The accepted biomarker of vitamin D status is the plasma levels of the hydroxylated form of vitamin D, 25-hydroxyvitamin D. Following synthesis in the skin, or absorption from the gastrointestinal tract, vitamin D is hydroxylated in the liver to form 25-hydroxyvitamin D. This form of vitamin D is biologically active and interacts with the vitamin D receptor. Metabolism of 25-hydroxyvitamin D proceeds in the kidney, where it can be further hydroxylated to 1,25-dihydroxyvitamin D, which also has biological activity. It is recommended that plasma levels of 25-hydroxyvitamin D be maintained between 40 and 80 ng/mL (100 and 200 nmol/L). However, current estimates suggest that intakes of vitamin D are too low to produce this sort of blood level. Foods that are high in vitamin D are not commonly eaten, and even if incorporated into a healthy diet still do not provide adequate vitamin D. There is therefore a reliance on exposure of sunlight to contribute to optimal vitamin D levels.
Acquiring enough vitamin D is therefore problematic for those living at high latitudes because for 6 months of the year, the angle of incidence of the sun might not be great enough to allow endogenous synthesis of vitamin D. For this reason supplements of around 2000 iu per day for adults are recommended during late autumn, winter and early spring. Estimates of the vitamin D intake to maintain vitamin D health in the absence of sun exposure have been set at around 400 iu per day (10 μg per day), a level that would prevent bone disease due to vitamin D deficiency. Further it has been established that plasma levels above 40 nmol/L assure protection from bone disease. However, analysis of populations have shown that based on intake 71 % of individuals are deficient in vitamin D, but when their plasma levels are measured only 19 % of the same individuals are deficient. Therefore a discrepancy exists between the intake of vitamin D and the plasma levels that are obtainable from that intake.
Sun exposure has been suggested to be responsible for this discrepancy. However, sun exposure cannot account for the discrepancy in its entirety because although vitamin D levels change with season, the plasma levels of vitamin D are still higher than can be accounted for with food intakes, even considering sunlight exposure. In addition such a uniform discrepancy is unlikely to be found in a heterogenous population exposed to different levels of sun exposure. More recently researchers have suggested other explanations to account for the fact that vitamin D plasma levels are higher in populations than can be accounted for by food sources of vitamin D. One suggestion is that preformed 25-hydroxyvitamin D is present in food, is bioavailable, and contributes significantly to plasma levels. Generally, foods have not been assessed for their preformed 25-hydroxyvitamin D concentrations but estimates suggest that much lower levels of 25-hydroxyvitamin D would be required to raise plasma levels compared to vitamin D.
Researchers have tried to assess the possible contribution from preformed 25-hydroxyvitamin D in the diets of free living populations1. For example, one group of researchers tried to estimate the contribution of 25-hydroxyvitamin from various foods to assess if it could explain the discrepancy between vitamin D intakes and plasma levels. The study authors attributed a potency factor of 5 to the preformed 25-hydroxyvitamin D in foods, an estimate based on previous researchers work. That is to say that preformed 25-hydroxyvitamin D in foods is 5 times a potent at raising 25-hydroxyvitamin D plasma levels than vitamin D. The results from the study showed that there was a notable increase in the vitamin D content of many foods when 25-hydroxyvitamin D levels were included. The authors suggested in a typical diet that this would equate to a 1.7 to 2.9 μg per day or a 15 to 30 % increase in intake of vitamin D which could reduce the discrepancy between intake and plasma levels, but not eliminate it.
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