Vitamin D
What it is
Vitamin D is a fat-soluble vitamin that functions as a hormone. It is produced in the skin on exposure to ultraviolet B radiation from sunlight, and obtained in smaller amounts from dietary sources including oily fish, egg yolks, and fortified foods.
Two dietary forms exist. Vitamin D3 (cholecalciferol) is derived from animal sources and produced in human skin. Vitamin D2 (ergocalciferol) is derived from plant sources and fungi. D3 is more effective at raising and sustaining serum 25-hydroxyvitamin D levels and is the form with the stronger evidence base. Where evidence is cited in this entry, it applies to D3 unless otherwise stated.
Deficiency is genuinely common. Estimates suggest that between 40 and 70 per cent of people in northern latitudes, including across the UK, have insufficient vitamin D levels, with prevalence highest in winter months and in individuals with darker skin pigmentation, limited sun exposure, or higher body weight.
What the evidence shows
Deficiency correction is where the evidence is strongest and most consistent. In individuals with confirmed deficiency, vitamin D3 supplementation reliably restores serum 25-hydroxyvitamin D to sufficient levels and resolves associated symptoms including fatigue, bone pain, and muscle weakness. This is well-established and not materially contested.
Immune function and respiratory infection has a moderate evidence base. A large individual participant data meta-analysis found a meaningful reduction in acute respiratory tract infections with daily or weekly vitamin D supplementation. The protective effect was substantially larger in individuals with low baseline status than in those who were already replete. Taking a supplement when you are already sufficient does not appear to confer the same benefit.
Mood and depression symptoms show early-stage evidence. A small number of RCTs suggest modest improvements in mood and perceived wellbeing, particularly in individuals with low baseline status. Effect sizes are small, studies are short, and findings are inconsistent. This is a promising research area rather than an established clinical effect.
Cognitive performance in generally healthy adults with normal vitamin D status has insufficient evidence. Studies are methodologically weak, findings are contradictory, and no well-powered RCT has demonstrated a meaningful cognitive benefit in replete individuals.
Cardiovascular disease prevention is not supported by the available trial evidence despite earlier observational associations. Two large, well-designed RCTs in healthy adults found no significant reduction in major cardiovascular events with supplementation.
What the evidence does not show
Vitamin D supplementation does not prevent cancer, cardiovascular disease, or autoimmune conditions in the general population. The observational associations that generated these hypotheses have not been replicated in large controlled trials.
Cognitive benefits in individuals with normal vitamin D status are not supported. The widespread commercial framing of vitamin D as a cognitive enhancer extends well beyond what the controlled trial evidence supports.
Supplementing without confirmed deficiency produces a smaller immune benefit than is commonly assumed. The immune function evidence is largely concentrated in individuals who are deficient at baseline.
Form and dose considerations
Vitamin D3 (cholecalciferol) is the appropriate form for supplementation. D2 (ergocalciferol) is less effective at raising and maintaining serum levels and should not be treated as equivalent to D3.
Trials supporting deficiency correction typically use doses between 1,000 and 4,000 IU per day. The dose required to reach and sustain adequate serum levels varies considerably between individuals, depending on baseline status, body weight, skin pigmentation, sun exposure, and genetic factors including VDR polymorphisms. Without a baseline blood test, it is not possible to choose an appropriate dose.
The upper tolerable intake for most adults is 4,000 IU per day. Toxicity at doses below this is rare but has been documented with sustained intake above 10,000 IU per day.
Who the evidence applies to
The deficiency correction evidence applies to individuals with confirmed deficiency. The benefit is largest in those with the lowest starting levels and diminishes as baseline status improves.
The immune function evidence applies most consistently to individuals with low baseline vitamin D status, older adults, and those with limited sun exposure. Effects in young, healthy, replete individuals are less consistent.
Genetic variation in the vitamin D receptor (VDR) gene affects individual response to supplementation and may explain some of the variability in trial outcomes across populations.
Pregnancy and breastfeeding represent a population where supplementation is generally recommended regardless of baseline status. Current UK guidance recommends 400 IU daily throughout pregnancy and breastfeeding. Anyone pregnant or breastfeeding should discuss dosing with their midwife or GP.
Safety and contraindications
Vitamin D is well tolerated at standard doses. The most important safety consideration is that deficiency should be confirmed before high-dose supplementation.
Individuals with primary hyperparathyroidism, sarcoidosis, or other conditions affecting calcium metabolism should seek medical advice before supplementing, as vitamin D increases calcium absorption. Vitamin D interacts with thiazide diuretics and some anticonvulsants. Anyone taking regular medication should check with their prescriber or pharmacist before supplementing.
What can reasonably be concluded
A serum 25-hydroxyvitamin D test before supplementing allows an appropriate dose to be chosen and avoids unnecessary supplementation in those who are already sufficient. Deficiency is common enough, particularly in northern latitudes in winter, that testing is a reasonable first step for most people rather than an overcautious one.
Vitamin D3 supplementation in confirmed deficiency is well-evidenced and appropriate. The immune function benefit is real but is most meaningful for those who are deficient. Claims extending the evidence to cardiovascular protection, cancer prevention, or cognitive enhancement in the general population are not supported by large controlled trials and should be treated with scepticism.