Native Americans do grow facial hair, but on average it tends to be sparser, finer, and slower to fill in compared to what is typical among men of European or Middle Eastern descent. The primary reason is genetic: a single variant in a gene called EDAR, which is nearly universal in Indigenous American populations, alters the developmental signaling that shapes hair follicles across the body, including the face. The story is more interesting than “one gene, less beard,” though, because that same variant simultaneously affects tooth shape, sweat gland density, and scalp hair thickness, hinting that reduced facial hair was likely a side effect of selection for something else entirely.
The EDAR Gene and What It Actually Does
The gene at the center of this story is EDAR, which encodes a receptor protein involved in a signaling pathway (EDA-EDAR-EDARADD) that operates during prenatal development. This pathway helps determine where hair follicles, sweat glands, and teeth form, and how large and active those structures become. A specific variant of this gene, known as V370A (the substitution of one amino acid for another at position 370), is one of the strongest signals of natural selection ever identified in the human genome. It is found at high frequency in East Asian populations and is essentially fixed in Native American populations, meaning nearly every individual carries it. By contrast, the variant is almost entirely absent in people of European and African descent.
1PubMed. The adaptive variant EDARV370A is associated with straight hair in East AsiansA large genome-wide association study of over 6,000 Latin Americans with mixed Indigenous, European, and African ancestry confirmed that the EDAR gene region is strongly associated with beard thickness. The same chromosomal region also showed connections to eyebrow thickness and the presence of a monobrow, reinforcing that this one stretch of DNA influences multiple hair-related traits at once.
2Nature Communications. A genome-wide association scan in admixed Latin Americans identifies loci influencing facial and scalp hair featuresWhat makes EDAR so consequential is that it does not just tweak one trait. It acts during a critical window of fetal development when the body is laying down the blueprint for skin appendages. Hair follicles on the face are part of this blueprint, and the V370A variant alters how those follicles are specified and sized. The result is follicles that produce finer, less dense facial hair in adulthood. Research in mouse models has shown that the EDA-EDAR pathway works in a tightly choreographed loop with other signaling systems to initiate and maintain hair follicle formation, so even a subtle change in EDAR activity can ripple outward.
3PubMed Central. Reciprocal requirements for EDA/EDAR/NF-kappaB and Wnt/beta-catenin signaling pathways in hair follicle inductionAndrogens Still Matter
Genetics set the blueprint, but hormones execute the construction. Beard growth in all humans is driven by androgens, particularly dihydrotestosterone (DHT). During puberty, rising androgen levels convert tiny, nearly invisible vellus hairs into thicker, pigmented terminal hairs on the face, chest, and elsewhere. This vellus-to-terminal switch is controlled by DHT binding to androgen receptors within the hair follicle’s dermal papilla. When that receptor is activated, the follicle enlarges and begins producing a coarser fiber.
4Clinical and Experimental Dermatology. Not quite naked: the bare necessities of human body hair evolutionNative American men have circulating androgens within normal human ranges. The difference is not in hormone levels but in how facial follicles respond to those hormones. Research has demonstrated that genetically identical hair follicles from different body sites can have dramatically different androgen responses, and that this variation is epigenetic rather than purely hormonal. Intermediate facial follicles exposed to male-level androgens will produce more hair, but their capacity to do so depends on the density and programming of the follicles already present.
5PubMed Central. Androgens trigger different growth responses in genetically identical human hair follicles in organ culture that reflect their epigenetic diversity in lifeIn practical terms, this means a Native American man’s facial follicles may be fewer in number and programmed to remain smaller, even though his testosterone levels would be perfectly capable of stimulating a full beard if the follicle architecture were different. The follicles are not broken or androgen-insensitive in a clinical sense; they are simply built to a different specification, one shaped by the EDAR variant and the developmental pathway it governs.
Why Evolution Favored This Variant
If reduced facial hair were the only thing the EDAR V370A variant did, it would be hard to explain why natural selection drove it to near-total prevalence across entire continental populations. Selection pressures strong enough to fix a variant that quickly usually need a meaningful survival or reproductive advantage. Reduced beard growth alone does not obviously provide one. The answer lies in the variant’s pleiotropy, the fact that it affects multiple traits simultaneously.
Among the most notable co-selected traits is increased eccrine sweat gland density. Research has identified genetic pathways that control the relative patterning of sweat glands and hair follicles on the skin, with higher sweat gland density coming at the cost of lower hair follicle density. The gene En1, identified through mouse studies, acts as a reciprocal switch between these two structures.
6PubMed Central. A genetic basis of variation in eccrine sweat gland and hair follicle densityThe EDAR V370A variant has been associated with greater sweat gland density in human carriers, which would have been a significant advantage for populations migrating through hot, humid environments. The ancestors of today’s Native Americans and East Asians likely passed through tropical and subtropical climates over thousands of years, and more efficient thermoregulation through sweating could have been the primary target of selection. Thinner facial and body hair would then have been a byproduct, carried along because the same developmental program that builds more sweat glands builds fewer and finer hair follicles.
Another co-selected trait is the distinctive shovel shape of upper incisor teeth, which is common in Asian and Native American populations but rare in Europeans and Africans. Studies in Japanese populations found that the number of EDAR 370A alleles an individual carries is strongly correlated with the degree of tooth shoveling.
7PubMed Central. A common variation in EDAR is a genetic determinant of shovel-shaped incisorsThicker scalp hair is yet another effect. The same variant associated with sparser beards produces coarser, straighter head hair with a rounder cross-section. A study of over 1,700 individuals from four East Asian populations found a strong association between V370A and straight hair type, with an additive effect.
1PubMed. The adaptive variant EDARV370A is associated with straight hair in East AsiansSo the package of traits that came with EDAR V370A includes thicker, straighter scalp hair; shovel-shaped incisors; more sweat glands; and reduced facial hair. Which of these was the actual target of selection remains debated, but the thermoregulation hypothesis has the most traction among researchers, partly because increased sweating efficiency has an obvious survival benefit and partly because the timing of the variant’s rise coincides with periods when ancestral populations inhabited warm climates.
Facial Structure Connections
The EDAR variant’s influence extends beyond hair and teeth. A separate genome-wide association study focused on facial morphology found that the same V370A variant is associated with reduced chin protrusion. The derived allele, which is essentially universal in Native Americans, was linked to a less projecting chin in a study of admixed Latin American individuals.
8Nature Communications. A genome-wide association scan implicates DCHS2, RUNX2, GLI3, PAX1 and EDAR in human facial variationThis finding is a reminder that EDAR operates during embryonic development when the face itself is being shaped, not just the skin structures on top of it. The signaling pathway specifies the location and size of ectodermal appendages, but it also interacts with the surrounding tissue architecture. A gene that changes how follicles, glands, and teeth develop in the facial region can, as a downstream consequence, influence the shape of the jaw and chin. Whether this particular connection has any functional significance or is just another pleiotropic side effect is an open question.
The Perception Problem
Part of the reason the question “why don’t Native Americans have facial hair?” is so commonly asked is that the popular perception overstates the case. Native American men are not hairless. Many grow mustaches, goatees, or patchy beards, particularly as they age. Historical accounts by European colonizers sometimes noted facial hair on Indigenous men, though these same accounts were filtered through cultural expectations and biases.
Several factors amplify the perception of hairlessness beyond what genetics alone would predict. First, many Indigenous cultures historically practiced deliberate hair removal on the face. Plucking facial hair with shell tweezers or other implements was a widespread grooming practice across numerous tribal groups in the Americas, well documented in the ethnographic record. When Europeans encountered cleanly plucked faces, they sometimes interpreted this as an inability to grow hair rather than a cultural choice to remove it.
Second, the comparison point matters enormously. European and Middle Eastern populations sit at the high end of the global spectrum for beard density. Men of East Asian descent also tend to have lighter beards than European men, for the same EDAR-related reasons, yet the question is asked less frequently about them, probably because colonialism and the specific history of Euro-Indigenous contact made the comparison more culturally salient in the Americas. If the baseline comparison were East Asian men rather than European men, the difference would seem far less dramatic.
Third, there is considerable individual variation within Native American populations. Some men grow substantial beards, particularly those with some degree of European admixture, which has been widespread across the Americas for over 500 years. The genome-wide association study in Latin Americans estimated average admixture proportions of roughly half European and half Native American in their sample, with substantial individual variation.
2Nature Communications. A genome-wide association scan in admixed Latin Americans identifies loci influencing facial and scalp hair featuresHow Admixture Changes the Picture
The genetics of beard growth are not all-or-nothing. Because the EDAR V370A variant has an additive effect, meaning each copy of the allele incrementally shifts the trait, individuals with mixed ancestry fall along a spectrum. A person who inherits one copy of the derived EDAR allele from a Native American parent and one ancestral copy from a European parent will tend to have intermediate beard thickness. With two copies of the derived allele, the effect on beard reduction is stronger.
The Latin American GWAS identified 18 signals of association with hair traits at genome-wide significance, ten of which were entirely new discoveries. Beard thickness was among the traits studied, and the signals were detectable precisely because the mixed-ancestry study population offered enough genetic variation to separate the contributions of different ancestral backgrounds. This kind of study design is powerful because it avoids confounding genetic effects with environmental or cultural ones: within the same community, under the same climate and diet, individuals with more Indigenous ancestry at the EDAR locus had thinner beards on average.
2Nature Communications. A genome-wide association scan in admixed Latin Americans identifies loci influencing facial and scalp hair featuresOther loci besides EDAR also contribute. The same study found associations between beard thickness and genetic markers in other chromosomal regions, confirming that facial hair is a polygenic trait, influenced by many genes simultaneously. EDAR is the single largest-effect gene identified so far, but it operates within a broader genetic context. This partly explains why two full-blooded Indigenous men from different tribal backgrounds might have noticeably different amounts of facial hair despite both carrying two copies of V370A.
Beards and Sexual Selection in Other Populations
An interesting counterpoint to the EDAR story is the research on why some populations developed thick beards in the first place. One hypothesis, sometimes called the pugilism hypothesis, proposes that beards may have evolved partly as protection during male-on-male physical competition. Research testing this idea found that hair-like fiber mats could absorb energy and reduce the force transmitted to underlying bone, and the authors noted that this protective function could explain why facial hair is associated with perceptions of social dominance and aggressiveness in populations where beards are common.
9PubMed Central. Impact Protection Potential of Mammalian Hair: Testing the Pugilism Hypothesis for the Evolution of Human Facial HairIf sexual selection for beards as signals of dominance did operate in some lineages, it would have been working against the grain in populations where EDAR V370A was already sweeping toward fixation for other reasons. The thermoregulatory advantage of more sweat glands and less body hair may have simply outweighed any benefit of thicker beards, or the cultural systems of these populations may have directed sexual selection along different lines entirely. Indigenous American cultures developed their own markers of attractiveness and social status that did not revolve around facial hair density, which would have further reduced any selective pressure to maintain thick beards.
What Happens Inside the Follicle
At the cellular level, the EDAR pathway intersects with other major signaling systems during follicle development. Research has shown that EDAR is actually a direct target of Wnt signaling, one of the fundamental pathways in embryonic development. Wnt signaling activates EDAR expression, and then EDAR-driven NF-κB signaling feeds back to maintain Wnt activity in the developing hair placode. Disrupting either side of this loop causes follicle development to go awry.
3PubMed Central. Reciprocal requirements for EDA/EDAR/NF-kappaB and Wnt/beta-catenin signaling pathways in hair follicle inductionThe V370A variant does not break this loop; it modifies it. The altered EDAR receptor produces enhanced signaling through the pathway, which paradoxically results in some follicle types becoming more robust (scalp hair gets thicker) while others become less so (facial and body hair becomes finer). The reason for this asymmetry likely lies in the different developmental timing and hormonal context of follicles at different body sites. Scalp follicles are specified early in fetal development and are not androgen-dependent, so enhanced EDAR signaling pushes them toward larger, thicker output. Facial follicles, by contrast, depend on a later androgen-driven switch to become terminal, and the follicular architecture shaped by EDAR during prenatal development determines how responsive they will be to that switch when puberty arrives.
Profiling studies of the EDA pathway during embryonic hair development have identified several downstream effectors, including components of the Sonic Hedgehog pathway and antagonists for both Wnt and BMP signaling.
10PubMed Central. Ectodysplasin regulates the lymphotoxin-beta pathway for hair differentiationThese cascading effects help explain why EDAR mutations that cause complete loss of function result in a medical condition called hypohidrotic ectodermal dysplasia, characterized by absent or severely reduced hair, teeth, and sweat glands across the entire body. The V370A variant is emphatically not a loss-of-function mutation. It is a gain-of-function change that enhances signaling, producing a suite of subtle shifts rather than a dramatic absence. The clinical condition and the normal variant sit at opposite ends of the same biological dial.
Individual Variation and Age
Even among men who carry two copies of the EDAR V370A variant, beard growth is not uniform. Facial hair tends to increase with age in all populations, and some Native American men develop more noticeable growth in their thirties, forties, and beyond, as cumulative androgen exposure gradually coaxes more follicles into producing visible hair. The pace of this process is slower and the ceiling is lower than in populations without the variant, but it is not static.
Diet, overall health, and stress can also modulate androgen levels and follicle sensitivity over time, though these effects are modest compared to the genetic baseline set by EDAR. Men with conditions that increase circulating androgens or DHT sensitivity may see somewhat more facial hair than their peers, while those with lower androgen levels may see less. None of these factors override the underlying follicle architecture, but they add noise to the picture, which is partly why blanket statements about any group’s facial hair capacity are always oversimplifications.
There is also the matter of other genes. The Latin American GWAS found multiple independent loci associated with beard thickness beyond EDAR, and these loci likely vary in frequency across different Indigenous populations. Two men with identical EDAR genotypes but different alleles at these other loci could end up with visibly different beards. The genetics of facial hair are polygenic enough that no single gene tells the full story, even one as powerful as EDAR.
2Nature Communications. A genome-wide association scan in admixed Latin Americans identifies loci influencing facial and scalp hair features