Vitamin D β the "sunshine vitamin" β is technically a hormone precursor produced in the skin following UVB radiation exposure and obtained in limited quantities through diet. It plays essential roles in calcium and phosphorus metabolism (maintaining bone density), immune regulation, muscle function, cardiovascular health, and neurological function. Despite its importance, vitamin D deficiency is estimated to affect approximately 1 billion people globally β making it one of the most prevalent nutritional deficiencies worldwide.
Causes of Deficiency
Vitamin D deficiency is particularly common in: people with darker skin (higher melanin content reduces UVB-driven synthesis); those living at high latitudes with limited sunlight exposure; individuals who cover skin for religious, cultural, or UV protection reasons; the housebound elderly; obese individuals (vitamin D sequesters in adipose tissue); those with fat malabsorption syndromes (Crohn's disease, coeliac disease, gastric bypass); exclusively breastfed infants without supplementation; and people working indoors with limited outdoor exposure. The conversion of vitamin D to its active form (calcitriol) requires functional kidneys and liver β chronic kidney or liver disease impairs this activation step independently of intake.
Consequences of Deficiency
Classic vitamin D deficiency causes rickets in children (impaired bone mineralisation, skeletal deformities) and osteomalacia in adults (bone pain, muscle weakness, fracture risk). More subtly, deficiency is associated with impaired calcium absorption, accelerating osteoporosis. Beyond musculoskeletal effects, low vitamin D status has been linked β with varying strength of evidence β to increased risk of respiratory infections, autoimmune diseases (multiple sclerosis, type 1 diabetes), depression, and certain cancers. Whether supplementation corrects these associations is an active research question; results from large trials (VITAL, D-HEALTH) are mixed, with some showing benefit for cancer mortality but not incidence.
Testing and Supplementation
Vitamin D status is measured by serum 25-hydroxyvitamin D [25(OH)D]. Deficiency is generally defined as below 20 ng/mL (50 nmol/L); insufficiency as 20β29 ng/mL; adequacy as 30β60 ng/mL. For deficiency, therapeutic supplementation of 50,000 IU weekly for 8β12 weeks typically restores levels, followed by maintenance dosing of 1,500β2,000 IU/day. The tolerable upper intake level is 4,000 IU/day for adults; toxicity (hypercalcaemia) from excessive supplementation is a real risk. Brief daily sunlight exposure (10β20 minutes on arms and legs, before applying sunscreen) contributes meaningfully to vitamin D synthesis without cancer risk at moderate doses.
Frequently Asked Questions
Which foods are high in vitamin D?
Dietary sources are limited but include: fatty fish (salmon 450β600 IU per serving; sardines, mackerel, tuna); egg yolks (40β50 IU per yolk); beef liver; fortified foods including many dairy products, plant milks, and breakfast cereals (100β200 IU per serving); and UV-exposed mushrooms, which can synthesise substantial vitamin D when sun-dried gills-up.
Should everyone take a vitamin D supplement?
Not necessarily. Those with adequate sun exposure and diverse diets may achieve sufficient levels without supplementation. However, given the prevalence of deficiency and the difficulty of obtaining adequate dietary vitamin D, many physicians recommend routine supplementation of 1,000β2,000 IU/day for adults β particularly during winter months, for darker-skinned individuals, and for the elderly. A blood test guides whether higher doses are needed.
Sources
- Holick MF. Vitamin D deficiency. NEJM. 2007.
- Manson JE, et al. VITAL trial. NEJM. 2019.
- NIH Office of Dietary Supplements. Vitamin D fact sheet. 2023.