Light skin is ahuman skin color that has a low level ofeumelanin pigmentation as an adaptation to environments of lowUV radiation.[1][2]Due to migrations of people in recent centuries, light-skinned populations today are found all over the world.[2][3] Light skin is most commonly found amongst the native populations ofEurope,East Asia,[4][5][6]West Asia,Central Asia,Siberia, andNorth Africa as measured throughskin reflectance.[7] People with light skin pigmentation are often referred to as "white"[8][9] although these usages can be ambiguous in some countries where they are used to refer specifically to certain ethnic groups or populations.[10]
Humans with light skin pigmentation have skin with low amounts ofeumelanin, and possess fewermelanosomes than humans withdark skin pigmentation. Light skin provides better absorption qualities of ultraviolet radiation, which helps the body to synthesize higher amounts ofvitamin D for bodily processes such as calcium development.[2][11] On the other hand, light-skinned people who live near theequator, where there is abundantsunlight, are at an increased risk offolate depletion. As a consequence of folate depletion, they are at a higher risk ofDNA damage,birth defects, and numerous types ofcancers, especiallyskin cancer.[12] Humans with darker skin who live further from thetropics may have lower vitamin D levels, which can also lead to health complications, both physical andmental, including miscarriage and a greater risk of developingschizophrenia.[13] These two observations form the "vitamin D–folate hypothesis", which attempts to explain why populations that migrated away from the tropics into areas of low UV radiation[14]evolved to have light skin pigmentation.[2][15][16]
The distribution of light-skinned populations is highly correlated with the low ultraviolet radiation levels of the regions inhabited by them. Historically, light-skinned populations almost exclusively lived far from the equator, in highlatitude areas with low sunlight intensity.[17]
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It is generally accepted thatdark skin evolved as a protection against the effect ofUV radiation;eumelanin protects against bothfolate depletion and directdamage to DNA.[2][20][21][22] This accounts for the dark skin pigmentation of Homo sapiens during their development in Africa; the major migrationsout of Africa to colonize the rest of the world were also dark-skinned.[23] It is widely supposed that light skin pigmentation developed due to the importance of maintainingvitamin D3 production in the skin.[24] Strongselective pressure would be expected for the evolution of light skin in areas of low UV radiation.[15]
After the ancestors of West Eurasians and East Eurasians diverged more than 40,000 years ago, lighter skin tones evolved independently in a subset of each of the two populations. In West Eurasians, theA111T allele of thers1426654polymorphism in the pigmentation geneSLC24A5 has the largest skin lightening effect and is widespread in Europe, South Asia, Central Asia, the Near East and North Africa.[25]
In a 2013 study, Canfield et al. established thatSLC24A5 sits in a block ofhaplotypes, one of which (C11) is shared by virtually all chromosomes that bear theA111T variant. This "equivalence" between C11 andA111T indicates that all people who carry this skin-lightening allele descend from a common origin: a single carrier who lived most likely "between the Middle East and the Indian subcontinent". Canfield et al. attempted to date theA111T mutation but only constrained the age range to before the Neolithic.[25] However, a second study from the same year (Basu Mallick et al.) estimated thecoalescent age (split date) for this allele to between ~28,000 and ~22,000 years ago.[26]
The second most important skin-lightening factor in West Eurasians is the depigmenting alleleF374 of thers16891982 polymorphism located in themelanin-synthesis geneSLC45A2. From its low haplotype diversity, Yuasa et al. (2006) likewise concluded that this mutation (L374F) "occurred only once in the ancestry of Caucasians".[27]
Summarising these studies, Hanel and Carlberg (2020) decided that the alleles of the two genesSLC24A5 andSLC45A2 which are most associated with lighter skin colour in modern Europeans originated inWest Asia about 22,000 to 28,000 years ago and these two mutations each arose in a single carrier.[23] This is consistent with Jones et al. (2015), who reconstructed the relationship between Near Eastern Neolithic farmers andCaucasus Hunter-Gatherers: two populations which carried the light skin variant ofSLC24A5. Analysing newly sequenced ancient genomes, Jones et al. estimated the split date at ~24,000 bp and localised the separation to somewhere south of the Caucasus.[28] However, a coalescent analysis of this allele by Crawford et al. (2017) gave a more narrowly constrained, and earlier, split date of ~29,000 years ago (with a 95% confidence window from 28,000 to 31,000 bp).[29]
The light skin variants ofSLC24A5 andSLC45A2 were present inAnatolia by 9,000 years ago, where they became associated with theNeolithic Revolution. From here, theircarriers spread Neolithic farming across Europe.[30] Lighter skin and blond hair also evolved in theAncient North Eurasian population.[31]
A further wave of lighter-skinned populations across Europe (and elsewhere) is associated with theYamnaya culture and theIndo-European migrations bearing Ancient North Eurasian ancestry and theKITLG allele for blond hair. Furthermore, theSLC24A5 gene linked with light pigmentation in Europeans was introduced into East Africa from Europe over five thousand years ago. These alleles can now be found in theSan,Ethiopians, andTanzanian populations with Afro-Asiatic ancestry.[25][32][33] TheSLC24A5 in Ethiopia maintains a substantial frequency withSemitic andCushitic speaking populations, compared withOmotic,Nilotic orNiger-Congo speaking groups. It is inferred that it may have arrived into the region via migration from the Levant, which is also supported by linguistic evidence.[34] In the San people, it was acquired from interactions with Eastern African pastoralists.[35] Meanwhile, in the case of East Asia and the Americas, a variation of theMFSD12 gene is responsible for lighter skin colour.[31] The modern association between skin tone and latitude is thus a relatively recent development.[23]
According to Crawford et al. (2017), most of the genetic variants associated with light and dark pigmentation appear to have originated more than 300,000 years ago.[36] African, South Asian and Australo-Melanesian populations also carry derived alleles for dark skin pigmentation that are not found in Europeans or East Asians.[32] 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.[32]
TheA111T mutation in theSLC24A5 gene predominates in populations withWestern Eurasian ancestry. The geographical distribution shows that it is nearly fixed in all of Europe and most of the Middle East, extending east to some populations in present-day Pakistan and Northern India. It shows a latitudinal decline toward the Equator, with high frequencies in North Africa (80%), and intermediate (40−60%) in Ethiopia and Somalia.[25]
Some authors have expressed caution regarding the skin pigmentation SNP predictions in early Paleolithic groups. According to Ju et al. (2021): "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. As an extreme example, Neanderthals and the Altai Denisovan individual show genetic scores that are in a similar range to Early Upper Paleolithic individuals, but it is highly plausible that these populations, who lived at high latitudes for hundreds of thousands of years, would have adapted independently to low UV levels. For this reason, we cannot confidently make statements about the skin pigmentation of ancient populations."[38]
A study from 2015 found that genes contributing to fair skin were nearly fixed in the Anatolian Neolithic Farmers: "The second strongest signal in our analysis is at the derived allele ofrs16891982 inSLC45A2, which contributes to light skin pigmentation and is almost fixed in present-day Europeans but occurred at much lower frequency in ancient populations. In contrast, the derived allele ofSLC24A5 that is the other major determinant of light skin pigmentation in modern Europe appears fixed in the Anatolian Neolithic, suggesting that its rapid increase in frequency to around 0.9 (90%) in Early Neolithic Europe was mostly due to migration."[39]
In 2018, a study was released showing many late Mesolithic Scandinavians from 9,500 years ago in Northern Europe had blonde hair and light skin, which was in contrast to some of their contemporaries, the darkerWestern Hunter Gatherers (WHG).[40] However, a 2024 paper found that phenotypically most of their studied WHG individuals carried the dark skin and blue eyes characteristic of WHGs, but some other WHGs in France they sequenced also had pale to intermediate skin pigmentation.[41] Another entry in 2018, showed that theEastern Hunter Gatherers (EHG), Scandinavian Hunter Gatherers (SHG), and the Baltic foragers, all had the derived alleles for light skin pigmentation.[42]
TheWestern Steppe Herders, an earlyBronze Age population are believed to have also contributed to the skin and hair pigmentation in Europe, having a dominant effect on the phenotypes ofNorthern Europeans in particular.[23]
Bagnasco, G et al. (2024), discovered that the phenotypic traits for a group ofEtruscans from 3,000 to 2,700 years ago showed a population with blue-eyes, light to dark brown hair, and pale white to intermediate skin tones.[43]
In 2015, it was discovered that 13,000 year old samples of Caucasus Hunter Gatherers (CHG) from Georgia carried the mutation and derived alleles for very fair skinned pigmentation similar to Early Farmers (EF). This trait was said to have a relatively long history in Eurasia and risen to high frequency during theNeolithic expansion, with its origin probably predating theLast Glacial Maximum (LGM).[44]
An individual from thePre-Pottery Neolithic inAin' Ghazal, Jordan had both of the major derived 'European' depigmentation alleles(AA, SLC45A2: rs16891982 and SLC24A5: rs1426654), while another only had one of theSLC24A5 ancestral genotypes(GG). It indicated evidence of a more northerly origin for this population, possibly indicating an influx from the region of northeastern Anatolia.[45]
A study on the populations of the Chalcolithic Levant (6,000-7,000 years ago), found that an allelers1426654 in theSLC24A5 gene which is one of the most important determinants of light pigmentation in West Eurasians, was fixed for the derived variants in all Levant Chalcolithic samples, suggesting that the light skinned phenotype may have been common in the community. The individuals also had high incidence of genomic markers associated with blue-eye color.[46][47]
A research paper in 2017 indicated Egyptians atAbusir el-Meleq from 2,590 to 2,023 years ago, had a derived variant for theSLC24A5 locus, which contributes to lighter skin pigmentation, and was shown to be at high frequency inNeolithic Anatolia, accordant with the sample's ancestral affinities.[48]Parabon NanoLabs (2021) based on this data from Schuenemann et al. (2017) usingwhole genome sequencing and advancedbioinformatics, further discovered that these ancient Egyptian samples instead had a light brown complexion, but carried the main gene for light skin. They stated the results were highly consistent with Schueneman et al.'s findings.[49]
In the same year, according to phenotype SNP analysis, the precolonialGuanche inhabitants of theCanary Islands were showing consistent traits such as light and medium skin, with dark hair and brown eyes.[50]
A paper conducted by Fregel, Rosa et al. (2018) showed that in North Africa,Late Neolithic Moroccans had the European/Caucasus derivedSLC24A5 mutation and other alleles and genes that predispose individuals to lighter skin and eye colours.[51]
In the 1960s, biochemist W. Farnsworth Loomis suggested that skin colour is related to the body's need forvitamin D. The major positive effect of UV radiation in land-livingvertebrates is the ability to synthesizevitamin D3 from it. A certain amount of vitamin D helps the body to absorb morecalcium which is essential for building and maintaining bones, especially for developingembryos. Vitamin D production depends on exposure to sunlight. Humans living at latitudes far from the equator developed light skin in order to help absorb more vitamin D. People with light (type II) skin can produce previtamin D3 in their skin at rates 5–10 times faster than dark-skinned (type V) people.[52][53][54][55][56]
In 1998, anthropologistNina Jablonski and her husband George Chaplin collected spectrometer data to measure UV radiation levels around the world and compared it to published information on the skin colour ofindigenous populations of more than 50 countries. The results showed a very high correlation between UV radiation and skin colour; the weaker the sunlight was in a geographic region, the lighter the indigenous people's skin tended to be. Jablonski points out that people living above the latitudes of 50 degrees have the highest chance of developing vitamin D deficiency. She suggests that people living far from the equator developed light skin to produce adequate amounts of vitamin D during winter with low levels of UV radiation. Genetic studies suggest that light-skinned humans have been selected for multiple times.[57][58][59]
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Polar regions of theNorthern Hemisphere receive little UV radiation, and even less vitamin D-producing UVB, for most of the year. These regions were uninhabited by humans until about 12,000 years ago. (In northern Fennoscandia at least, human populations arrived soon after deglaciation.)[60] Areas likeScandinavia andSiberia have very low concentrations of ultraviolet radiation, and indigenous populations are all light-skinned.[2][53]
However, dietary factors may allow vitamin D sufficiency even in dark skinned populations.[61][62] Many indigenous populations acrossNorthern Europe andNorthern Asia survive by consumingreindeer, which they follow andherd. Reindeer meat, organs, andfat contain large amounts of vitamin D which the reindeer get from eating substantial amounts oflichen.[63] Some people of thepolar regions, like theInuit (Eskimos), retained their dark skin; they ate Vitamin D-richseafood, such as fish and sea mammalblubber.[64]
Furthermore, these people have been living in the far north for less than 7,000 years. As their founding populations lacked alleles for light skin colour, they may have had insufficient time for significantly lower melanin production to have beenselected for by nature after being introduced by random mutations.[65] "This was one of the last barriers in the history of human settlement," Jablonski states. "Only after humans learned fishing, and therefore had access to food rich in vitamin D, could they settle regions ofhigh latitude." Additionally, in the spring, Inuit would receive high levels of UV radiation as reflection from the snow, and their relatively darker skin then protects them from the sunlight.[2][15][11]
Two other main hypotheses have been put forward to explain the development of light skin pigmentation: resistance to cold injury, and genetic drift; now both of them are considered unlikely to be the main mechanism behind the evolution of light skin.[2]
The resistance to cold injury hypothesis claimed that dark skin was selected against in cold climates far from the equator and in higher altitudes as dark skin was more affected byfrostbite.[66] It has been found that reaction of theskin to extreme cold climates has actually more to do with other aspects, such as the distribution ofconnective tissue and distribution of fat,[67][68] and with the responsiveness of peripheralcapillaries to differences in temperature, and not with pigmentation.[2]
The supposition that dark skin evolved in the absence of selective pressure was put forward by theprobable mutation effect hypothesis.[69] The main factor initiating the development of light skin was seen as a consequence ofgenetic mutation without an evolutionaryselective pressure. The subsequent spread of light skin was thought to be caused byassortive mating[68] and sexual selection contributed to an even lighter pigmentation in females.[70][71] Doubt has been cast on this hypothesis, as more random patterns of skin colouration would be expected in contrast to the observed structural light skin pigmentation in areas of low UV radiation.[59] Theclinal (gradual) distribution of skin pigmentation observable in the Eastern hemisphere, and to a lesser extent in the Western hemisphere, is one of the most significant characteristics of human skin pigmentation. Increasingly lighter skinned populations are distributed across areas with incrementally lower levels of UV radiation.[72][73]
Variations in theKITL gene have been positively associated with about 20% of melanin concentration differences between African and non-African populations. One of the alleles of the gene has an 80% occurrence rate in Eurasian populations.[74][75] TheASIP gene has a 75–80% variation rate among Eurasian populations compared to 20–25% in African populations.[76] Variations in theSLC24A5 gene account for 20–25% of the variation between dark and light skinned populations of Africa,[77] and appear to have arisen as recently as within the last 10,000 years.[78] The Ala111Thr or rs1426654 polymorphism in the coding region of the SLC24A5 gene reaches fixation inEurope, but is found across the globe, particularly among populations inNorthern Africa, theHorn of Africa,West Asia,Central Asia andSouth Asia.[79][80][81]
The derived Ala111Thr allele in the SLC24A5 gene locus known to be associated with lighter skin pigmentation was in top selection signals in theWolayta, and the select alleles of single-nucleotide polymorphisms rs1426654 and rs1834640 characteristic of fair complexions in Eurasian populations were of high frequency (47.9%) in this Omotic-speaking Ethiopian population.[82] A higher proportion of these genes MYEF2-SLC24A5 were seen in high altitude (Amhara and Tigray) compared with the low-altitude (Afar) Ethiopians, with also elevated European admixture proportions observed in the high altitude tribes. The authors did not rule out the possibility that these European alleles were differentially selected in high-altitude populations due to unknown selective pressures.[83]
Africans carrying Eurasian ancestry like the Toubou were shown to have signals atHERC2 rs1129038, a major contributor to blue eye color in Europeans, as well as a signal at SLC24A5 rs1834640, a major contributor to pigmentation.[84]
Melanin is a derivative of theamino acidtyrosine.Eumelanin is the dominant form of melanin found inhuman skin. Eumelanin protects tissues and DNA from radiation damage byUV light. Melanin is produced in specialized cells calledmelanocytes, which are found in the lowest level of theepidermis.[85] Melanin is produced inside small membrane-bound packages calledmelanosomes. Humans with naturally occurring light skin have varied amounts of smaller and sparsely distributed eumelanin and its lighter-coloured relative,pheomelanin.[57][86] The concentration of pheomelanin varies highly within populations from individual to individual, but it is more commonly found among lightly pigmented Europeans, East Asians, and Native Americans.[24][87]
For the same body region, individuals, independently of skin colour, have the same amount of melanocytes (however variation between different body parts is substantial), but organelles which contain pigments, called melanosomes, are smaller and less numerous in light-skinned humans.[88]
For people with very light skin, the skin gets most of its colour from the bluish-white connective tissue in thedermis and from thehaemoglobin associatedblood cells circulating in thecapillaries of the dermis. The colour associated with the circulating haemoglobin becomes more obvious, especially in the face, whenarterioles dilate and become tumefied with blood as a result of prolongedphysical exercise or stimulation of thesympathetic nervous system (usuallyembarrassment oranger).[89] Up to 50% of UVA can penetrate deeply into the dermis in persons with light skin pigmentation with little protective melanin pigment.[63]
The combination of light skin,red hair, andfreckling is associated with high amount of pheomelanin, little amounts of eumelanin. Thisphenotype is caused by aloss-of-function mutation in the melanocortin 1 receptor (MC1R) gene.[90][91] However, variations in the MC1R gene sequence only have considerable influence on pigmentation in populations where red hair and extremely light skin is prevalent.[59] The gene variation's primary effect is to promote eumelanin synthesis at the expense of pheomelanin synthesis, although this contributes to very little variation in skin reflectance between different ethnic groups.[92] Melanocytes from light skin cells cocultured withkeratinocytes give rise to a distribution pattern characteristic of light skin.[93]
Freckles usually only occur in people with very lightly pigmented skin. They vary from very dark to brown in colour and develop a random pattern on the skin of the individual.[94] Solarlentigines, the other types of freckles, occur among old people regardless of skin colour.[2] People with very light skin (types I and II) make very little melanin in their melanocytes, and have very little or no ability to produce melanin in the stimulus of UV radiation.[95] This can result in frequent sunburns and a more dangerous, but invisible, damage done toconnective tissue andDNA underlying the skin. This can contribute topremature aging andskin cancer.[96][97] The strongly red appearance of lightly pigmented skin as a response to high UV radiation levels is caused by the increased diameter, number, and blood flow of the capillaries.[24]
People with moderately pigmented skin (Types III-IV) are able to produce melanin in their skin in response to UVR. Normaltanning is usually delayed as it takes time for the melanins to move up in theepidermis. Heavy tanning does not approach the photoprotective effect against UVR-inducedDNA damage compared to naturally occurringdark skin,[98][99] however it offers great protection against seasonal variations in UVR. Gradually developed tan in the spring prevents sunburns in the summer. This mechanism is almost certainly the evolutionary reason behind the development of tanning behaviour.[2]
Skin pigmentation is an evolutionary adaptation to the various UV radiation levels around the world. There are health implications of light-skinned people living in environments of high UV radiation. Various cultural practices increase problems related to health conditions of light skin, for examplesunbathing among the light-skinned.[2]
Humans with light skin pigmentation living in low sunlight environments experience increasedvitamin D synthesis compared to humans with dark skin pigmentation due to the ability to absorb more sunlight. Almost every part of the human body, including the skeleton, the immune system, and brain requires vitamin D. Vitamin D production in the skin begins when UV radiation penetrates the skin and interacts with a cholesterol-like molecule produce pre-vitamin D3. This reaction only occurs in the presence of medium length UVR, UVB. Most of the UVB and UVC rays are destroyed or reflected by ozone, oxygen, and dust in the atmosphere. UVB reaches the Earth's surface in the highest amounts when its path is straight and goes through a little layer of atmosphere.
The farther a place is from the equator, the less UVB is received, and the potential to produce of vitamin D is diminished. Some regions far from the equator do not receive UVB radiation at all between autumn and spring.[63] Vitamin D deficiency does not kill its victims quickly, and generally does not kill at all. Rather it weakens the immune system, the bones, and compromises the body's ability to fight uncontrolled cell division which results in cancer. A form of vitamin D is a potent cell growth inhibitor; thus chronic deficiencies of vitamin D seem to be associated with higher risk of certain cancers. This is an active topic of cancer research and is still debated.[63] The vitamin D deficiency associated with dark skin leads to higher levels of schizophrenia in such populations residing in northerly latitudes.[100]
With the increase of vitamin D synthesis, there is a decreased incidence of conditions that are related to common vitamin D deficiency conditions of people with dark skin pigmentation living in environments of low UV radiation:rickets,osteoporosis, numerouscancer types (includingcolon andbreast cancer), and immune system malfunctioning. Vitamin D promotes the production ofcathelicidin, which helps to defend humans' bodies against fungal, bacterial, and viralinfections, includingflu.[2][3] When exposed to UVB, the entire exposed area of body's skin of a relatively light skinned person is able to produce between 10 and 20000 IU of vitamin D.[63]
Light-skinned people living in high sunlight environments are more susceptible to the harmful UV rays of sunlight because of the lack ofmelanin produced in the skin. The most common risk that comes with high exposure to sunlight is the increased risk ofsunburns. This increased risk has come along with the cultural practice of sunbathing, which is popular among light-skinned populations. This cultural practice to gain tanned skin if not regulated properly can lead to sunburn, especially among very lightly skinned humans. The overexposure to sunlight also can lead tobasal cell carcinoma, which is a common form ofskin cancer.
Another health implication is thedepletion of folate within the body, where the overexposure to UV light can lead tomegaloblastic anemia. Folate deficiency in pregnant women can be detrimental to the health of their newborn babies in the form ofneural tube defects,miscarriages, andspina bifida, a birth defect in which thebackbone andspinal canal do not close before birth.[101] The peak of neural tube defect occurrences is the highest in the May–June period in theNorthern Hemisphere.[2] Folate is needed forDNA replication in dividing cells and deficiency can lead to failures of normalembryogenesis andspermatogenesis.[2][3][53]
Individuals with lightly pigmented skin who are repeatedly exposed to strong UV radiation, experience faster aging of the skin, which shows in increased wrinkling and anomalies of pigmentation. Oxidative damage causes the degradation of protective tissue in thedermis, which confers the strength of the skin.[24] It has been postulated that white women may developwrinkles faster than black women aftermenopause because white women are more susceptible to sun damage throughout life. Dr. Hugh S. Taylor, ofYale School of Medicine, concluded that the study could not prove the findings but they suspect the underlying cause. Light-coloured skin has been suspected to be one of the contributing factors that promote wrinkling.[102][103]
The genomic data further allowed us to study the physical appearance of SHGs; for instance, they show a combination of eye color varying from blue to light brown and light skin pigmentation. This is strikingly different from the WHGs-who have been suggested to have the specific combination of blue eyes and dark skin and EHGs-who have been suggested to be brown-eyed and light-skinned.
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.
On the basis of coalescent analysis with sequence data from the Simons Genomic Diversity Project (SGDP), the time to most recent common ancestor (TMRCA) of most Eurasian lineages containing the rs1426654 (A) allele is 29 thousand years ago (ka) [95% critical interval (CI), 28 to 31 ka], consistent with previous studies.
the Toubou have ~30% Eurasian ancestry from a population similar to the Greeks, who have 13% derived alleles at rs4988235, suggesting an expectation of ~3.9% of the derived allele simply from admixture. We similarly found in the Toubou signals at HERC2 (MIM: 605837) rs1129038 a major contributor to blue eye color in Europeans35 (Toubou derived allele frequency [DAF] ¼ 0.014; Greek DAF ¼ 0.33; Yoruba, Sara, and Laal DAF ¼ 0), as well as a signal at SLC24A5 (MIM: 609802) rs1834640, a major contributor to pigmentation36 (Toubou DAF ¼ 0.19; Greek DAF ¼ 0.99; Yoruba, Sara, and Laal DAF ¼ 0–0.04).
{{citation}}: CS1 maint: location missing publisher (link)A separate observation that the offspring of migrants with dark skin who migrate to cold climates have an increased risk of schizophrenia may also be due to low vitamin D during gestation and early life as dark skin requires greater sunlight exposure to make adequate levels of the vitamin D prehormone.