There are two sources of vitamin D: sunlight (resulting in skin synthesis of vitamin D) and the diet. Vitamin D exists as either vitamin D2 (ergocalciferol) or vitamin D3 (cholecalciferol). Vitamin D2 is widely distributed in plants and fungi, derived from UV irradiation of the plant sterol ergosterol. Vitamin D3 is formed from the action of UV irradiation on 7-dehydrocholesterol in the skin of animals including humans. Skin production is, quantitatively, a more important source of vitamin D than the diet because there are not many rich food sources of vitamin D. However, dietary sources are essential when exposure to sunlight is limited.
Vitamin D is not classically a vitamin but a pro-hormone, acting as a precursor to one of the hormones involved in calcium homeostasis. Vitamin D is metabolised first to 25 hydroxyvitamin D (25OHD) and then to the active hormone 1,25-dihydroxyvitamin D (1,25(OH)2D) in the liver and kidney. In this form it works as a hormone regulating calcium and phosphorus metabolism, which are essential for bone mineralisation. Calcium homeostasis is also important for neuromuscular function.
Deficiency of vitamin D results in poor calcification of the skeleton. Prolonged deficiency of vitamin D during periods of bone growth in children leads to rickets. Rickets can cause bone pain, poor growth and deformities of the skeleton, such as bowed legs, curvature of the spine, and thickening of the ankles, wrists and knees. Children with rickets are also more likely to fracture their bones. Poor vitamin D status and rickets in children used to be commonplace in the UK but fortification and supplementation policies implemented after the Second World War made rickets a disease of the past. However, in recent years, cases are again being reported, particularly in some ethnic minority groups.
In adults, vitamin D is required to maintain healthy bone. Deficiency can lead to osteomalacia, commonly presenting with aching bones and muscles, and proximal muscle weakness, which makes standing up and walking difficult and results in a marked waddling gait. Osteoporosis is not directly due to vitamin D deficiency but vitamin D may be helpful in managing the disease. There is limited evidence for links between vitamin D status and other non-musculoskeletal health outcomes, including cardiovascular disease, hypertension, autoimmune diseases (e.g. multiple sclerosis and type 1 diabetes), neuropsychological function and cancer. This evidence-base mainly includes observational studies and so findings may be confounded by other factors or due to reverse causality (i.e. the illness is the cause, and not the consequence, of low vitamin D status).
Poor vitamin D status is defined by the Scientific Advisory Committee on Nutrition (SACN) as a blood level of 25 hydroxyvitamin D (25OHD) below 25 nmol/L, although definitions vary internationally. Low vitamin D status is commonplace in the UK, with approximately 20% of the population having serum concentrations below the 25 nmol/L level (NDNS 2008-12). Low vitamin D status is particularly prevalent in institutionalised adults over the age of 65 years [38% of men and 37% of women (assessed in NDNS 1994/95 only)], girls aged 11-18 years (24%) and men aged 19-64 years (24%) (NDNS 2008-12). As sunlight is the major source, status tends to be lower in the winter/spring than summer/autumn, and lower in Scotland than England.
In the UK some groups of people are vulnerable to vitamin D deficiency, such as those with dark skin, those who do not spend much time outdoors (e.g. institutionalised or housebound people) and those who habitually cover the skin. Currently the UK government recommends that the following groups of people take vitamin D supplements: pregnant and lactating women (10 µg per day); infants and children aged under 4 years (7-8.5 µg per day); people aged 65 years and older (10 µg per day); those with limited exposure to the sun (10 µg per day); and people of Asian origin (10 µg per day). However, an update to these recommendations has been proposed by SACN in their Draft Vitamin D and Health report (2015), which suggests that a reference nutrient intake (RNI) should be set for the whole UK population aged 4 years and over at 10 µg per day. SACN reported that there was insufficient data to set RNIs for infants and children aged 0-3 years. As a precaution, a ’Safe Intake’ of vitamin D was proposed for these ages: 8.5-10 μg/day for ages 0 to < 1 year (including exclusively breast-fed infants) and 10 μg/day for ages 1 to < 4 years.
Most vitamin D is obtained through the action of sunlight on skin during the summer months. The latitude and strength of the sun in the UK means that the skin can make vitamin D only between 11 am and 3 pm, during the months of April to October.
Dietary sources of vitamin D in the UK are natural food sources, fortified foods and supplements. Foods that contain significant amounts of vitamin D include oily fish, eggs, fortified cereals, meat and fat spreads; further information can be found here. Human milk contains low levels of vitamin D, but infant formula is fortified with 0.001-0.0025 mg/100 kcal.
Skin synthesis of vitamin D is self-regulated and so long sun exposure does not lead to excessive vitamin D production. Excessive dietary vitamin D intake can have toxic effects and may lead to hypercalcaemia (high calcium level in the blood). Hypercalcaemia can result in deposition of the excess calcium in soft tissues and demineralisation of bones, and heart and kidney damage. The European Food Safety Authority (EFSA) (2012) has set the Tolerable Upper Intake Level of vitamin D at 100 µg/day.
In light of the topicality of vitamin D, Nutrition Bulletin and the Journal of Human Nutrition and Dietetics have collaborated to produce a Virtual Issue (published January 2016) on this topic. Entitled Vitamin D – Population Requirements, Intake and Status: Implications for Health, this includes thirteen papers, all of which are free to download, and can be accessed via the Nutrition Bulletin website