|Written by Chris Masterjohn|
|Updated 15 December 2011|
When sunlight of the ultraviolet-B (UVB) wavelength strikes the skin, it is absorbed by 7-dehydrocholesterol, a steroid and precursor to cholesterol, splitting open one of its carbon rings and thus converting it into the secosteroid previtamin D3. While 7-dehydrocholesterol is tucked tightly within the lipids of skin cell membranes, previtamin D3 is an unstable compound that over a brief period of time converts into vitamin D3, causing it to be released from the cell membrane.12 Vitamin D3 then travels into the blood where it binds to vitamin D-binding protein (DBP).16 Eventually, it is delivered to the liver where it is converted into its primary storage form, calcidiol, which is likewise transported in the blood by DBP.8
Full-body exposure of pale skin to summer sunshine for 30 minutes without clothing or sunscreen can result in the synthesis of between 10,000 and 20,000 IU of vitamin D. Two mechanisms, however, prevent the body from synthesizing an excessive amount of vitamin D: first, a given area of skin can only produce a certain amount of vitamin D before it reaches an equilibrium in which vitamin D is degraded by sunlight as fast as it is synthesized; second, after repeated exposure to sun, the pigment melanin accumulates, which decreases the formation of vitamin D.8 Although the various degradation products of excess vitamin D have generally been presumed to be inactive, several of them exert biological activity in skin cells, where they may prevent hyperproliferative disorders such as psoriasis.17
The amount of UVB radiation available depends on the angle at which the sun's rays strike the earth, the presence of clouds and buildings, ozone and aerosol pollution, altitude and reflective surfaces such as snow.18Because of the effect of the sun's angle, Webb and colleagues showed in 1988 that, even in completely clear skies, synthesis of vitamin D in the skin is impossible for four months of the year in Boston, Massachusetts and six months of the year in Edmonton, the capital of Alberta, Canada. The Webb team found that such a "vitamin D winter" occurred during at least part of the year at any latitude greater than 34 degrees.19 More recently, one group of researchers used a computer model to suggest that in the nearly unattainable condition of truly clear skies, the vitamin D winters are shorter than Webb's team suggested, but that under some environmental conditions, vitamin D winters can occur even at the equator.18
8. Adams. Hollis. "Vitamin D: Synthesis, Metabolism and Clinical Measurement." In Coe, F. L. Favus, M. J.Disorders of Bone and Mineral Metabolism: 2nd Edition, Baltimore, MD: Lippincott Williams and Wilkins, 2002. (Review)
16. Haddad, J. G. Matsuoka, L. Y. Hollis, B. W. Hu, Y. Z. Wortsman, J. "Human Plasma Transport of Vitamin D after Its Endogenous Synthesis," J Clin Invest., 1993; 91: 2552-2555.
17. Chen, T. C. Persons, K. S. Lu, Z. Mathieu, J. S. Holick, M. F. "An evaluation of the biologic activity and vitamin D receptor binding affinity of the photoisomers of vitamin D3 and previtamin D3," J. Nutr. Biochem., 2000; 11: 267-272.
18. Engelsen, et al., "Symposium-in-Print: UV Radiation, Vitamin D and Human Health: An Unfolding Controversy: Daily Duration of Vitamin D Synthesis in Human Skin with Relation to Latitude Total Ozone, Altitude, Ground Cover, Aerosols and Cloud Thickness," Photochemistry and Photobiology, 81 (2005) 1287-1290.
19. Webb, A. R. Kline, L. Holick, M. F. "Influence of season and latitude on the cutaneous synthesis of vitamin D3: exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin," J Clin Endocrinol Metab., 1988; 67(2): 373-8/