The hypothesis is that depigmentation of the skin occurred by selection because of the decreased UVR to promote synthesis of vitamin D. The synthesis of the pre vitamin D3 occurs through photosynthesis. Darkly pigmented skin slows the process of vitamin D3 production. Depigmentation evolved to allow vitamin D3 synthesis outside tropical regions away from the equator. Depigmentation is the lightening of the skin to permit higher synthesis of vitamin D3. There is a requirement of vitamin D3 in low UVB environments that requires a need for UVB photons which have influenced the selection for high skin pigmentation. The role of latitude and location to the equator influences the role of pigmentation in producing vitamin D3 is important in adaptation
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Depigmentation allows for increased levels of absorbance of vitamin D. This is likely due to the fact pigmented skin acts as a high resistor to UV rays as the environment has selected for this. Therefore moving away from the equator where the UVR is less intense depigmentation evolved as a way to reduce the resistance so more UVB radiation can be absorbed for vitamin D3 synthesis (Murray, 1934). For the humans living inside the tropics pigmentation evolved as an adaption to protect against too much exposure to UVR which is harmful. Loomis (1967) explains how the higher pigmentation is correlated to lower levels of radiation from UV rays. This supports the hypothesis that latitude and location relative to the equator is correlated with skin pigmentation. As people migrated out of the tropics the depigmentation became advantageous for producing vitamin D by the skin as the concentration of melanin allows the UVB to be absorbed. There is one exception to this rule however which Loomis (1967) explains is the Eskimos. They are located out of the tropics and would be expected to possess depigmentation however this is not the case, it is suggested that due to the diet of rich vitamin D3 sources that this adaptation is not necessary in prevention from …show more content…
This is disproved due to the fact that the process involved has protective mechanisms to prevent the excess critical build up of vitamins (Jablonski and Chaplin, 2000). The depigmentation hypothesis has its biggest challenger in Robins (1991). His explanation for vitamin D deficiencies is the outcome from “industrialization, urbanisation and overpopulation” (Robins, 1991). He disagrees that there is a causal link linking depigmentation in humans skin to the biosynthesis of vitamin D3. His argument is that rickets is unsupported by any source of evidence that it would be able to arise in spite of skin pigmentation (Robins, 1991). However there is evidence to dispute this, there is many records of cases of rickets and similar deficiency diseases occurring due to lack of vitamin D3 sources for highly pigmented people (Jablonski and Chaplin, 2000). The evidence disputes the challenge from Robins by providing cases where pigmentation levels are directly affected by UVR exposure to synthesis vitamin D3. The other evidence disputing Robins argument is explained by Jablonski and Chaplin through the vitamin D3 storage capabilities. There is only a possibility in situations where it is only possible if the vitamin D3 intake is high enough from whatever
Depigmentation allows for increased levels of absorbance of vitamin D. This is likely due to the fact pigmented skin acts as a high resistor to UV rays as the environment has selected for this. Therefore moving away from the equator where the UVR is less intense depigmentation evolved as a way to reduce the resistance so more UVB radiation can be absorbed for vitamin D3 synthesis (Murray, 1934). For the humans living inside the tropics pigmentation evolved as an adaption to protect against too much exposure to UVR which is harmful. Loomis (1967) explains how the higher pigmentation is correlated to lower levels of radiation from UV rays. This supports the hypothesis that latitude and location relative to the equator is correlated with skin pigmentation. As people migrated out of the tropics the depigmentation became advantageous for producing vitamin D by the skin as the concentration of melanin allows the UVB to be absorbed. There is one exception to this rule however which Loomis (1967) explains is the Eskimos. They are located out of the tropics and would be expected to possess depigmentation however this is not the case, it is suggested that due to the diet of rich vitamin D3 sources that this adaptation is not necessary in prevention from …show more content…
This is disproved due to the fact that the process involved has protective mechanisms to prevent the excess critical build up of vitamins (Jablonski and Chaplin, 2000). The depigmentation hypothesis has its biggest challenger in Robins (1991). His explanation for vitamin D deficiencies is the outcome from “industrialization, urbanisation and overpopulation” (Robins, 1991). He disagrees that there is a causal link linking depigmentation in humans skin to the biosynthesis of vitamin D3. His argument is that rickets is unsupported by any source of evidence that it would be able to arise in spite of skin pigmentation (Robins, 1991). However there is evidence to dispute this, there is many records of cases of rickets and similar deficiency diseases occurring due to lack of vitamin D3 sources for highly pigmented people (Jablonski and Chaplin, 2000). The evidence disputes the challenge from Robins by providing cases where pigmentation levels are directly affected by UVR exposure to synthesis vitamin D3. The other evidence disputing Robins argument is explained by Jablonski and Chaplin through the vitamin D3 storage capabilities. There is only a possibility in situations where it is only possible if the vitamin D3 intake is high enough from whatever