Vitamin D is a steroidal hormone that plays an important role in calcium homeostasis, bone formation and resorption via its interaction with the parathyroid gland, kidneys and the intestines.
Vitamin D is synthesised in the skin after exposure to sunlight via ultraviolet B (UVB) radiation and is our main source of vitamin D. UVB photons penetrate into the skin and are absorbed by 7-dehydrocholesterol leading to the formation of an unstable previtamin D that is converted to form vitamin D3 (cholecalciferol). Vitamin D2 (ergocalciferol) is the form of vitamin D that is present in plants and is used to fortify foods. Both forms of vitamin D enter the circulation bound to a protein and metabolized by the liver to form 25-hydroxyvitamin D (calcidiol), which is the major form of vitamin D in the blood and a substrate for the production of 1, 25 dihydroxyvitamin D, and a hormonally active metabolite.
Food sources of vitamin D include oily fish, eggs and dairy and fortified foods such as orange juice, milk, some cereals and breads, but food sources are inadequate to supply our requirements with only a few minutes of sunlight exceeding dietary sources. Cod liver oil also contains a variable amount of vitamin D but also contains vitamin A which is antagonistic and thwarts vitamin D’s protective effects so is not recommended.
Vitamin D exerts its biological effects through its receptors and targets more than 200 human genes in a wide variety of tissues. Without adequate vitamin D3 the small intestine absorbs no more than 10-15% of dietary calcium, whereas adequate dietary vitamin D3 can absorb 30% and efficiency increases to 80% during growth, lactation, and pregnancy. Without adequate vitamin D3 and calcium absorption, the bone-deforming disease, rickets can develop especially in breast-fed infants.
Some studies have linked vitamin D deficiency with several auto-immune disorders including insulin-dependent diabetes mellitus, multiple sclerosis, inflammatory bowel disease, systemic lupus erthyematosus rheumatoid arthritis and asthma,as well as cancer, periodontal disease, osteoporosis, macular degeneration, autism, mental illness, cardiovascular disease and hypertension. Hypertensive patients exposed to UVB radiation for 3 months have shown a decrease in their diastolic and systolic readings, whereas those patients that were not exposed had no change in their readings. The mechanism might be due to the ability of vitamin D3 to down-regulate renin and angiotensin, a system that regulate blood pressure.
Immune cells have a wide distribution of vitamin D receptors and have an effect on cell proliferation and differentiation, making vitamin D an important immune system regulator. Vitamin D may also up-regulate a naturally occurring broad spectrum antibiotic known as cathelicidin and deficiency of cathelicidin might be secondary to vitamin D deficiency and be associated with the common cold and influenza.
Vitamin D deficiency has also been linked to muscular weakness and myalgia (muscle pain). Vitamin D deficiencies can sometimes be misdiagnosed as fibromylagia and vitamin D supplementation may lead to resolution of symptoms.
The use of some medication such as corticosteroids can alter vitamin D metabolism and reduce levels as does anticonvulsants, cimetidine, theophylline and orlistat; whereas medications such as diuretics and statins can increase levels. Patients on medication should be monitored for 25-hydroxy vitamin D3 when taking in excess of 2000 IUs.
Vitamin D deficiency is also a common finding in infants that are solely breastfed and who do not receive vitamin D supplementation and in adults, who have increased skin pigmentation, wear sunscreen or limit outdoor activities or keep covered up in sunlight.
Sunscreens efficiently absorb UVB radiation with factor 8 reducing cutaneous production of previtamin D3 by 95% and factor 15 by 99%. Melanin, a pigment produced in sunlight, is a natural sunscreen that developed to protect humans from blistering solar radiation. People with dark skin pigmentation, therefore are less efficient than white skin at producing vitamin D and require 10-50 times the exposure to sunlight than a white person. Cutaneous vitamin D production is absent early and late in the day and during the winter months or where the skies are polluted or cloudy. Aging decreases the amount of vitamin D produced in the skin by 75% by the age of 70 years but can still achieve increased blood concentrations of vitamin D3 through exposure to sunlight.Obesity is also associated with vitamin D deficiency, as vitamin D is deposited in body fat stores and is non-bioavailable.
Depending on latitude, hour of the day and other factors such as an individual’s age, 20 minutes of sun exposure may produce up to 20,000 units of vitamin D, which may be sufficient to supply sufficient levels for an adult for 25 days, which is equivalent to 200 glasses of milk.Toxicity from excessive sun exposure has not been found and this is probably due to the skins ability to regulate levels.
Cancer Research UK advises that individuals should stay below their sunburn threshold to minimise the risk of skin cancer, but state that exposing the skin during the summer months during the midday sun (11 am until 3 pm) for short periods without burning stimulates vitamin D synthesis.
Deficiency is widespread and may partly be due to recommendations to use sunscreen and avoid sun exposure.Window glass in homes and cars and clothing effectively block UVB radiation even in summer.The recommended daily intake is insufficient in the absence of sunlight and requires a minimum of 1000 IU vitamin D per day to maintain a healthy concentration of 25-hydroxy vitamin D3 (its active form) in the blood and could require as much as 7000 IU.
Obtaining and properly interpreting a serum 25 hydroxy-vitamin D3 level is the only way to be sure to know what the levels are. Testing should be carried out twice per year, at the end of summer for a peak level and early spring and can be done via www.vitamindtest.org.uk. Supplementing may require testing at more regular intervals until you are in the optimal range and to monitor levels. The reference range (37.5 to 50 nmol/L) may be insufficient and evidence points to a value closer to 80 or 90 nmol/L.  Toxicity is possible with oral supplementation, however, toxicity is rare.The amount of vitamin D needed varies depending on body weight, body fat, age, skin colour, season, latitude and sun exposure.For every 15 kg of body weight, 1000 IU may be needed and patients with serious diseases may require more.
Vitamin D and toxicity
In chronic toxicity, urine calcium and then serum calcium will begin to increase when 25 hydroxy vitamin D3 exceed 150 ng/mL and is associated with hypercalcemia, resulting in calcification of the internal organs, especially the kidneys. However, most people would have to take in excess of 10,000 IUs per day for many months. Full recovery is possible on stopping vitamin D and with strict sun-avoidance.
Check out your vitamin D levels www.vitamindtest.org.uk
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