Vitamin D is one of the most studied micronutrients of the past two decades and one of the most commonly deficient. Estimates from the WHO and various national health surveys suggest that over one billion people worldwide have insufficient vitamin D levels — including large proportions of populations in sunny countries, not just northern latitudes.
This creates a paradox that confuses many people: if the body makes vitamin D from sunlight, why are so many people deficient? And what does the evidence say about supplementation?
What Vitamin D Actually Does
Calling it a "vitamin" is technically a misnomer. Vitamin D3 (cholecalciferol) is a prohormone — it's synthesised in the skin under UV-B radiation and then converted in the liver to 25-hydroxyvitamin D (25(OH)D), which is the form measured in blood tests. The kidneys then convert this to 1,25-dihydroxyvitamin D (calcitriol), the biologically active form.
Vitamin D receptors are present in virtually every tissue in the body. Its established roles include:
- Calcium and phosphorus absorption — the original, textbook function. Deficiency causes rickets in children and osteomalacia in adults.
- Bone mineralisation — beyond just calcium absorption, vitamin D regulates the bone remodelling process.
- Immune function — vitamin D modulates both innate and adaptive immunity. Deficiency is associated with increased susceptibility to respiratory infections.
- Muscle function — deficiency is a recognised cause of proximal muscle weakness and contributes to fall risk in older adults.
- Mood regulation — receptors in the brain and correlations with depression have been observed in multiple studies, though causality remains debated.
Beyond these established roles, epidemiological studies have associated low vitamin D with higher rates of cardiovascular disease, type 2 diabetes, multiple sclerosis, and several cancers. The mechanistic pathways are plausible, but randomised controlled trials have been less convincing than the observational data — a recurring theme in vitamin D research.
Why Sunlight Isn't Enough for Most People
The body can synthesise substantial vitamin D from UV-B radiation — in ideal conditions. Those conditions are rarer than most people assume:
- Latitude: Above roughly 35°N or below 35°S (which includes most of Europe, all of Canada, much of the US), the sun angle in winter means that UV-B wavelengths are largely filtered by the atmosphere. From October to March in London or Berlin, you can't synthesise meaningful vitamin D from sun exposure regardless of how much time you spend outdoors.
- Time of day: UV-B synthesis requires a solar elevation angle above ~45°. This generally means mid-day exposure (roughly 10am–3pm). Morning and evening sun produces essentially no vitamin D synthesis.
- Skin colour: Melanin reduces UV-B penetration. People with darker skin tones require substantially longer sun exposure to produce equivalent vitamin D — a significant factor given that many populations with darker skin now live at northern latitudes.
- Sunscreen: SPF 30 reduces vitamin D synthesis by approximately 95%. Appropriate use of sunscreen for skin cancer prevention conflicts with vitamin D production.
- Age: The capacity to synthesise vitamin D from sunlight decreases with age. An 80-year-old produces about 25% as much vitamin D per unit of UV-B exposure as a 20-year-old.
- BMI and body fat: Vitamin D is fat-soluble. Higher body fat is associated with greater sequestration of vitamin D in adipose tissue, reducing bioavailability.
The combination of these factors means that even people who spend time outdoors — in moderately sunny climates — may not be synthesising enough vitamin D during winter months, and many people have chronically low levels year-round.
What the Blood Test Means: Reference Ranges Explained
Vitamin D status is measured as serum 25(OH)D. The numbers matter, and they're a source of genuine controversy among experts:
25(OH)D Blood Level Reference Guide
| Level (nmol/L) | Level (ng/mL) | Status | Clinical Significance |
|---|---|---|---|
| <25 | <10 | Severe deficiency | Risk of rickets/osteomalacia; significant immune impairment |
| 25–50 | 10–20 | Deficiency | Below virtually all guidelines; bone health and immune function compromised |
| 50–75 | 20–30 | Insufficiency | The contested zone — some bodies define "sufficient" here; most researchers disagree |
| 75–125 | 30–50 | Sufficiency | Target range for most researchers; associated with optimal bone, immune, and muscle outcomes |
| 125–150 | 50–60 | High normal | Within safe range; some immune research suggests benefits up to this level |
| >250 | >100 | Potential toxicity | Hypercalcaemia risk; not achievable from food or typical supplementation alone |
The controversy is significant: the Institute of Medicine (IOM, now the National Academy of Medicine) defines sufficiency as ≥50 nmol/L (20 ng/mL), while organisations like the Endocrine Society, Vitamin D Council, and many researchers argue for ≥75–80 nmol/L (30–32 ng/mL). This difference in threshold definition is why some studies conclude "most people are sufficient" while others conclude "most people are deficient" — they're measuring the same data against different benchmarks.
"The IOM's 20 ng/mL threshold was set to ensure bone health in 97.5% of the population. It was never intended as an optimal level for non-skeletal outcomes." — Dr. Michael Holick, Boston University School of Medicine
Dietary Sources: Food Is Not the Answer
Very few foods contain meaningful amounts of vitamin D. The short list:
- Fatty fish (salmon, mackerel, herring, sardines): 400–1,000 IU per serving — the best dietary source
- Cod liver oil: ~450 IU per teaspoon (plus vitamin A — don't overdo it)
- Egg yolks: 40–50 IU each (hens raised outdoors or under UV produce considerably more)
- UV-exposed mushrooms: Highly variable; commercially grown mushrooms in the dark contain almost none
- Fortified foods: Milk, plant milks, and some cereals in fortified countries — typically 40–100 IU per serving
To reach 2,000 IU from diet alone, you'd need to eat salmon daily. Most people don't. This is why supplementation is the practical tool for maintaining adequate vitamin D levels, particularly in winter or at northern latitudes.
D3 vs D2: Which Form to Take
Supplements come in two forms:
Vitamin D3 (cholecalciferol): The form produced by the skin. More effectively raises and maintains serum 25(OH)D levels. The preferred form in essentially all clinical guidance.
Vitamin D2 (ergocalciferol): Plant-derived, historically used in prescription formulations. Less potent and shorter-lived in the body. Increasingly avoided in favour of D3.
If you're vegan: D3 is typically derived from lanolin (sheep wool). Vegan D3 from lichen is available and equally effective — look for it specifically.
What Dose? The Evidence
Dosing recommendations vary widely. Context matters:
Maintenance (if blood levels are already adequate): 1,000–2,000 IU daily is sufficient for most adults during months of low sun exposure. Population studies suggest that 1,000 IU raises serum 25(OH)D by approximately 10–25 nmol/L, though individual response varies considerably.
Correction of deficiency: If your 25(OH)D is below 50 nmol/L, a loading protocol of 4,000–6,000 IU daily for 8–12 weeks is appropriate, followed by re-testing and maintenance dosing. Some guidelines use short-term higher doses (e.g., 50,000 IU weekly for 8 weeks as a prescription-only intervention).
Upper safe limit: The IOM sets the Tolerable Upper Intake Level at 4,000 IU/day for most adults. The Endocrine Society considers 10,000 IU/day safe for short-term use under supervision. Vitamin D toxicity (hypercalcaemia) from supplementation alone is rare but possible at sustained very high doses (>10,000 IU/day long-term).
The practical recommendation for most adults: 2,000 IU of D3 daily in autumn and winter, with a blood test every 1–2 years to confirm adequacy. If your level is below 50 nmol/L, discuss a corrective protocol with your doctor.
The Vitamin K2 Question
You'll encounter many supplements pairing D3 with vitamin K2. The rationale: vitamin D increases calcium absorption, and vitamin K2 (particularly the MK-7 form) is involved in directing calcium to bones rather than arteries. The concern is that high-dose vitamin D supplementation without adequate K2 might contribute to arterial calcification.
The evidence here is mechanistically plausible but not definitive in RCT data. The practical reality: if you're taking standard doses (1,000–4,000 IU daily), the theoretical risk is low. If you're eating a reasonably varied diet including any fermented foods, aged cheese, or egg yolks, you're getting some K2 from food. Many practitioners recommend pairing them for peace of mind, and the combination supplements are widely available.
What to Do Right Now
- Get tested — a 25(OH)D blood test (widely available, often covered by standard health panels) tells you where you actually stand. Guessing doesn't work; individual variation in vitamin D status is enormous.
- Supplement D3 in autumn/winter — if you live above 35°N or below 35°S, assume you need supplementation from October through March regardless of sun exposure.
- Start at 2,000 IU/day unless your test shows deficiency, in which case use higher doses under medical guidance.
- Take it with fat — vitamin D is fat-soluble. Taking it with your largest meal improves absorption by approximately 50%.
- Don't rely on food alone — except for serious fatty fish consumption, dietary vitamin D is insufficient to maintain adequate levels.
Vitamin D is one of the few supplements with strong evidence behind it, a genuine population-level deficiency problem, and a straightforward, inexpensive correction. The case for routine supplementation at temperate and northern latitudes is solid. The case for getting tested first is even stronger — so you're treating a known number, not guessing.