Vitamin D deficiency is a state in which the body's vitamin D availability is insufficient for normal physiological needs, particularly the regulation of calcium and phosphate metabolism and maintenance of healthy bone mineralisation. Vitamin D can be obtained from dietary sources and supplements and can also be produced in the skin when ultraviolet B radiation converts a precursor into vitamin D3.
The liver converts vitamin D to 25-hydroxyvitamin D, commonly called 25-hydroxyvitamin D or 25-OH-D, which is the main blood marker used to assess vitamin D status. The kidneys and other tissues can convert it into the biologically active hormone 1,25-dihydroxyvitamin D. Deficiency can impair calcium absorption and bone mineralisation and, when severe or prolonged, contribute to rickets in children or osteomalacia in adults.
Sunlight exposure is an important source of vitamin D, but the amount produced depends on latitude, season, time of day, skin pigmentation, clothing, sunscreen use, age and other factors. Ultraviolet B radiation must reach the skin for meaningful cutaneous synthesis. At higher latitudes, including much of northern Europe, winter sunlight may be insufficient for substantial vitamin D production. Older adults generally have reduced capacity to synthesise vitamin D in the skin. People who spend little time outdoors or whose skin is usually covered may also have increased risk. However, deliberate excessive ultraviolet exposure is not recommended as a method of obtaining vitamin D because ultraviolet radiation causes skin damage and increases skin-cancer risk.
Dietary intake can contribute to vitamin D status, although relatively few foods naturally contain large amounts. Oily fish provides vitamin D, and some foods such as spreads, cereals or plant-based alternatives may be fortified depending on national practices. Supplements can provide vitamin D when dietary and environmental sources are insufficient or when a person belongs to a group at increased risk. Requirements and public-health recommendations vary by country because they reflect differences in latitude, food fortification, population risk and health policy. A balanced nutritional approach therefore considers both dietary sources and appropriate supplementation rather than assuming that sunlight alone will always provide sufficient vitamin D.
Risk factors for vitamin D deficiency include limited sunlight exposure, older age, darker skin pigmentation in regions with relatively low ultraviolet exposure, covering most of the skin, institutionalisation or prolonged indoor living, malabsorption disorders and certain medical conditions. Obesity can also be associated with lower circulating vitamin D concentrations because vitamin D is fat-soluble and can be distributed into adipose tissue. Disorders affecting the liver or kidneys can interfere with vitamin D metabolism. Some medicines, including certain anticonvulsants, can alter vitamin D metabolism. Infants have particular nutritional considerations because they have limited vitamin D stores and requirements relative to body size, which is why many countries provide specific supplementation guidance for infancy.
Symptoms of vitamin D deficiency can be absent, particularly when deficiency is mild. Significant deficiency can cause bone pain, muscle weakness and increased susceptibility to fractures because inadequate vitamin D disrupts mineralisation and calcium-phosphate homeostasis. In children, severe deficiency can cause rickets, characterised by impaired bone development and deformities. In adults, osteomalacia involves defective mineralisation of newly formed bone and can cause diffuse bone pain, muscle weakness and increased fracture risk. Severe deficiency can also contribute to hypocalcaemia and secondary hyperparathyroidism. These manifestations are distinct from osteoporosis, which involves reduced bone mass and altered bone strength but does not simply mean that the bones have failed to mineralise because of vitamin D deficiency.
Vitamin D status is assessed primarily using serum 25-hydroxyvitamin D rather than the active hormone 1,25-dihydroxyvitamin D in routine deficiency assessment. The active hormone is tightly regulated and can remain normal or even increase when vitamin D stores are inadequate, so it is not generally the preferred measure of nutritional vitamin D status. Interpretation of 25-hydroxyvitamin D concentrations requires awareness that laboratory methods, reference ranges and definitions of deficiency can differ.
Testing is not necessarily required for every person, particularly when national guidance recommends supplementation based on established risk factors. Testing is more relevant when deficiency is suspected to be severe, symptoms are present, there is a bone disorder, malabsorption is suspected or treatment response is uncertain.
Treatment depends on severity and clinical circumstances. Mild or uncomplicated deficiency may be addressed with an appropriate vitamin D supplement, while significant deficiency or symptomatic osteomalacia may require a higher-dose replacement regimen under clinical supervision. Calcium intake and other nutritional factors may also need consideration because vitamin D works partly by promoting intestinal calcium absorption. Excessive vitamin D supplementation is not harmless. Very high doses can cause vitamin D toxicity, leading to hypercalcaemia, which can produce nausea, vomiting, weakness, excessive thirst, frequent urination, confusion and kidney complications. Treatment should therefore use appropriate doses rather than assuming that progressively higher intake provides progressively greater benefit.
Vitamin D deficiency is best understood as a specific nutritional and metabolic problem rather than a universal explanation for fatigue, pain or poor health. Adequate vitamin D is important for calcium metabolism and skeletal health, and correcting genuine deficiency can prevent or treat important bone disorders. Associations between vitamin D status and many other conditions have been investigated, but observational associations do not necessarily mean that supplementation prevents those diseases, and routine high-dose supplementation should not be justified solely by broad claims about immunity, cardiovascular health or general wellbeing. Appropriate prevention and treatment depend on individual risk, national guidance, diet, environmental exposure, medical conditions and safe supplementation.
