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Vitamin D and Health

SACN_Vitamin_D_and_Health_report

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2.75 Another RCT 21 (Cashman et al., 2014a) investigated the effect of habitual calcium intake on serum<br />

25(OH)D concentration. <strong>Health</strong>y adults (n=125; age, ≥ 50y; mean calcium intake=814 mg/d) were<br />

stratified according to habitual calcium intake (< 700 compared with > 1000 mg/d; mean intakes, 496<br />

& 1437 mg/d for low <strong>and</strong> high calcium intake groups respectively) <strong>and</strong> received either vitamin D 3<br />

(20 µg/800 IU per day) or placebo for 15 weeks throughout winter. Mean serum 25(OH)D<br />

concentration increased significantly (p≤ 0.005) in the vitamin D 3 group <strong>and</strong> decreased significantly in<br />

the placebo group (p≤ 0.002) <strong>and</strong> were of the same magnitude irrespective of calcium intake. These<br />

findings suggest that calcium intake does not modify the requirement for vitamin D within the range<br />

of calcium intakes studied. However, since this study was conducted in adults without metabolic bone<br />

disease, the findings may not be applicable to children (who have higher calcium requirements<br />

because of increased metabolism) or to those with metabolic bone disease.<br />

Physiological requirements by life-stage<br />

Infants<br />

2.76 <strong>Vitamin</strong> D, together with calcium <strong>and</strong> phosphorus, is required during infancy <strong>and</strong> early childhood<br />

(< 3y) to meet the dem<strong>and</strong>s of rapid growth for healthy skeletal development. Prolonged deficiency<br />

of vitamin D during periods of bone growth in children leads to a failure or delay of endochondral<br />

calcification at the growth plates of the long bones which results in rickets <strong>and</strong> an accumulation of<br />

excess unmineralised osteoid (bone matrix) in all bones; the low mineral to bone matrix ratio in bone<br />

results in osteomalacia (Pettifor, 2012). The main signs of rickets are skeletal deformity with bone pain<br />

or tenderness; <strong>and</strong> muscle weakness. Deficiencies of calcium <strong>and</strong> phosphorus can also cause rickets.<br />

Children <strong>and</strong> Adolescents<br />

2.77 Adolescence is a critical developmental period for bone health when there is rapid growth. <strong>Vitamin</strong> D<br />

is important for bone accretion during this time of skeletal development. Although rickets is most<br />

commonly observed during infancy <strong>and</strong> in young children, it can also occur during the pubertal growth<br />

spurt <strong>and</strong> adolescence. Children presenting with rickets have histological features of both rickets <strong>and</strong><br />

osteomalacia. Once the growth plates of the long bones have fused during adolescence, only features<br />

of osteomalacia are found (Pettifor, 2012). Insufficient vitamin D during this time could also affect<br />

bone mineral density <strong>and</strong> lead to children <strong>and</strong> adolescents not achieving their full potential at peak<br />

bone mass.<br />

Adults<br />

2.78 In adults, vitamin D is required to maintain healthy bone. Deficiency can lead to osteomalacia,<br />

presenting as muscle weakness <strong>and</strong> bone tenderness or pain in the spine, shoulder, ribs or pelvis (DH,<br />

1991; DH, 1998).<br />

2.79 In addition to evidence suggesting a link between vitamin D status <strong>and</strong> rickets/osteomalacia,<br />

numerous epidemiological studies have reported associations between vitamin D status <strong>and</strong> other<br />

musculoskeletal <strong>and</strong> non-musculoskeletal health outcomes. Relationships between vitamin D status<br />

<strong>and</strong> health outcomes are considered in chapter 6.<br />

21 This study was specifically commissioned by the Department of <strong>Health</strong> to inform SACN’s review of the DRVs for vitamin D.<br />

16

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