Malignant tumour of the skin, including some of the most common human cancers. Though recognizable at an early stage, it has a significant death rate. Light-skinned people have the highest risk but can reduce it by limiting exposure to sunlight and to ionizing radiation. The most common types arise in the epidermis (outer skin layer) and have become more frequent with the thinning of the atmosphere's ozone layer. The most serious form is melanoma, which is frequently fatal if not treated early with surgery. Cancers arising from the dermis are rare; the best-known is Kaposi sarcoma.
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A section through the skin. The tough, dead cells of the outer epidermal surface (corneal layer) elipsis
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Melanin comes in two types: pheomelanin (red) and eumelanin (very dark brown). 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 each parent. Each gene comes in several alleles, resulting in a great variety of different skin tones.
The evolution of the different skin tones is thought to have occurred as follows: the haired primate ancestors of humans, like modern great apes, had light skin under their hair. When Hominids evolved relative hairlessness (the most likely function of which was to facilitate perspiration), 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 selection 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. Sexual selection and diet may have played a part in the evolution of skin tone diversity, as well.
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 fish-based diet provides plenty of vitamin D.
Dark skin (melanin) protects against ultraviolet light; this light causes mutations in skin cells, which in turn cause skin cancers. Light-skinned persons have about a tenfold greater risk of dying from skin cancer under equal sunlight exposure, with redheads having the greatest risk. Furthermore, dark skin prevents radiation of UV-A rays from destroying the essential folic acid, derived from B vitamins. Folic acid (or folate) is needed for the synthesis of DNA in dividing cells and folate deficiency in pregnant women are associated with birth defects.
While dark skin better preserves vitamin B, it can also lead to vitamin D deficiency at higher latitudes which in turn can cause fatal cancers affecting the colon, lung and prostate. Dark-skinned people are also at higher risk for rickets, cardiovascular disease, diabetes and multiple sclerosis..To address this issue, some countries have programs to ensure fortification of milk with vitamin D.
The advantage of light skin at high latitudes is that it allows more sun absorption, leading to increased production of vitamin D3, necessary for calcium absorption and bone growth. The lighter skin of women at higher latitudes most likely results from the higher calcium needs of women during pregnancy and lactation. However, some have postulated that it may also derive from sexual selection (this hypothesis may derive from current social conditions in which light skinned people set the beauty standard).
Albinism is a condition characterized by the absence of melanin, resulting in very light skin, eyes, and hair; it is caused by an inability to synthesize tyrosine, and has a genetic basis.
Differences in skin tone are the most readily perceptible phenotypical distinction of human populations, and hence has historically lent itself to color terminology for race, often to the effect of darker skin being seen as being of lowest social value, and lighter skin of highest. However, according to classical scholar Frank Snowden, the Egyptians and Greeks (et al.) assigned relatively neutral connotations to skin color variation because conquest rather than skin color was the major determinant of slave status.
The tone of human skin can vary from a dark brown to nearly a colorless pigmentation, which may appear reddish due to the blood in the skin. Europeans have lighter skin, hair, and eyes than any other group on Earth. For practical purposes, such as exposure time for sun tanning, six skin types are distinguished following Fitzpatrick (1975), listed in decreasing lightness:
|type||also called||tanning behavior||hair and eye color||von Luschan scale|
|I||very light, also "Celtic"||Often burns, rarely tans.||Tends to have freckles, red or fair hair, blue or green eyes.||1-5|
|II||light, or light-skinned European||Usually burns, sometimes tans||Tends to have light hair, blue or brown eyes.||6-10|
|III||light intermediate, or dark-skinned European or "average Caucasian"||Sometimes burns, usually tans.||Tends to have brown hair and eyes.||11-15|
|IV||dark intermediate, also "Mediterranean" or "Olive"||Sometimes burns, often tans.||Tends to have dark brown eyes and hair.||16-20|
|V||dark or "Brown" type||Naturally black-brown skin||Often has dark brown eyes and hair.||21-28|
|VI||very dark, or "Black" type||Naturally black-brown skin||Usually has black-brown eyes and hair.||29-36|
Types I to IV are all subsumed under "white". Types V and VI do not natively occur in Europe, North Asia, Northern America, or indeed significantly north of the Tropic of Cancer, while types I to IV do not natively occur in Sub-Saharan Africa or Australia. North Africa, Southwest and South Asia natively have intermediate types III to V.
In attempting to discover the mechanisms that have generated such a wide variation in human skin tone, 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
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:
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 hominid 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 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, prior to Homo Sapien colonization of extra-African territories, humans had dark skin given that they lived for extended periods of time where the sunlight is intense. As some humans migrated north, over time they developed light skin.
The retention of the ancestral trait at the equator is due to natural selection for melanin pigment production which serves to protect the body from harmful UV rays (Jablonski 2006). Notably, given that hair is a part of the skin, the retention is also analogous to that which occurred for Natural afro-hair prior to pre-Holocene admixture events among people who settled in India and Australia. However, certain evidence suggests that, unlike skin color, Afro hair ceased to be under strong selection once dark skin arose ~1 million years ago (Harding 2000) (rather, it remained as a vestigial trait among Africans, Andamanese, and Melanesians and changed to straight in the north for adaptive reasons--see hair texture). In fact, dark skin is so selectively advantageous at the equator that initially light skinned native Americans who migrated to Mexico and/or South America experienced renewed selective pressure towards the evolution of dark skin.
According to (Norton et al., 2006), light skin observed in Europeans (with deep Red and/or yellowish skin tones), non-Indian Southeast Asians, East Asians and North Africa (Maghreb) is due to independent genetic mutations in at least three loci. They concluded that light pigmentation is at least partially due to sexual selection, however Jablonski postulates that the predominant reason revolved around the facilitation of vitamin D production in northern Eurasia (see hair texture).
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, 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, pg.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 the sampled 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 certain (European) 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 (and other equatorial) 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. Also, close examination of the haplotype variation among the non-Europeans (including East Asians) suggested that, among most non-European non-Africans, the most common variants were in the silent mutation positions (Harding et al 2000 p 1355). Thus, at least at this locus, most non-Europeans share the ancestral function. The fact that relatively light skinned east Asians varied little genetically from dark skinned Africans at this locus supports the fact that skin color is a complex trait determined by several genes. Thus light skin among east Asians occurs by way of a different genetic mechanism than that among Europeans.
With regards to Europeans, the next question to ask would be: why were there zero differences and no divergences in the amino acid sequences of the receptor protein among the Africans (and other equatorial groups) while there were 18 differences among the populations in Ireland, England, and Sweden? (Harding et al., 2000, pp.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 Sweden. Even the mutations that produce red hair with little ability to tan were non-lethal in the northern latitudes. 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 five 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. argues that based on cave paintings, Europeans may have been dark as recently as 13,000 years ago. The painters depicted themselves as having darker complexions than the animals they hunted.
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. Folate breakdown in sun-exposed skin is inhibited by the presence of melanin and is essential for human fetal development. It is likely that folate conservation played an important role in the selection of dark skin in the ancient African ancestors of modern humans. 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 .
However, the progeny of those humans who migrated North away from the intense African sun had another evolutionary constraint: vitamin D availability. Human requirements for vitamin D (cholecalciferol) are in part met through photoconversion of a precursor to vitamin D3. As humans migrated north from the equator, they were exposed to less intense sunlight, in part because of the need for greater use of clothing to protect against the colder climate. Thus, under these conditions, evolutionary pressures would tend to select for lighter-skinned humans as there was less photodestruction of folate and a greater need for photogeneration of cholecalciferol. Tracking back the statistical patterns in variations in DNA among all known people sampled who are alive on the Earth today, it appears that
Millington GWM. (2006) Proopiomelanocortin (POMC): the cutaneous roles of its melanocortin products and receptors. Clin Exp Dermatol 31: 407-412.
Millington GWM, Levell NJ. (2007) From genesis to gene-sequencing: historical progress in the understanding of skin color. Intl J Dermatol 46: 103-105.
Species distribution and physiological characterization of Acinetobacter genospecies from healthy human skin of tribal population in India.(Original Article)
Oct 01, 2007; Byline: S. Yavankar, K. Pardesi, B. Chopade Background: Various reports on distribution of Acinetobacter spp. from healthy human...
Injury-induced innate immune response in human skin mediated by transactivation of the epidermal growth factor receptor.(Research article)(medical research)(includes statistical table)
Jul 01, 2006; We found that sterile wounding of human skin induced epidermal expression of the antimicrobial (poly)peptides human...