The evolutionary significance of vitamin D, skin pigment, and ultraviolet light.

Vitamin D is essential for normal growth, calcuim absorption, and skeletal development. Vitamin D deficiency can cause death, immobilization, or pelvic deformities which prevent normal childbirth. In the past these problems were extremely common in North America and Europe, and were only elminated by adding vitamin D to food. Prior to that, variations in available vitamin D affected health, survival and reproductive efficiency sufficiently to have evolutionary significance. Vitamin D is naturally present in few foods; most comes from the photo-conversion of 7-dehydrocholesterol in skin. The limiting factor in this conversion is the availability of ultraviolet light less than310 nm. Seasonal and geographic variations in natural ultraviolet radiation cause parallel variations in blood vitamin D levels, intestinal calcuim absorption, and clinical vitamin D deficiency. These physiological variations can be abolished by exposure to comparable artificial ultraviolet radiation, or by dietary vitamin D supplements. Ultraviolet radiation less than310 nm is absorbed by skin pigment, but is also increases skin pigmentation. This has led to the hypothesis that skin pigment regulates skin vitamin D production. Little direct evidence exists to test this reasonable hypothesis, but necessary and sufficient conditions for establishing it can be outlined. Until this hypothesis is experimentally tested, it is impossible to evaluate the corollary hypothesis: that racial variations in the efficiency of cutaneous vitamin D production restricted the evolution of dark-skinned peoples to tropical latitudes and thereby caused the geographic distribution of the races.

[1]  B. Trappler,et al.  ŒSTROGENS IN ISCHÆMIC HEART-DISEASE , 1976, The Lancet.

[2]  M. Gupta,et al.  Spontaneous cure of vitamin-D deficiency in Asians during summer in Britain. , 1974, Lancet.

[3]  J. Round,et al.  Seasonal Changes in Human Plasma Levels of 25-Hydroxyvitamin D , 1974, Nature.

[4]  F. Cockburn,et al.  Enamel hypoplasia of the teeth associated with neonatal tetany: a manifestation of maternal vitamin-D deficiency. , 1973, Lancet.

[5]  J. Forfar,et al.  Antenatal factors associated with neonatal hypocalcaemic convulsions. , 1973, Lancet.

[6]  H. DeLuca,et al.  Regulation of vitamin D metabolism and function. , 1973, Physiological reviews.

[7]  M. Wills,et al.  Effect of increased dietary phytic acid on cholecalciferol requirements in rats. , 1972, The Lancet.

[8]  J. Haddad,et al.  COMPETITIVE PROTEIN-BINDING RADIOASSAY FOR 25-HYDROXYCHOLECALCIFEROL1 , 1971 .

[9]  W. Loomis Skin-Pigment Regulation of Vitamin-D Biosynthesis in Man , 1967, Science.

[10]  R. Smith,et al.  DETERMINANTS OF SERUM ANTIRACHITIC ACTIVITY. SPECIAL REFERENCE TO INVOLUTIONAL OSTEOPOROSIS. , 1964, The American journal of clinical nutrition.

[11]  H. G. Jenkins,et al.  Applications of Germicidal, Erythemal and Infrared Energy , 1948, Nature.

[12]  F. Benford,et al.  Quantitative studies of the effectiveness of ultraviolet radiation of various wave-lengths in rickets. , 1938 .

[13]  H. Bekemeier [Evolution skin pigmentation and cutaneous vitamin D photosynthesis]. , 1969, Deutsche Medizinische Wochenschrift.

[14]  I. Magnus,et al.  RESPONSE OF HUMAN SKIN TO ULTRAVIOLET LIGHT. , 1968 .

[15]  H. DeLuca Mechanism of action and metabolic fate of vitamin D. , 1967, Vitamins and hormones.