Vitamin A, deficiency

In this period, the empirical healing of certain diseases by foods was estabUshed. Examples (3) were the treatment of night blindness (vitamin A deficiency) with hver ia many cultures over centuries, of beriberi (vitamin deficiency) by use of unpoHshed rice by the Japanese navy, of scurvy (vitamin C deficiency) by citms fmits ia the British navy or piae needle extracts by North American natives, and pellagra (niacia deficiency) by a dietary shift away from corn-based foods ia many countries. Other, nondietary empirical treatments iavolved, eg, exposure of children ia northern latitudes to sunlight to cute tickets (vitamin D deficiency) (4). 

Biological, spectroscopic, and chromatographic methods have been used to assay vitamin A and the carotenoids. Biological methods have traditionally been based on the growth response of vitamin A—deficient rats. The utiUty and shortcomings of this test have been reviewed (52,53). This test has found apphcabiUty for analogues of retinol (54,55). Carotenoids that function as provitamin A precursors can also be assayed by this test (56). 

In humans, vitamin A deficiency manifests itself in the following ways night blindness, xerophthalmia, Bitot s spots, and corneal involvement and ulceration. Changes in the skin have also been observed. Although vitamin A deficiency is seen in adults, the condition is particularly harmful in the very young. Often, this results from malnutrition (56). 

On a vitamin A-deficient diet, mucus-secreting tissues become keratinized. This condition tends to occur in the trachea, the skin, the saUvary glands, the cornea, and the testes. When this occurs in the cornea, it can be followed by blindness. Vitamin A deficiency is the principal cause of blindness in the very young. This problem is particularly acute in the third world (8). 

A deficiency of this vitamin caused by a low dietary intake of vitamin B12 is rare because the vitamin is found in meats, milk, eggs, and cheese. The body is also able to store this vitamin a deficiency, for any reason, will not occur for 5 to 6 years. 

Anand et al. 1987). The authors hypothesized that the ocular effects associated with endosulfan may be a result of prolonged hypertension (although no data on blood pressure were presented, and there is no other information to indicate that chronically administered endosulfan induces hypertension) or an endosulfan-induced vitamin A deficiency (which was observed in this study). Although the rabbit may represent a uniquely sensitive species, the possibility that long-term exposure of persons at hazardous waste sites to endosulfan may result in adverse effects on ocular tissues cannot be eliminated. 

Some hydroxy metabolites of coplanar PCBs, such as 4-OH and 3,3 4,5 -tet-rachlorobiphenyl, act as antagonists of thyroxin (Chapter 6, Section 6.2.4). They have high affinity for the thyroxin-binding site on transthyretin (TTR) in plasma. Toxic effects include vitamin A deficiency. Biomarker assays for this toxic mechanism include percentage of thyroxin-binding sites to which rodenticide is bound, plasma levels of thyroxin, and plasma levels of vitamin A. 

Vitamin A Deficiency Is a Major Public Health Problem Worldwide... 

The progeny, called Golden Rice , has received massive publicity for its potential to alleviate vitamin A deficiency in developing countries (Potrykus,... 

Patients with vitamin A deficiency may report visual disturbances, night blindness, and dry skin. 

Connective tissue disease Substance abuse Stevens-Johnson syndrome Immunocompromised Atopic dermatitis Gonococcal infection Vitamin A deficiency... 

Iron-deficiency anaemia results from a discrepancy between iron availability and the amount required for production of red blood cells. The causes of acquired iron deficiency in so-called underdeveloped and developed countries must be differentiated. In underdeveloped countries, the main causes of iron deficiency are (a) the poor availability of iron in the diet due to low haem and high fibre and phytate content (D Souza et ah, 1987), and (b) chronic blood loss due to hookworm, schistosomiasis and malaria (Stoltzfus et ah, 1997 Olsen et ah, 1998 Dreyfuss et ah, 2000). Inflammation and vitamin A deficiency often interfere with the above causes of iron deficiency, causing a mixed type of anaemia. In underdeveloped countries diet improvement, iron fortification of natural foods and eradication of parasites will have a much higher impact than will refinement of diagnostic procedures and therapy of iron-deficiency anaemia. 

Vitamin A deficiency affects more than 100 million children around the world (Miller and others 2002) and thus remains an important public health problem in many countries. Vitamin A is essential for vision, reproduction, growth, immune function, and general health of humans (van Lieshout and others 2001). The major sources of vitamin A in the human diet are retinyl esters (preformed vitamin A) found in foods of animal origin and provitamin A carotenoids from fruits and vegetables. Unfortunately, foods containing preformed vitamin A (meat, milk, eggs, etc.) are frequently too expensive for some economically deprived developing countries, and therefore dietary carotenoids are the main source of vitamin A in these countries. 

McGowan SE. 2007. Vitamin A deficiency increases airway resistance following C-fiber stimulation. Respir Physiol Neurobiol 157 281-289. 

Miller M, Humphrey J, Johnson E, Marinda E, Brookmeyer R and Katz J. 2002. Why do children become vitamin A deficient J Nutr 132 2867-2880. 

Chhabra, A. and S.P. Arora. 1989. Histological alterations in certain tissues of goats fed zinc- and vitamin A-deficient diets. Indian Jour. Anim. Sci. 59 1045-1048. 

P2a. Peck, S. M., Chargin, L., and Sobotka, H., Keratosis follicularis (Darier s disease). A vitamin A deficiency disease. Arch. Dermatol, and Syphilol. 43, 223-229 (1941). 

Williams RJ, Pelton RB. Individuality in nutrition effects of vitamin A-deficient and other deficient diets on experimental animals. Proceedings of the National Academy of Sciences USA 1966 55 12634. 

Here is a case in which too much of a good thing is not a good thing. Excess vitamin A is toxic, particularly to the liver. The UL is 3 mg/day for adult men and women, only three or four times greater than the RDIs. Most health food stores sell P-carotene supplements. Unless you have reason to believe that you are at risk of vitamin A deficiency, there is no reason to use these supplements. 

A deficiency of vitamin A results in night blindness. A chronic deficiency results in a thickening of membranes in the cornea which, if untreated, can lead to blindness through perforation of the cornea and loss of the lens. It is estimated that half a million children develop blindness due to vitamin A deficiency every year. Refeeding malnourished children can produce a deficiency of vitamin A (see below). 

Very low reserves of vitamin A. This leads to an important effect of refeeding. The requirement for vitamin A increases when the children are supphed with protein so that they can quickly become vitamin A deficient, resulting in blindness (see above). Hence, the vitamin must be administered with the protein. 

Vitamin A is essential for growth and development of cells and tissues. In its active form, retinoic acid (RA), it controls the regular differentiation as a ligand for retinoic acid receptors (RAR, RXR) and is involved in the integration (gap junction formation) of cell formations (Biesalski, 1996 Biesalski et al, 1999). Vitamin A plays a substantial role, especially in the respiratory epithelium and the lung. During moderate vitamin A deficiency, the incidence for diseases of the respiratory tract is considerably increased and repeated respiratory infections can be influenced therapeutically by a moderate vitamin A supplementation (Biesalski et ah, 2001 Greenberg et ah, 1997 John et ah, 1997). 

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