Vitamin A- Benefits, Deficiency Symptoms And Food Sources
Alternative names :- Beta carotene, Retinol
A growth factor present in fat was demonstrated independently by two groups in 1913: McCollum and Davis, and Osborne and Mendel. Later, Goldblatt and Zilva found two factors in cod-liver oil: one, now known as vitamin A, was easily inactivated by heat in the presence of air, while the other, now known as vitamin D, was more resistant to heat. They also showed that the growth-promoting factor in spinach, provitamin A or carotene, did not prevent rickets.
Vitamin A and carotene can be obtained from either animal or vegetable sources. The animal form is divided between retinol and dehydroretinol whereas the vegetable carotene can be split into four very potent groups - alpha-carotene, beta-carotene, gamma-carotene and crypto-carotene. With enough beta-carotene available in the body, the body can manufacture its own vitamin A.
Benefits and functions of Vitamin A
Vitamin A is an anti-oxidant, a compound that may protect against disease by neutralizing unstable oxygen molecules, called free radicals , within the body. Vitamin A is absorbed as retinyl ester along with fat from the proximal small intestine. The absorption is more rapid in men than in women. A lower plasma response to retinylesters in women may be due to a more efficient chylomicron remnant cIearance. Commercially available water-dispersible forms of oral vitamin A are absorbed independent of fat absorption.
Vitamin A is poorly absorbed during diarrhea. Absorption is also decreased with intestinal roundworm, hookworm and Giardia lamblia infestations. Oral administration of non-absorbable mineral oils, like liquid paraffin, dissolves vitamin A which is then excreted unabsorbed.
Beta carotene absorption increases with high fat diet. Dividing the beta carotene daily dose into three meals (instead of one) enhances absorption without increasing dietary fat. It may also reduce breast cancer.
Recommended dosage of Vitamin A
The Recommended Dosage for vitamin A are :-
Deficiency symptoms of Vitamin A
Experimental deficiency is produced when the diet is deficient in both retinol and carotene. The resulting hyperkeratosis and impaired dark adaptation are corrected by 150 micrograms of retinol or.300 micrograms of beta carotene.
Deficiency occurs when the intake of vitamin A, or its precursor carotene, is poor. It is common in economically less-privileged countries, especially in children, due to inadequate intake. This is aggravated by a low-protein diet which reduces the synthesis of retinol-binding protein. Mothers in these countries should be encouraged to breastfeed their children for at least two years, with the addition of good quality weaning food at about 4-6 months. Vitamin A deficiency is also known to occur in well-to-do families with plentiful food, where the children refuse to eat vegetables and fruits.
Vitamin A deficiency is seldom seen in isolation. A child supplemented with vitamin A also needs protection from nutritional deficiency. Green leafy foods are rich sources, not only of carotene but also of vitamin C, iron, folic acid and calcium. All these are deficient among developing country populations.
Deficient fat ingestion- may impair carotene absorption. Intestinal malabsorption, fatty diarrhea, and habitual intake of liquid paraffin cause vitamin A deficiency. In advanced liver disease, such as cirrhosis of the liver-and biliary obstruction, there is vitamin A deficiency. Alcoholic liver injury depletes vitamin A stores in the liver.
Food sources of Vitamin A
The ultimate source of the vitamin A is carotene. The carotene content is high in green vegetables (spinach), yellow vegetables (carrots, tomatoes). and yellow. fruits (papaya, mangoes). It is difficult to calculate the carotenoid content, which is determined by the degree of ripening of fruits or vegetables and the method of storage and preparation. The content increases considerably with stages of ripening. Carotenoids in mango total 12.5 g per 100 g fresh pulp; about 60% is present as beta carotene, which is higher than in any other fruit.
Commercial vitamin A is extracted from the livers of fish like the shark, and from cod and halibut in colder regions. Halibut-liver oil is the richest source of vitamin A, containing 200 micrograms (700 IU; 0.7 micromol) per drop, while a teaspoon each of cod and shark-liver oil contains 600 micrograms (2000 IU; 2.2 micromol) and 300 micrograms (1000 IU; 1.1 micromol), respectively.
Hypervitaminosis A occurs with massive intake of vitamin A. It has occurred in explorers eating the livers of fish (halibut) or polar bears, and in those consuming 100-150 ml of halibut-liver oil. Toxicity occurs with consumption of 25,000-50,000 IU/day for several months, occurring earlier in people who have deranged liver function, and low serum albumin and retinol-binding protein, as also in those taking alcohol. Circulating retinol esters dissolved in lipids (and not in retinol-binding protein) are injurious to cell membranes.
Even the recommended dose of 500 IV daily may result in liver toxicity. Emulsified vitamin A is more toxic than the conventional form. Excessive carotene is not injurious and does not cause hypervitaminosis.
Early evidence of vitamin A toxicity includes loss of appetite, nausea, vomiting, irritability, fatigue, weight loss, inflammation and cracking of lips, dry skin, desquamation, itching, and hair loss. Later, it results in enlargement of the liver and spleen, with jaundice, ascites (water in the peritoneal cavity), esophageal varices (distended veins) which may bleed, and increased transaminases. Headache, subcutaneous swelling, pain in joints and bones, and tenderness of long bones may occur; high serum calcium may be noted.
In children there is premature closure of the epiphyses, stunted growth, and raised intracranial pressure that mimics brain tumor; this may progress to hydrocephalus. Congenital deformities occur if high doses are administered during pregnancy.
Serum retinyl esters may be raised, but almost half the affected patients have normal levels. Liver biopsy may show fatty changes and cirrhosis; those with milder liver damage improve when vitamin A is discontinued.
The toxic symptoms of hypervitaminosis A disappear on stopping vitamin A administration.
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