The evolution of light skin color: role of vitamin D disputed.

Abstract

Vitamin D is essential for calcium and phosphorus homeostasis and for the growth, development, and structural integrity of the skeleton. Over 90% of the body’s requirements for vitamin D derive from cutaneous photosynthesis, with dietary sources accounting for the remainder. Ultraviolet-B radiation (UVB) penetrates the epidermis where it photolyses 7-dehydrocholesterol to previtamin D3, which is then converted to vitamin D3. The latter is translocated to the circulation via the dermal vasculature; it is hydroxylated (enzymatically) in the liver to 25-hydroxyvitamin D (25-OHD) and then in the kidneys to 1,25-dihydroxyvitamin D (1,25-(OH)2D) (Holick, 2007). Although the serum 25-OHD concentration gives the best index of an individual’s vitamin D status, 1,25-(OH)2D is the most active form biologically in mediating the effects on intestine (calcium absorption) and bone. The serum concentration of 1,25-(OH)2 Di s tightly regulated and is not ordinarily dependent on sun exposure or diet. Severe vitamin D deficiency causes nutritional rickets in children and adolescents, and osteomalacia and osteoporosis in adults. Rickets is caused by defective mineralization of the collagen matrix in newly formed osteoid tissue, with resultant bone softening. It is characterized by crippling deformities (notably bowing of the lower limb bones and narrowing of the pelvic outlet), muscle weakness, and, in neonates born to vitamin D-deficient mothers, by potentially fatal hypocalcaemia (manifesting as convulsions, heart failure) (Wharton and Bishop, 2003; Holick, 2006b). Rickets is a sunlight deprivation disease, which emerged on an epidemic scale during the industrial revolution, when cities in Europe and North America were enveloped in a perpetual twilightlike haze of coal smoke. By the end of the 19th century, up to 90% of children in these centers suffered from rickets.