Osteomalacia in adults and rickets in children occur as a result of vitamin D deficiency or from a disturbance in its metabolism (see Table 3.3). The frequency of occurrence depends on the distribution of the populations affected. In the nineteenth century nutritional rickets were endemic in industrial cities of Britain due to the poor diet and environmental conditions of children. As a result of effective public health measures privational rickets virtually disappeared from the UK by 1940 (Maxwell, 2001). However, in the 1960s low vitamin D status was found to be common among immigrant Asian children, adolescents and women living in the UK due to a combination of factors including the type of vegetarian diet, which was high in phytate from unleavened breads (see section 3.11), low calcium intake and limited exposure to sunlight. A striking reduction in Asian rickets occurred in Glasgow when free vitamin D supplements were introduced for children up to 18 years old (Smith, 2000).
The elderly, especially those over 75 years, may have 25-OHD levels less than 12 nmol/L during the winter months because they expose insufficient skin to the sun during the summer months. Fifteen elderly people, living at 37° latitude who formerly went outside infrequently, were studied over a 4 week period while spending 0, 15 and 30 minutes on a veranda exposing the face and legs to sunlight. At the end of the study period, plasma 25-OHD levels increased by
After nutritional vitamin D deficiency, coeliac and renal diseases are the most important causes of osteomalacia and rickets. In coeliac disease there is a patchy enteropathy of the gut which can potentially lead to fat malabsorption. The efficient absorption of fat is essential for the absorption of fat-soluble vitamins, thus in patients with inadequate sunlight exposure, vitamin D deficiency can occur. Patients with kidney diseases are also susceptible to vitamin D deficiency as the enzyme necessary to convert 25-OHD to the metabolically active vitamin D metabolite, 1,25-OHD, is located in the kidney.
A follow-up study in Finland of 10 821 people born in Oulu and Lapland in 1966 showed that those who received recommended supplements of vitamin D during their first year of life were 80% less likely to develop type 1 diabetes over the next 30 years. Type 1 diabetes is thought to be an autoimmune disease caused when immune system cells attack insulin-producing cells in the pancreas. Vitamin D is known to be an immune system suppressant and the authors believe that vitamin D might somehow inhibit this autoimmune reaction (Hypponen et al, 2001). Finnish children are less exposed to sunlight than those in more southerly countries, hence most receive vitamin D supplements. It is also suggested that mothers' worries over UV exposure and skin cancer may also be contributing to world-wide increases in type I diabetes. There is evidence that parents are restricting children's exposure to sunlight by using more sun-screen than previously and this might have played a part. Early infections with enterovirus and childhood obesity were also associated with increased risks of type 1 diabetes (Hypponen et al, 2001). Nevertheless, none of the above explains the molecular role in the pathogenesis of type 1 diabetes and more work is needed in the area.
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