25-hydroxyvitamin D is the primary circulating form of vitamin D and the most reliable indicator of vitamin D status in the body. This metabolite reflects total vitamin D input from sun exposure, dietary intake, and supplementation, with a half-life of approximately 2-3 weeks. Vitamin D undergoes hydroxylation in the liver to form 25-hydroxyvitamin D, which circulates bound to vitamin D binding protein. This metabolite serves as the substrate for production of the active hormone 1,25-dihydroxyvitamin D in the kidneys and other tissues, playing crucial roles in calcium homeostasis, bone health, and immune function.
25-hydroxyvitamin D is the primary circulating form of vitamin D and the standard measure of vitamin D status. It plays essential roles in calcium homeostasis, bone mineralization, immune modulation, and gene expression across multiple tissue types. Deficiency is widespread globally, including in otherwise healthy populations.
Levels below 20 ng/mL are classified as deficient; 20-29 ng/mL as insufficient (Endocrine Society criteria). Deficiency is associated with reduced bone mineral density, increased fracture risk, impaired immune function, and fatigue. Toxicity (typically >100 ng/mL) can cause hypercalcemia but is rare and almost exclusively due to supplementation.
Vitamin D receptors are expressed in skeletal muscle tissue, and adequate levels are linked to muscle contractility and neuromuscular function. Athletes training primarily indoors, at northern latitudes, or with limited sun exposure are at elevated risk for insufficiency. Seasonal variation in vitamin D levels is well-documented, with nadirs typically occurring in late winter.
Turnaround Time
3 days (up to 12 days)
Fasting Required
No
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