Vitamin D can be obtained from either the diet or from the sun. Good dietary sources of vitamin D are limited to those of animal origin, with the main source being the oils of fish. The animal form of vitamin D is called cholecalciferol. Vegetables do produce and contain vitamin D, but levels are generally low and the bioavailability of the plant form of vitamin D, ergocalciferol, is not as high for cholecalciferol. A much more reliable and efficient way of obtaining vitamin D is though the conversion of cholesterol to vitamin D in the skin. This reaction is catalysed by the ultraviolet light from the sun, and so regular sun exposure is required in order to allow subcutaneous vitamin D production. Living at high latitudes therefore increases the risk of vitamin D deficiency because dietary sources of vitamin D are limited and sun strength is too weak in the winter months. As a result many individuals living at high latitudes obtain insufficient vitamin D between autumn and spring.
Generally it is recognised that many individuals living in Western Europe and North America suffer from insufficient vitamin D status. Sun exposure is discouraged during the summer, and many therefore do not undergo any significant sun exposure. Vitamin D levels therefore never recover from their nadir in the winter months and as a result a semi-permanent vitamin D status is present in large numbers of individuals. Increasingly, poor vitamin D status is being linked to a number of diseases, particularly relating to the immune system and blood glucose control. This is because in its role as a hormone, vitamin D is required for the correct function of insulin and for correct immune function. Vitamin D deficiency may also cause elevations in parathyroid hormone, because vitamin D metabolism is regulated by parathyroid hormone. Parathyroid hormone excess may in turn affect subchondral bone formation and this may result is poor remodelling of joint tissue, particularly the cartilage.
One group of researchers1 has investigated the association between serum levels of 25-hydroxyvitamin D and levels of parathyroid hormone, separately and in combination, with the progression of knee osteoarthritis in middle aged and elderly subjects. The mean concentration of 25-hydroxyvitamin D was only 26.2 ng/mL (a level that would indicate vitamin D insufficiency) and 16 % of the subjects had serum 25-hydroxyvitamin D levels below 15 ng/mL (a level which would indicate a clinical vitamin D deficiency). Subjects with vitamin D levels below 15 ng/mL had a 2-fold increased risk of knee osteoarthritis progression compared to subjects with 25-hydroxyvitamin D concentrations above 15 ng/mL. Parathyroid hormone levels were not associated with osteoarthritis progression rates individually. However, high parathyroid hormone levels (above 73 pg/mL) in combination with a vitamin D deficiency was associated with a 3-fold increased risk of osteoarthritis progression.
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