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Vitamin D and Health

SACN_Vitamin_D_and_Health_report

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a) biochemical indicators of vitamin D status <strong>and</strong> the validity of the values used to assess<br />

risk of deficiency <strong>and</strong> excess;<br />

b) association between vitamin D status <strong>and</strong> health outcomes at all life stages <strong>and</strong> the<br />

effects of biological modifiers;<br />

c) the contribution of cutaneous vitamin D synthesis to vitamin D status in the UK taking<br />

account of factors that modify skin exposure to sunlight; risks of skin damage <strong>and</strong><br />

other adverse health outcomes associated with sunlight exposure;<br />

d) potential adverse effects of high vitamin D intakes; <strong>and</strong><br />

e) relative contributions made by dietary vitamin D intake (from natural food sources,<br />

fortified foods <strong>and</strong> supplements) <strong>and</strong> cutaneous vitamin D synthesis, to the vitamin D<br />

status of the UK population.<br />

10.7 Data from RCTs, then prospective studies, when available, were preferred for setting DRVs but data<br />

from other study types were also considered (including case-control, cross-sectional studies <strong>and</strong> case<br />

reports).<br />

Biology & metabolism<br />

10.8 The first step in endogenous vitamin D synthesis is the conversion by solar UVB radiation of 7-DHC to<br />

previtamin D in the skin. The dose response is not linear, which means that longer exposures do not<br />

lead to proportionally greater previtamin D synthesis. Previtamin D 3 is thermodynamically unstable<br />

<strong>and</strong> is converted at body temperature to vitamin D 3 which enters the circulation <strong>and</strong> is transported to<br />

the liver bound to vitamin D binding protein.<br />

10.9 Dietary vitamin D is lipid soluble <strong>and</strong> is incorporated within enterocytes into chylomicrons that are<br />

secreted into lymph <strong>and</strong> transported through the lymphatic system to the systemic circulation to the<br />

liver.<br />

10.10 <strong>Vitamin</strong> D is converted to its active metabolite 1,25(OH) 2 D in two hydroxylation steps: firstly to<br />

25(OH)D in the liver <strong>and</strong> then to 1,25(OH) 2 D in the kidney. 25(OH)D is the major circulating<br />

metabolite of vitamin D. Its concentration in serum reflects vitamin D supply from cutaneous<br />

synthesis <strong>and</strong> the diet.<br />

10.11 <strong>Vitamin</strong> D accumulates in both adipose tissue <strong>and</strong> muscle. Details about accumulation <strong>and</strong><br />

mobilisation of vitamin D from adipose tissue <strong>and</strong> other tissues such as muscle are not clear at this<br />

time.<br />

10.12 Polymorphisms in genes encoding proteins involved in vitamin D metabolism have been identified<br />

which might influence serum 25(OH)D concentrations <strong>and</strong> functional outcomes but the nutritional<br />

implications of such findings is not clear.<br />

Biomarkers of exposure<br />

10.13 The active metabolite of vitamin D, 1,25(OH) 2 D, is not a suitable indicator of vitamin D exposure<br />

because it is homeostatically regulated <strong>and</strong> has a short half-life (< 4 hours). Serum 25(OH)D<br />

concentration is widely considered to be the best indicator of total vitamin D exposure (from the diet<br />

<strong>and</strong> sunlight) because it has a long half-life in the circulation (about 2-3 weeks) <strong>and</strong> is not subject to<br />

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