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Human skin color
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Human skin color
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Extended Coloured (Afrikaans: Kleurlinge or Bruinmense) family from South Africa showing some spectrum of human skin coloration.

Human skin color ranges from the darkest brown to the lightest hues. Differences in skin color among individuals is caused by variation in pigmentation, which is largely the result of genetics (inherited from one's biological parents), and in adults in particular, due to exposure to the sun, disorders, or some combination thereof. Differences across populations evolved through natural selection and sexual selection, because of social norms and differences in environment, as well as regulation of the biochemical effects of ultraviolet radiation penetrating the skin.[1]

Human skin color is influenced greatly by the amount of the pigment melanin present. Melanin is produced within the skin in cells called melanocytes; it is the main determinant of the skin color of darker-skin humans. The skin color of people with light skin is determined mainly by the bluish-white connective tissue under the dermis and by the hemoglobin circulating in the veins of the dermis. The red color underlying the skin becomes more visible, especially in the face, when, as a consequence of physical exercise, sexual arousal, or the stimulation of the nervous system (e.g. due to anger or embarrassment), arterioles dilate.[2] Color is not entirely uniform across an individual's skin; for example, the skin of the palm and the soles of the feet is lighter than most other skin; this is more noticeable in darker-skinned people.

There is a direct correlation between the geographic distribution of ultraviolet radiation (UVR) and the distribution of indigenous skin pigmentation around the world. Areas that receive higher amounts of UVR, generally located closer to the equator or at higher altitudes, tend to have darker-skinned populations. Areas that are far from the tropics and closer to the poles have lower intensity of UVR, which is reflected in lighter-skinned populations.[3] By the time modern Homo sapiens evolved, all humans were dark-skinned.[1][4] Some researchers suggest that human populations over the past 50,000 years have changed from dark-skinned to light-skinned and that such major changes in pigmentation may have happened in as little as 100 generations (≈2,500 years) through selective sweeps.[5] Natural skin color can also darken as a result of tanning due to exposure to sunlight. The leading theory is that skin color adapts to intense sunlight irradiation to provide partial protection against the ultraviolet fraction that produces damage and thus mutations in the DNA of the skin cells.[6]

The social significance of differences in skin color has varied across cultures and over time, as demonstrated with regard to social status and discrimination.

Melanin and genes

[edit]
See also: Melanin
One possible structure of Eumelanin.

Melanin is produced by cells called melanocytes in a process called melanogenesis. Melanin is made within small membrane–bound packages called melanosomes. As they become full of melanin, they move into the slender arms of melanocytes, from where they are transferred to the keratinocytes. Under normal conditions, melanosomes cover the upper part of the keratinocytes and protect them from genetic damage. One melanocyte supplies melanin to thirty-six keratinocytes according to signals from the keratinocytes. They also regulate melanin production and replication of melanocytes.[5] People have different skin colors mainly because their melanocytes produce different amount and kinds of melanin.

The genetic mechanism behind human skin color is mainly regulated by the enzyme tyrosinase, which creates the color of the skin, eyes, and hair shades.[7][8] Differences in skin color are also attributed to differences in size and distribution of melanosomes in the skin.[5] Melanocytes produce two types of melanin. The most common form of biological melanin is eumelanin, a brown-black polymer of dihydroxyindole carboxylic acids, and their reduced forms. Most are derived from the amino acid tyrosine. Eumelanin is found in hair, areola, and skin, and the hair colors gray, black, blond, and brown. In humans, it is more abundant in people with dark skin. Pheomelanin, a pink to red hue is found in particularly large quantities in red hair,[9] the lips, nipples, glans of the penis, and vagina.[10]

Both the amount and type of melanin produced is controlled by a number of genes that operate under incomplete dominance.[11] One copy of each of the various genes is inherited from each parent. Each gene can come in several alleles, resulting in the great variety of human skin tones. Melanin controls the amount of ultraviolet (UV) radiation from the sun that penetrates the skin by absorption. While UV radiation can assist in the production of vitamin D, excessive exposure to UV can damage health.

Evolution of skin color

[edit]
Further information: Melanocortin 1 receptor

Time scale of skin color evolution

[edit]

Loss of body hair in Homo links to the thermoregulation through perspiration heat dissipation required for activity in hot open environments[12] and endurance running.[13] Humans as primates have a particular need for this thermoregulation since unlike other mammals they lack a carotid rete that allows precooling of blood to the brain, an organ extremely sensitive to changes in body temperature.[14] Given endurance running and its needs for thermoregulation arose with H. erectus,[15] this links hairlessness with the origin of H. erectus[13] about 2 million years ago.[16]

As hominids gradually lost their fur between 1.2 and 4 million years ago, to allow for better cooling through sweating, their naked skin was exposed to sunlight. In the tropics, natural selection favoured dark-skinned human populations as high levels of skin pigmentation protected against the harmful effects of sunlight. Indigenous populations' skin reflectance (the amount of sunlight the skin reflects) and the actual UV radiation in a particular geographic area is highly inversely correlated, which supports this idea. Genetic evidence also supports this notion, demonstrating that around 1.2 million years ago there was a strong evolutionary pressure which acted on the development of dark skin pigmentation in early members of the genus Homo.[17] Hairlessness exposes folate circulating subcutaneously and in the dermis to degradation from UV-radiation.[18] The effect of sunlight on folic acid levels has been crucial in the development of dark skin and favored the emergence of skin pigmentation in order to protect from folate depletion due to the increased exposure to sunlight.[6][19]

In 2017, a study showed that both dark and light pigmentation alleles arose before the origin of modern humans,[20] with the older version of the variants in many cases being associated with lighter skin.[21] The earliest hominid ancestors of humans most likely had pale non-pigmented skin covered with dark black hair, like the chimpanzee and other great apes.[22][23]

With the evolution of hairless skin, abundant sweat glands, and skin rich in melanin, early humans could walk, run, and forage for food for long periods of time under the hot sun without brain damage due to overheating, giving them an evolutionary advantage over other species.[5] Research on the MC1R alleles using assumptions about past population size and an absence of population bottlenecks suggests the allele for dark skin present in modern Africans arose at least by 1.2 million years ago.[24]

This was the genotype inherited by anatomically modern humans, but retained only by part of the extant populations, thus forming an aspect of human genetic variation. About 100,000–70,000 years ago, some anatomically modern humans (Homo sapiens) began to migrate away from the tropics to the north where they were exposed to less intense sunlight. This was possibly in part due to the need for greater use of clothing to protect against the colder climate. Under these conditions there was less photodestruction of folate and so the evolutionary pressure working against the survival of lighter-skinned gene variants was reduced. In addition, lighter skin is able to generate more vitamin D (cholecalciferol) than darker skin, so it would have represented a health benefit in reduced sunlight if there were limited sources of vitamin D.[25] Hence the leading hypothesis for the evolution of human skin color proposes that:

  1. From the origin of hairlessness and exposure to UV-radiation to less than 100,000 years ago, archaic humans, including archaic Homo sapiens, were dark-skinned.
  2. As some Homo sapiens populations began to migrate, the evolutionary constraint keeping skin dark decreased proportionally to the distance north a population migrated, resulting in a range of skin tones within northern populations, although the bulk of humans remained dark-skinned.
  3. At some point, some northern populations experienced positive selection for lighter skin due to the increased production of vitamin D from sunlight and the genes for darker skin disappeared from these populations.
  4. Subsequent migrations into different UV environments and admixture between populations have resulted in the varied range of skin pigmentations we see today.

The genetic mutations leading to light skin, though partially different among East Asians and Western Europeans,[26] suggest the two groups experienced a similar selective pressure after settlement in northern latitudes.[27]

The theory is partially supported by a study into the SLC24A5 gene which found that the allele associated with light skin in Europe "determined […] that 18,000 years had passed since the light-skin allele was fixed in Europeans" but may have originated as recently as 12,000–6,000 years ago "given the imprecision of method" ,[28] which is in line with the earliest evidence of farming.[29] Paleolithic Cro-Magnon groups, as well as Early Holocene Western and central European hunter-gatherers (Western Hunter Gatherers) have been suggested to have been dark skinned based on DNA analysis,[30] with a number of the most prominent light-skin tone gene variants found in modern Europeans being introduced by Anatolian Neolithic Farmers that migrated into Europe beginning around 9,000 years ago,[31] with selection pressure for lighter skin intensifying from the Neolithic period onwards.[31][32]

Research by Nina Jablonski suggests that an estimated time of about 10,000 to 20,000 years is enough for human populations to achieve optimal skin pigmentation in a particular geographic area but that development of ideal skin coloration may happen faster if the evolutionary pressure is stronger, even in as little as 100 generations. The length of time is also affected by cultural practices such as food intake, clothing, body coverings, and shelter usage which can alter the ways in which the environment affects populations.[5]

Evolutionary model of human pigmentation in three continental populations. The colors of the branches roughly indicate the generalized skin pigmentation level of these populations.[33]

Population and admixture studies suggest a three-way model for the evolution of human skin color, with dark skin evolving in early Homo sapiens in Africa and light skin evolving only recently after modern humans had expanded out of Africa. For the most part, the evolution of light skin has followed different genetic paths in Western and Eastern Eurasian populations; however, some mutations associated with lighter skin have estimated origin dates after humans spread out of Africa but before the divergence of the two lineages.[34]

According to Crawford et al. (2017), most of the genetic variants associated with light and dark pigmentation in African populations appear to have originated more than 300,000 years ago.[35] African, South Asian and Australo-Melanesian populations also carry derived alleles for dark skin pigmentation that are not found in Europeans or East Asians.[36] Huang et al. 2021 found the existence of "selective pressure on light pigmentation in the ancestral population of Europeans and East Asians", prior to their divergence from each other. Skin pigmentation was also found to be affected by directional selection towards darker skin among Africans, as well as lighter skin among Eurasians.[37] Crawford et al. (2017) similarly found evidence for selection towards light pigmentation prior to the divergence of West Eurasians and East Asians.[36]

Functional considerations

[edit]

Elias et. al. in 2010 showed a superior barrier function in darkly pigmented skin. Most protective functions of the skin, including the permeability barrier and the antimicrobial barrier, reside in the stratum corneum and the researchers surmise that the stratum corneum has undergone the most genetic change since the loss of human body hair. Natural selection would have favored mutations that protect this essential barrier; one such protective adaptation is the pigmentation of interfollicular epidermis, because it improves barrier function as compared to non-pigmented skin.[38]

The authors argue that lack of significant differences between modern light-skinned and dark-skinned populations in vitamin D deficiency, early death from UV-induced cancers and birth defects — as well as instances of light and dark populations living side-by-side in areas with similar UV — suggest the standard model is insufficient to explain the strong selection drive for pigmented skin.[38] Jablonski rejects this theory on the grounds that the human tanning response is driven by UV-B exposure, not xeric stress, and that the positive selection for vitamin D production is "well-established".[4]

Genetics

[edit]
See also: Human genetic variation and Race and genetics

To some extent, skin color is determined independently of eye and hair color, as can be seen from variation in skin coloration in human populations.[39][40][34]

For skin color, heritability is very high, even though it can be modified by exposure to sunlight.[26]

A recent systematic study found 169 genes involved in human skin coloration. Most of the genes were involved in melanosome biogenesis, endosomal transport, and gene regulation. Notably, the function of these genes was verified in tissue culture experiments using CRISPR-Cas9 knockouts, showing that these genes are indeed involved in melanin production.[41]

Dark skin

[edit]
Main article: Dark skin

All modern humans share a common ancestor who lived around 200,000 years ago in Africa.[42] Comparisons between known skin pigmentation genes in chimpanzees and modern Africans show that dark skin evolved along with the loss of body hair about 1.2 million years ago and that this common ancestor had dark skin.[43] Investigations into dark-skinned populations in South Asia and Melanesia indicate that skin pigmentation in these populations is due to the preservation of this ancestral state and not due to new variations on a previously lightened population.[44]

MC1R

[edit]
MC1R (rs885479)

The melanocortin 1 receptor (MC1R) gene is primarily responsible for determining whether pheomelanin and eumelanin are produced in the human body. Research shows at least 10 differences in MC1R between African and chimpanzee samples and that the gene has probably undergone a strong positive selection (a selective sweep) in early Hominins around 1.2 million years ago.[45] This is consistent with positive selection for the high-eumelanin phenotype seen in Africa and other environments with high UV exposure.[43][44]

Light skin

[edit]
Main article: Light skin
History of human skin pigmentation in Eurasia based on genetics

For the most part, the evolution of light skin has followed different genetic paths in European and East Asian populations.

KITLG

[edit]
KITLG (rs1881227)

The KIT ligand (KITLG) gene is involved in the permanent survival, proliferation and migration of melanocytes.[46] A mutation in this gene, A326G (rs642742[47]), has been positively associated with variations of skin color in African-Americans of mixed West African and European descent and is estimated to account for 15–20% of the melanin difference between African and European populations.[48][49] and occurs in over 80% of European and Asian samples, compared with less than 10% in African samples.[48]

ASIP

[edit]

Studies have found two alleles in the vicinity of ASIP Agouti signalling peptide are associated with skin color variation in humans. One, rs2424984,[50] has been identified as an indicator of skin reflectance in a forensics analysis of human phenotypes across Caucasian, African-American, South Asian, East Asian, Hispanic and Native American populations[51] and is about three times more common in non-African populations than in Africa.[52] The other allele, 8188G (rs6058017[53]) is significantly associated with skin color variation in African-Americans and the ancestral version occurs in only 12% of European and 28% of East Asian samples compared with 80% of West African samples.[54]

Europe

[edit]

A number of genes have been positively associated with the skin pigmentation difference between European and non-European populations. Mutations in SLC24A5 and SLC45A2 are believed to account for the bulk of this variation and show very strong signs of selection. A variation in TYR has also been identified as a contributor.

Research indicates the selection for the light-skin alleles of these genes in Europeans is comparatively recent, having occurred later than 20,000 years ago and perhaps as recently as 12,000 to 6,000 years ago.[34] In the 1970s, Luca Cavalli-Sforza suggested that the selective sweep that rendered light skin ubiquitous in Europe might be correlated with the advent of farming and thus have taken place only around 6,000 years ago;[28] This scenario found support in a 2014 analysis of Mesolithic (7,000 years old) hunter-gatherer DNA from La Braña, Spain, which showed a version of these genes not corresponding with light skin color.[55]

In 2015, researchers analysed for light skin genes in the DNA of 94 ancient skeletons ranging from 8,000 to 3,000 years old from Europe and Russia. They found c. 8,000-year-old hunter-gatherers in Spain, Luxembourg, and Hungary were dark skinned while similarly aged hunter gatherers in Sweden were light skinned (having predominately derived alleles of SLC24A5, SLC45A2 and also HERC2/OCA2). Neolithic farmers entering Europe at around the same time were intermediate, being nearly fixed for the derived SLC24A5 variant but only having the derived SLC45A2 allele in low frequencies. The SLC24A5 variant spread very rapidly throughout central and southern Europe from about 8,000 years ago, whereas the light skin variant of SLC45A2 spread throughout Europe after 5,800 years ago.[56][57]

Some authors have expressed caution regarding the skin pigmentation predictions. According to Ju et al. (2021), in a study addressing 40,000 years of modern human history, stated:

"Relatively dark skin pigmentation in Early Upper Paleolithic Europe would be consistent with those populations being relatively poorly adapted to high-latitude conditions as a result of having recently migrated from lower latitudes. On the other hand, although we have shown that these populations carried few of the light pigmentation alleles that are segregating in present-day Europe, they may have carried different alleles that we cannot now detect."[58]

SLC24A5
[edit]

Solute carrier family 24 member 5 (SLC24A5) regulates calcium in melanocytes and is important in the process of melanogenesis.[59] The SLC24A5 gene's derived Ala111Thr allele (rs1426654[60]) has been shown to be a major factor in light skin pigmentation and is common in Western Eurasia.[51] Recent studies have found that the variant represents as much as 25–40% of the average skin tone difference between Europeans and West Africans.[26][61] This derived allele is a reliable predictor of phenotype across a range of populations.[62][63] It has been the subject of recent selection in Western Eurasia, and is fixed in European populations.[34][64][65]

SLC45A2
[edit]

Solute carrier family 45 member 2 (SLC45A2 or MATP) aids in the transport and processing of tyrosine, a precursor to melanin. It has also been shown to be one of the significant components of the skin color of modern Europeans through its Phe374Leu (rs16891982[66]) allele that has been directly correlated with skin color variation across a range of populations.[67][68][62][51][63] This variation is ubiquitous in European populations but extremely rare elsewhere and shows strong signs of selection.[64][65][69]

TYR
[edit]

The TYR gene encodes the enzyme tyrosinase, which is involved in the production of melanin from tyrosine. It has an allele, Ser192Tyr (rs1042602[70]), found solely in 40–50% of Europeans[26][34] and linked to light-colored skin in studies of South Asian[63] and African-American[71] populations.

East Asia

[edit]

A number of genes known to affect skin color have alleles that show signs of positive selection in East Asian populations. Of these, only OCA2 has been directly related to skin color measurements, while DCT, MC1R and ATRN are marked as candidate genes for future study.

OCA2
[edit]
OCA2 (rs12913832)

Oculocutaneous albinism II (OCA2) assists in the regulation of pH in melanocytes. The OCA2 gene's derived His615Arg (rs1800414[72]) allele has been shown to account for about 8% of the skin tone difference between African and East Asian populations in studies of an East Asian population living in Toronto and a Chinese Han population. This variant is essentially restricted to East Asia, with highest frequencies in Eastern East Asia (49–63%), midrange frequencies in Southeast Asia, and the lowest frequencies in Western China and some Eastern European populations.[73][74]

Candidate genes
[edit]

A number of studies have found genes linked to human skin pigmentation that have alleles with statistically significant frequencies in Chinese and East Asian populations. While not linked to measurements of skin tone variation directly, dopachrome tautomerase (DCT or TYRP2 rs2031526[75][76]), melanocortin 1 receptor (MC1R) Arg163Gln (rs885479[77][78]) and attractin (ATRN[26]) have been indicated as potential contributors to the evolution of light skin in East Asian populations.

Tanning response

[edit]

Tanning response in humans is controlled by a variety of genes. MC1R variants Arg151Sys (rs1805007[79]), Arg160Trp (rs1805008[80]), Asp294Sys (rs1805009[81]), Val60Leu (rs1805005[82]) and Val92Met (rs2228479[83]) have been associated with reduced tanning response in European and/or East Asian populations. These alleles show no signs of positive selection and only occur in relatively small numbers, reaching a peak in Europe with around 28% of the population having at least one allele of one of the variations.[44][84] A study of self-reported tanning ability and skin type in American non-Hispanic Caucasians found that SLC24A5 Phe374Leu is significantly associated with reduced tanning ability and also associated TYR Arg402Gln (rs1126809[85]), OCA2 Arg305Trp (rs1800401[86]) and a 2-SNP haplotype in ASIP (rs4911414[87] and rs1015362[88]) to skin type variation within a "fair/medium/olive" context.[89]

Albinism

[edit]
Main article: Albinism in humans

Oculocutaneous albinism (OCA) is a lack of pigment in the eyes, skin and sometimes hair that occurs in a very small fraction of the population. The four known types of OCA are caused by mutations in the TYR, OCA2, TYRP1, and SLC45A2 genes.[90]

Age

[edit]

In hominids, the parts of the body not covered with hair, like the face and the back of the hands, start out pale in infants and turn darker as the skin is exposed to more sun. All human babies are born pale, regardless of what their adult color will be. In humans, melanin production does not peak until after puberty.[5]

The skin of children becomes darker as they go through puberty and experience the effects of sex hormones.[91] This darkening is especially noticeable in the skin of the nipples, the areola of the nipples, the labia majora in females, and the scrotum in males. In some people, the armpits become slightly darker during puberty. The interaction of genetic, hormonal, and environmental factors on skin coloration with age is still not adequately understood, but it is known that men are at their darkest baseline skin color around the age of 30, without considering the effects of tanning.[5]

Human skin color fades with age. Humans over the age of thirty experience a decrease in melanin-producing cells by about 10% to 20% per decade as melanocyte stem cells gradually die.[92] The skin of face and hands has about twice the amount of pigment cells as unexposed areas of the body, as chronic exposure to the sun continues to stimulate melanocytes. The blotchy appearance of skin color in the face and hands of older people is due to the uneven distribution of pigment cells and to changes in the interaction between melanocytes and keratinocytes.[5]

Sexual dimorphism

[edit]

Women from some darker-skinned populations may have lighter skin than men so their bodies can absorb more vitamin D during pregnancy, which improves calcium absorption.[25] In light skinned populations, namely those of European descent, multiple different studies using up-to-date and robust statistical methods find that women have similar skin color as men.

It is unknown why skin color is sexually dimorphic in some populations. Prior to menopause, women may have darker skin than men due to the female sex hormone estrogen increasing skin pigmentation.[93] To the extent that women's skin is darker than men's results in lower rates of skin cancer in women than men.[94]

In populations where women have lighter skin than men, it has been hypothesized that the requirement for high amounts of calcium during pregnancy and lactation may be related to the dimorphism. Breastfeeding newborns, whose skeletons are growing, require high amounts of calcium intake from the mother's milk (about 4 times more than during prenatal development),[95] part of which comes from reserves in the mother's skeleton.[5]

Adequate vitamin D resources are needed to absorb calcium from the diet, and it has been shown that deficiencies of vitamin D and calcium increase the likelihood of various birth defects such as spina bifida and rickets. Natural selection may have led to females with lighter skin than males in some indigenous populations because women must get enough vitamin D and calcium to support the development of fetus and nursing infants and to maintain their own health.[5] However, some authors have cast doubt on the theory that vitamin D synthesis is related to the sexual dimorphism of human skin color in these populations.[96]

The sexes also differ in how their skin color changes over time.[93] Women's pigmentation in certain parts of their body, such as the areola and nipples, changes throughout the menstrual cycle and during pregnancy. Between 50 and 70% of pregnant women will develop the "mask of pregnancy", which refers to the browning and yellowing of the cheeks, upper lips, and forehead that occurs during pregnancy.[5] This is caused by increases in estrogen, and it can also develop in women who take birth control pills or due to hormone replacement therapy.[97]

Disorders of pigmentation

[edit]

Uneven pigmentation of some sort affects most people, regardless of bioethnic background or skin color. Skin may either appear lighter, or darker than normal, or lack pigmentation at all; there may be blotchy, uneven areas, patches of brown to gray discoloration or freckling. Apart from blood-related conditions such as jaundice, carotenosis, or argyria, skin pigmentation disorders generally occur because the body produces either too much or too little melanin.

Depigmentation

[edit]
Main article: Depigmentation

Albinism

[edit]

Some types of albinism affect only the skin and hair, while other types affect the skin, hair and eyes, and in rare cases only the eyes. All of them are caused by different genetic mutations. Albinism is a recessively inherited trait in humans where both pigmented parents may be carriers of the gene and pass it down to their children. Each child has a 25% chance of being albino and a 75% chance of having normally pigmented skin.[98] One common type of albinism is oculocutaneous albinism or OCA, which has many subtypes caused by different genetic mutations. Albinism is a serious problem in areas of high sunlight intensity, leading to extreme sun sensitivity, skin cancer, and eye damage.[5]

Albinism is more common in some parts of the world than in others, but it is estimated that 1 in 70 humans carry the gene for OCA. The most severe type of albinism is OCA1A, which is characterized by complete, lifelong loss of melanin production, other forms of OCA1B, OCA2, OCA3, OCA4, show some form of melanin accumulation and are less severe.[5] The four known types of OCA are caused by mutations in the TYR, OCA2, TYRP1, and SLC45A2 genes.[90]

Albinos often face social and cultural challenges (even threats), as the condition is often a source of ridicule, racism, fear, and violence. Many cultures around the world have developed beliefs regarding people with albinism. Albinos are persecuted in Tanzania by witchdoctors, who use the body parts of albinos as ingredients in rituals and potions, as they are thought to possess magical power.[99]

Vitiligo

[edit]
Former Chief Justice of India, P. Sathasivam, has vitiligo.

Vitiligo is a condition that causes depigmentation of sections of skin. It occurs when melanocytes die or are unable to function. The causes of vitiligo are not clear, but research suggests several possibilities, including autoimmune reactions, genetic make-up, oxidative stress, and neural or viral causes.[100] The incidence worldwide is less than 1%.[101] Individuals affected by vitiligo sometimes suffer psychological discomfort because of their appearance.[5]

Hyperpigmentation

[edit]

Increased melanin production, also known as hyperpigmentation, can be a few different phenomena:

  • Melasma describes the darkening of the skin. A type of Melasma is Chloasma, the skin discolorations caused by hormones. These hormonal changes are usually the result of pregnancy, birth control pills or estrogen replacement therapy.
  • Solar lentigo, also known as "liver spots" or "senile freckles", refers to darkened spots on the skin caused by aging and the sun. These spots are quite common in adults with a long history of unprotected sun exposure.

Aside from sun exposure and hormones, hyperpigmentation can be caused by skin damage, such as remnants of blemishes, wounds or rashes.[102] This is especially true for those with darker skin tones.

The most typical cause of darkened areas of skin, brown spots or areas of discoloration is unprotected sun exposure. Once incorrectly referred to as liver spots, these pigment problems are not connected with the liver.

On lighter to medium skin tones, solar lentigenes emerge as small- to medium-sized brown patches of freckling that can grow and accumulate over time on areas of the body that receive the most unprotected sun exposure, such as the back of the hands, forearms, chest, and face. For those with darker skin colors, these discolorations can appear as patches or areas of ashen-gray skin.

Exposure to the sun

[edit]
See also: Sun tanning
A suntanned arm showing darker skin where it has been exposed. This pattern of tanning is often called a farmer's tan.

Melanin in the skin protects the body by absorbing solar radiation. In general, the more melanin there is in the skin the more solar radiation can be absorbed. Excessive solar radiation causes direct and indirect DNA damage to the skin and the body naturally combats and seeks to repair the damage and protect the skin by creating and releasing further melanin into the skin's cells. With the production of the melanin, the skin color darkens, but can also cause sunburn. The tanning process can also be created by artificial UV radiation.

There are two different mechanisms involved. Firstly, the UVA-radiation creates oxidative stress, which in turn oxidizes existing melanin and leads to rapid darkening of the melanin, also known as IPD (immediate pigment darkening). Secondly, there is an increase in production of melanin known as melanogenesis.[103] Melanogenesis leads to delayed tanning and first becomes visible about 72 hours after exposure. The tan that is created by an increased melanogenesis lasts much longer than the one that is caused by oxidation of existing melanin. Tanning involves not just the increased melanin production in response to UV radiation but the thickening of the top layer of the epidermis, the stratum corneum.[5]

A person's natural skin color affects their reaction to exposure to the sun. Generally, those who start out with darker skin color and more melanin have better abilities to tan. Individuals with very light skin and albinos have no ability to tan.[104] The biggest differences resulting from sun exposure are visible in individuals who start out with moderately pigmented brown skin: the change is dramatically visible as tan lines, where parts of the skin which tanned are delineated from unexposed skin.[5]

Modern lifestyles and mobility have created mismatch between skin color and environment for many individuals. Vitamin D deficiencies and UVR overexposure are concerns for many. It is important for these people individually to adjust their diet and lifestyle according to their skin color, the environment they live in, and the time of year.[5] For practical purposes, such as exposure time for sun tanning, six skin types are distinguished following Fitzpatrick (1975), listed in order of decreasing lightness:

Fitzpatrick scale

[edit]
Main article: Fitzpatrick scale

The following list shows the six categories of the Fitzpatrick scale in relation to the 36 categories of the older von Luschan scale:[105][106]

Type Also called Sunburning Tanning behavior Von Luschan's chromatic scale
I Light, pale white Always Never 0–6
II White, fair Usually Minimally 7–13
III Medium white to light brown Sometimes Uniformly 14–20
IV Olive, moderate brown Rarely Easily 21–27
V Brown, dark brown Very rarely Very easily 28–34
VI Very dark brown to black Never Rarely 35–36

Dark skin with large concentrations of melanin protects against ultraviolet light and skin cancers; light-skinned people have about a tenfold greater risk of dying from skin cancer, compared with dark-skinned persons, under equal sunlight exposure. Furthermore, UV-A rays from sunlight are believed to interact with folic acid in ways that may damage health.[107] In a number of traditional societies the sun was avoided as much as possible, especially around noon when the ultraviolet radiation in sunlight is at its most intense. Midday was a time when people stayed in the shade and had the main meal followed by a nap, a practice similar to the modern siesta.

Geographic variation

[edit]

Approximately 10% of the variance in skin color occurs within regions, and approximately 90% occurs between regions.[108] Because skin color has been under strong selective pressure, similar skin colors can result from convergent adaptation rather than from genetic relatedness; populations with similar pigmentation may be genetically no more similar than other widely separated groups. Furthermore, in some parts of the world where people from different regions have mixed extensively, the connection between skin color and ancestry has substantially weakened.[109] In Brazil, for example, skin color is not closely associated with the percentage of recent African ancestors a person has, as estimated from an analysis of genetic variants differing in frequency among continent groups.[110]

In general, people living close to the equator are highly darkly pigmented, and those living near the poles are generally very lightly pigmented. The rest of humanity shows a high degree of skin color variation between these two extremes, generally correlating with UV exposure. The main exception to this rule is in the New World, where people have only lived for about 10,000 to 15,000 years and show a less pronounced degree of skin pigmentation.[5]

In recent times, humans have become increasingly mobile as a consequence of improved technology, domestication, environmental change, strong curiosity, and risk-taking. Migrations over the last 4000 years, and especially the last 400 years, have been the fastest in human history and have led to many people settling in places far away from their ancestral homelands. This means that skin colors today are not as confined to geographical location as they were previously.[5]

Social status, colorism and racism

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Main article: Discrimination based on skin color
Skin colors according to von Luschan's chromatic scale

According to classical scholar Frank Snowden, skin color did not determine social status in ancient Egypt, Greece or Rome. These ancient civilizations viewed relations between the major power and the subordinate state as more significant in a person's status than their skin colors.[111][page needed]

Some social groups favor specific skin coloring. The preferred skin tone varies by culture and has varied over time. A number of indigenous African groups, such as the Maasai, associated pale skin with being cursed or caused by evil spirits associated with witchcraft. They would abandon their children born with conditions such as albinism and showed a sexual preference for darker skin.[112]

Many cultures have historically favored lighter skin for women. Before the Industrial Revolution, inhabitants of the continent of Europe preferred pale skin, which they interpreted as a sign of high social status. The poorer classes worked outdoors and got darker skin from exposure to the sun, while the upper class stayed indoors and had light skin. Hence light skin became associated with wealth and high position.[113] Women would put lead-based cosmetics on their skin to whiten their skin tone artificially.[114] However, when not strictly monitored, these cosmetics caused lead poisoning.

Colonization and enslavement was a cause of discrimination due to skin color and racism.[115] Slavery in the Americas led to the perception that lighter-skinned African-Americans were more intelligent and cooperative. Such lighter-skinned individuals had a greater likelihood of receiving preferential treatment from overseers and for opportunities for higher education.[116] The preference for fair skin remained prominent until the end of the Gilded Age, but racial stereotypes about worth and beauty persisted throughout the 20th century.[117]

A preference for fair or lighter skin continues in some countries, including Latin American countries where whites form a minority.[118] In Brazil, a dark-skinned person is more likely to experience discrimination.[119]

Significant exceptions to a preference for lighter skin started to appear in Western culture in the mid-20th century.[120] Though sun-tanned skin was once associated with the sun-exposed manual labor of the lower class, the associations became dramatically reversed during this time—a change usually credited to the trendsetting Frenchwoman Coco Chanel (1883–1971) presenting tanned skin as fashionable, healthy, and luxurious.[121]

Many people within the United States regard tanned skin as both more attractive and healthier than pale or very dark skin.[122][123][124] Pale skin has become associated with indoor office-work while tanned skin has become associated with increased leisure time, sportiness and good health that comes with wealth and higher social status.[113] Studies have also emerged indicating that the degree of tanning is directly related to how attractive a young woman is.[125][126]

Skin whitening

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Main article: Skin whitening
Skin lightening soaps

In South Asia, society regards fair skin as more attractive and associates dark skin with lower class status. This results in a massive market for skin-whitening creams.[127] Fairer skin-tones also correlate to higher caste-status in the Hindu social order—although the system is not based on skin tone.[128] Actors and actresses in Indian cinema tend to have light skin tones, and Indian cinematographers have used graphics and intense lighting to achieve more "desirable" skin tones.[129] Fair skin tones are advertised as an asset in Indian marketing.[130]

In 2013, 77% of Nigerian women, 52% of Senegalese women, and 25% of Malian women were using lightening products.[131][132] In 2020, Der Spiegel reported that in Ghana, "When You Are Light-Skinned, You Earn More", and that "[s]ome pregnant women take tablets in the hopes that it will lead their child to be born with fair skin. Some apply bleaching lotion [...] to their babies, in the hopes that it will improve their child's chances."[133]

Skin-whitening products have remained popular over time, often due to historical beliefs and perceptions about fair skin. Sales of skin-whitening products across the world grew from $40 billion to $43 billion in 2008.[134] In South and East Asian countries, people have traditionally seen light skin as more attractive, and a preference for lighter skin remains prevalent. In ancient China and Japan, for example, pale skin can be traced back to ancient drawings depicting women and goddesses with fair skin tones.[citation needed] In ancient China, Japan, and Southeast Asia, pale skin was seen as a sign of wealth. Thus skin-whitening cosmetic products are popular in East Asia.[135]

In 2010, four out of ten women surveyed in Hong Kong, Malaysia, the Philippines and South Korea used a skin-whitening cream, and more than 60 companies globally compete for Asia's estimated $18 billion market.[136] Changes in regulations in the cosmetic industry led to skin-care companies introducing harm-free skin lighteners. In Japan, the geisha have a reputation for their white-painted faces, and the appeal of the bihaku (美白), or "beautiful white", ideal leads many Japanese women to avoid any form of tanning.[137]

There are exceptions to this, with Japanese fashion trends such as ganguro emphasizing tanned skin. Skin whitening is also not uncommon in Africa,[138][139] and several research projects have suggested a general preference for lighter skin in the African-American community.[140] In contrast, one study on men of the Bikosso tribe in Cameroon found no preference for attractiveness of females based on lighter skin color, bringing into question the universality of earlier studies that had exclusively focused on skin-color preferences among non-African populations.[141]

See also

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References

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Further reading

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Human skin color

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Human skin color encompasses the spectrum of pigmentation observed across populations, from very light to very dark, arising primarily from differential production of by epidermal melanocytes as an to varying radiation (UVR) intensities. This pigmentation is governed by the relative amounts of two melanin types: eumelanin, which imparts brown to black hues and predominates in darker skin for UV protection against DNA damage and folate degradation, and pheomelanin, which contributes reddish-yellow tones more prevalent in er skin tones. In equatorial regions with high UVR, darker constitutive pigmentation evolved to mitigate risks and , whereas in higher latitudes with scant UVR, lighter skin facilitates sufficient dermal penetration for photosynthesis essential for calcium absorption and skeletal health. Genetic analyses reveal a polygenic basis involving at least 15-20 loci under , with variants like those in SLC24A5 and SLC45A2 showing signatures of positive selection for outside , underscoring the clinal yet population-specific patterns of variation rather than discrete racial categories.31324-7) Controversies persist regarding the precise timing of pigmentation shifts during human migrations and the relative influences of versus UVR-driven , though empirical genomic data affirm UVR as the dominant selective pressure.

Biological foundations

Melanin production and types

is synthesized by melanocytes, specialized pigment-producing cells derived from cells and located primarily in the basal layer of the . These cells generate within subcellular organelles known as melanosomes, which are then transferred to adjacent for distribution throughout the skin. The process, termed melanogenesis, is regulated by hormonal signals such as alpha-melanocyte-stimulating hormone (α-MSH) and environmental factors like ultraviolet radiation. The melanin biosynthesis pathway commences with the amino acid L-tyrosine, which serves as the primary substrate. The rate-limiting enzyme tyrosinase catalyzes the initial steps: hydroxylation of L-tyrosine to L-3,4-dihydroxyphenylalanine (L-DOPA), followed by oxidation to dopaquinone. Dopaquinone is a pivotal intermediate; in the absence of sulfhydryl groups like cysteine, it undergoes cyclization and polymerization to form eumelanin precursors, while conjugation with cysteine diverts the pathway toward pheomelanin synthesis. Additional enzymes, including tyrosinase-related protein 1 (TYRP1) and dopachrome tautomerase (DCT or TYRP2), facilitate downstream modifications, particularly in eumelanin production. Two principal types of contribute to human pigmentation: eumelanin and pheomelanin. Eumelanin exists in black and brown variants, forming insoluble polymers that impart dark pigmentation and provide robust photoprotection against radiation. Pheomelanin, in contrast, consists of red-yellow pigments that are sulfur-containing and associated with lighter tones, freckling, and increased UV sensitivity. The relative proportions of these melanins, influenced by genetic and environmental factors, determine phenotypic variation in color; higher eumelanin-to-pheomelanin ratios correlate with darker complexions. While occurs in the brain, it plays no direct role in cutaneous pigmentation.

Role in protection and physiology

Melanin pigmentation in human skin functions primarily as a photoprotective mechanism against ultraviolet (UV) radiation. Eumelanin, the dominant pigment in darker skin tones, absorbs UV photons across UVB (280-315 nm) and UVA (315-400 nm) spectra, converting their energy into heat and thereby limiting penetration to deeper epidermal and dermal layers. This reduces the incidence of UV-induced DNA lesions, such as cyclobutane pyrimidine dimers, which are precursors to mutations implicated in non-melanoma skin cancers like basal and squamous cell carcinomas. Constitutive melanin levels correlate inversely with skin cancer risk, with epidemiological data showing rates up to 100-fold higher in lighter-skinned populations exposed to high UV environments compared to darker-skinned ones. Beyond direct cellular damage, melanin shields against UV-mediated photodegradation of (vitamin B9), a critical cofactor in one-carbon for , , and repair. UVB exposure degrades up to 50% of circulating folate in lightly pigmented skin within minutes, potentially impairing through increased risks of defects, sperm abnormalities, and spontaneous abortions; darker pigmentation mitigates this loss, preserving folate bioavailability under chronic high-UV conditions. Experimental exposures confirm that melanized skin maintains folate stability, supporting the that folate protection drove the evolution of in equatorial regions. In physiological trade-offs, higher density inversely affects cutaneous synthesis, as it competes for the same UVB wavelengths (290-320 nm) needed to photoisomerize into previtamin D3, the precursor to active 1,25-dihydroxy. Lightly pigmented skin permits 5-10 times greater production per unit UV exposure than darkly pigmented skin, an adaptation favoring prevention and skeletal health in low-UV latitudes where solar zenith angles limit UVB availability below 35°N/S for much of the year. Consequently, darkly pigmented individuals in northern environments exhibit 2-20 fold lower serum 25-hydroxy levels without supplementation, heightening risks of and immune dysregulation. Acute tanning exemplifies inducible physiological protection, wherein UV exposure upregulates activity and eumelanin deposition within 48-72 hours, enhancing UV absorbance by 2-3 fold and distributing as supranuclear caps over nuclei to further attenuate DNA exposure. This facultative response, mediated by melanocortin-1 receptor signaling, provides adaptive buffering against intermittent solar intensity spikes, though chronic exposure still accrues damage in all types. While some studies propose minor thermoregulatory influences—darker absorbing slightly more visible for heat retention in cooler climates— evaporative cooling via sweat glands dominates thermal , rendering pigmentation's role ancillary compared to UV-related functions.

Genetic determinants

Core genes regulating pigmentation

The core genes regulating human skin pigmentation primarily influence synthesis within melanocytes, melanosome maturation, and the balance between eumelanin (dark ) and pheomelanin (light, reddish ). These genes encode proteins critical for the enzymatic pathway converting to , ion transport in melanosomes, and signaling for production. Variants in these genes explain a substantial portion of pigmentation variation, with some alleles showing signatures of positive selection in response to ultraviolet levels. TYR (tyrosinase) encodes the rate-limiting enzyme that catalyzes the initial steps of biosynthesis from , producing dopaquinone as a precursor for both eumelanin and pheomelanin. Loss-of-function mutations in TYR cause type 1 (OCA1), resulting in absent or minimal pigmentation and increased UV sensitivity. The R402Q variant modulates melanogenesis efficiency and shows global frequency variation, contributing to differences in constitutive skin color. MC1R (melanocortin 1 receptor) acts as a G-protein-coupled receptor on melanocyte surfaces, responding to alpha-melanocyte-stimulating hormone (α-MSH) to elevate cyclic AMP levels, which promotes eumelanin over pheomelanin production. Loss-of-function variants, such as R151C, R160W, and D294H, are prevalent in Europeans (up to 80-100% in red-haired individuals) and lead to fair skin, freckling, and red hair by favoring pheomelanin, while increasing skin cancer risk due to reduced photoprotection. SLC24A5 encodes a potassium-dependent sodium-calcium exchanger localized to membranes, influencing calcium and activity to regulate content. The rs1426654 A (Thr111) is nearly fixed (>95%) in European populations and associated with lighter by reducing eumelanin production; it accounts for up to 25-38% of pigmentation difference between Europeans and Africans, with evidence of selection in low-UV environments for synthesis. This also appears at lower frequencies in some East African and South Asian groups. SLC45A2 (MATP) functions as a proton-dependent transporter in melanosomes, maintaining optimal pH for activity and eumelanin polymerization. The rs16891982 G (Phe374/Leu374) predominates in Europeans (>90%) and correlates with lighter skin tones by impairing melanin maturation; it emerged post-Neolithic admixture and shows epistatic interactions with SLC24A5 to amplify effects. OCA2 regulates melanosomal pH and tyrosine transport, affecting melanin loading into melanosomes and overall pigment density. The rs1800407 G allele (Arg419Gln) reduces function, leading to lighter skin and blue eyes, with higher frequencies in Europeans and East Asians; it interacts with nearby HERC2 variants to modulate expression, contributing to ~15-20% of iris color variance that parallels skin pigmentation clines. These genes exhibit polygenic effects, with additive and epistatic interactions explaining ~30-50% of skin color in diverse populations, as validated by genome-wide association studies and functional assays in models.

Polygenic and variation

Human skin pigmentation is a classic example of polygenic , governed by the additive and interactive effects of multiple genetic loci rather than a single Mendelian , resulting in a continuous of phenotypes rather than discrete categories. These loci are primarily autosomal, and Y-DNA haplogroups C, D, E, J, O, Q, and R are not directly associated with skin color adaptations, as they trace paternal ancestry but do not influence pigmentation phenotypes. Skin color variation is driven by autosomal genes (e.g., SLC24A5, SLC45A2, OCA2, MC1R) under selection for UV protection and vitamin D synthesis. Each contributing typically exerts a small quantitative effect on production, type (eumelanin versus pheomelanin), melanosome packaging, or transfer to keratinocytes, leading to graded variation in constitutive skin reflectance and color. Early models proposed 3–6 major genes, but modern genomic analyses reveal involvement of dozens to hundreds of loci, with effects varying by population ancestry due to differing frequencies and linkage disequilibria. Heritability estimates for skin color, derived from twin and studies, range from 0.55 to 0.83 within populations, indicating substantial genetic control amid environmental influences like UV exposure. Genome-wide association studies (GWAS) have mapped over 100 loci associated with pigmentation variation across diverse ancestries, including signals near genes like TYR, OCA2, SLC45A2, and /OCA2, though effect sizes diminish beyond the strongest variants. A 2023 functional genetic screen in melanocytes identified 169 genes modulating levels, 135 of which were novel to pigmentation research, underscoring the breadth of polygenic architecture and pathways like biogenesis and endosomal trafficking. These loci collectively explain 20–40% of phenotypic variance in self-reported or measured skin color in large cohorts, with polygenic risk scores enabling prediction but limited by incomplete capture of rare variants and epistatic interactions. Within-population variation arises from segregation and recombination of these alleles, producing bell-shaped distributions of (e.g., measured via ), where intermediate tones predominate. Between-population differences stem from shifts under selection, yet substantial overlap exists; for example, African-ancestry groups show higher variance due to diverse haplotypes at loci like SLC24A5, while European-ancestry groups exhibit narrower ranges fixed for lightening alleles. Admixture introduces novel combinations, as seen in Latin American cohorts where 18 GWAS signals highlight of lighter tones via distinct genetic paths. In admixed populations within majority-light societies, if admixed individuals preferentially partner with lighter-skinned people due to demographics, social patterns, or preferences, average skin tones can shift lighter over generations by increasing the frequency of light alleles. and gene-environment interactions further modulate outcomes, but the polygenic framework emphasizes incremental allelic contributions over deterministic "color genes."

Recent genetic discoveries

In 2023, a genome-wide CRISPR-Cas9 screen in human melanocytes identified 169 genes influencing production, including 135 previously unassociated with pigmentation, such as KLF6 (regulating melanosome maturation) and COMMD3 (modulating melanosomal ). These genes, enriched in pathways like transcription regulation and endosomal transport, account for additional polygenic variation in skin color and exhibit signatures of local adaptation in diverse populations. A genome-wide association study (GWAS) in 48,433 East Asians quantified skin color via CIE Lab* metrics and pinpointed 23 genomic loci, 11 of which were novel, including GLIS1, SEM1, GAB2, and a nonsynonymous variant (rs2511188) in USP35. This work underscored population-specific polygenic architectures, with SNP heritability estimates of 23-24% and evidence of interactions with environmental factors like sun exposure, diverging from European-centric findings. Advances in ancient DNA analysis include a 2025 probabilistic method using genotype likelihoods from low-coverage sequencing data (<8×), applied to 348 Eurasian genomes spanning 45,000 years, which improved prediction accuracy over prior tools like HIrisPlex-S. This revealed nonlinear shifts toward lighter pigmentation, with Neolithic farmers contributing key alleles (e.g., SLC24A5 rs1426654) but persistence of dark skin variants into later periods due to gene flow. Recent population-specific variants include CYB561A3 (co-localizing with TYRP1 in melanosomes, 2024), GNPAT rs75356281 (enhancing tanning in Tibetans, 2022), and PAH rs10778203 (reducing tanning in East Asians via impaired tyrosine synthesis, 2024). These findings highlight ongoing refinement of the ~26 known pigmentation genes and expand understanding of adaptive diversity beyond core loci like OCA2 and SLC45A2.

Evolutionary development

Origins in early humans

Early Homo sapiens, originating in Africa approximately 300,000 years ago, exhibited dark skin pigmentation as the ancestral condition. This phenotype, characterized by high levels of eumelanin, provided essential protection against intense ultraviolet radiation (UVR) prevalent in equatorial environments, mitigating risks of skin cancer, DNA damage, and folate degradation critical for reproductive health. The evolution of such dark pigmentation likely followed the loss of body hair in earlier hominins around 1.2 to 1.8 million years ago, exposing skin to solar radiation and necessitating melanin-based shielding. Genetic evidence from pigmentation loci supports this dark ancestral state. Variants promoting high melanin production, including those in genes like MC1R and TYR, predate the emergence of modern humans and remain prevalent in sub-Saharan African populations, indicating fixation through natural selection in high-UV settings. In contrast, alleles associated with lighter skin, such as derived mutations in SLC24A5 and SLC45A2, originated later and are absent or rare in early African sapiens genomes, underscoring that depigmentation arose as an adaptation to reduced UVR post-migration. Ancient DNA and comparative genomics further corroborate uniformity in early human pigmentation. Reconstructions from fossil-associated proxies and phylogenetic analyses show no evidence of widespread light skin in African Homo sapiens prior to dispersals, with dark pigmentation serving as the baseline for subsequent variations driven by latitude and diet. While some pre-sapiens hominins may have exhibited pigmentation diversity, the transition to hairless, dark-skinned forms in and persisting into sapiens reflects causal pressures from UV exposure and vitamin D synthesis balance in sunny habitats.

Timeline of adaptations post-migration

Following the out-of-Africa migration of anatomically modern humans approximately 60,000–70,000 years ago, dispersing populations initially retained darkly pigmented skin suited to equatorial ultraviolet (UV) radiation levels. Genetic evidence from ancient DNA confirms that early non-African groups, including those entering Eurasia, exhibited dark pigmentation similar to sub-Saharan Africans, as high melanin protected against UV damage while body hair loss necessitated it for folate preservation. Selection pressures in higher-latitude environments with reduced UV-B penetration then drove convergent depigmentation to enhance cutaneous vitamin D production, with adaptations manifesting on timescales of thousands of years rather than immediate responses. In Europe, ancient DNA analyses reveal that Upper Paleolithic hunter-gatherers (circa 40,000–10,000 years ago) predominantly carried alleles for dark skin, with the derived light-skin variant at SLC24A5 (rs1426654) appearing sporadically but not fixed until later. Selective sweeps for depigmentation alleles in SLC24A5, SLC45A2, and occurred between 11,000 and 19,000 years ago, coinciding with post- recolonization and dietary shifts reducing vitamin D intake from marine sources. By the Neolithic period (starting ~8,000 years ago), frequencies of light-skin variants increased, particularly with the arrival of Anatolian farmers carrying SLC24A5, though Western hunter-gatherers showed variable but often darker profiles; full fixation of multiple alleles in northern Europeans likely completed during the (~5,000–4,000 years ago). Parallel adaptations in East Asia involved distinct genetic pathways, with the OCA2 gene (notably rs1800407 and rs1800414 variants) playing a central role in reducing eumelanin and achieving lighter constitutive pigmentation independently of European mechanisms. Ancient DNA from Tianyuan Man (~40,000 years ago) indicates intermediate pigmentation, suggesting initial retention of darker traits post-migration, while selection for lighter skin intensified ~15,000–30,000 years ago amid low-UV continental interiors. East Asian depigmentation, characterized by weaker tanning responses alongside baseline lightness, reflects adaptation to seasonal UV variability and agricultural reliance, with high allele frequencies fixed by the Holocene. Populations migrating to intermediate or equatorial regions, such as (~50,000 years ago) and the (~15,000–20,000 years ago), largely conserved darker skin due to sustained high-UV exposure, though minor variations arose from local selection or drift; for instance, some Native American groups show slight depigmentation linked to SLC24A5 introgression. These post-migration timelines underscore polycentric evolution, where depigmentation proceeded rapidly under strong selection (estimated selection coefficients ~0.01–0.1) but variably across lineages, constrained by migration bottlenecks and admixture.

Environmental selection pressures

Ultraviolet radiation (UVR) from sunlight constitutes the primary environmental selection pressure shaping human skin pigmentation, with intensity varying by latitude and altitude. In equatorial regions, high UVR levels exert strong selective pressure for darker skin to mitigate photodegradation of folate, a B vitamin critical for DNA synthesis and reproductive success; UVR exposure degrades folate in lightly pigmented skin, leading to reduced fertility and developmental defects. Darker eumelanin-rich skin absorbs UVR, preventing its penetration to deeper dermal layers where folate circulates, thereby preserving folate levels and conferring a fitness advantage in high-UV environments. Additionally, high UVR promotes skin cancer and DNA damage, further favoring melanized skin that acts as a natural sunscreen, reducing non-melanoma skin cancer risk by up to 1000-fold in darkly pigmented individuals compared to lightly pigmented ones under equivalent exposure. In higher latitudes, where UVR is attenuated by atmospheric scattering and seasonal variation, the selective pressure reverses to favor lighter skin pigmentation to facilitate cutaneous vitamin D synthesis. Vitamin D, produced via UVR-induced conversion of 7-dehydrocholesterol in the skin, is essential for calcium absorption and skeletal health; insufficient production in darkly pigmented individuals at low UVR latitudes increases rickets prevalence, particularly in growing children and pregnant women, impairing mobility and reproduction. Mathematical models estimate selection coefficients as high as 0.3 for depigmentation alleles in northern environments, indicating rapid evolutionary adaptation within 10,000-20,000 years post-migration. This latitudinal cline in pigmentation aligns closely with surface UVR indices, with darker skin predominant between 15°N and 15°S and progressively lighter tones toward the poles, underscoring UVR's dominant role over other factors like diet or temperature. The vitamin D-folate duality hypothesis posits a balancing selection where pigmentation optimizes both nutrient protections: excess UVR depletes folate without sufficient vitamin D risk, while deficient UVR limits vitamin D without folate threat. Empirical data from global populations confirm this, showing no significant deviation from UVR predictions even accounting for clothing or shelter, though cultural practices may modulate pressures in modern contexts. Secondary pressures, such as oxidative stress from high-altitude UVR or arid environments, may amplify selection in specific locales but remain subordinate to latitudinal UVR gradients. Genetic scans reveal pigmentation loci under positive selection correlating with ancestral UVR exposure, validating environmental causation over neutral drift.

Population distributions

Latitudinal gradients and clines

Human skin pigmentation displays a marked latitudinal gradient, with darker skin tones prevailing in equatorial regions and lighter tones increasing toward higher latitudes. This pattern manifests as continuous clines, featuring gradual shifts in pigmentation across geographic space rather than discrete categories. Measurements of skin reflectance, an inverse proxy for melanin content, reveal a strong correlation with absolute latitude: reflectance rises systematically from low values near the equator (darker skin) to higher values at polar latitudes (lighter skin), with correlation coefficients exceeding 0.7 in global datasets. The gradient arises from natural selection balancing ultraviolet radiation (UVR) exposure: high equatorial UVR favors eumelanin-rich dark skin to shield against DNA damage, folate degradation, and skin cancer, while low UVR at higher latitudes selects for lighter skin to permit adequate UVB absorption for vitamin D production in the epidermis. This distribution reflects two countervailing clines shaped by UVR gradients, which track latitude primarily through atmospheric scattering and absorption of solar radiation; equatorial zones receive up to 50% more UVB than polar regions annually. Although latitude proxies UVR effectively, pigmentation aligns more precisely with surface UVB levels, accounting for local modifiers like altitude and cloud cover that can disrupt pure latitudinal trends in isolated areas. Population-level data from diverse ancestries confirm these clines, with genetic variants in pigmentation loci exhibiting allele frequency gradients mirroring skin color variation along latitudinal axes.

Regional genetic signatures

Average skin pigmentation differs among major continental ancestry groups: sub-Saharan African ancestry typically shows the darkest tones (highest eumelanin, Fitzpatrick V–VI), with the lowest skin reflectance values among Nilo-Saharan pastoralists in eastern Africa such as the Nilotic Dinka and Nuer from South Sudan; European ancestry the lightest (lowest melanin, Fitzpatrick I–III, often with freckling/red hair); East Asian ancestry intermediate to light with yellower undertones (Fitzpatrick III–IV); Native American/Oceanian ancestry varies latitudinally, darker in equatorial regions (e.g., Indigenous Australians and Bougainville Melanesians comparable to or darker than the darkest sub-Saharan groups) and lighter in higher latitudes. Populations like the Senegalese and Chopi from Mozambique exhibit dark skin but are not among the absolute darkest. Substantial overlap exists across distributions, with tanning and admixture blurring boundaries. Human skin pigmentation exhibits distinct regional genetic signatures shaped by local selection pressures and historical migrations, with specific alleles at key loci showing pronounced frequency differences across continents. In European-descended populations, the derived alleles of SLC24A5 (rs1426654 A, encoding Ala111Thr) and SLC45A2 (rs16891982 G) predominate, reaching frequencies exceeding 90-98%, which substantially reduce eumelanin production and enable lighter skin tones adapted to lower ultraviolet radiation environments. These variants are rare or absent in sub-Saharan African populations (frequencies near 0%) and occur at low levels (typically <20%) in East Asians, highlighting convergent evolution for depigmentation via distinct genetic paths. East Asian populations display lighter skin pigmentation through alternative genetic mechanisms, primarily involving variants in OCA2 (such as rs1800407) and MFSD12, which modulate melanosome function and melanin synthesis independently of the European SLC24A5/SLC45A2 pathway. For instance, the OCA2 derived allele contributes to reduced pigmentation in Han Chinese and Japanese cohorts, with effect sizes comparable to European loci but without overlap in the primary variants under selection. KITLG polymorphisms also show elevated derived allele frequencies in East Asians (~70-80%), further fine-tuning pigmentation levels suited to temperate latitudes. In contrast, sub-Saharan Africans maintain predominantly ancestral alleles across these loci, preserving high eumelanin levels through melanin-promoting variants in genes like MFSD12 and DDB1, which exhibit signatures of positive selection for dark skin protection against intense solar exposure. Admixed regions like South Asia and the Americas reveal intermediate signatures reflecting ancestry proportions; for example, South Asians often carry partial European-like SLC24A5 alleles (frequencies 10-50%) alongside indigenous dark-skin variants, resulting in clinal variation. In Native American populations, East Asian-derived pigmentation alleles predominate, but low frequencies of light-skin variants (<2%) underscore limited independent adaptation post-migration. Genome-wide studies confirm polygenic contributions, with over 170 pigmentation-associated variants under selection in West Eurasians, versus distinct sets in Africans and East Asians, emphasizing regional specificity over universal drivers. These patterns, validated through ancient DNA and contemporary genotyping, illustrate how genetic architecture partitions global pigmentation diversity.

Ancient DNA evidence

Ancient DNA (aDNA) analyses have enabled reconstruction of skin pigmentation phenotypes in prehistoric populations by genotyping key variants associated with melanin production and distribution, such as those in SLC24A5, SLC45A2, and TYR. These studies employ probabilistic models to handle low-coverage genomes typical of aDNA, predicting categories like dark, intermediate, or light skin based on allele frequencies. Early work by Wilde et al. (2014) examined prehistoric Europeans and detected positive selection on light-skin alleles in SLC45A2 (rs16891982), SLC24A5 (rs1426654), and TYR (rs1042602) over the last 5,000 years, with frequencies increasing from near absence in Mesolithic hunter-gatherers to predominance in modern populations. In Europe, aDNA from early Upper Paleolithic individuals, such as those from ~45,000 years ago, indicates predominantly dark skin, consistent with retention of ancestral dark pigmentation from African origins. Hunter-gatherers around 8,500 years ago in regions like Spain and Luxembourg lacked derived light-skin alleles in SLC24A5 and SLC45A2, suggesting dark to intermediate tones. The introduction of SLC24A5 via Anatolian Neolithic farmers ~8,000 years ago initiated depigmentation, but SLC45A2 remained rare until ~5,800 years ago, when its frequency rose sharply, likely through admixture with steppe pastoralists like the Yamnaya. A 2020 analysis of 1,158 West Eurasian genomes spanning 40,000 years confirmed directional selection on a subset of large-effect variants, driving a significant decline in polygenic scores for dark pigmentation (P < 1 × 10⁻⁴). A comprehensive 2025 study of 348 Eurasian aDNA samples over 45,000 years quantified the slow shift: 100% dark skin in Paleolithic samples (12 individuals), 81% dark in Mesolithic (53 samples), 73% dark in Neolithic (93 samples), dropping to 51% dark by Bronze Age (43 samples), with intermediate tones bridging to lighter phenotypes. Dark skin persisted in ~63% of ancient Europeans across tens of thousands of years, with lighter traits becoming majority only in the last ~3,000 years, particularly in northern and central regions. In Eastern Europe and Iberia, dark phenotypes remained common into later periods. Beyond Europe, aDNA supports independent light skin evolution in East Asians, with selection intensifying after divergence from Native Americans ~20,000 years ago, involving distinct variants not shared with Europeans. These findings underscore that while migration and admixture introduced alleles, ongoing natural selection—evidenced by allele frequency changes beyond demographic shifts—shaped pigmentation, privileging variants enhancing vitamin D synthesis in low-UV environments.

Individual physiological factors

Age and developmental changes

During embryonic development, melanocytes originate from neural crest cells and begin migrating to the epidermis between the 10th and 14th weeks of gestation, establishing the foundational pattern for pigmentation, though active melanin synthesis remains limited in utero. Newborn infants across all human populations exhibit paler skin relative to their genetic adult pigmentation potential, as melanocyte function and eumelanin production are not fully activated at birth; this results in a transient lighter appearance even in individuals destined for darker constitutive tones. Postnatally, epidermal pigmentation darkens progressively through infancy and childhood via increased melanocyte proliferation, melanosome maturation, and melanin deposition, with noticeable shifts toward redder and darker hues in the first months followed by sustained intensification of yellow-brown components; by late childhood or puberty, skin typically approaches stable adult coloration as hormonal influences further enhance melanin output. In adulthood, pigmentation remains relatively constant under baseline conditions, but chronological aging from around age 30 onward involves a decline in melanocyte numbers—estimated at 10-20% per decade—accompanied by hypertrophy of surviving cells, yielding an overall pallor and translucency despite potential focal hyperpigmentations from photoaging, such as lentigines, which arise from uneven melanin accumulation rather than uniform darkening.

Sexual dimorphism

In most human populations, females exhibit lighter skin pigmentation than males, a pattern observed across diverse ethnic groups through spectrophotometric measurements of skin reflectance. Studies indicate that unexposed female skin is typically 2-3 percentage points higher in reflectance (appearing paler) compared to male skin, with this difference emerging around puberty and persisting into adulthood. This dimorphism is consistent but varies slightly by population; for instance, it holds in both light- and dark-skinned groups, though males tend to be browner and ruddier overall due to higher hemoglobin influence on tone. The magnitude of this sex difference in pigmentation is small but statistically significant, often quantified via metrics like the Individual Typology Angle or melanin index, where females score lower on pigmentation intensity. Experimental data from diverse samples, including Europeans, Africans, and Asians, confirm females' relative lightness even after controlling for age and sun exposure, suggesting a genetic or hormonal basis rather than purely environmental. Hormonal factors, such as estrogen's inhibitory effect on melanocyte activity, contribute to this pattern, as evidenced by lighter skin during pregnancy or with oral contraceptives. Evolutionary explanations for female lighter skin include sexual selection, where preferences for paler female skin may have amplified dimorphism, potentially correlating with latitude as populations adapted to varying UV environments—stronger dimorphism farther from the equator. Alternatively, physiological demands posit that females require enhanced vitamin D synthesis for reproductive health, favoring lighter skin to maximize cutaneous production under lower UV conditions, given higher needs during gestation and lactation. These hypotheses are supported by cross-population data but remain debated, with genetic analyses showing sex-specific effects in pigmentation loci like MC1R.

Sun exposure and facultative pigmentation

Facultative pigmentation refers to the adaptive, reversible darkening of human skin in response to ultraviolet (UV) radiation exposure, primarily through increased melanin production beyond the genetically determined constitutive baseline. This process, commonly known as tanning, serves as a photoprotective mechanism by enhancing UV absorption and scattering in the epidermis, thereby reducing penetration to deeper layers and mitigating DNA damage in keratinocytes and melanocytes. UV radiation, particularly UVB (280-320 nm), triggers DNA photoproducts like cyclobutane pyrimidine dimers in skin cells, prompting a signaling cascade involving p53 activation that stimulates melanocyte proliferation and melanogenesis. The tanning response manifests in two distinct phases: immediate pigment darkening (IPD) and delayed tanning (DT). IPD occurs within minutes of UVA (320-400 nm) exposure, resulting from the oxidation and redistribution of preexisting melanin and pheomelanin without new synthesis; it peaks in 1-2 hours and fades within days. DT, induced mainly by UVB, begins 48-72 hours post-exposure and persists for weeks, involving de novo melanin production where melanocytes increase tyrosinase activity, synthesize eumelanin-rich melanosomes, and transfer them to suprabasal keratinocytes, thickening the epidermal cap and altering melanosome distribution. Repetitive UV exposure can amplify visible pigmentation up to 7-10-fold, though actual melanin content rises only about twofold, due to enhanced dispersion and reduced degradation. Tanning capacity varies significantly by Fitzpatrick skin phototype, reflecting baseline melanin levels and melanogenic responsiveness. Types I-II (light skin) exhibit minimal or absent tanning, with high susceptibility to burning as UV induces inflammation before sufficient melanogenesis; types III-IV (intermediate) tan gradually after initial erythema; while types V-VI (dark skin) tan profusely with rare burning, leveraging robust constitutive pigmentation for rapid facultative enhancement. Despite photoprotection—melanin reducing UV-induced DNA strand breaks by up to 40-fold in darker melanocytes—tanning signifies underlying cellular damage, elevating risks of mutations leading to basal cell carcinoma (24% increased risk from indoor tanning), squamous cell carcinoma (58%), and melanoma. Thus, while evolutionarily adaptive, chronic facultative pigmentation correlates with cumulative UV genotoxicity rather than harmless bronzing.

Pigmentation anomalies

Hypopigmentation disorders

Hypopigmentation disorders are medical conditions characterized by decreased melanin synthesis, abnormal melanosome function, or destruction of melanocytes, leading to patches of lighter skin relative to an individual's baseline pigmentation or generalized pallor. These disorders arise from genetic mutations, autoimmune processes, or syndromic associations, often presenting congenitally or in early childhood, and may involve skin, hair, and ocular tissues. Diagnosis typically relies on clinical examination, Wood's lamp evaluation to highlight hypopigmented areas, and genetic testing for confirmation. Oculocutaneous albinism (OCA) represents a group of autosomal recessive disorders caused by mutations in genes essential for melanin production, such as TYR (OCA1), OCA2 (OCA2), or TYRP1 (OCA3), resulting in absent or reduced melanin in skin, hair, and eyes. Affected individuals exhibit very pale skin, white or light hair, and iris translucency, with symptoms including nystagmus, reduced visual acuity, and photophobia due to foveal hypoplasia and optic nerve misrouting. Prevalence varies globally but is estimated at approximately 1 in 17,000 individuals across all forms. OCA increases risks of sunburn and skin cancer from UV exposure, necessitating rigorous photoprotection. Vitiligo, an acquired autoimmune disorder, involves T-cell mediated destruction of melanocytes, producing well-demarcated depigmented macules and patches, often symmetrical and progressive, affecting up to 2% of the population worldwide with onset typically before age 30. It manifests in non-segmental (generalized) or segmental forms, with genetic predisposition linked to variants in NLRP1, PTPN22, and HLA loci, alongside environmental triggers like stress or trauma (Koebner phenomenon). Associated comorbidities include thyroid autoimmunity and type 1 diabetes, reflecting broader immune dysregulation. Piebaldism is a rare autosomal dominant condition due to mutations in the KIT proto-oncogene, impairing melanocyte migration from during embryogenesis, yielding stable congenital leukoderma with a characteristic white forelock (poliosis) and symmetrical depigmented patches on the forehead, trunk, and extremities, sparing the eyes and mucosa. Hyperpigmented borders may surround lesions, but progression does not occur, and intellectual function remains unaffected, distinguishing it from other depigmenting disorders. Prevalence is low, with sporadic cases reported globally. Hypopigmented macules, or ash-leaf spots, occur in over 90% of individuals with tuberous sclerosis complex (TSC), an autosomal dominant neurocutaneous syndrome from TSC1 or TSC2 mutations disrupting mTOR signaling, which secondarily affects melanocyte function and yields lancet-shaped hypopigmented lesions visible under Wood's lamp from infancy. These macules serve as an early diagnostic criterion but are not pathognomonic, appearing in 0.6-13% of the general pediatric population without TSC. In TSC, they accompany other features like facial angiofibromas and seizures, with hypopigmentation reflecting localized melanin reduction rather than melanocyte absence. Other hypopigmentation disorders include Hermansky-Pudlak syndrome, where biallelic mutations in lysosomal trafficking genes (e.g., HPS1-10) cause oculocutaneous albinism alongside platelet dysfunction and pulmonary fibrosis, and hypomelanosis of Ito, a mosaic disorder from postzygotic mutations leading to swirling hypopigmented whorls often with neurological involvement. These highlight the spectrum from isolated cutaneous traits to multisystem genetic defects.

Hyperpigmentation conditions

Hyperpigmentation conditions encompass a range of disorders marked by excessive melanin deposition in the skin, resulting in darker patches or generalized darkening, often stemming from genetic mutations that dysregulate melanocyte proliferation, migration, or melanogenesis pathways. These anomalies contrast with normal variation in skin color by involving aberrant signaling, such as overactivation of KIT ligand or cAMP-mediated pathways, leading to uneven or progressive pigmentation changes. While some arise secondarily to inflammation or endocrine dysfunction, inherited forms highlight direct genetic causality, with mutations in genes like KITLG amplifying melanin production through enhanced receptor tyrosine kinase activity. Familial progressive hyperpigmentation (FPH), an autosomal dominant disorder, manifests as irregular hyperpigmented patches present at birth or emerging in early infancy, gradually spreading to cover large areas of the body without associated health risks beyond cosmetic impact. Caused by gain-of-function mutations in the KITLG gene on chromosome 12q22, these alterations increase KIT signaling, promoting melanocyte survival and eumelanin synthesis, as evidenced in affected families where skin biopsy reveals increased dermal melanin. A distinct subtype, FPH1 (OMIM 614233), underscores the role of this locus in progressive dermal accumulation. Dyschromatosis symmetrica hereditaria (DSH) features hyperpigmented and hypopigmented macules primarily on the dorsal hands and feet, onset in infancy, linked to autosomal dominant mutations in ADAR (encoding adenosine deaminase acting on RNA), which disrupts RNA editing and indirectly affects melanin regulation via altered gene expression in melanocytes. Clinical presentation includes freckle-like spots with genetic penetrance varying by allele, confirmed through sequencing in pedigrees showing symmetric distribution. Incontinentia pigmenti, an X-linked dominant condition lethal in most male fetuses, progresses through vesicular, verrucous, and hyperpigmented stages, with the latter yielding swirling brown lines along Blaschko's lines due to NEMO (IKBKG) mutations impairing NF-κB signaling, which normally curbs melanocyte apoptosis and inflammation. Affecting primarily females, it involves mosaic X-inactivation, leading to clonal hypermelanosis alongside potential ocular or dental anomalies. LEOPARD syndrome, part of the RASopathies, presents with multiple lentigines—small, tan-brown hyperpigmented macules—alongside cardiac defects, caused by heterozygous loss-of-function mutations in PTPN11, RAF1, or BRAF genes on the , which paradoxically enhance melanogenesis in skin despite growth inhibition elsewhere. Lentigines appear in childhood, increasing with age, with histopathological evidence of epidermal melanocyte hyperplasia. Dowling-Degos disease involves reticulate hyperpigmentation in flexural areas like axillae and neck, autosomal dominant inheritance via KRT5 mutations disrupting keratinocyte-melanocyte interactions, resulting in thin, elongated rete ridges laden with melanin. Onset post-puberty, it features speckled brown macules without systemic involvement, distinguishable by dermatoscopy showing filiform digitations. Carney complex includes cutaneous hyperpigmentation through profuse lentigines and blue nevi, driven by inactivating mutations in PRKAR1A, which encodes protein kinase A regulatory subunit, leading to cAMP dysregulation and unchecked melanocyte stimulation akin to McCune-Albright syndrome mechanisms. Pigmentation appears early, often with endocrine overactivity, confirmed in genetic cohorts showing 70-80% penetrance for skin findings.

Assessment methods

Phenotypic scales and metrics

Phenotypic scales for human skin color primarily assess constitutive pigmentation through visual comparison or self-reported traits, with the Fitzpatrick skin phototype scale being the most established in clinical dermatology. Developed in 1975 by Thomas B. Fitzpatrick, it classifies skin into six types (I-VI) based on the tendency to burn and tan upon ultraviolet exposure: Type I involves pale skin that always burns and never tans, while Type VI features deeply pigmented skin that never burns and tans profoundly. This scale correlates with melanin content and UV sensitivity but relies on subjective recall, limiting reproducibility, particularly for types IV-VI where distinctions blur due to minimal burning variation. The von Luschan chromatic scale, introduced in the early 20th century by anthropologist Felix von Luschan, uses 36 opaque glass tiles of graduated hues from pale yellow (type 1) to dark brown (type 36) for direct visual matching against forearm skin under standardized lighting. It aimed for anthropological quantification of pigmentation gradients but suffers from inter-observer variability and insensitivity to subtle undertones like redness or yellowness. More recent visual tools include the Monk Skin Tone Scale, which expands representation for diverse tones beyond traditional Western-centric models, and the Eumelanin Human Skin Colour Scale, dividing constitutive color into five eumelanin-based quintiles for objective description without ethnic proxies. These address gaps in inclusivity but remain prone to perceptual biases. Objective metrics employ instrumentation for precision, circumventing human judgment. Reflectance spectrophotometry devices, such as the Mexameter, compute a melanin index (MI) by analyzing light absorption at specific wavelengths (e.g., 880 nm for melanin), yielding numerical values where higher MI indicates greater pigmentation density. Colorimetry derives CIELAB values—L* for lightness (100 white to 0 black), a* for red-green, b* for yellow-blue—from tristimulus measurements, enabling derived metrics like the Individual Typology Angle (ITA = arctan[(L* - 50)/b*]), which objectively stratifies phototypes: ITA >55° for very light, < -30° for dark. These methods quantify epidermal melanin noninvasively and reproducibly, correlating strongly with histological eumelanin levels, though they require calibration for skin site and hydration effects. Limitations include cost and accessibility, favoring clinical over population studies, yet they provide causal insights into pigmentation as a melanin-driven trait rather than vague perceptual categories.

Genetic and molecular tools

Targeted genotyping of single nucleotide polymorphisms (SNPs) in genes involved in melanogenesis serves as a primary molecular tool for assessing the genetic basis of human skin color variation. Common SNPs include rs1426654 in SLC24A5, which encodes a melanosome maturation protein and is associated with lighter skin in Europeans due to the derived A allele fixed at high frequency (>98%) in these populations, and rs16891982 in SLC45A2, where the G allele correlates with reduced pigmentation. Techniques such as TaqMan assays, which utilize allele-specific probes during real-time PCR to detect these SNPs with high specificity and throughput, enable precise genotyping from minimal DNA samples. Genome-wide association studies (GWAS) identify novel pigmentation loci by scanning thousands of SNPs across genomes from diverse cohorts, revealing over 100 associated variants that collectively explain a portion of skin color , though polygenic effects predominate. Next-generation sequencing (NGS) facilitates comprehensive analysis, including whole-exome or targeted panel sequencing of pigmentation genes like TYR, OCA2, MC1R, and KITLG, allowing detection of rare variants and structural changes influencing production. Polygenic risk scores (PRS) integrate multiple SNPs to predict pigmentation phenotypes, with models demonstrating up to 25% variance explained in European-ancestry groups for skin color metrics. In forensic applications, multiplex SNP panels such as those in the VISAGE Enhanced Tool or HIrisPlex-S system combine pigmentation markers with ancestry informative SNPs to infer skin color from degraded DNA, achieving categorical predictions like "light," "medium," or "dark" with population-specific accuracy. These tools underscore the polygenic architecture of skin pigmentation, where no single variant is deterministic, and environmental factors modulate expression, but genetic data provide causal insights into evolutionary adaptations. Limitations include reduced predictive power across admixed or non-European populations due to linkage disequilibrium differences and incomplete variant coverage.

Scientific debates and misconceptions

Biological vs. social interpretations

Human skin pigmentation is a polygenic trait with high heritability, estimated at 0.80-0.96 across diverse populations, underscoring its primary biological determination through genetic variants influencing melanin production and distribution. Genome-wide association studies have identified at least 135 genes associated with variation in skin, hair, and eye color, with key loci such as SLC24A5, SLC45A2, and OCA2 showing strong signals of positive selection in response to ultraviolet radiation gradients. Evolutionary analyses indicate that darker constitutive pigmentation predominated in early modern humans near the equator to shield against folate depletion and DNA damage from high UV exposure, while depigmentation alleles emerged and fixed in higher-latitude populations around 10,000-40,000 years ago to optimize cutaneous vitamin D synthesis under low UV conditions. This adaptive divergence manifests in clinal but ancestry-correlated patterns, where genetic ancestry predicts pigmentation with over 90% accuracy in admixed individuals. Social constructivist interpretations, prevalent in certain humanities and discourses, posit that categorizations of skin color variation—often tied to racial taxonomies—derive not from inherent biological discontinuities but from arbitrary cultural, historical, and power-laden classifications without objective genetic underpinnings. Advocates of this view, such as those emphasizing race as a "regulatory kind" shaped by societal norms rather than fixed essences, argue that observed pigmentation gradients reflect fluid social meanings rather than evolved adaptations, dismissing genetic clustering as insufficient for delineating discrete biological races. These perspectives often prioritize environmental and cultural explanations for group-level differences, attributing disparities in pigmentation-related health outcomes (e.g., rates) to socioeconomic factors over genetic predispositions. The tension between these frameworks highlights a methodological divide: biological realism relies on empirical genomic and paleogenomic data demonstrating convergent selection on pigmentation loci across isolated populations, such as independent SLC24A5 mutations in Europeans and some South Asians, which refute claims of pigmentation as purely arbitrary or non-heritable. In contrast, constructivist accounts have been critiqued for selectively interpreting genetic continuity (e.g., within-Africa variation) to undermine inter-population differences, despite principal component analyses of global genomes showing pigmentation traits aligning with continental ancestry groups at rates exceeding 95%. This discord reflects broader institutional tendencies in academia, where biological interpretations of visible traits like skin color face scrutiny for potential misuse in historical pseudosciences, leading some sources to favor constructivism despite contradictory molecular evidence from peer-reviewed research. Rigorous , grounded in , affirms that while social factors modulate perceptions and outcomes, the proximate mechanisms of pigmentation remain biologically mediated, with trumping constructivist null hypotheses in twin and admixture studies.

Controversies in racial classification

The classification of human races using skin color as a primary criterion has sparked significant , particularly regarding whether such categorization reflects discrete biological groups or merely superficial clinal variation along geographic gradients. Skin pigmentation exhibits a latitudinal cline, with darker tones predominant near the and lighter tones at higher latitudes, driven by adaptations to ultraviolet radiation levels. However, this continuity does not preclude differentiation; multiple pigmentation loci display elevated FST values—measures of differentiation—between continental groups, indicating localized selection pressures that align pigmentation with ancestry clusters. For instance, the SLC24A5 gene variant associated with lighter skin is fixed or near-fixed in European-derived populations (frequency >98%) but absent or rare in sub-Saharan African groups (frequency <1%), underscoring substantial allele frequency divergence. A central controversy arises from Richard Lewontin's 1972 apportionment of human genetic diversity, which demonstrated that about 85% of variation at individual loci occurs within populations rather than between them, prompting claims that traits like skin color cannot justify racial taxonomy as they are "skin deep" and lack deeper genetic correlates. This view has been challenged by A.W.F. Edwards as "Lewontin's fallacy," arguing that while single-locus data show high within-group variance, multivariate analysis of correlated markers across the genome enables probabilistic assignment of individuals to ancestral populations with high accuracy, comparable to traditional racial groupings. Empirical support comes from STRUCTURE analyses of genomic data, which consistently recover clusters corresponding to African, European, East Asian, and other continental ancestries, where average skin pigmentation differs markedly due to fixed or high-frequency variants in genes like MC1R, OCA2, and KITLG. Critics of biological racial concepts, often from anthropological perspectives, contend that such clustering overlooks admixture and cultural overlays, yet forensic applications demonstrate practical utility: ancestry estimation from skeletal traits predicts pigmentation and biogeographical origin with accuracies exceeding 80% in admixed populations. In forensic anthropology, skin color inference via ancestry profiling remains contentious, with some practitioners shifting terminology from "race" to "ancestry" to emphasize geographic origins over social constructs, while acknowledging that phenotypic traits like pigmentation serve as proxies for genetic clusters shaped by evolutionary history. Proponents highlight successes in case resolutions, such as identifying remains through pigmentation-compatible ancestry, but detractors argue this reinforces outdated racial essentialism, ignoring that no single trait like skin color encapsulates the full spectrum of human variation. Despite these critiques, genome-wide studies reveal that pigmentation genes contribute disproportionately to inter-population differentiation, with FST values for key SNPs often in the top percentiles of the genome, suggesting that skin color, while polygenic and variable, retains validity as an ancestral marker when integrated with other data. This tension reflects broader ideological influences in academia, where empirical genetic clustering is sometimes downplayed to avoid implications of inherent group differences, prioritizing social interpretations over causal evolutionary mechanisms.

Critiques of environmental determinism

Critiques of in human skin pigmentation emphasize that while (UV) radiation exerts selective pressure, pigmentation distributions cannot be fully explained by current local environmental conditions alone, as historical, genetic, and ecological factors introduce significant deviations from predicted patterns. Proponents of a strict UV-driven model anticipate a tight between , UV intensity, and skin darkness, with darker constitutive pigmentation evolving in high-UV equatorial regions for protection against DNA damage and folate degradation, and lighter pigmentation in high-latitude areas to optimize synthesis. However, empirical observations reveal exceptions, such as relatively dark-skinned populations in low-UV environments, attributable to recent migrations that limit adaptation time. For example, retain dark pigmentation despite residing in temperate zones with reduced UV exposure, reflecting ancestry from equatorial migrants approximately 50,000 years ago and insufficient generational span for substantial under relaxed selection. Arctic populations like the provide a prominent case, exhibiting values indicative of darker pigmentation (around 40-50% in measurements) despite latitudes above 60°N where annual UV doses are minimal. This discrepancy arises because Inuit ancestors migrated from Beringian regions only 4,000-6,000 years ago, a timeframe too brief for the fixation of alleles under vitamin D-limited selection, compounded by genetic bottlenecks that preserved tropical-derived variants. Dietary adaptations further undermine deterministic predictions: Inuit reliance on vitamin D-rich marine foods (e.g., seal blubber providing up to 1,000 IU per 100g) circumvents the need for enhanced cutaneous synthesis, relaxing selective pressure for lighter skin and allowing ancestral darkness to persist. Similar patterns occur among some Native American groups in regions, where post-Columbian admixture and short post-migration history (10,000-15,000 years in the ) yield intermediate pigmentation not fully aligned with local UV clines. Additional limitations include micro-environmental variations and non-UV influences that disrupt macro-scale correlations. Effective UV exposure varies with factors like , levels, altitude, and surface reflectivity (e.g., amplifying UVB by up to 80% in summers), decoupling pigmentation from alone. Genetic analyses confirm independent depigmentation trajectories—SLC24A5 mutations dominant in Europeans but absent in East Asians, who rely on OCA2/ variants—highlighting , drift, and incomplete rather than equilibrium responses to environment. Critics, including analyses of global datasets, note that up to 20-30% of pigmentation variance defies strict UV predictions, with or pleiotropic effects on traits like immune function potentially contributing, as evidenced by rapid sweeps post-Out-of-Africa (e.g., SLC45A2 fixation in Europeans within 10,000 years). These factors underscore causal realism: environment shapes selection coefficients, but realized phenotypes emerge from phylogenetic inheritance and stochastic processes, not deterministic environmental matching.

Cultural perceptions

Historical attitudes across societies

In ancient Egyptian artistic conventions, males were typically rendered with reddish-brown skin tones symbolizing exposure to the sun from outdoor labor, while females appeared with lighter yellowish hues indicative of indoor seclusion and higher status. This differentiation reflected socioeconomic roles rather than a rigid , though darker-skinned to the south were stereotyped in art as foreigners with distinct features. Similarly, in ancient , deviations from normative appearance, such as anomalies or diseases, were interpreted as ominous signs portending or ritual impurity, linking physical traits to divine disfavor. Greco-Roman societies observed variations in skin color among populations like , described as dark-skinned, but lacked systematic based on a black-white binary; evaluations centered on and over pigmentation. texts noted ' dark skin as a natural trait tied to , without inherent inferiority, and Roman literature similarly prioritized and status, with encompassing diverse ethnicities irrespective of color. Darker complexions were sometimes associated with robustness or , as in athletic ideals, but foreignness or barbarism drove attitudes more than hue alone. In ancient and , lighter skin correlated with upper castes, who avoided manual outdoor toil, fostering preferences for fairness in marriage and predating European contact, though colonial rule amplified these via administrative classifications linking tone to . Chinese historical records from the onward favored pale skin among elites as a marker of refinement and scholarly pursuits shielded from manual labor, with darker tones evoking laborers or southern "barbarians"; texts like those on Kunlun slaves dehumanized very dark ns as uncivilized, yet free traders from received varied, often neutral regard based on utility. Medieval European attitudes toward darker skin, encountered via trade or pilgrimage, emphasized novelty or biblical associations like the "blessed" in Acts, yielding positive depictions in art such as portrayed as black; prejudice, when present, stemmed from religious otherness or enslavement origins rather than color per se, with no evidence of endogenous racial slavery. In sub-Saharan African societies pre-colonially, skin color held minimal divisive role, as intra-group variations were normalized and status derived from lineage or prowess, though lighter tones occasionally signaled foreign prestige via Arab trade. Across these contexts, preferences for lighter often signaled class privilege—denoting avoidance of sun-exposed drudgery—while darker tones evoked labor or environmental , though such patterns varied by , , and without universal condemnation.

Color preferences and mate selection

Empirical studies in suggest that preferences for lighter tones in potential mates, particularly among women, may function as cues to , , and , as lighter pigmentation correlates with reduced lifetime sun exposure and thus lower . This preference is hypothesized to drive in human color, with women exhibiting lighter tones than men on average across populations, reinforced by male choosiness for traits signaling reproductive viability. Subtle variations in skin coloration, influenced by factors like intake and oxygenation, further modulate perceived attractiveness, with yellower or golden hues often rated higher due to associations with dietary . Twin studies indicate moderate in mate preferences for color, estimated at 0.43 for women and 0.55 for men, with women showing stronger toward fairer tones—over 80% preferring —while men favor medium tones more variably. In experimental ratings, both sexes rate faces with average or slightly lighter-than-average as most attractive, linking paler complexions to perceptions of youthfulness and rather than extreme associated with illness. These patterns hold across diverse samples, suggesting an innate component, though cultural amplification occurs where lighter skin signals or indoor lifestyles indicative of resource access. Historical and sociological data reveal cohort-specific trends: in early 20th-century U.S. populations, lighter-skinned women experienced higher rates and partner quality, reflecting preferences tied to perceived purity and status, whereas darker-skinned men gained relative advantages in mate access over time as economic opportunities shifted. Cross-ethnoracial studies confirm tone influences partner selection, with lighter tones conferring advantages in intergroup pairings, particularly for women from lower-status groups, though effects diminish when controlling for socioeconomic factors. Such preferences persist despite modern interventions, underscoring their robustness beyond socialization alone.

Modern colorism and interventions

Modern colorism manifests as preferential treatment for individuals with lighter skin tones, often resulting in socioeconomic disadvantages for those with darker skin within the same ethnic or racial groups. Empirical studies indicate that darker-skinned Black Americans experience lower , income levels, and job prestige compared to lighter-skinned counterparts. In employment contexts, field experiments have demonstrated against darker-skinned applicants in rental housing markets, with lighter-skinned individuals receiving more favorable responses. Similarly, in marital outcomes, lighter skin tone among correlates with higher marriage rates and more favorable partner selection, reflecting persistent cultural preferences rooted in historical hierarchies. Globally, colorism drives widespread use of skin lightening products, particularly in regions with high prevalence such as , where meta-analyses report 27.1% of respondents engaging in regular skin bleaching. The international market for these products reached $8 billion in , projected to grow significantly, underscoring the economic scale of colorist preferences despite associated health risks like dermal damage from corticosteroids. In and , usage rates among women exceed 40% in some countries, often linked to aspirations for , beauty standards, and perceived professional advantages. Interventions aimed at combating colorism include educational programs in schools to challenge skin tone biases and policy efforts to prohibit discriminatory hiring practices based on appearance. However, peer-reviewed evaluations of their effectiveness remain limited, with calls for targeted strategies involving teachers, students, and families to mitigate internalized preferences. Awareness campaigns have raised visibility, but empirical data on sustained behavioral change or reduced disparities is scarce, highlighting the challenge of addressing deeply ingrained cultural norms.

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