A hormone, not really a vitamin. It controls how much calcium and phosphate you absorb.
Mechanisms, studies and evidence grades for each claim above.
Vitamin D is really a hormone the body makes itself. UVB light turns a cholesterol precursor in the skin (7-dehydrocholesterol) into vitamin D3. The liver converts it to 25-hydroxyvitamin D, the storage form measured in blood tests. Then the kidney turns that into the active hormone calcitriol (1,25-dihydroxyvitamin D), but only as much as PTH calls for. Both conversion enzymes need magnesium.1,2
Calcitriol binds the vitamin D receptor (VDR), a zinc-finger transcription factor, and switches on the genes for moving minerals into the body:
When that fails, collagen keeps being laid down but doesn't harden. In children that causes rickets (bowed legs, delayed growth). In adults it causes osteomalacia (soft, aching bones and weak muscles). PTH rises to make up the difference and pulls calcium out of the skeleton.1 Vitamin K2 then activates osteocalcin to lock calcium into bone matrix.
What trials show. Treating real deficiency prevents and cures rickets and osteomalacia. That isn't in dispute. Adding vitamin D on top of adequate status does much less. In the VITAL trial, 25,871 healthy US adults took 2,000 IU/day or placebo for about 5 years. There was no reduction in fractures, and no reduction in cancer or major cardiovascular events either.3,4 Most VITAL participants weren't deficient at the start. The lesson: vitamin D fixes a shortage but doesn't boost bone beyond normal.
↑ back to summaryImmune cells carry the VDR and also have their own conversion enzyme. When a macrophage detects bacteria through its Toll-like receptors, it switches on both. It takes 25-hydroxyvitamin D from the blood, makes calcitriol inside the cell and uses it to produce cathelicidin (LL-37), an antimicrobial peptide that kills bacteria including tuberculosis. Blood with low 25-hydroxyvitamin D couldn't support this response well in the lab.5 This local system works regardless of the kidney's hormone control, which is why the storage level in blood matters to immune cells.
On the adaptive side, calcitriol pushes T cells away from inflammatory Th1/Th17 responses and toward regulatory T cells, and makes dendritic cells more tolerant. That's the basis for interest in vitamin D and autoimmune disease.
Human trials:
Sun on skin is the normal source. Food supplies little except oily fish. But UVB is filtered out by the atmosphere when the sun is low. In a classic study, winter sunlight in Boston (42°N) made no vitamin D3 in skin samples from November to February. In Edmonton (52°N) the gap ran from October to March.8 Above about 37°N, roughly a line through San Francisco, Kansas and Virginia, winter sun doesn't make meaningful vitamin D, and status falls through the winter. Hence the approach on this page: sunlight in summer, a supplement in winter. See Sunlight.
The RDA is 600 IU/day (800 IU over 70), set for bone health with minimal sun. Many clinicians aim for a blood level of 30 ng/mL (75 nmol/L) and use 1,000–2,000 IU/day in winter to reach it.2 The upper limit is 4,000 IU/day. Pair it with magnesium, which is needed for both conversion steps, and K2, which directs calcium into bone.
Rickets in children; osteomalacia in adults (aching bones, especially the shins and lower back, and weakness in the thigh and hip muscles that makes climbing stairs hard); raised PTH with gradual bone loss; and, from the trials above, probably more respiratory infections.1 People most at risk have darker skin at high latitudes, cover most of their skin, spend little time outdoors, are older (skin makes less vitamin D with age), are obese (vitamin D is stored in fat) or have fat malabsorption.
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