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Vitamin D deficiency is defined as a serum concentration Succimer in the new 2011 report on dietary requirements concludes that dietary reference intake for vitamin D can only be established according to bone health outcomes, not according to other outcomes (e.g. respiratory health), for which the evidence is still insufficient. The report estimated that children over 1?year old need at least 600?IU of vitamin D a day, with a maximum upper limit of 2500?IU for children aged 1�C3?years, 3000?IU for children from 4 to 8?years old, and 4000?IU/day for children aged 9 or more years old (15). The current Guidelines from the Section on Breastfeeding and the Committee on Nutrition RSL3 nmr of the American Academy of Pediatrics recommend a minimum daily intake of 400?IU of vitamin D for all infants, children, and adolescents, starting soon after birth (16). On the other hand, Holick (14, 17) estimated that teenagers and adults need at least 2000?IU of vitamin D a day to meet their body��s requirements. Concerning serum levels, the 2011 IOM Committee targeted a serum level of at least 50?nmol/L of 25(OH)D as meeting the needs of nearly all children, in agreement with the Pediatric Endocrine Society (18). Taken together, these considerations show the lack of any AG-221 nmr general consensus on what serum vitamin D levels are necessary for global health or the doses to recommend for its supplementation (15). It has also been suggested that current cutoffs may underestimate the real needs. A potential obstacle to the clinical use of vitamin D may be its possible (albeit rare) hypercalcemic effect, and that is why drug developers are exploring active vitamin D analogs that minimize the risk of hypercalcemia (19). In addition, data from modern genomewide association studies show that at least three different genes (encoding three key enzymes, 7-DHC reductase, the liver 25-hydroxylase CYP2R1, and CYP24A1) contribute to the variability in serum vitamin D concentrations. These genes may also influence response to vitamin D supplementation, as recently demonstrated by Schlingmann et?al., who described a mutation in CYP24A1 that explained the greater sensitivity to vitamin D of patients with idiopathic infantile hypercalcemia. As the authors suggested, such a mutation could be a genetic risk factor for the onset of symptomatic hypercalcemia triggered by vitamin D prophylaxis in apparently healthy infants. We should also remember these issues when considering vitamin D supplementation (20).