Resurrection of vitamin D deficiency and rickets

J Clin Invest. 2006 Aug;116(8):2062-72. doi: 10.1172/JCI29449.


The epidemic scourge of rickets in the 19th century was caused by vitamin D deficiency due to inadequate sun exposure and resulted in growth retardation, muscle weakness, skeletal deformities, hypocalcemia, tetany, and seizures. The encouragement of sensible sun exposure and the fortification of milk with vitamin D resulted in almost complete eradication of the disease. Vitamin D (where D represents D2 or D3) is biologically inert and metabolized in the liver to 25-hydroxyvitamin D [25(OH)D], the major circulating form of vitamin D that is used to determine vitamin D status. 25(OH)D is activated in the kidneys to 1,25-dihydroxyvitamin D [1,25(OH)2D], which regulates calcium, phosphorus, and bone metabolism. Vitamin D deficiency has again become an epidemic in children, and rickets has become a global health issue. In addition to vitamin D deficiency, calcium deficiency and acquired and inherited disorders of vitamin D, calcium, and phosphorus metabolism cause rickets. This review summarizes the role of vitamin D in the prevention of rickets and its importance in the overall health and welfare of infants and children.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Calcium / metabolism
  • Child
  • Child, Preschool
  • Dihydroxycholecalciferols / metabolism
  • Female
  • Humans
  • Hydroxycholecalciferols / metabolism
  • Male
  • Phosphorus / metabolism
  • Prevalence
  • Rickets / epidemiology*
  • Rickets / etiology
  • Rickets / genetics
  • Rickets / radiotherapy
  • Ultraviolet Rays
  • Vitamin D / radiation effects
  • Vitamin D Deficiency / epidemiology*
  • Vitamin D Deficiency / radiotherapy


  • Dihydroxycholecalciferols
  • Hydroxycholecalciferols
  • Vitamin D
  • Phosphorus
  • Calcium