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.

Bibliographic Collection: 
MOCA Reference, APE
Publication Type: Journal Article
Authors: Webb, A R; Kline, L; Holick, M F
Year of Publication: 1988
Journal: J Clin Endocrinol Metab
Volume: 67
Issue: 2
Pagination: 373-8
Date Published: 1988 Aug
Publication Language: eng
ISSN: 0021-972X
Keywords: Alberta, Boston, Cholecalciferol, Dehydrocholesterols, Humans, In Vitro Techniques, Photochemistry, Seasons, Skin, Sunlight, Ultraviolet Rays

Sunlight has long been recognized as a major provider of vitamin D for humans; radiation in the UVB (290-315 nm) portion of the solar spectrum photolyzes 7-dehydrocholesterol in the skin to previtamin D3, which, in turn, is converted by a thermal process to vitamin D3. Latitude and season affect both the quantity and quality of solar radiation reaching the earth's surface, especially in the UVB region of the spectrum, but little is known about how these influence the ability of sunlight to synthesize vitamin D3 in skin. A model has been developed to evaluate the effect of seasonal and latitudinal changes on the potential of sunlight to initiate cutaneous production of vitamin D3. Human skin or [3 alpha-3H]7-dehydrocholesterol exposed to sunlight on cloudless days in Boston (42.2 degrees N) from November through February produced no previtamin D3. In Edmonton (52 degrees N) this ineffective winter period extended from October through March. Further south (34 degrees N and 18 degrees N), sunlight effectively photoconverted 7-dehydrocholesterol to previtamin D3 in the middle of winter. These results quantify the dramatic influence of changes in solar UVB radiation on cutaneous vitamin D3 synthesis and indicate the latitudinal increase in the length of the "vitamin D winter" during which dietary supplementation of the vitamin may be advisable.

DOI: 10.1210/jcem-67-2-373
Alternate Journal: J. Clin. Endocrinol. Metab.