Dark skin is a naturally occurring human skin colour rich in eumelanin pigments and having a dark colour. People with relatively dark skin are referred to as brown, and those with very dark skin are often referred to as black, although this usage can be ambiguous in some countries where it is also used to specifically refer to different ethnic groups or populations.
Evolution of dark skin pigmentation began around 1.2 million years ago in light-skinned early hominid species after they moved from the equatorial rainforest to the sunny savannas. In the heat of the savannas, better cooling mechanisms were required, which were achieved by the loss of body hair and development of more efficient sweating. The loss of body hair led to the development of dark skin pigmentation, which acted as a mechanism of natural selection against folate depletion, and to a lesser extent, DNA damage. The primary factor contributing to the evolution of dark skin pigmentation was the breakdown of folate in reaction to ultraviolet radiation; the relationship between folate breakdown induced by ultraviolet radiation and reduced fitness as a failure of normal embryogenesis and spermatogenesis led to the selection of dark skin pigmentation. By the time modern Homo sapiens evolved, all humans were dark-skinned.
Humans with dark skin pigmentation have skin naturally rich in melanin (especially eumelanin), and have more melanosomes which provide a superior protection against the deleterious effects of ultraviolet radiation. This helps the body to retain its folate reserves and protects against damage to the DNA.
Dark-skinned people who live in high latitudes with mild sunlight are at an increased risk – especially in the winter – of vitamin D deficiency. As a consequence of vitamin D deficiency, they are at a higher risk of developing rickets, and numerous types of cancers, and possibly cardiovascular disease and low immune system activity.
The global distribution of generally dark-skinned populations is strongly correlated with the high ultraviolet radiation levels of the regions inhabited by them. These populations almost exclusively live near the equator, in tropical areas with intense sunlight: Australia, Melanesia, New Guinea, South Asia and Sub-Saharan Africa. Studies into these populations indicates that dark skin is a retention of the pre-existing high UV adapted state of modern humans before the Out of Africa migration and not a later evolutionary adaptation. Due to mass migration and increased mobility of people between geographical regions in the recent past, dark-skinned populations today are found all over the world.
- 1 Evolution
- 2 Biochemistry and genetics
- 3 Health implications
- 4 Geographic distribution
- 5 Culture
- 6 See also
- 7 References
People who lived in areas of intense sunlight developed dark skin colouration to protect against ultraviolet light and to protect their body mainly from folate depletion. Evolutionary pigmentation of the skin was caused by ultraviolet (UV) radiation of the sun. As hominids gradually lost their fur (between 4.5 and 2 million years ago) to allow for better cooling through sweating, their naked and lightly pigmented 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 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. The effect of sunlight on folic acid levels has been crucial in the development of dark skin.
Humans' earliest ancestors, just like their closest relatives – chimpanzees – today, had light skin. About 7 million years ago human and chimpanzee lineages diverged, and between 4.5 and 2 million years ago early humans moved out of rainforests to the savannas of East Africa. They not only had to cope with more intense sunlight but had to develop a better cooling system. It was harder to get food in the hot savannas and as mammalian brains are prone to overheating – 5 or 6 °C rise in temperature can lead to heatstroke – so there was a need for the development of better heat regulation. The solution was sweating and loss of body hair.
Sweating dissipated heat through evaporation. Early humans, like chimpanzees now, had few sweat glands, and most of them were located in the palms of the hand and the soles of feet. At times, individuals with more sweat glands were born. These humans could search for food and hunt for longer periods before being forced back to the shades. The more they could forage, more and healthier offspring they could produce, and higher the chance they had to pass on their genes for abundant sweat glands. With less hair, sweat could evaporate more easily and cool the body of humans faster. But this less-hairy skin proved to be a problem for humans living in areas of intense UV radiation. As heavy UV radiation has harmful effects, the solution was to develop dark skin as a protection. A few million years of evolution later, early humans had sparse body hair and more than 2 million sweat glands in their body.
Hairlessness, however, is particularly vulnerable to be damaged by ultraviolet light. Scientists have long assumed that humans evolved melanin in order to absorb or scatter harmful sun radiation. Some researchers assumed that melanin protects against skin cancer. While high UV radiation can cause skin cancer, the development of cancer usually occurs after child bearing age. As natural selection favours individuals with traits of reproductive success, skin cancer had little effect on the evolution of dark skin. Previous hypotheses suggested that sunburned nipples impeded breastfeeding, but a slight tan is enough to protect mothers against this issue.
A 1978 study examined the effect of sunlight on folate – a vitamin B complex – levels. The study found that even short periods of intense sunlight are able to halve folate levels if someone has light skin. Low folate levels are correlated with neural tube defects, such as anencephaly and spina bifida. UV rays can strip away folate, which is important to the development of healthy foetuses. In these abnormalities children are born with incomplete brain or spinal cord. Nina Jablonski, a professor of anthropology and expert on evolution of human skin coloration, found several cases in which mother’s visits to tanning studios were connected to neural tube defects in early pregnancy. She also found that folate was crucial to sperm development; some male contraception drugs are based on folate inhibition. It has been found that folate may have been the driving force behind the evolution of dark skin.
As humans dispersed from equatorial Africa to low UVR areas and higher altitudes sometime between 120,000 and 65,000 years ago, dark skin posed as a disadvantage. Populations with light skin pigmentation evolved in climates of little sunlight. Light skin pigmentation protects against vitamin D deficiency. It is known that dark-skinned people who have moved to climates of limited sunlight can develop vitamin D related conditions such as rickets, and different forms of cancer.
The main other hypotheses that have been put forward through history to explain the evolution of dark skin coloration relate to increased mortality due skin cancers, enhanced fitness as a result of protection against sunburns, and increasing benefits of due to antibacterial properties of eumelanin.
Darkly pigmented, eumelanin-rich skin protects against DNA damage caused by the sunlight. This is associated with lower skin cancer rates among dark-skinned populations. The presence of pheomelanin in light skin increases the oxidative stress in melanocytes, and this combined with the limited ability of pheomelanin to absorb UVR contributes to higher skin cancer rates among light-skinned individuals. The damaging effect of UVR on DNA structure and the entailing elevated skin cancer risk is widely recognized. However, these cancer types usually affect people at the end or after their reproductive career and could have not been the evolutionary reason behind the development of dark skin pigmentation. Of all the major skin cancer types, only malignant melanoma have a major effect in a person's reproductive age. The mortality rates of melanoma has been very low (less than 5 per 100 000) before the mid-20th century. It has been argued that the low melanoma mortality rates during reproductive age cannot be the principal reason behind the development of dark skin pigmentation.
Studies have found that even serious sunburns could not affect sweat gland function and thermoregulation. There are no data or studies that support that sunburn can cause damage so serious that can affect reproductive success.
Another group of hypotheses contended that dark skin pigmentation developed as antibacterial protection against tropical infectious diseases and parasites. Although it is true that eumelanin has antibacterial properties, its importance is secondary as a physical absorbed to protect against UVR induced damage. This hypothesis is not consistent with the evidence that most of the hominid evolution took place in savanna environment and not in tropical rainforests. Humans living in hot and sunny environments have darker skin than humans who live in wet and cloudy environments. The antimicrobial hypothesis also does not explain why some populations (like the Inuits or Tibetans) who live far from the tropics and are exposed to high UVR have darker skin pigmentation than their surrounding populations.
Biochemistry and genetics
Dark-skinned humans have high amount of melanin found in their skin. Melanin is derivative of the amino acid tyrosine. Eumelanin is the dominant form of melanin found in human skin. Eumelanin protects tissues and DNA from radiation damage of UV light. Melanin is produced in specialized cells called melanocytes, which are found at the lowest level of the epidermis. Melanin is produced inside small membrane-bound packages called melanosomes. People with naturally occurring dark skin have melanosomes which are clumped, large, and full of eumelanin. A four-fold difference in naturally occurring dark skin gives seven to eightfold protection against DNA damage, but even the darkest skin colour cannot protect against all damage to DNA.
Dark skin offers great protection against UVR because of its eumelanin contect, its superb UVR-absorbing capabilites of large melanosomes, and because eumelanin can be mobilized faster and brought to the surface of the skin from the deeps of the epidermis. For the same body region, light- and dark-skinned individuals have similar numbers of melanocytes (there is considerable variation between different body regions), but pigment-containing organelles, called melanosomes, are larger and more numerous in dark-skinned individuals. Keratocytes from dark skin cocultured with melanocytes give rise to a melanosome distribution pattern characteristic of dark skin. Melanosomes are not in aggregated state in darkly pigmented skin compared to lightly pigmented skin. Due to the heavily melanised melanosomes in darkly pigmented skin, it can absorb more energy from UVR and thus offers better protection against sunburns and by absorption and dispersion UV rays. Darkly pigmented skin protects against direct and indirect DNA damage. Photodegration occurs when melanin absorbs photons. Recent research suggest that the photoprotective effect of dark skin is increased by the fact that melanin can capture free radicals, such as hydrogen peroxide, which are created by the interaction of UVR and layers of the skin. Heavily pigmented melanocytes have greater capacity to divide after UVR irradiation, which suggests that they receive less damage to their DNA. Despite this, UVB damages the immune system even in darker skinned individuals due to its effect on Langerhans cells. The stratum corneum of people with dark or heavily tanned skin is more condensed and contains more cornified cell layers than in lightly pigmented humans. These qualities of dark skin enhance the barrier protection function of the skin.
Although darkly pigmented skin absorbs about 30 to 40% more sunlight than lightly pigmented skin, dark skin does not increase the body's internal heat intake in conditions of intense solar radiation. Solar radiation heats up rather the body's surface and not the interior. Furthermore, this amount of heat is negligible compared the heat produced when muscles are actively used during exercise. Regardless of skin colour, humans have excellent capabilities to dissipate heat through sweating. Half of the solar radiation reaching the Earth’s surface is in the form of infrared light and is absorbed similarly regardless of skin coloration.
In people with naturally occurring dark skin, the tanning occurs with the dramatic mobilization of melanin upward in the epidermis and continues with the increased production of melanin. This accounts for the fact that dark-skinned people get visibly darker after one or two weeks of sun exposure, and then lose their colour after months when they stay out of the sun. Darkly pigmented people tend to exhibit less signs of aging in their skin than the lightly pigmented because their dark skin protects them from most photoaging.
Skin colour is a polygenic trait, which means that several different genes are involved in determining a specific phenotype. Many genes work together in complex, additive, and non-additive combinations to determine the skin colour of an individual. The skin colour variations are normally distributed from light to dark, as it is usual for polygenic traits.
Data collected from studies on MC1R gene has shown that there is a lack of diversity in dark-skinned African samples in the allele of the gene compared to non-African populations. This is remarkable given that the number of polymorphisms for almost all genes in the human gene pool is greater in African samples than in any other geographic region. So, while the MC1Rf gene does not significantly contribute to variation in skin colour around the world, the allele found in high levels in African populations probably protects against UV radiation and was probably important in the evolution of dark skin.
Skin colour seems to vary mostly due to variations in a number of genes of large effect as well as several other genes of small effect (TYR, TYRP1, OCA2, SLC45A2, SLC24A5, MC1R, KITLG and SLC24A4). This does not take into account the effects of epistasis, which would probably increase the number of related genes. Variations in the SLC24A5 gene account for 20–25% of the variation between dark and light skinned populations of Africa, and appear to have arisen as recently as within the last 10,000 years. The Ala111Thr or rs1426654 polymorphism in the coding region of the SLC24A5 gene reaches fixation in Europe, and is also common among populations in North Africa, the Horn of Africa, West Asia, Central Asia and South Asia.
Skin pigmentation is an evolutionary adaptation to various UVR levels around the world. As a consequence there are many health implications that are the product of population movements of humans of certain skin pigmentation to new environments with different levels of UVR. Modern humans are often ignorant of their evolutionary history at their peril. Cultural practices that increase problems of conditions among dark-skinned populations are traditional clothing and vitamin D-poor diet.
Advantages of dark skin pigmentation in high sunlight environments
Dark pigmented people living in high sunlight environments are at an advantage due to the high amounts of melanin produced in their skin. The dark pigmentation protects from DNA damage and absorbs the right amounts of UV radiation needed by the body, as well as protects against folate depletion. Folate is water soluble vitamin B complex which naturally occurs in green, leafy vegetables, whole grains, and citrus fruits. Women need folate to maintain healthy eggs, for proper implantation of eggs, and for the normal development of placenta after fertilization. Folate is needed for normal sperm production in men. Furthermore, folate is essential for fetal growth, organ development, and neural tube development. Folate breaks down in high intense UVR. Dark-skinned women suffer the lowest level of neural tube defects. Folate plays an important role in DNA production and gene expression. It is essential for maintaining proper levels of amino acids which make up proteins. Folate is used in the formation of myelin, the sheath the covers nerve cells and makes it possible to send electrical signals quickly. Folate is also plays an important role in the development of many neurotransmitters, e.g. serotonin which regulates appetite, sleep, and mood. Serum folate is broken down by UV radiation or alcohol consumption. Because the skin is protected by the melanin, dark pigmented people have a lower chance of developing skin cancer and conditions related to folate deficiency, such as neural tube defects.
Disadvantages of dark skin pigmentation in low sunlight environments
Dark-skinned people living in low sunlight environments have been recorded to be very susceptible to vitamin D deficiency due to reduced vitamin D synthesis. A dark-skinned person requires about six times as much UVB than lightly pigmented persons. This is not a problem near the equator; however, it can be a problem at higher latitudes. For humans with dark skin in climates of low UVR, it can take about two hours to produce the same amount of vitamin D as humans with light skin produce in 15 minutes. Dark-skinned people having a high body-mass index and not taking vitamin D supplements were associated with vitamin D deficiency. Vitamin D plays an important role in regulating the human immune system and chronic deficiencies in vitamin D can make humans susceptible to specific types of cancers and many kinds of infectious diseases. Vitamin D deficiency increases the risk of the developing tuberculosis fivefold and also contributes to the development of breast, prostate, and colorectal cancer. The most prevalent disease to follow vitamin D deficiency is rickets, the softening of bones in children potentially leading to fractures and deformity. Rickets is caused by reduced vitamin D synthesis that causes an absence of vitamin D, which then causes the dietary calcium to not be properly absorbed. This disease in the past was commonly found among dark-skinned Americans of the southern part of the United States who migrated north into low sunlight environments. The popularity of sugary drinks and decreased time spent outside have contributed to significant rise of developing rickets. Deformities of the female pelvis related to severe rickets impair normal childbirth, which leads to higher mortality of the infant, mother, or both. Vitamin D deficiency is most common in regions with low sunlight, especially in the winter. Chronic deficiencies in vitamin D may also be linked with breast, prostate, colon, ovarian, and possibly other types of cancers. The casual relationship between cardiovascular disease and vitamin D deficiency also suggest link between health of cardiac and smooth muscle. Low vitamin D levels have also been linked to impaired immune system and brain functions. In addition, recent studies have linked vitamin D deficiency to autoimmune diseases, hypertension, multiple sclerosis, diabetes, and incidence of memory loss. Outside the tropics UVR has to penetrate through a thicker layer of atmosphere, which results in most of the UVB reflected or destroyed en route; because of this there is less potential for vitamin D biosynthesis in regions far from the equator. Higher amount of vitamin D intake for dark-skinned people living in regions with low levels of sunlight are advised by doctors to follow vitamin D rich diet or take vitamin D supplements.
There is a correlation between the geographic distribution of UV radiation (UVR) and the distribution of skin pigmentation around the world. Areas that have higher amounts of UVR have darker-skinned populations, generally located nearer the equator. Areas that are further away from the equator generally closer to the poles have a lower concentration of UVR, and contain lighter-skinned populations. This is the result of human evolution which contributed to variable melanin content in the skin to adapt to certain environments. A larger percentage of dark skinned people are found in the Southern Hemisphere because latitudinal land mass distribution is disproportionate. The present distribution of skin colour variation does not completely reflect the correlation of intense UVR and dark skin pigmentation due to mass migration and movement of peoples across continents in the recent past.
Dark-skinned populations inhabiting South Asia, Africa, Melanesia, Papua New Guinea and Australia all live in some of the areas with the highest UV radiation in the world, and have evolved very dark skin pigmentations as protection from the harmful sun rays. Evolution has restricted humans with darker skin in tropical latitudes, especially in non-forested regions, where ultraviolet radiation from the sun is usually the most intense. Different dark-skinned populations are not necessarily closely related genetically. Before the modern mass migration, it is has been argued that the majority of dark pigmented people lived within 20º of the equator.
Natives of Buka and Bougainville at the northern Solomon Islands in Melanesia and the Chopi people of Mozambique in the southeast coast of Africa have darker skin than other surrounding populations. (The native people of Bougainville, Papua New Guinea, have some of the darkest skin pigmentation in the world.) Although these people are widely separated they share similar physical environments. In both regions, they experience very high UVR exposure from cloudless skies near the equator which is reflected from water or sand. Water reflects, depending on colour, about 10 to 30% of UVR, that falls on it. People in these populations spend long hours fishing on the sea. Because it is impractical to wear extensive clothing in a watery environment culture and technology does little to buffer UVR exposure. The skin takes a very large amount of UVR radiation. These populations are probably near or at the maximum darkness that human skin can achieve.
More recent research has found that human populations over the past 50,000 years have changed from dark-skinned to light-skinned and vice versa. Only 100-200 generations ago, the ancestors of most people living today likely also resided in a different place and had a different skin color. According to Nina Jablonski, darkly pigmented modern populations in South India and Sri Lanka are an example of this, having redarkened after their ancestors migrated down from areas much farther north. Scientists originally believed that such shifts in pigmentation occurred relatively slowly. However, researchers have since observed that changes in skin coloration can happen in as little as 100 generations (~2,500 years), with no intermarriage required. The speed of change is also affected by clothing, which tends to slow it down.
The Aborigines of Australia, as with all humans, are descendents of African migrants, and their ancestors may have been among the first major groups to leave Africa around 50,000 years ago. Despite early migrations, genetic evidence has pointed out that the indigenous peoples of Australia are genetically very dissimilar to the dark-skinned populations of Africa and that they are more closely related to Eurasian populations.
The term black initially has been applied as a reference to the skin pigmentation of the aborigines of Australia; today it has been embraced by aboriginal activists as a term for shared culture and identity, regardless of skin colour.
Melanesia, a subregion of Oceania, whose name means "black islands", have several islands that are inhabited by people with dark skin pigmentation. The islands of Melanesia are located immediately north and northeast of Australia as well as east coast of Papua New Guinea. The western end of melanesia, from New Guinea through the Solomon Islands were first colonized by humans about 40 000 to 29 000 years ago.
In the world, blond hair is exceptionally rare outside Europe, and Southwest Asia, especially among dark-skinned populations. However, Melanesians are one of dark-skinned human populations known to have naturally occurring blond hair.
The indigenous Papuan people of New Guinea have dark skin pigmentation and have inhabited the island for at least 40,000 years. Due to their similar phenotype and the location of New Guinea being in the migration route taken by Indigenous Australians, it was generally believed that Papuans and Aboriginal Australians shared a common origin. However, a 1999 study failed to find clear indications of a single shared genetic origin between the two populations, suggesting multiple waves of migration into Sahul with distinct ancestries.
Sub-Saharan Africa is the region in Africa situated south of the Sahara where a large number of dark-skinned populations live. Dark-skinned groups on the continent have the same receptor protein as Homo ergaster and Homo erectus had. According to scientific studies, populations in Africa also have the highest skin colour diversity. High levels of skin colour variation exists between different populations in Sub-Saharan Africa. These differences depend in part on general distance from the equator, illustrating the complex interactions of evolutionary forces which have contributed to the geographic distribution of skin color at any point of time.
Due to frequently differing ancestry among dark-skinned populations, the presence of dark skin in general is not a reliable genetic marker, including among groups in Africa. For example, Wilson et al. (2001) found that most of their Ethiopian samples showed closer genetic affinity with light-skinned Armenians and Norwegians than with dark-skinned Bantu populations. Mohamoud (2006) likewise observed that their Somali samples were genetically more similar to Arab populations than to other African populations.
The preference or disfavour for darker skin has varied depending on geographical area and time. Today, darker skin is viewed as fashionable and as a sign of well-being in some societies. This resulted in the development of tanning industry in several countries. However, in some countries, dark skin is not seen as highly desirable or indicative of higher class, especially among women.
- dark-skinned Princeton University "naturally having skin of a dark color"
- "Dark-skinned". Dictionary.com. Retrieved 10 December 2012. "having skin rich in melanin pigments"
- Muehlenbein, Michael (2010). Human Evolutionary Biology. Cambridge University Press. pp. 192–213.
- Dictionary.com: black 3.a "a member of any of various dark-skinned peoples" 21.a"pertaining or belonging to any of the various populations characterized by dark skin pigmentation"
- Oxford Dictionaries. April 2010. Oxford University Press. "belonging to or denoting any human group having dark-coloured skin" "black" (accessed 6 August 2012).
- Dictionary.com: black 3.a "a member of any of various dark-skinned peoples" 21.a"specifically thedark-skinned peoples of Africa, Oceania, or Australia."
- "Global Census". American Anthropological Association. Retrieved 10 December 2012.
- Oxford Dictionaries. April 2010. Oxford University Press. "especially of African or Australian Aboriginal ancestry" "black" (accessed 6 August 2012).
- James, Mackers (1828-11-08). "Proclamation". Classified Advertising. Trove. Retrieved 10 December 2012.
- Nina, Jablonski (2004). "The evolution of human skin and skin color". Annual Review of Anthropology 33: 585–623. doi:10.1146/annurev.anthro.33.070203.143955. "genetic evidence [demonstrate] that strong levels of natural selection acted about 1.2 mya to produce darkly pigmented skin in early members of the genus Homo"
- Bower, C.; Stanley (1992). "The role of nutritional factors in the aetiology of neural tube defects". Journal of Paediatrics and Child Health 28: 12–16.
- Minns, R.A. (1996). "Folic acid and neural tube defects". Spinal Cord 34: 460–465.
- Copp et al. (1998). "Embryonic mechanisms underlying the prevenetion of neural tube defects by vitamins". Mental Retardation and Developmental Disabilities Research Reviews 4: 264–268.
- Molloy et al. "Folate status and neural tube defects". BioFactors 10: 291–294.
- Lucock, M. "Folic acid: nutritional biochemistry, molecular biology, and role in disease processes". Molecular Genetics and Metabolism. 71 (1–2): 121–138.
- William et al. "Decline in the prevalence of spina bifida and anencephaly by race/ethnicity:1995–2002". Pediatrics 116: 580–586.
- Nielsen et al. "The importance of the depth distribution of melanin in skin for DNA protection and other photobiological processes". Journal of Photochemistry and Photobiology B: Biology 82: 194–198.
- Jane, Higdon. "Vitamin D". Micronutrient Information Center. Linus Pauling Institute. Retrieved 10 December 2012.
- Jablonski, N.G.; Chaplin (2000). "The evolution of human skin coloration". Journal of Human Evolution 39: 57–106. doi:10.1006/jhev.2000.0403.
- Harding, R; Healy, E; Ray, A; Ellis, N; Flanagan, N; Todd, C; Dixon, C; Sajantila, A et al. (2000). "Evidence for Variable Selective Pressures at MC1R". The American Journal of Human Genetics 66 (4): 1351–61. doi:10.1086/302863. PMC 1288200. PMID 10733465.
- O'Neil, Dennis. "Skin Color Adaptation". Human Biological Adaptability: Skin Color as an Adaptation. Palomar. Retrieved 10 December 2012.
- O'Neil, Dennis. "Overview". Modern Human Variation. Palomer. Retrieved 10 December 2012.
- Nina, Jablonski (2004). "The evolution of human skin and skin color". Annual Review of Anthropology 33: 585–623. doi:10.1146/annurev.anthro.33.070203.143955.
- Gina, Kirchweger. "The Biology of Skin Color: Black and White". Evolution Library. PBS. Retrieved 10 December 2012.
- Jablonski, N.G. (2006). Skin: a Natural History. Berkeley: University of California Press.
- Dawkins, Richard (2004). The Ancestor's Tale.
- Montagna, W. "The consequences of having naked skin". Birth Defects: Original Article Series 17: 1–7.
- Langbein et al. (2005). "Characterization of a novel human type II epithelial keratin K1b, specifically expressed in eccrine sweat glands". Journal of Investigative Dermatology 125: 428–444.
- Blum, H.F. (1961). "Does the melanin pigment of human skin have adaptive value?". Quarterly Review of Biology 36: 50–63.
- Rigel, D.S. "Cutaneous ultraviolet exposure and its relationship to the development of skin cancer". Journal of American Academy of Dermatology 58: S129–S132.
- Jemal et al. "Recent trends in cutaneous melanoma incidence among white in the United States". Journal of National Cancer Institute 93: 678–683.
- Jablonski, Nina. "Department of Anthropology at Penn State". Penn State University. Retrieved 14 December 2012.
- Tim Appenzeller, Nature Human migrations: Eastern odyssey 485, 24–26 doi:10.1038/485024a 2 May 2012
- Jablonski, Nina (2012). Living Color. Berkeley, Los Angeles, London: University of California Press. ISBN 978-0-520-25153-3.
- "Effects of Ecology and Climate on Human Physical Variations". Retrieved 10 December 2012.
- Miyamura et al. (2007). "Regulation of human skin pigmentation and responses to ultraviolet radiation". BioFactors 20: 2–13.
- Saraiya et al. (2004). "Interventions to prevent skin cancer by reducing exposure to ultraviolet radiation: a systematic review". American Journal of Preventive Medicine 27: 422–466.
- Agar, N.; Young A. R. (2005). "Melanogenesis: a photoprotective response to DNA damage?". Mutation Research 571: 121–132.
- Pfeifer et al. (2005). "Mutations induced by ultraviolet light". Mutation Research 571: 19–31.
- Rouzaud et al. (2005). "MC1R and the response of melanocytes to ultraviolet radiation". Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 133–152 571.
- Brenner, M.; Hearing V. J. (2008). "The protective role of melanin against UV damage in human skin". Photochemistry and Photobiology 84: 539–549.
- Van Nieuwpoort et al. (2004). "Tyrosine-induced melanogenesis shows differences in morphologic and melanogenic preferences of melanosomes from light and dark skin types". Journal of Investigative Dermatology 122: 1251–1255.
- Kielbassa et al. (2000). "DNA damaged induced by ultraviolet and visible light and its wavelength dependence". Methods in Enzymology 319: 436–445.
- Cleaver and Crowely (2002). "UV damage, DNA repair and skin carcinogenesis". Frontiers in Bioscience 7: 1024–1043.
- Sinha et al. (2002). "UV-induced DNA damage and repair: a review". Photochemical and Photobiological Science 1(4): 225–236.
- Schreier et al. (2007). "Thymine dimerization in DNA is an ultrafast photoreaction". Science 315 (5812): 625–629.
- Epel et al. (1999). "Development in the floating world: defenses of eggs and embryos against damage from UV radiation". American Zoologist 39: 271–278.
- Haass, N.K.; et al. (2005). "Adhesion, migration and communications in melanocytes and melanoma". Pigment Cell Research 18: 150–159.
- Thong, H.Y.; et al. (2003). "The patterns of melanosome distribution in keratinocytes of human skin as one determining factor of skin colour". British Journal of Dermatology 149: 498–505.
- Tadokoro, T; et al. (2005). "Mechanisms of skin tanning in different racial/ethnic groups in response to ultraviolet radiation". Journal of Investigative Dermatology 124: 1326–1332.
- Minwala, S; et al. (2001). "Keratinocytes Play a Role in Regulating Distribution Patterns of Recipient Melanosomes In Vitro". Journal of Investigative Dermatology 117: 341–347.
- Szabo, G; et al. "Racial differences in the fate of melanosomes in human epidermis". Nature 222: 1081–1082.
- Lewis, Ricki (2012). Human genetics : concepts and applications (10th ed. ed.). New York, NY: McGraw-Hill Co. pp. 135–136. ISBN 978-0-07-352530-3.
- "Skin Color".
- Rana, B.K.; et al. (1999). "High polymorphism at the human melanocortin 1 receptor locus". Genetics 151: 1547–1557.
- "Effects of Ecology and Climate on Human Physical Variations".
- Khan, Razib (2009). "Genetics of human pigmentation: Gene expression". Discover Magazine. Retrieved 11 December 2012.
- Lamason, R. L.; Mohideen, MA; Mest, JR; Wong, AC; Norton, HL; Aros, MC; Jurynec, MJ; Mao, X et al. (2005). "SLC24A5, a Putative Cation Exchanger, Affects Pigmentation in Zebrafish and Humans". Science 310 (5755): 1782–17886. doi:10.1126/science.1116238. PMID 16357253.
- Gibbons, A. (2007). "AMERICAN ASSOCIATION OF PHYSICAL ANTHROPOLOGISTS MEETING: European Skin Turned Pale Only Recently, Gene Suggests". Science 5823 (5823): 364a. doi:10.1126/science.316.5823.364a. PMID 17446367.
- "Graphical display of Allele Frequencies for Ala111Thr". Allele Frequency Database. Retrieved 10 October 2012.
- "ALFRED - Polymorphism Information - Ala111Thr". Allele Frequency Database. Retrieved 10 October 2012.
- Pagani, Luca; Toomas Kivisild, Ayele Tarekegn, Rosemary Ekong, Chris Plaster, Irene Gallego Romero, Qasim Ayub, S. Qasim Mehdi, Mark G. Thomas, Donata Luiselli, Endashaw Bekele, Neil Bradman, David J. Balding, Chris Tyler-Smith (21 June 2012). "Ethiopian Genetic Diversity Reveals Linguistic Stratification and Complex Influences on the Ethiopian Gene Pool". The American Journal of Human Genetics 91 (1): Volume 91, Issue 1, 83–96, 21 June 2012. doi:10.1016/j.ajhg.2012.05.015. Retrieved 20 July 2013.
- "Dark-skinned immigrant urged to take vitamin D". CBC News. Retrieved 10 December 2012.
- Buccimazza, S. S.; C. D. Molteno, T. T. Dunnem, and D. L. Viljoen (1994). "Prevalence of neural tube defects in Cape Town, South Africa". Teratology 50 (3): 194–199.
- "Dark-skinned immigrants urged to take vitamin D".
- Oglesby, Erika. "Darker Skin? More Vitamin D, Please!". Care2. Retrieved 1 January 2013.
- Murray, F. G. (1934). "Pigmentation, sunlight, and nutritional disease". American Anthropologist 36 (3): 438–445.
- Loomis, W. F. (1967). "Skin-pigment regulation of vitamin-D biosynthesis in man". Science 157 (3788): 501–506.
- "Vitamin D and the evolution of human depigmentation". American Journal of Physical Anthropology 139 (4): 451–461. 2009.
- Vieth, R (2003). In Bone Loss and Osteoporosis: an Anthropological Perspective. Kluwer Academic/Plenum Press. pp. 135–150.
- Garland, C.F.; Garland, F.C., Gorham, E.D., et al. (2006). "The Role of Vitamin D in Cancer Prevention". Journal of Public Health 96: 252–261.
- Fleet, J.C. (2008). "Molecular actions of vitamin D contributing to cancer prevention". Molecular Aspects of Medicine 29: 388–396.
- Grant, W.B. (2008). "Solar ultraviolet irradiance and cancer incidence and morality". Advances in Experimental Medicine and Biology 624: 16–30.
- Chen, T.C.; et al. (2007). "Factors that influence the cutaneous synthesis and dietary sources of vitamin D". Archives of Biochemistry and Biophysics 460: 213–217.
- Kim, D.H.; et al. (2008). "Prevalence of hypovitaminosis D in cardiovascular diseases". American Journal of Cardiology 102: 1540–1544.
- McGrath, J.J.; et al. (2004). "Vitamin D – implications for brain development". Journal of Steroid Biochemistry and Molecular Biology. 89–90: 557–560.
- Harms, M.; et al. (2008). "Developmental vitamin D deficiency alters adult behaviour in 129/SvJ and C57BL/6J mice". Behavioural Brain Research 187: 343–350.
- "How to get your vitamin D".
- "Your Health".
- "Vitamin D deficiency and skin sun exposure".
- Villarosa, Linda. "Why Black People Need More Vitamin D". The Root. Retrieved 1 January 2013.
- "Micronutrient Information Center". Linus Pauling Institute. Retrieved 1 January 2013.
- Marks, Jonathan. "Interview with Jonathan Marks". Race – The Power of an Illusion. PBS. Retrieved 3 January 2013. "Certainly dark skin is present all over the world in different populations. Indigenous Australians, indigenous peoples of India, indigenous peoples of Africa are all very darkly pigmented even though they're not particularly closely related."
- "Modern human variation: overview".
- "Ultraviolet radiation albedo of natural surfaces". Journal of Environmental Engineering and Landscape Management 16 (2): 83–88. 2008.
- Krulwich, Robert (2 February 2009). "Your Family May Once Have Been A Different Color". NPR. Retrieved 4 July 2013.
- "Aboriginal Genome".
- "A Proclamation".
- Andrew Bolt On Trial On Racism Charges
- "Papua Web".
- "Origins and dispersals of Pacific peoples: Evidence from mtDNA phylogenesis of the pacific rat". Proceedigns of the National Academy of Science 101 (24): 9167–9172. 2004.
- Norton, H. L.; J. S. Friedlaender, D. A. Merriwether, G. Koki, C S. Mgone, and M. D. Shriver (2006). "Skin and hair pigmentation variation in island Melanesia". American Journal of Physical Anthropology 130 (2): 254–268.
- Sindya N. Bhanoo (3 May 2012). "Another Genetic Quirk of the Solomon Islands: Blond Hair". The New York Times. Retrieved 3 May 2012.
- Dupree, L. "Afghānistān: (iv.) ethnography". In Ehsan Yarshater. Encyclopædia Iranica (Online Edition ed.). United States: Columbia University. Retrieved 5 November 2011.
- Alan J. Redd and Mark Stoneking (1999). "Peopling of Sahul: mtDNA Variation in Aboriginal Australian and Papua New Guinean Populations". American Journal of Human Genetics 65: 808–828. PMC 1377989.
- "Modern human variation: overview".
- "Black Africa".
- Rogers, A.R.; et al. (2004). "Genetic variation at the MC1R locus and the time loss of human body hair". Current Anthropology 45: 105–124. doi:10.1086/381006.
- Relethford, JH (2000). "Human skin color diversity is highest in sub-Saharan African populations". Human biology; an international record of research 5 (72): 773–80. PMID 11126724.
- Wilson, James F.; Weale, Michael E.; Smith, Alice C.; Gratrix, Fiona; Fletcher, Benjamin; Thomas, Mark G.; Bradman, Neil; Goldstein, David B. (2001). "Population genetic structure of variable drug response". Nature Genetics 29 (3): 265–9. doi:10.1038/ng761. PMID 11685208. "62% of the Ethiopians fall in the ﬁrst cluster, which encompasses the majority of the Jews, Norwegians and Armenians, indicating that placement of these individuals in a ‘Black’ cluster would be an inaccurate reﬂection of the genetic structure. Only 24% of the Ethiopians are placed in the cluster with the Bantu"
- Mohamoud, A. M. (October 2006). "P52 Characteristics of HLA Class I and Class II Antigens of the Somali Population". Transfusion Medicine 16 (Supplement s1): 47. doi:10.1111/j.1365-3148.2006.00694_52.x. Retrieved 4 July 2013.