Vitamin A deficiency
Vitamin A deficiency exists when the chronic failure to eat sufficient amounts of vitamin A or beta-carotene results in levels of blood-serum vitamin A that are below a defined range. Beta-carotene is a form of pre-vitamin A, whichis readily converted to vitamin A in the body. Night blindness is the firstsymptom of vitamin A deficiency. Prolonged and severe vitamin A deficiency can produce total and irreversible blindness.
Vitamin A (called retinol in mammals) is a fat-soluble vitamin. The recommended dietary allowance (RDA) for vitamin A is 1.0 mg/day for the adult man and0.8 mg/day for the adult woman. Since beta-carotene is converted to vitamin Ain the body, the body's requirement for vitamin A can be supplied entirely by beta-carotene. Six mg of beta-carotene are considered to be the equivalentof 1 mg of vitamin A. The best sources of vitamin A are eggs, milk, butter, liver, and fish, such as herring, sardines, and tuna. Beef is a poor source ofvitamin A. Plants do not contain vitamin A, but they do contain beta-carotene and other carotenoids. The best sources of beta-carotene are dark-green, orange, and yellow vegetables; spinach, carrots, oranges, and sweet potatoes are excellent examples. Cereals are poor sources of beta-carotene.
Vitamin A is used for two functions in the body. Used in the eye, it is a component of the eye's light-sensitive parts, containing rods and cones, that allow for night-vision or for seeing in dim-light circumstances. Vitamin A (retinol) occurs in the rods. Another form of Vitamin A, retinoic acid, is used in the body for regulating the development of various tissues, such as the cells of the skin, and the lining of the lungs and intestines. Vitamin A is important during embryological development, since, without vitamin A, the fertilized egg cannot develop into a fetus.
Vitamin A deficiency occurs with the chronic consumption of diets that are deficient in both vitamin A and beta-carotene. When vitamin A deficiency existsin the developed world, it tends to happen in alcoholics or in people with diseases that affect the intestine's ability to absorb fat. Examples of such diseases are celiac disease (chronic nutritional disorder), cystic fibrosis, and cholestasis (bile-flow failure or interference). Vitamin A deficiency occurred in infants during the early 1900s in Denmark. The deficiency resulted when milk fat was made into butter for export, leaving the by-product (skimmedmilk) for infant feeding. Vitamin A deficiency has taken place in infants inimpoverished populations in India, where the only foods fed to the infants were low in beta-carotene. Vitamin A deficiency is also common in areas like Southeast Asia, where polished rice, which lacks the vitamin, is a major part of the diet.
The earliest symptom of vitamin A deficiency is night blindness. Prolonged deficiency results in drying of the conjunctiva (the mucous membrane that linesthe inner surface of the eyelids and extends over the forepart of the eyeball). With continued vitamin A deficiency, the drying extends to the cornea (xerophthalamia). The cornea eventually shrivels up and becomes ulcerated (keratinomalacia). Superficial, foamy gray triangular spots may appear in the whiteof the eye (Bitot's spots). Finally, inflammation and infection occur in theinterior of the eye, resulting in total and irreversible blindness.
Vitamin A status is measured by tests for retinol. Blood-serum retinol concentrations of 30-60 mg/dl are considered in the normal range. Levels that fallbelow this range indicate vitamin A deficiency. Night blindness is measured by a technique called electroretinography. Xerophthalamia, keratinomalacia, and Bitot's spots are diagnosed visually by trained medical personnel.
Vitamin A deficiency can be prevented or treated by taking vitamin supplements or by getting injections of the vitamin. The specific doses given are oralretinyl palmitate (110 mg), retinyl acetate (66 mg), or injected retinyl palmitate (55 mg) administered on each of two successive days, and once a few weeks later if symptoms are not relieved.
The prognosis for correcting night blindness is excellent. Xerophthalamia canbe corrected with vitamin A therapy. Ulcerations, tissue death, and total blindness, caused by severe vitamin A deficiency, cannot be treated with vitamin A.
Vitamin A deficiency can be prevented by including foods rich in vitamin A orbeta-carotene as a regular component of the diet; liver, meat, eggs, milk, and dairy products are examples. Foods rich in beta-carotene include red peppers, carrots, pumpkins, as well as those just mentioned. Margarine is rich inbeta-carotene, because this chemical is used as a coloring agent in margarineproduction. In Africa, Indonesia, and the Philippines, vitamin A deficiencyis prevented by public health programs that supply children with injections of the vitamin.
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