Vitamin D deficiency mainly causes two health problems namely rickets and osteomalacia. Other disorders due to vitamin D deficiency include bowed legs, skeletal deformation and rachitic rosary. Though vitamin D can be synthesized from sun light, the mounting evidence of skin cancer due to exposure to sunlight is forcing the general population and scientists alike to switch to dietary source of vitamin D.
Vitamin D deficiency is present even in developed countries including USA. The third National Health and Nutrition Examination Survey (NHANES III) has shown that in United States the vitamin D deficiency is prevalent throughout the nation.
The clinical manifestations of vitamin D may be due to deficient production of vitamin D in the skin, diets with low vitamin D content, increase loss of vitamin D, impairment in activation of vitamin D or resistance to effects of 1,25(OH)2D (1,25dihydroxycholecalciferol).
The causes of impaired vitamin D action may be due to:
- Vitamin D deficiency (diet with poor vitamin D content, mal absorption or less production of vitamin D in skin)
- increase loss of vitamin D (impaired enterohepatic circulation, increased metabolism due to drugs like rifampin, barbiturates and phenytoin)
- Target organ resistance (mutation of vitamin D receptors or drugs like phenytoin)
- impaired 1-alpha hydroxylation (renal failure, hypoparathyroidism, 1-alpha hydroxylase mutation, X-linked hypophosphatemic rickets, osteomalacia and antifungal drugs like ketokonazole)
- Impaired 25, hydroxylation (liver disease and drug like isoniazid).
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Excess intake of vitamin A for long duration can lead to vitamin A toxicity, unlike water-soluble vitamins, which do not have toxicity due to removal of excess water soluble vitamins through urine as they are water soluble. Vitamin A toxicity occurs when more than recommended daily allowance or RDA is taken for long time. The RDA of vitamin A for normal healthy adult is 600 mcg of retinol.
Vitamin A toxicity was first reported among Arctic explorers who ate liver of polar bear and vitamin A toxicity is also seen if it is given at very high dose of more than 150 mgs in adults and 100 mgs in children. The vitamin A toxicity is seen more commonly is Eskimos, because they eat polar bear liver and seal livers, both are very rich in vitamin A. the staple diet of Eskimo is made up of rich source of vitamin A.
Excess intake of vitamin A in the form of retinol or any other form can lead to nausea, vomiting, anorexia and sleep disturbances. These are followed by desquamation of skin, enlargement of the liver and papillar edema. Increased intracranial pressure, vertigo, diplopia, bulging fontanels in children, seizures, and exfoliative dermatitis are the common symptoms of vitamin A toxicity and in severe cases it may cause death. Other common symptoms include dry skin, cheilosis, glossitis, vomiting, alopecia, bone demineralization and pain, hypercalcemia, lymph node enlargement, hyperlipidemia, amenorrhea etc. The toxicity of vitamin A mainly occurs if excess amount of vitamin A is consumed for long time from animal sources. Excess plant vitamin A usually does not lead to severe toxicity. Excess beta carotene as found in carrots and other yellow vegetables can lead to yellow coloration of plasma and skin (called carotenemia), but this do not appear to be harmful or dangerous. But excess plant carotinoids should be avoided as it can increase chance of lung cancer in smokers. Hypothyroid patients are more susceptible to the development of carotenemia due to impaired breakdown of carotene to vitamin A. Reduction of carotenes from the diet results in the disappearance of skin yellowing and carotenemia over a period of 30–60 days in these patients. Read more…