Dietary Calcium Deficiency and Rickets

Abstract

The chapter reviews the role of low dietary calcium intakes in the pathogenesis of nutritional rickets in children. Calcium requirements in children are primarily determined by the skeletal demands for calcium during growth and the efficiency of intestinal calcium absorption to meet these demands. In large parts of the developing world, calcium intakes in children are considered to be low at approximately 300 mg/day. There is good evidence to indicate that children adapt to these low intakes by increasing fractional calcium absorption when the vitamin D status is adequate and by reducing renal calcium excretion. Nevertheless, despite these adaptive processes, calcium deficiency rickets has been described in children from a number of countries, such as South Africa, Nigeria, Bangladesh, and India. Calcium intakes in these children have been estimated to be approximately 200 mg/day. Biochemically, the hallmark is a marked elevation of serum 1,25-dihydroxyvitamin D [1,25(OH)2D] concentrations in association with hypocalcemia and elevated alkaline phosphatase concentrations. 25-Hydroxyvitamin D [25(OH)D] concentrations are lower than in non-rachitic children but generally above levels usually associated with vitamin D deficiency rickets. A number of studies have documented healing of the disease by the supplementation of dietary calcium alone. There is increasing evidence to suggest that vitamin D requirements in children are influenced by their calcium requirements and the calcium content of the diet. Thus nutritional rickets has a spectrum of causes with dietary calcium deficiency being at one end of the spectrum and pure vitamin D deficiency at the other. In between a combination of relative vitamin D insufficiency and low dietary calcium intakes combine to exacerbate the development of rickets.