Toxicity of vitamin

The chronic toxicity of viteimin A is a more general cause for concern prolonged emd regular inteike of more them about 7,500 to 9,000 / g per day by adults (and significantly less for children) causes signs and symptoms of toxicity affecting  

The skin excessive dryness, seeding emd chapping of the skin, desquamation, and alopecia. 

The central nervous system headache, nausea, ataxia, emd emorexia, edl eissociated with increased cerebrospinal fluid pressure. 

The liver hepatomegedy, hyperlipidemia, emd histological changes in the liver, including increased collagen formation. Alcohol potentiates the hepatotoxicity of vitamin A. 

Prudent upper levels of habitutd intake of retinol tne shown in Table 2.5. 

Bones joint pains, thickening of the long bones, hypercalcemia, and calcification of soft tissues, but with reduced bone mineral density. High intakes of vitamin A are associated with an increased rate of loss of bone mineral density with age, and some studies have shown that intakes above 1,500 /xg per day are associated with increased incidence of osteoporosis and hip fracture, although other studies have not shown any relationship between vitamin A intake and osteoporosis (Institute of Medicine, 2001). At high levels of intake, vitamin A both stimulates bone 

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Toxicity of vitamin K has not been well defined. Jaundice may occur in a newborn if large dosages of vitamin K are given to the mother before birth. Although kemicterus may result, this can be prevented by using vitamin K. 

Vitamin E (a-tocopherol) is most abundantly available in wheat germ oil and in small quantities in cereals, nuts, spinach, and egg yolk. Deficiency of vitamin E normally does not occur. Large doses of vitamin E are used to reduce the toxicity of vitamin A. Prolonged use causes delay in wound healing but significant... 

Table 1.10 Toxicity of Vitamins Upper Limits of Habituai Consumption and Toierabie Upper Limits of intake...

Guldager (1936) measured the toxicity of vitamin D in a large number of experiments on rats on a good Ca and P diet and found the borderline dose in growing rats to be between 300 and 700 I.U. daily. When 700 I.U. were administered, calcium-salt precipitates were observed in the kidneys without exception. 

Nieman and Obbink (1954) have provided an extensive review of the subchronic toxicity of vitamin A preparations and of retinol that appeared in the literature up to the early 1950s. The studies described were carried out in a variety of animal species but primarily in the rat dosages ranged from 3 to 180 mg retinol equivalents/day and the duration of treatment varied from a few days to several weeks. 

De Francisco A, Chakraborty J, Chowdhury HR, Yunus M, Baqui AH, Siddique AK, Sack RB. Acute toxicity of vitamin A given with vaccines in infancy. Lancet 1993 342(8870) 526-7. 

In the experiments of Stamler (1956) experimental toxemia was produced in rats on a diet containing 5 % cod liver oil, with about 100 I.U. per gram of vitamin D. This dose is about ten times as high as is used in normal rat rations. As cod liver oil contains some highly unsaturated fatty acids which possibly have a toxic effect and may aggravate an essential fatty acid deficiency, one cannot be certain which of these two dietary factors is the more essential for the toxemic effect. Sinclair (1957, 1958a) demonstrated a greater toxicity of vitamin D when the rats were deficient in essential unsaturated fatty acids. 

The toxicity of vitamin C is very low and doses of 10 g/day appear to be quite safe. The major concern at high doses is the risk of the formation of calcium oxalate kidney stones and it might be wise not to take calcium supplements with vitamin C. The increase of oxalate levels, even at high doses, only increases by about 50%. The evidence for rebound effects where, following withdrawal of high-dose therapy, vitamin C levels fall and for in vivo mutagenicity is not conclusive. The worst effects of vitamin C at high dose appear to be GI disturbances and diarrhoea. 

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