Vitamin D, Calcium Homeostasis, and Skeleton Accretion in Children

Abstract

Overt vitamin D deficiency early in life has classically been associated with the etiology of rickets. Recent interest has focused on vitamin D insufficiency and calcium homeostasis and bone health. A review of the literature suggests that the relationship between vitamin D status and calcium utilization has some important differences with life stage and race. In contrast to adults, serum 1,25-dihydroxyvitamin D, but not serum 25-hydroxyvitamin D, predicts calcium absorption in growing children. PTH suppression with increasing serum 25-hydroxyvitamin D varies with race in adolescents. A limitation of our understanding of vitamin D status on calcium homeostasis in children relates to the cross-sectional nature of the evidence and interventions that typically use too little vitamin D supplementation to affect status. Vitamin D status has predicted changes in BMD during growth, and higher doses have been associated with increased bone area and BMC of the hip in pubertal girls with low baseline vitamin D status. Bone accretion is related to calcium status, sexual maturity, race, and genetics. Current cross-sectional studies in children suggest that vitamin D status is less important for bone accrual than for bone health in adults. Intervention studies are needed to identify responsive groups.

Dairy and Bone Health

“…Studies on the effects of vitamin D supplementation or status on bone health have yielded mixed results in children [22] and Dairy and Bone Health 84S VOL. 28, NO.…”

Maternal high-fat diet: effects on offspring bone structure

“…Such associations suggest a possible role for maternal and foetal nutrition in determining peak bone mass and fracture risk in later life. The observation of altered skeletal structure as a consequence of undernutrition during a critical stage of early life, as exemplified by rickets, demonstrates that skeletal development can be disrupted by severe dietary change [10]. Cohort studies of female twins, including monozygous twins, showed significant intra-pair concordance between birth weight and bone mass.…”

Pediatric vitamin D and calcium nutrition in developing countries

“…Fibroblast growth factor 23, elevated in patients with some tumors and hypophosphatemic forms of rickets, can also suppress 1-hydroxylation [34]. 1,25-Dihydroxyvitamin D binds to vitamin D receptors in the intestine to stimulate transcellular absorption of calcium and phosphorus [35]. In addition, there is separate paracellular calcium absorption which depends on the dietary calcium content but not on 1,25-dihydroxyvitamin D [35].…”

“…1,25-Dihydroxyvitamin D binds to vitamin D receptors in the intestine to stimulate transcellular absorption of calcium and phosphorus [35]. In addition, there is separate paracellular calcium absorption which depends on the dietary calcium content but not on 1,25-dihydroxyvitamin D [35]. Inadequate calcium intake could cause insufficient intestinal calcium absorption through both the trans-cellular and the para-cellular routes to meet the needs of the body.…”