Vitamin D deficiency in children on the rise…

So, what is vitamin D and what does it do…

Dietary sources of vitamin D is found only in a few natural foods such as fatty fish (e.g. herring and mackerel), liver, milk and eggs being the main sources. Vegetables, fruits and nuts do not contain detectable amounts of Vitamin D. In the UK all margarines, some processed milks and some breakfast cereals are fortified with Vitamin D.

Vitamin D is formed in skin through the action of ultraviolet light, which catalyses the synthesis of vitamin D3 from 7-dehydrocholesterol.  Vitamin D2 is formed by ultraviolet light-induced conversion of ergosterol from plants, fungi and lower life forms.

Both vitamin D3 and D2 are used in a number of food supplements, including fish oil products. And amounts range from 2.5 to 12.5 mcg per day.


The hormonal metabolite of vitamin D regulates calcium and phosphate metabolism  via three target tissues: small intestine, bone and kidney.  In the small intestine, parathyroid hormone/vitamin D regulates calcium uptake from the gut.  In the kidney, this active form of vitamin D regulates calcium resorption in the proximal tubule.  Vitamin D has a role in the maintenance of the mechanical integrity and structure of the skeleton. Vitamin D is involved in the maintenance of plasma calcium levels via bone resorption and formation.

Consequences of deficiency:

Prolonged vitamin D deficiency during periods of bone growth in children results in “rickets”.  In the UK, the prevalence of rickets was substantially diminished following the mandatory fortification of margarine and the introduction of modified cows milk powder fortified with vitamin D. The signs of rickets include pigeon chest, bowed femurs and separated knees.  In adults, osteomalacia – the defective mineralisation of the bone – may be due  vitamin D deficiency or impaired vitamin D formation.

Reported beneficial effects:

Vitamin D metabolites have been reported to induce cell differentiation and reduce cell proliferation, and hence it has been suggested that they could protect against both prostate and colon cancers on the basis of these to in vitro observations as well as epidemiological evidence.  There is also some evidence that vitamin D supplementation may be of potential benefit in the treatment of the autoimmune disease rheumatoid arthritis, in the inhibition of the progression of multiple sclerosis, the amelioration of symptoms of inflammatory bowel disease and the decreased risk of bone loss and fracture incidence in older women.

Absorption, distribution, metabolism and excretion:

Vitamin D is absorbed from the small intestine in association with lipids and circulated in the body via the lymph. Vitamin D int he plasma (either from diet or skin) is bound to a protein synthesised in the liver, vitamin D-binding protein (DBP), for transport to the liver – the main site of metabolic activation or vitamin D3.  A portion of all the vitamin D reaching the liver is 25-hydroxylated and release into the circulation.  Thus, circulating levels of 25-(OH) – vitamin D, the principle circulating metabolite, are under homeostatic control and are proportional to the size of the liver stores.  Vitamin D absorption is not affected by vitamin D status.

Adverse effects of excessive consumption:

Excess vitamin D may lead to hypercalaemia and hypercalciuria, which results in the deposition of calcium in soft tissues (e.g. kidney, bronchi and arteries), diffuse deminerlisation of bones and irreversible cardiovascular adverse effects.  It has been suggested that excess vitamin D may be linked to heart disease but there is limited evidence for this association.  Vitamin D at moderate levels of intake may facilitate renal stone formation in individuals who are predisposed.

Vitamin D2 and D3 are assumed to have equal levels of efficacy and adverse effects in humans.  In animals, excess vitamin D caused hypercalcaemia and adversely  affects the reproductive performance in rodents and rabbits.

Taken from: Vitamins and Minerals – An overview of benefits and safety. Dr. Derek Shrimpton and Professor David Richardson. Commissions by the  HFMA (Health Food Manufacturers’ Association). 2003.



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