SHBG production while stimulating testosterone production. The result is a vicious cycle: more free testosterone, more DHT, more hair loss, and worse metabolic health.
The Treatment Landscape
Given that dormant follicles aren't dead follicles, treatments for pattern hair loss aim to either block DHT or stimulate those sleeping follicles back into action.
Finasteride, sold under brand names like Propecia, blocks the type II version of five-alpha reductase, preventing testosterone from being converted to DHT. It works—studies show increased hair counts at two and four years of continued use—but it works better at the crown than at the temples, and it doesn't reverse advanced baldness. A related drug called dutasteride blocks both type I and type II five-alpha reductase and may be more effective, though it's only approved for hair loss treatment in Korea and Japan, not the United States.
Minoxidil, originally developed as a blood pressure medication, promotes hair growth through mechanisms that remain unclear. It dilates blood vessels, but whether that's the reason it helps hair grow is unknown. What is known is that it works better when combined with other treatments.
The combination approach has proven most effective. Studies show that combining finasteride with minoxidil produces better results than either alone. Adding low-level laser therapy or microneedling—creating tiny punctures in the scalp to stimulate healing responses—improves outcomes further.
Hair transplant surgery offers the most dramatic results but doesn't address the underlying process. Surgeons move follicles from the DHT-resistant areas—the sides and back of the head, the Hippocratic wreath—to the balding areas. These transplanted follicles keep their genetic resistance to DHT, which is why transplants are permanent. But the native hair around them continues to thin, sometimes requiring additional procedures.
The Age Paradox
Pattern hair loss gets worse with age, but here's the strange thing: androgen levels fall as men age.
Testosterone decreases. DHT decreases. The enzymes that convert one to the other decrease. The receptors that respond to androgens in the scalp decrease. Sex hormone-binding globulin, which should be protective, actually increases. By age eighty, the ratio of testosterone to SHBG has fallen by as much as eighty percent compared to young adulthood.
All of these changes should protect against hair loss. They don't.
Several explanations have been proposed. One is that local DHT production in the scalp increases with age even as systemic levels fall—balding scalps show higher levels of five-alpha reductase than non-balding scalps. Another is cumulative damage: decades of DHT exposure cause progressive damage to the dermal papilla cells that regulate hair growth. These cells show higher levels of DNA damage and earlier senescence in bald scalps.
There's also the threshold effect. Free testosterone in an eighty-year-old man has fallen to about twice the level found in a twenty-year-old woman. That's still enough to drive hair loss. Studies suggest that testosterone levels need to fall to about thirty percent of normal male levels—roughly what you'd find in a woman—before hair loss stops progressing. Sixty percent, the approximate level in elderly men, is sufficient to continue the process.
The Deeper Question
Pattern hair loss sits at the intersection of genetics, hormones, metabolism, and aging in ways we're only beginning to understand. The same metabolic dysfunction that predicts heart disease and diabetes shows up early as a receding hairline. The same hormones that drive puberty quietly begin a decades-long process of follicular miniaturization.
For anyone experiencing early hair loss, the medical recommendation is clear: get screened for diabetes and metabolic syndrome. The hair loss itself may be cosmetically distressing, but it may also be signaling something more important about your metabolic health.
And for the millions who simply want their hair back, the science offers hope. Those follicles haven't died. They're waiting. The challenge is figuring out how to wake them up.