title: Vitamin D: evolutionary, physiological and health perspectives.
abstract: Vitamin D, the sunshine vitamin, has been important not only for the evolution of a healthy calcified vertebrate skeleton but it also evolved into a hormone that has a wide diversity of biologic effects. During exposure to sunlight the ultraviolet B radiation converts 7-dehydrocholesterol to previtamin D(3) which in turn rapidly isomerizes to vitamin D(3). Once formed, vitamin D(3) is metabolized in the liver to 25-hydroxyvitamin D(3) and in the kidneys to its active form 1,25-dihydroxyvitamin D(3). 1,25-dihydroxyvitamin D(3) interacts with its vitamin D receptor in calcium regulating tissues to regulate calcium metabolism and bone health. It is now recognized that most cells in the body have a vitamin D receptor and they also have the capability of producing 1,25-dihydroxyvitamin D(3) which in turn is capable of regulating a wide variety of genes that have important functions in regulating cell growth, modulating immune function and cardiovascular health. Epidemiologic evidence and prospective studies have linked vitamin D deficiency with increased risk of many chronic diseases including autoimmune diseases, cardiovascular disease, deadly cancers, type II diabetes and infectious diseases. Vitamin D deficiency and insufficiency have been defined as a 25-hydroxyvitamin D <20 ng/ml and 21-29 ng/ml respectively. For every 100 IU of vitamin D ingested the blood level of 25-hydroxyvitamin D, the measure vitamin D status, increases by 1 ng/ml. It is estimated that children need at least 400-1000 IU of vitamin D a day while teenagers and adults need at least 2000 IU of vitamin D a day to satisfy their body's vitamin D requirement. It is estimated that 1 billion people worldwide are vitamin D deficient or insufficient. Correcting and preventing this deficiency could have an enormous impact on reducing health costs worldwide.
authors.affiliation: Department of Medicine, Section of Endocrinology, Nutrition, and Diabetes, Vitamin D, Skin and Bone Research Laboratory, Boston University Medical Center, Boston, MA, USA. mfholick@bu.edu
authors.forename: Michael F
authors.initials: MF
authors.lastname: Holick
mesh_terms: D000818:Animals; D001851:Bone Diseases, Metabolic / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D002118:Calcium / Q000378:metabolism; D019587:Dietary Supplements; D006706:Homeostasis; D006801:Humans; D018673:Nutrition Policy; D009751:Nutritional Requirements; D009752:Nutritional Status; D010758:Phosphorus / Q000378:metabolism; D014807:Vitamin D / Q000502:physiology* / Q000627:therapeutic use; D014808:Vitamin D Deficiency / Q000188:drug therapy / Q000453:epidemiology* / Q000503:physiopathology* / Q000517:prevention & control
chemical_list: D014807:Vitamin D; D010758:Phosphorus; D002118:Calcium