Introduction

Although rickets and osteomalacia were described in England as early as the middle of the seventeenth century, it is only at the beginning of the twentieth century that vitamin D (D) (D refers to both D3 or cholecalciferol and D2 or ergocalciferol) was discovered by Mellanby and McCollum who, in their studies on experimental rickets, were able to show that cod liver oil contained antirickets activity. Although genetically determined forms of the disease still exist, nutritionally induced rickets has largely disappeared in North America due to the enrichment of several foods in D2 or D3. However, studies in institutionalized and elderly populations indicate that depletion is still quite prevalent in these groups.

Normal vitamin D physiology

Vitamin D metabolism

D3 is an endogenous secosteroid synthesized in the skin plasma membrane where the ultraviolet B rays of the sun induce a photochemical reaction and a rearrangement of 7-dehydrocholesterol or provitamin D3 to give rise to the secosteroid previtamin D3 structure. Under the influence of body heat, previtamin D3 undergoes a slow and reversible isomerization accompanied by a change in the structure configuration of the molecule leading to the production of vitamin D3 of endogenous origin. D3 is then exported to the systemic circulation where, with D of dietary sources, it circulates in serum bound to the vitamin D binding protein (DBP), or is stocked in fat or muscle.