Vitamin D is a hormone that is produced in the skin through exposure to ultraviolet light. Being a hormone, vitamin D plays an important role in metabolic regulation, the main part of which centres of calcium homeostasis. In this regard, vitamin D and its metabolites increase calcium absorption from the gut to raise plasma levels of calcium ions. Increasingly it is being recognised that the vitamin D status of many living in high latitude countries is inadequate, due to long periods of weak sunlight. Vitamin D is also present in foods and dietary intakes can contribute significantly to vitamin D status. However, the foods containing vitamin D are limited and therefore even diets rich in vitamin D foods cannot make up the shortfall created by limited sun exposure. As a result supplements are now recommended to maintain adequate vitamin D status, with up to 2000 IU per day suggested for a typical adult through the winter months. It is therefore interesting to review the studies investigating vitamin D absorption from supplements.
In one such study1, vitamin D absorption was investigated in healthy subjects in comparison to subjects with fat malabsorption syndrome. Oral vitamin D supplements of 50,000 IU (1.25 mg) of vitamin D2 (ergocalciferol) per day were administered to the subjects and their plasma levels of vitamin D measured. The subjects with fat malabsorption included Crohn’s disease, cystic fibrosis, villous atrophy, scleroderma and ulcerative colitis sufferers who had baseline 25-hydroxyvitamin D concentrations of between 10 and 37 ng/mL. Administration of vitamin D to the healthy subjects caused the initial vitamin D concentration which was below 10 ng/mL to rise within a 4 hour period. By 12 hours post administration peak 25-hydroxyvitamin D concentrations had reached 70 and 80 ng/mL in the subjects, before gradually declining to baseline over the course of 7 days. Other healthy subjects were then used to confirm these data, and again the subjects showed large rises in 25-hydroxyvitamin D from around 5 ng/mL to over 50 ng/mL within 12 hours.
However, this pattern was not repeated with all the subjects suffering from fat malabsorption. While two of the subjects did show a rise similar to the healthy subjects (a peak 25-hydroxyvitamin D concentration of 60 ng/mL after 12 hours) the other patients did not respond to oral vitamin D. Therefore subjects with fat malabsorption or other malabsorption diseases may required careful monitoring regarding their vitamin D status. Because vitamin D is fat soluble, an inability to absorb fat clearly has the potential to prevent the absorption of fat soluble vitamins such as vitamin D. Vitamin D is a relatively nonpolar sterol, and therefore it must be solubilised by incorporation into bile salt micelles to allow absorption in the aqueous phase. This process is absent from subject with fat malabsorption and this negatively affects vitamin D absorption. Normal pancreatic and biliary secretions are therefore necessary for optimal vitamin D absorption even if administration is via high dose supplements.
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