Vitamin D can be obtained from two sources, the diet and subcutaneous production. Generally dietary vitamin D is not present in high concentrations in commonly eaten foods. Therefore it is believed that most individuals rely mainly on sunlight to produce vitamin D subcutaneously. Vitamin D is not a true vitamin, but a steroid hormone with a complex metabolism. Once in the circulation from either subcutaneous production or dietary sources, vitamin D is hydroxylated in the liver to form 25-hydroxyvitamin D [25(OH)D], the biomarker usually used to assess vitamin D status. Subsequently 25-hydroxyvitamin D is further hydroxylated in the kidney to form 1,25-dihydroxyvitamin D [1,25(OH2)D] which functions in cellular regulation. Variations in the serum concentrations of 25-hydroxyvitamin D have been attributed largely to seasonal variations in sunlight exposure and this has lead to the conclusion that much of the unsupplemented vitamin D status of individuals is accounted for by solar exposure.
However, this assertion has been questioned by researchers because winter vitamin D status does not drop low enough to account for the lack of sunlight, but remains higher than can be attributed to known food sources. This has lead to speculation that winter levels are maintained by adipose stores of vitamin D, but this assertion has not been fully tested and is controversial. In fact, adipose tissues concentrations are not high enough to sustain the serum concentrations of 25-hydroxyvitamin D seen throughout winter. The discrepancy between variations in serum levels of vitamin D and dietary intakes and sunlight exposure levels has caused researchers to analyse the individual 25-hydroxyvitamin D status data from previous studies in order to explain the discordance1. Using 8 studies involving 3000 individuals the researchers extrapolated supplemental dose response curves to zero concentrations values for serum 25-hydroxyvitamin D to allow estimates of contributions from solar sources of vitamin D.
The results of this study are interesting because they change the previous assertion that solar synthesis of vitamin D is the major driver of 25-hydroxyvitamin D status. Total input including diet and solar synthesis of 25-hydroxyvitamin D ranged from 778 IU per day to 2667 IU per day in hospitalised and healthy caucasian individuals, respectively. As has been shown previously, obese individuals and those of African origin had lower 25-hydroxyvitamin D concentrations that those of normal weight and caucasians, respectively. Seasonal oscillations in 25-hydroxyvitamin D ranged from 5.20 to 11.4 nmol/L (2.08 to 4.56 ng/mL) which equated to a mean subcutaneous synthesis of vitamin D of 209 to 651 IU per day at summer peak. The authors of this study calculated that the contribution of solar input to the total basal input of vitamin D was only 25 % with the largest summer peak being 485 IU per day. Therefore the previous contribution of solar activity to vitamin D status may have been overestimated.
The argument that adipose tissue storage of vitamin D is not a major contributor to winter 25-hydroxyvitamin D serum concentrations is based on three pieces of evidence. Firstly, measurements of adipose tissue show low levels of vitamin D that could not sustain serum levels throughout the winter. Secondly, large doses of vitamin D do not result in large amounts of stored vitamin D but most is used immediately. Thirdly, based on this study, the actual production of vitamin D in the summer is small, which questions if this amount could actually build up a store of the vitamin in adipose tissue. The authors suggested instead that preformed 25-hydroxyvitamin D might be provided by the diet through unknown sources, and that this is a major contributor to vitamin D status. The authors estimated that the dietary intake and subcutaneous synthesis left a gap of 40 μg per day of vitamin D (1600 IU per day) to explain serum concentrations, and that this could be accounted for by ~6-10 μg per day of preformed 25-hydroxyvitamin D.
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