Why Are Some People Hairy? Genetics, Hormones, and More

How hairy you are comes down to a tug-of-war between your genes and your hormones, with the sensitivity of individual hair follicles acting as the referee. Everyone is born with roughly the same number of hair follicles, somewhere around five million, but wide variation in hair thickness, color, length, and distribution means two people can look dramatically different. The real question is not whether you have follicles (you do, nearly everywhere) but what those follicles are doing: producing fine, nearly invisible vellus hairs or thick, pigmented terminal hairs. That distinction is driven by androgens, genetic programming, and a surprising number of other factors that can change across your lifetime.

You Have More Hair Than You Think

A common misconception is that “hairier” people simply have more hair follicles. In reality, humans and chimpanzees have roughly the same hair follicle density across most of the body. The difference is the type of hair those follicles produce. Chimpanzee infants grow thick, pigmented terminal hairs across nearly their entire body, while human infants only produce terminal hair on the scalp, eyelashes, and eyebrows.¹ The rest of a human baby’s body is covered in vellus hair: short (under 2 mm), fine (under 30 micrometers in diameter), and usually unpigmented. In macaques, hair density is roughly two to 21 times higher than in either humans or chimps depending on the body region, but human and chimp densities are surprisingly similar.²

So the follicles are there. What makes some people visibly hairier than others is how many of those vellus follicles get switched over to producing terminal hair. That conversion is the central event in body hair variation, and it depends on three main players: androgens, the genetic blueprint of each follicle, and the follicle’s local sensitivity to hormonal signals.

Androgens Run the Show, But Not in a Straightforward Way

Androgens are the primary hormones responsible for converting vellus follicles into terminal ones during and after puberty. Testosterone and its more potent derivative, dihydrotestosterone (DHT), bind to androgen receptors inside follicle cells and switch on genes that change follicle behavior. Pubic and axillary hair appear relatively early in puberty as testosterone and adrenal hormones rise, though these hairs seem to respond more slowly to the initial neuroendocrine changes than other pubertal milestones.³ Over the following years, chest, back, limb, and facial hair gradually thicken in response to rising androgen levels, more so in males than females because of the higher androgen concentrations involved.

Here is where things get strange. The same androgen, DHT, promotes thick terminal hair growth on the beard and chest but causes the opposite effect on the scalp, where it miniaturizes follicles and drives pattern hair loss. This biological paradox has puzzled researchers for decades.⁴ DHT has been shown to induce early hair regression, follicle miniaturization, and hair density loss in scalp follicles, effects that can be partly reversed by blocking the androgen receptor.⁵ Meanwhile, beard follicles thrive under the same hormonal signal.

The resolution to this paradox lies in what happens inside the follicle after the androgen receptor is activated. Different body sites have different co-activator proteins that modulate how the cell responds to androgens. A molecule called Hic-5/ARA55 is expressed at high levels in dermal papilla cells from the beard and from balding frontal scalp tissue, but at low levels in cells from the non-balding back of the head. Blocking Hic-5/ARA55 suppressed androgen receptor activity by roughly 65 to 71 percent in beard and balding-scalp cells, while it had no significant effect in occipital (non-balding) scalp cells.⁶ In short, follicles in different body regions are wired to react to the same hormone in opposite ways, and the molecular environment inside each follicle determines whether DHT means “grow” or “shrink.”

Your Genetic Blueprint Sets the Range

Hormones are only half the story. Genes determine how many of your follicles are primed to respond to androgens, and they set the baseline thickness and growth rate of your hair. A large genome-wide association study in Latin American populations identified 18 genetic signals linked to various hair traits, including scalp hair shape, balding, eyebrow thickness, beard thickness, monobrow tendency, and even hair greying.⁷ Many of these were the first genetic loci ever reported for those specific traits, which gives you a sense of how recently scientists have begun mapping the genetics of body hair in detail.

A more recent study in East Asian populations pinpointed three genetic loci tied to hair density, implicating genes involved in hair follicle development.⁸ One variant correlated with lower expression of a gene called NRP2 but higher hair density, hinting at a counterintuitive regulatory mechanism where less of a certain protein actually means more visible hair. These findings reinforce something dermatologists have observed clinically for a long time: hair density and distribution differ across ethnic groups in ways that genetics can now start to explain.

Population-level studies confirm these differences directly. Research comparing body hair characteristics across ethnic groups found that Caucasian and North African men had a significantly higher proportion of hair follicles in the active growth phase on cheek and upper-lip regions (above 85 percent) compared to men of African or Chinese descent.⁹ Hair growth rates on the body ranged widely, from about 180 to 485 micrometers per day depending on the site. These are substantial differences and they track with what most people observe anecdotally: body hair patterns vary meaningfully across family lineages and populations, not just between individuals.

Follicle Sensitivity Explains Why Hormones Alone Are Not Enough

Two people with identical androgen levels can have completely different amounts of body hair. The missing piece is follicle sensitivity, which is governed by the density and activity of androgen receptors within each follicle’s dermal papilla cells. Androgen receptors have been confirmed to be present and functionally required in human hair follicles, and genetically identical follicles from different body sites can respond in opposite ways to the same androgen signal.¹⁰ The researchers who demonstrated this attributed the divergent responses to epigenetic diversity: follicles carry the same DNA but have different chemical tags on that DNA depending on their anatomical location, causing different genes to be accessible in different spots.

This is why some women with polycystic ovary syndrome (PCOS) develop pronounced facial and body hair while others with similar androgen levels do not. Hirsutism in PCOS is associated with both androgen excess and the individual response of the pilosebaceous unit (the follicle and its associated oil gland) to androgens.¹¹ Some women develop hirsutism despite having androgen levels that fall within the normal range, simply because their follicles are more sensitive to whatever androgens are present. The enzyme 5-alpha reductase type II, which converts testosterone to the more potent DHT locally within the follicle, plays a key role here. Higher local activity of that enzyme means more DHT at the follicle level, even if blood levels look unremarkable.¹²

When Excess Hair Signals a Medical Condition

There is an important distinction between “naturally hairy” and hair growth that signals an underlying hormonal or genetic problem. Hirsutism refers specifically to the growth of coarse terminal hair in a male-pattern distribution in women, and it results from excess androgen production, often from ovarian or adrenal sources.¹³ PCOS is the most common cause, but hirsutism can also arise from non-classic congenital adrenal hyperplasia, idiopathic hyperandrogenism (where androgen levels are elevated but no tumor or syndrome is identified), or enhanced peripheral conversion of androgen precursors to testosterone.¹⁴ In some cases, hirsutism is idiopathic or triggered by medications.

Hypertrichosis is a separate condition altogether. Unlike hirsutism, it is not driven by androgens and it does not follow a male-pattern distribution. Hypertrichosis is defined as excessive hair growth beyond normal variation for a person’s age, sex, and ethnicity, affecting areas that are not predominantly androgen-dependent. Congenital forms are rare and frequently accompany other clinical features including developmental delay, epilepsy, or complex body malformations.¹⁵ If someone notices sudden generalized hair growth that does not match the typical androgen-driven pattern, it warrants medical evaluation to rule out an underlying disorder.

Clinicians measure hirsutism severity using the modified Ferriman-Gallwey score, which grades hair density across nine body areas.¹⁶ This standardized scoring system helps distinguish normal variation from clinically meaningful excess and guides decisions about whether hormonal workup or treatment is needed.

How Hair Changes Across Your Lifetime

Body hair is not static. The puberty-driven conversion of vellus to terminal hairs is the most dramatic shift, but changes continue throughout life. In men, body hair often continues to thicken and spread through the twenties and into the thirties, well after puberty is technically complete. Ear and nose hairs get coarser with age, and back hair may not appear until middle age in some men.

In women, menopause reshapes the landscape significantly. A population-based study found that body hair loss after menopause was strongly correlated with increasing age and was most pronounced at androgen-sensitive sites. The researchers identified two distinct patterns: a diffuse pattern in which generalized scalp thinning tracked with body hair loss and older age, and a frontal pattern in which scalp thinning at the hairline was associated with higher facial hair scores and relatively younger postmenopausal age.¹⁷ In other words, falling estrogen levels allow residual androgens to exert more influence on facial follicles, which is why some women notice new chin or upper-lip hairs after menopause even as hair elsewhere thins.

Medications That Make You Hairier (or Less So)

Several drugs can shift body hair in either direction. The medications most commonly responsible for hirsutism include testosterone, danazol, anabolic steroids, and glucocorticoids. Hypertrichosis, the non-androgen-driven form of excess hair growth, is a well-known side effect of cyclosporin, minoxidil, and diazoxide.¹⁸ Minoxidil is a particularly interesting case. It was originally developed as a blood-pressure medication, and generalized hair growth was an unwanted side effect. It is now the active ingredient in many over-the-counter hair growth products, but when applied inappropriately or absorbed systemically, it can cause diffuse hypertrichosis. A documented case involved a two-year-old boy who developed generalized excess hair growth after just two months of treatment with topical minoxidil foam.¹⁹

The ability of minoxidil to reverse follicle miniaturization has been demonstrated in a mouse model grafted with human scalp skin from patients with pattern hair loss. Treatment with minoxidil or platelet-rich plasma induced the enlargement of miniaturized follicles back to terminal-sized follicles, confirming that the vellus-to-terminal conversion is not strictly a one-way street.²⁰ This plasticity means that under the right pharmacological conditions, follicles can be nudged back and forth between producing fine vellus hairs and thick terminal ones.

Why Humans Lost Most of Their Body Hair in the First Place

The loss of dense body hair is one of the most visible anatomical changes separating modern humans from other primates. Several hypotheses have been proposed, including improved thermoregulation for endurance running, sexual selection favoring less-hairy mates, enhanced parasite detection (parasites are easier to spot and remove on bare skin), and reduced ectoparasite loads overall.²¹ The thermoregulation hypothesis has gained particular traction. Humans traded dense body hair for an enormously expanded eccrine (sweat) gland system. Human eccrine gland density averages about tenfold higher than that of both macaques and chimpanzees across nearly all body regions.²

Scalp hair, however, was retained and for good reason. Thermal modeling using a heated mannequin has confirmed that scalp hair significantly reduces heat gain from solar radiation. Tightly curled hair provides the most effective protection, minimizing the amount of sweat needed to offset incoming solar heat.²² This finding suggests that the curly hair morphology common in equatorial populations is itself a thermoregulatory adaptation, not merely an aesthetic trait.

The Follicle’s Microbial Neighbors

A newer line of research is examining how the microbial communities living on skin and within hair follicles influence hair growth. Hair follicles are recognized sites of microbial colonization, and the resident bacteria and fungi interact with immune cells to help regulate local inflammation and homeostasis. Shifts in the follicular microbiome have been described in some inflammatory skin conditions, suggesting a connection between microbial imbalance and hair disorders.²³ Whether these microbial communities play a meaningful role in determining normal body hair distribution, rather than just hair disease, remains an open question. The field is young enough that anyone offering firm answers about the microbiome and hairiness is getting ahead of the data.

Hair Variation Across Body Sites

Not all body hair is created equal, even on the same person. Pubic hair shafts and medullas are significantly thicker than those of axillary or scalp hair, a finding confirmed by histomorphological analysis.²⁴ Axillary hair grows at rates close to those of terminal scalp hairs but differs in texture and diameter. These regional differences are maintained by site-specific signaling environments: each follicle operates within a local cocktail of growth factors, hormones, and molecular signals that varies from one patch of skin to the next. The signaling pathways that regulate hair follicle cycling, including Wnt, BMP, Notch, and Hedgehog, are expressed at different levels and different times depending on the follicle’s location.²⁵

This site-specific programming is also why hair removal results differ by body area. Laser hair removal works best on thick, dark terminal hairs with deep follicles, which is why it tends to be more effective on legs and underarms than on the fine vellus hairs of the forearms or face. The same biology that makes some body regions hairier also makes them more responsive to certain treatments, while the lighter, finer hairs that make up most human body coverage resist intervention precisely because their follicles are small and shallow.