Màu da

mật độ các màu da trên thế giới

Màu da loài người có thể có nhiều sắc, từ rất đậm cho đến rất nhạt gần như không màu (và ở những người này, da có nước màu trắng hồng do màu máu ẩn hiện lên trên). Màu sắc của da là do lượng sắc tố melanin trong da, nhiều thì làm da đậm đen lại, ít thì làm da nhạt đi. Nói chung phái nữ có ít melanin hơn phái nam.

Người có tổ tiên sinh sống vùng nắng nhiều, nhiệt độ cao có da đậm đen, trong khi da người có tổ tiến sống vùng ít nắng, ôn đới trắng hơn. Tuy nhiên càng về sau này càng có sự pha trộn giữa các sắc dân, nên màu da có nhiều sắc khác nhau.

Sắc tố Melanin và gen

Melanin comes in two types: pheomelanin (red) and eumelanin (dark brown to nearly 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 tones.

Dark skin protects against those skin cancers that are caused by 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 does not block sunlight as effectively, leading to increased production of vitamin D₃, necessary for calcium absorption and bone growth. The lighter skin of women may result from the higher calcium needs of women during pregnancy and lactation.

The evolution of the different skin tones is thought to have occurred as follows: the haired ancestors 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 does not exert much evolutionary pressure.) When humans migrated to less sun-intensive regions in the north, low vitamin D₃ levels became a problem and light skin color re-emerged.

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

The Inuit and Yupik are special cases: 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 very light skin and hair; it is caused by a genetic mutation.

Skin tone has sometimes been used in an (often controversial) attempt to define human races; see also racism. On a cultural level, color metaphors for race have evolved based upon genetic variations in human skin color and changing customs or traditions of what arbitrary criteria and the amount of categories to use.

Các nghiên cứu về màu da loài người

The tone of human skin varies from dark brown to nearly colorless, which appears pale pink due to the blood in the skin. In attempting to discover the mechanisms that have generated such a wide variation in human skin tone, Nina Jablonski and George Chaplin (2000) discovered that there is a high correlation between the tone of 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 skin tone (W) 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 skin tone lightness W is related to the annual UV available for skin exposure AUV according to

$W=70-{\frac {AUV}{10}}$

(Jablonski and Chaplin (2000), p. 67, formula coefficients have been rounded to one-figure accuracy) where the skin tone lightness W 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 lightness maximum of 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 tone:

1. 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
2. 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 gene pool so that within a thousand years, the skin of their descendants living today has turned dark or turned light 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 rich in vitamin D, such as fish, so that there was no necessity for their skin to lighten to let enough UV under their skin to synthesize the vitamin D that humans need for healthy bones.

In considering the tone 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 tone different from the skin tone of today's chimpanzees—namely light-skinned under black hair. But as humans evolved to lose their body hair a parallel evolution permitted human populations to turn their base skin tone dark or light 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 light skin, though they retained within the gene pool the capability to develop dark skin when they migrated to areas with intense sunlight again, such as across the Bering Strait and south to the Equator. [1]

Những ý kiến khác ngược

Ashley Robins (1991) has argued that the light skin of indigenous peoples living north of 40° north latitude need not arise necessarily from the natural selection pressures on those humans to synthesize enough vitamin D. Robins argues that people with dark skin can get enough vitamin D if they spend enough time in the spring and summer sun, and he hypothesizes that the fatty tissues of humans would store enough vitamin D to maintain health during the northern-most winters. [2]

Tại sao có người da trắng?

Several genes have been invoked to explain variations of skin tones in humans, including ASIP, MATP, TYR, and OCA2 [3]. A recently discovered gene, SLC24A5 has been shown to account for a substantial fraction of the difference in the average of 30 or so melanin units between Europeans and Africans.

Wide variations in human skin tones have been correlated with mutations in another 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 stimulates 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 membrane to inside the cell--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 membrane the hormone signal from the pituitary gland to produce the melanin that makes human skin very dark. Many variations in the amino acid sequence of this receptor protein result in lighter or darker skin.

The human MC1R gene consists of a string of 954 nucleotides, where each nucleotide is one of the four bases Adenine (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 tone of all the Africans' skin was dark. 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 dark. 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 lighter 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 lighter. However, the mutation rate toward lighter skin in the progeny of those African individuals who had moved North to areas with weaker sun was comparable to the mutation rate of the folks whose ancient ancestors grew up in Sweden. Hence, Harding concluded that the lightness 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 to determine the most probable progression of the skin tone of human ancestors over the last 5 million years. Comparing the MC1R nucleotide sequences for chimpanzees and humans in various regions of the earth, Rogers concluded that the common ancestors of all humans had light skin tone under dark hair--similar to the skin tone and hair color pattern of today's chimpanzees. That is 5 million years ago, the human ancestors' dark hair protected their light 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 light.

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 lightness 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 dark, and the intense sun killed off the progeny with any lighter 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 dark 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 dark 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 light over time because the evolutionary constraint that keeps Africans' skin dark generation after generation decreases generally the further North a people migrates (Rogers 2004). This latest assertion (3) however, does not take into account the period of time over which this mutation is to take place. The dependence on this period of time will make Rogers' thesis either hold as the period of time accommodates to the variability observed, or sway. No studies have yet been made to try to find out this rate of mutation.

Xem thêm

• Albinism
• Von Luschan's chromatic scale
• Complexion
• Hyperpigmentation
• Human physical appearance
• Human migration
• Pigmentocracy
• Race
• Sunlight
• Sun tanning

Tham khảo

• Harding, Rosalind M., Eugene Healy, Amanda J. Ray, Nichola S. Ellis, Niamh Flanagan, Carol Todd, Craig Dixon, Antti Sajantila, Ian J. Jackson, Mark A. Birch-Machin, and Jonathan L. Rees. 2000. "Evidence for variable selective pressures at MC1R." American Journal of Human Genetics 66: 1351-1361.
• Jablonski, Nina G., and George Chaplin. 2000. "The evolution of human skin coloration." Journal of Human Evolution 39: 57-106. (in pdf format)
• Jablonski, Nina G., and George Chaplin. 2002. "Skin deep." Scientific American 287 (4) (October): 74-82.
• Rees, J.L., and N. Flanagan. 1999. "Pigmentation, melanocortins, and red hair." Q. J. Med." 92: 125-131.
• Robins, A.H. 1991. Biological Perspectives on Human Pigmentation. Cambridge: Cambridge University Press. [4]
• Rogers, Alan R., David Iltis, and Stephen Wooding. 2004. "Genetic variation at the MC1R locus and the time since loss of human body hair." Current Anthropology 45 (1): 105-108.
• Lamason RL, Mohideen MA, Mest JR, Wong AC, Norton HL, Aros MC, Jurynec MJ, Mao X, Humphreville VR, Humbert JE, Sinha S, Moore JL, Jagadeeswaran P, Zhao W, Ning G, Makalowska I, McKeigue PM, O'donnell D, Kittles R, Parra EJ, Mangini NJ, Grunwald DJ, Shriver MD, Canfield VA, Cheng KC (2005). SLC24A5, a putative cation exchanger, affects pigmentation in zebrafish and humans. Science 310 (5755): 1782-6. PMID 16357253

Liên kết ngoài

• Nicholas Wade. 2003. "Why Humans and Their Fur Parted Ways." New York Times (Science Times) (August 19). Summary of clues to the saga in which humans evolved to lose their hair and had to adjust, including turning from light skin to dark skin, together with an estimation of the time at which humans invented clothing.

• Frank W Sweet The Paleo-Etiology of Human Skin Tone
  • Proposes that the advent of agriculture and a grain diet low in vitamin D gave Northern Europeans their very pale skin.
  • Says skin tone is regulated by 5 genes and suggests Native Americans lost some genes in passage through the Arctic, preventing them from evolving very dark skin in equatorial America.
  • Gives some history of global skin tone maps, noting that Biasutti map is out of date.

• Key gene 'controls skin tone' SLC24A5 gene controls up to 38% of the tonal range in people with mixed European and West African ancestry
• Three parameters determining skin tone: 1) increased vegetation blocks the sun and induces lighter tone untanned under-arm skin over millennia, 2) increased persistence of snow on the ground induces darker tone untanned under-arm skin over millennia, and 3) increased flux of solar radiation resulting from closeness to the equator induces darker tone untanned skin over millennia.