Human skin colour can range from almost black to pinkish white in different people. In general, people with ancestors from sunny regions have darker skin than people with ancestors from regions with less sunlight. (However, this is complicated by the fact that there are people whose ancestors come from both sunny and less-sunny regions; and these people may have skin colors across the spectrum). On average, women have slightly lighter skin than men.

Skin colour is determined by the amount and type of the pigment melanin in the skin. Melanin comes in two types: phaeomelanin (red to yellow) and eumelanin (dark brown to black). Both amount and type are determined by four to six genes which operate under incomplete dominance. One copy of each of those genes is inherited from the father and one from the mother. Each gene comes in several alleles, resulting in a great variety of different skin colours.

Dark skin protects against skin cancer, mutations in skin cells induced by ultraviolet light. Light-skinned persons have about a tenfold greater risk of dying from skin cancer under equal sun conditions. Furthermore, dark skin prevents UV-A radiation from destroying the essential B vitamin folate. Folate is needed for the synthesis of DNA in dividing cells and too low levels of folate in pregnant women are associated with birth defects.

While dark skin protects vitamin B, it can lead to a vitamin D deficiency. The advantage of light skin is that it lets more sunlight through, which leads to increased production of vitamin D3, necessary for calcium absorption and bone growth. The lighter skin of women results from the higher calcium needs of women during pregnancy and lactation.

The evolution of the different skin colours is thought to have occurred as follows: the haired ancestor of humans, like modern great apes, had light skin under their hair. Once the hair was lost, they evolved dark skin, needed to prevent low folate levels since they lived in sun-rich Africa. (The skin cancer connection is probably of secondary importance, since skin cancer usually kills only after the reproductive age and therefore doesn't exert much evolutionary pressure.) When humans migrated to sun-poorer regions in the north, low vitamin D3 levels became a problem and light skin colour evolved.

Dark-skinned people who live in sun-poor regions often lack vitamin D3, one reason for the fortification of milk with vitamin D in some countries.

The Inuit are a special case: even though they live in an extremely sun-poor environment, they have retained their relatively dark skin. This can be explained by the fact that their traditional animal-based diet provides plenty of vitamin D.

Albinism is a condition characterized by the absence of melanin, resulting in white skin and hair; it is caused by a genetic mutation.

Skin color has sometimes been used in an (often controversial) attempt to define human races; see also racism.

Research on Skin Colour Variability

The colour of human skin varies from dark brown to pale pink. In attempting to discover the mechanisms that have generated such a wide variation in human skin colour, Nina Jablonski and George Chaplin (2000) discovered that there is a high correlation between the coloration of the human skin of indigenous peoples and the average annual ultraviolet (UV) radiation available for skin exposure where the indigenous peoples live. Accordingly, Jablonski and Chaplin plotted the whiteness (W) of skin coloration of indigenous peoples who have stayed in the same geographical area for the last 500 years versus the annual UV available for skin exposure (AUV) for over 200 indigenous persons and found that whiteness W of skin coloration is related to to the annual UV available for skin exposure AUV according to (Jablonski and Chaplin (2000), p. 67, formula coefficients have been rounded to one-figure accuracy) where the whiteness W of skin coloration is measured as the percentage of light reflected from the upper inner arm at which location on humans there should be minimal tanning of human skin due to personal exposure to the sun; a lighter skinned human would reflect more light and would have a higher W number. Judging from the above linear fit to the empirical data, the theoretical maximum whitest human skin would reflect only 70 per cent of incident light for a hypothetical indigenous human-like population that lived where there was zero annual UV available for skin exposure (AUV = 0 in the above formula). Jablonski and Chaplin evaluated average annual UV available for skin exposure AUV from satellite measurements that took into consideration the measured daily variation in the thickness of the ozone layer that blocked UV hitting the earth, measured daily variation in opacity of cloud cover, and daily change in angle at which the sunlight containing UV radiation strikes the earth and passes through different thicknesses of earth's atmosphere at different latitudes for each of the different human indigenous peoples' home areas from 1979 to 1992.Jablonski and Chaplin proposed an explanation for the observed variation of untanned human skin with annual UV exposure. By Jablonski and Chaplin's explanation, there are two competing forces affecting human skin color:

the melanin that produces the darker tones of human skin serves as a light filter to protect against too much UV light getting under the human skin where too much UV causes sunburn and disrupts the synthesis of precursors necessary to make human DNA; versus
humans need at least a minimum threshold of UV light to get deep under human skin to produce vitamin D, which is essential for building and maintaining the bones of the human skeleton.
Jablonski and Chaplin note that when human indigenous peoples have migrated, they have carried with them a sufficient human gene pool so that within a thousand years, the skin of their descendants living today has turned dark or turned white to adapt to fit the formula given above--with the notable exception of dark-skinned peoples moving north, such as to populate the seacoast of Greenland, to live where they have a year-round supply of food, such as fish, rich in vitamin D, so that there was no necessity for their skin to turn white to let enough UV under their skin to synthesize the vitamin D that humans need for healthy bones.

In considering the color of human skin in the long span of human evolution, Jablonski and Chaplin note that there is no empirical evidence to suggest that the human ancestors six million years ago had a skin color different from the skin color of today's chimpanzees¡ªnamely pale-skinned under black hair. But as humans evolved to lose their body hair a parallel evolution permitted human populations to turn their base skin colour dark or white over a period of less than a thousand years to adjust to the competing demands of 1) increasing eumelanin to protect from UV that was too intense and 2) reducing eumelanin so that enough UV would penetrate to synthesize enough vitamin D. By this explanation, in the time that humans lived only in Africa, humans had dark skin to the extent that they lived for extended periods of time where the sunlight is intense. As some humans migrated north, over time they developed white skin, though they retained within the gene pool the capability to develop black skin when they migrated to areas with intense sunlight again, such as across the Bering Strait and south to the Equator.

Origins of Black Skin in Humans

Scientists have correlated the wide variations in human skin color with the mutations in one gene, the MC1R gene (Harding et al 2000:1351). The "MC1R" label for the gene stands for melanocortin 1 receptor, where

"melano" refers to black,
"melanocortin" refers to the hormone stimulant produced by the pituitary gland that orders cells to produce the melanin that makes skin cells black,
the "1" in the MC1R gene name specifies the first family of melanocortin genes, and
"receptor" indicates that the protein from the gene serves as a signal relay from outside the cell wall to inside the cell wall--to the place in the cell where the black melanin is synthesized.
Accordingly, the MC1R gene specifies the amino acid sequence in the receptor protein that relays through the cell wall the hormone signal from the pituitary gland to produce the melanin that makes human skin black. Many variations in the amino acid sequence of this receptor protein result in whiter or darker skin.

The human MC1R gene consists of a string of 954 nucleotides, where each nucleotide is one of the four bases Adenosine (A), Guanine (G), Thymine (T), or Cytosine (C). But 261 of the nucleotides in the MC1R gene can change with no effect on the amino acid sequence in the receptor protein produced from the gene. For example, the nucleotide triplets GGT, GGC, GGA, and GGG are all synonymous and all produce the amino acid Glycine, ( See DNA Codon Table ) so a mutation in the third position in the triplet GGT is a "silent mutation" and has no effect on the amino acid produced from the triplet. Harding et al (2000:1355) analyzed the amino acid sequences in the receptor proteins from 106 individuals from Africa and 524 individuals from outside Africa to find why the color of all the Africans' skin was black. Harding found that there were zero differences among the Africans for the amino acid sequences in their receptor proteins, so the skin of each individual from Africa was black. In contrast, among the non-African individuals, there were 18 different amino acid sites in which the receptor proteins differed, and each amino acid that differed from the African receptor protein resulted in skin lighter than the skin of the African individuals. Nonetheless, the variations in the 261 silent sites in the MC1R were similar between the Africans and non-Africans, so the basic mutation rates among the Africans and non-Africans were the same. Why were there zero differences and no divergences in the amino acid sequences of the receptor protein among the Africans while there were 18 differences among the populations in Ireland, England, and Sweden?

Harding (2000:1359-1360) concluded that the intense sun in Africa created an evolutionary constraint that reduced severely the survival of progeny with any difference in the 693 sites of the MC1R gene that resulted in even one small change in the amino acid sequence of the receptor protein--because any variation from the African receptor protein produced significantly whiter skin that gave less protection from the intense African sun. In contrast, in Sweden, for example, the sun was so weak that no mutation in the receptor protein reduced the survival probability of progeny. Indeed, for the individuals from Ireland, England, and Sweden, the mutation variations among the 693 gene sites that caused changes in amino acid sequence was the same as the mutation variations in the 261 gene sites at which silent mutations still produced the same amino acid sequence. Thus, Harding concluded that the intense sun in Africa selectively killed off the progeny of individuals who had a mutation in the MC1R gene that made the skin whiter. However, the mutation rate toward whiter skin in the progeny of those African individuals who had moved North to areas with weaker sun was comparable to the MC1R mutation rate of the white folks whose ancient ancestors grew up in Sweden. Hence, Harding concluded that the whiteness of human skin was a direct result of random mutations in the MC1R gene that were non-lethal at the latitudes of Ireland, England, and Sweden. Even the mutations that produce red hair with little ability to tan were non-lethal in the northern latitudes.

Rogers, Iltis, and Wooding (2004) examined Harding's data on the variation of MC1R nucleotide sequences for people of different ancestry on the earth to determine the most probable progression of the skin color of human ancestors over the last 5 million years. Comparing the MC1R nucleotide sequences for humans and chimpanzees in various regions of the earth, Rogers concluded that the common ancestors of all humans on earth had white skin color under dark hair--similar to the skin and hair color pattern of today's chimpanzees. That is 5 million years ago, the human ancestors' dark hair protected their white skin from the intense African sun so that there was no evolutionary constraint that killed off the progeny of those who had mutations in the MC1R nucleotide sequences that made their skin white.

However, over 1.2 million years ago, judging from the numbers and spread of variations among human and chimpanzee MC1R nucleotide sequences, the human ancestors in Africa began to lose their hair and they came under increasing evolutionary pressures that killed off the progeny of individuals that retained the inherited whiteness of their skin. By 1.2 million years ago, all people having descendants today had exactly the receptor protein of today's Africans; their skin was black, and the intense sun killed off the progeny with any whiter skin that resulted from mutational variation in the receptor protein (Rogers 2004:107).

However, the progeny of those humans who migrated North away from the intense African sun were not under the evolutionary constraint that keeps human skin black generation after generation in Africa. Tracking back the statistical patterns in variations in DNA among all known people sampled who are alive on the earth today, Rogers concluded the following: 1) from 1.2 million years ago for a million years, the ancestors of all people alive today were as black as today's Africans, 2) for that period of a million years, human ancestors lived naked without clothing, and 3) the descendants of any people who migrate North from Africa will mutate to become white over time because the evolutionary constraint that keeps Africans' skin black generation after generation decreases generally the further North a people migrates .