Micronutrients And The Evolution Of Skin Pigmentation

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Two key micronutrients may have played a critical role in the evolution of skin coloration. Pigmentation with melanin is an adaptive response that is maintained by natural selection. The vitamin D hypothesis states that pale skins were necessary outside tropical latitudes to facilitate vitamin D biosynthesis within the skin from low levels of UV light. Thus, depigmentation evolved as humankind radiated out of the tropics where a dark skin protected against excess, even toxic, synthesis of vitamin D (18). More recently, Jablonski and Chaplin (19) formulated a superbly elegant paradigm to show how degradation of UV labile folic acid (20) might impair reproductive success by destroying a molecule critical to cell division (Figures 2.2 and 2.3), and that arresting vitamin D3 synthesis in the skin at high latitudes could further impair reproductive success by altering calcium homeosta-sis (Figure 2.4). They conclude that natural selection has produced two opposing clines of skin coloration. One based on folate that photoprotects in a gradation from dark pigmentation at the equator to fair skin at the poles. The second cline, based on vitamin D3 photosynthesis, shows a gradation from low pigmentation at the poles to dark coloration at the equator. At the central nexus of these two clines, populations exhibit an increased capability for developing facultative pigmentation to cope with changing seasonal UV levels.

Of course, skin pigmentation is multifactorial with genes such as MC1R (melanocortin-1 receptor gene), in particular, being a major determinant of skin and hair pigmentation (21). This gene is highly polymorphic in fair-skinned populations, but less so in dark-skinned African populations (19). Other genes such as MATP (membrane-associated transporter protein) contain SNPs that are also strongly associated with variation in human pigmentation (22). However, it is also worthy to note that wholly intracellular folates in the form of tetrahydro-, 5,10-methylenetetrahydro-, or 10-formyltetrahydrofolate tend to be particularly labile, and these are the forms required for nucleotide biosynthesis and cellular replication (23). UV scission of these coenzymes may be particularly harmful in respect to reproductive efficiency. We have previously shown that UV-B light at 312 nm with a calculated energy of 91.78 kcal/mol profoundly enhances oxidation of monoglutamyl 5-methyltetrahydrofolate (plasma form of folate) to 5-methyldihydrofolate, with a subsequent and irreversible loss of vitamin activity via C9-N10 bond scission, forming a pterin residue and p-aminobenzoylglutamate (20). Recent research from the author's

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