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Place · Level 3
从阳光抵达皮肤 · 到肝脏改名 · 到肾脏点火 · 最后服务全身
synergy · 3
D imports calcium; K2 routes it to bone, not arteries.
The VITAL trial design itself was omega-3 + D co-intervention; overall depression/immune/CV hard endpoints null, but subgroup + exploratory analyses showed signal in low-baseline populations. Clinical: not 'supplement everyone' — combine only when correcting documented deficiency.
Bischoff-Ferrari 2019: RT + adequate vitamin D doubles strength gains vs RT alone. VDR is expressed in skeletal muscle and modulates protein synthesis.
cofactor · 7
Both vitamin-D activation steps need magnesium as cofactor.
Vitamin D's final activation step (CYP27B1) happens in the kidney. As kidney function falls that step stalls, 1,25(OH)₂D drops, and calcium-phosphate control goes with it — the chemical starting point of CKD mineral-bone disease.
The nutritional base for bone is 1000-1200 mg/day of calcium (food first, supplements only for the gap) plus enough vitamin D — D governs whether that calcium is absorbed and laid down, and it is not something high doses buy.
Vitamin D decides whether the calcium you eat is absorbed at all: the target is 25(OH)D held between 30 and 50 ng/mL, reached with food, sun and supplements where needed. Below that line, more calcium mostly does not stay.
VDR is expressed in skeletal muscle; adequate D status amplifies MPS response to protein feeding (Mason 2013 RCT). Deficiency correlates with reduced strength and fall risk, especially in older adults.
Alveolar macrophages deal with pathogens crossing the mucus layer partly through the antimicrobial peptide LL-37, whose expression vitamin D upregulates — this is where the vitamin-D-and-airway association lands at cell level.
Vitamin D's effect in sarcopenia shows up mainly in the deficient: correcting to sufficiency improves strength and reduces falls. Topping up someone already sufficient buys no more, which matches the conclusion on the bone line.
regulates · 6
Calcitriol opens the active intestinal calcium channel. No D = no absorption.
Phosphorus, calcium, vitamin D, PTH, and FGF23 form a mineral-homeostasis axis.
1,25(OH)₂D modulates cathelicidin + defensin via VDR in macrophages/T-cells. Martineau 2017 BMJ meta (N=10,933): supplementation cuts respiratory infections ~12% in low-baseline individuals.
A 25(OH)D under 20 ng/mL is worth checking and correcting in a fatigue work-up — but pushing past sufficiency buys no more energy, and that is the direction people usually get wrong.
Vitamin D shaves a little off BPPV recurrence but is nowhere near a cure — repositioning is still the treatment; D at most discounts the relapse rate. Do not carry this over to vitamin D and falls or fractures, which large trials have substantially revised in the past decade.
Two different things: filling a gap is worth doing — correcting a deficiency may marginally help respiratory infection — while topping up someone already sufficient adds nothing. Immunity is not better-when-higher; supplements restore normal, they do not push past it.