Vitamin D deficiency occurs when the body does not have enough vitamin D to maintain normal physiological functions, particularly calcium and phosphate regulation and healthy bones and muscles. Vitamin D is unusual among vitamins because the body can manufacture it in the skin after exposure to ultraviolet B radiation from sunlight, while smaller amounts can come from food and supplements. Deficiency therefore does not necessarily mean that a person eats too little vitamin D. It can result from insufficient sunlight exposure, inadequate dietary intake, impaired absorption, impaired conversion or activation of vitamin D, increased physiological requirements, or combinations of these factors. The amount of sunlight needed varies with season, latitude, skin pigmentation, clothing, outdoor activity and other circumstances.
In the UK, insufficient sunlight is an important cause because ultraviolet B radiation is inadequate for reliable vitamin D production during much of the year. NHS guidance states that most people should be able to make enough vitamin D from sunlight between roughly late March or early April and the end of September, whereas sunlight between October and early March is generally insufficient for this purpose. People who spend little time outdoors are consequently at increased risk. This includes people who are housebound or frail, people living in residential or care settings and people whose circumstances substantially restrict exposure of their skin to daylight.
Skin pigmentation affects vitamin D synthesis because melanin reduces the amount of ultraviolet B radiation reaching the skin cells responsible for producing vitamin D. People with dark skin can therefore require more ultraviolet exposure to produce a comparable amount of vitamin D than people with lighter skin, although individual variation is substantial. NHS guidance identifies people with African, African-Caribbean or South Asian backgrounds as groups who may not make enough vitamin D from sunlight and therefore advises consideration of year-round supplementation for these groups. This does not mean that skin colour alone determines vitamin D status, because outdoor exposure, season, clothing, age, diet and health also influence the final concentration.
Dietary insufficiency can contribute to deficiency because relatively few foods naturally contain substantial amounts of vitamin D. Useful sources include oily fish such as salmon, sardines, trout, herring and mackerel, as well as egg yolks, red meat, liver and some fortified foods. In the UK, ordinary cow's milk is generally not a major vitamin D source because it is not routinely fortified in the same way as milk in some other countries. People whose diets contain few vitamin-D-containing or fortified foods can therefore have a lower intake, particularly when sunlight exposure is also limited. Restrictive diets may require particular attention to reliable fortified foods or appropriate supplementation.
Some people develop vitamin D deficiency despite adequate exposure and dietary intake because their bodies cannot absorb or metabolise vitamin D normally. Fat-malabsorption disorders can reduce absorption of fat-soluble vitamin D because vitamin D is absorbed along with dietary fat. Conditions affecting the intestine, pancreas or bile system, and some gastrointestinal surgeries, can therefore increase risk. Chronic liver or kidney disease can also interfere with the conversion of vitamin D into biologically active metabolites. The distinction matters because simply taking more dietary vitamin D may not correct a deficiency when the underlying problem is impaired absorption, altered metabolism or organ dysfunction.
Certain medicines can affect vitamin D metabolism and contribute to deficiency, particularly medicines that increase the breakdown of vitamin D or interfere with its metabolism. Examples described in clinical literature include some anticonvulsants and other long-term medicines, although the significance depends on the drug, dose, duration and individual circumstances. Increased physiological demand can also matter. Infants, children during growth, pregnant people and some other groups may have different requirements or risks. Obesity is associated with lower circulating vitamin D concentrations in many populations, partly because vitamin D can become distributed into a larger volume of body tissue. These relationships do not mean that any one factor inevitably causes deficiency.
Age can contribute through several mechanisms. Older skin is generally less efficient at producing vitamin D after ultraviolet exposure, and older people may spend less time outdoors or have less skin exposed to sunlight. Institutionalisation, reduced mobility and chronic illness can compound these factors. Covering most of the skin with clothing can similarly reduce cutaneous vitamin D production. Sunscreen reduces ultraviolet B penetration and therefore can theoretically reduce vitamin D synthesis, but sun protection remains important because excessive ultraviolet exposure causes sunburn, premature skin ageing and skin cancer. Vitamin D deficiency should therefore be addressed through appropriate dietary intake and supplementation rather than deliberately seeking harmful ultraviolet exposure.
Vitamin D deficiency is therefore usually multifactorial rather than attributable to one simple cause. The important distinction is between insufficient vitamin D production or intake and conditions that interfere with absorption or metabolism. Mild biochemical deficiency may produce no obvious symptoms, while severe or prolonged deficiency can impair bone mineralisation and cause rickets in children or osteomalacia and bone pain in adults. UK guidance recommends that everyone consider a daily vitamin D supplement during autumn and winter, with year-round supplementation recommended for several groups at increased risk of deficiency. Supplements should be used at appropriate doses because vitamin D is fat-soluble and excessive intake can itself cause toxicity.
