See original article by Ladhani et al (pp 781–4) Mineralisation of osteoid tissue of bone is dependent on a suitable supply of mineral, both calcium and phosphate, to that tissue. Failure to provide sufficient mineral results in osteomalacia which, in growing bone with its attendant growth plates and unfused epiphyses, is manifest as rickets. Although vitamin D deficiency is not the only cause of rickets (nutritional calcium deficiency has also recently been proposed as an important factor1), it has historically been a major cause of morbidity.2 Vitamin D is mainly derived from the action of sunlight on 7-dehydrocholesterol in the skin, and vitamin D deficiency is more likely to occur in individuals with darker skins or in those whose skin is extensively covered.3 Vitamin D is converted via two enzymatic reactions to the active metabolite, 1,25-dihydroxyvitamin D (1,25-(OH)2D), whose principal actions are to stimulate absorption of calcium by the gut and promote mineralisation of bone. Failure to do so adequately may therefore result in osteomalacia and rickets; it also limits peak bone mass4 and contributes to involutional osteoporosis.5 Vitamin D deficiency in pregnant mothers also limits fetal growth.6 In addition, vitamin D may have an important part to play in preventing other diseases such as hypertension, various cancers, and type 1 diabetes.5 Rickets is not a new disease. It was first described by an English physician, Dr Daniel Whistler, in 1645, although it is known to have existed well before that.7 It has long been recognised that lack of exposure to adequate amounts of sunlight was a major cause of vitamin D deficiency rickets which, following the industrial revolution, became a significant cause of morbidity especially in the urbanised cities of the north of England and Scotland. As the …