Vitamin D deficiency is one of the most common nutrient deficiencies worldwide — and one of the most over-attributed. Genuine deficiency produces real, measurable problems in bone and muscle. Many other symptoms popularly blamed on low vitamin D have weak or mixed trial support. Knowing the difference saves money and prevents missed diagnoses.
⚠️ Medical disclaimer: This is education, not medical advice. Do not start high-dose vitamin D without a blood test, especially with sarcoidosis, hyperparathyroidism, kidney stones or kidney disease.
Bone pain and tenderness. Osteomalacia — soft, poorly mineralised bone — causes deep, aching pain in the pelvis, ribs, lower back and legs, often with tenderness on pressing the shin or sternum.
Proximal muscle weakness. Difficulty rising from a chair, climbing stairs, or a waddling gait. Vitamin D receptors are present in skeletal muscle, and severe deficiency produces a recognisable myopathy that improves with repletion.
Increased fracture and fall risk in older adults. Correcting deficiency, usually alongside adequate calcium, reduces fracture risk in deficient populations. Supplementing people who are already replete does not.
Rickets in children. Bowed legs, delayed growth, wrist and rib swelling, delayed tooth eruption. Rare but still occurring, particularly in exclusively breastfed infants without supplementation and in children with darker skin at high latitudes.
Secondary hyperparathyroidism. Not a symptom you feel, but a lab pattern: falling 25(OH)D drives PTH up to maintain calcium, accelerating bone turnover.
These are frequently reported by people with low levels, but randomized supplementation trials have been inconsistent:
The honest framing: fix a documented deficiency because deficiency itself is harmful, not because supplementation reliably fixes non-skeletal symptoms.
| Risk factor | Why |
|---|---|
| Latitude above ~37° in winter | UVB too weak for cutaneous synthesis for several months |
| Darker skin pigmentation | Melanin reduces UVB-driven synthesis |
| Limited sun exposure | Indoor work, covering clothing, housebound, care homes |
| Age over 65 | Reduced skin synthesis capacity |
| Obesity | Sequestration in adipose tissue lowers circulating levels |
| Malabsorption | Coeliac, Crohn's, cystic fibrosis, bariatric surgery |
| Chronic kidney or liver disease | Impaired hydroxylation steps |
| Certain medications | Anticonvulsants, glucocorticoids, some antiretrovirals |
| Exclusively breastfed infants | Breast milk is low in vitamin D — supplementation is standard advice |
Ask for serum 25(OH)D, not 1,25-dihydroxyvitamin D (which is regulated tightly and can look normal in deficiency).
| 25(OH)D | nmol/L | ng/mL | Interpretation |
|---|---|---|---|
| Severe deficiency | <25 | <10 | Risk of osteomalacia/rickets |
| Deficiency | <30 | <12 | Treat |
| Insufficiency | 30–50 | 12–20 | Likely inadequate for bone health |
| Adequate | 50–125 | 20–50 | Sufficient for nearly everyone |
| High | >125 | >50 | No added benefit; monitor |
| Potentially toxic | >375 | >150 | Hypercalcaemia risk |
Check alongside calcium, phosphate, ALP and PTH if deficiency is significant — that panel distinguishes simple deficiency from parathyroid or renal disease. Our guide to reading blood work covers how these markers interact.
Retest 3 months after starting supplementation; 25(OH)D has a half-life of roughly 2–3 weeks and levels plateau by about 8–12 weeks.
Maintenance (adults, no deficiency): 10–25 µg (400–1,000 IU)/day. Many public health bodies recommend 10 µg/day through autumn and winter for the whole population at northern latitudes.
Insufficiency (30–50 nmol/L): 25–50 µg (1,000–2,000 IU)/day, retest at 3 months.
Documented deficiency (<30 nmol/L): typical clinical protocols use a loading regimen — for example around 300,000 IU total spread over 6–10 weeks — followed by maintenance. This should be prescribed and monitored, not self-administered.
Form: vitamin D3 (cholecalciferol) raises 25(OH)D more effectively than D2 (ergocalciferol) at equivalent doses. Daily dosing outperforms large intermittent boluses for most outcomes.
Obesity: higher doses are usually needed — often 1.5–3× the standard amount to reach the same serum level.
| Food | Serving | Approx. vitamin D |
|---|---|---|
| Wild salmon | 100 g | 10–25 µg (400–1,000 IU) |
| Farmed salmon | 100 g | 5–10 µg (200–400 IU) |
| Mackerel, sardines | 100 g | 5–10 µg |
| Cod liver oil | 5 ml | ~11 µg (440 IU) |
| Egg yolk | 1 large | ~1 µg (40 IU) |
| UV-exposed mushrooms | 100 g | 5–10 µg |
| Fortified milk/plant milk | 250 ml | 2–3 µg |
| Fortified cereal | 40 g | 1–2 µg |
Diet alone rarely corrects a deficiency — that is the practical reason supplementation exists.
Sunlight: roughly 10–20 minutes of midday summer sun on arms and legs produces meaningful amounts for lighter skin at mid-latitudes; darker skin needs several times longer. Glass blocks UVB, and above ~37° latitude synthesis effectively stops from late autumn to early spring.
Upload your blood work to Nutrtion.io — the app reads your 25(OH)D alongside calcium, ferritin and B12, shows how each marker has moved between tests, and turns the gaps into specific food and supplement targets.
How long until I feel better after starting vitamin D? Bone pain and muscle weakness from genuine deficiency typically improve over 4–12 weeks. If nothing changes by three months with a corrected level, look for another cause.
Can I get enough vitamin D from food alone? Only with regular oily fish or cod liver oil. Most people at higher latitudes cannot.
Is 1,000 IU a day enough? For maintenance in most adults, yes. For correcting documented deficiency, usually no.
Does sunscreen cause deficiency? In real-world use, sunscreen has little measurable effect on vitamin D status; skin cancer prevention takes priority.
Should everyone get tested? Population-wide screening is not recommended. Test if you have risk factors, unexplained bone or muscle symptoms, osteoporosis, malabsorption, or a relevant medication history.