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Retinol, the dietary form of vitamin A, is a fat-soluble, antioxidant vitamin important in vision and bone growth. It belongs to the family of chemical compounds known as retinoids. Retinol is ingested in a precursor form; animal sources (milk and eggs) contain retinyl esters, whereas plants (carrots, spinach) contain pro-vitamin A carotenoids. Hydrolysis of retinyl esters results in retinol while pro-vitamin A carotenois can be cleaved to produce retinal. Retinal, also known as retinaldehyde, can be reversibly reduced to produce retinol or it can be irreversibly oxidized to produce retinoic acid. The best described active retinoid metabolites are 11-cis-retinal and the all-trans and 9-cis-isomers of retinoic acid.
In 1913, Elmer McCollum, a biochemist at the University of Wisconsin, and colleague Marguerite Davis identified a fat-soluble nutrient in butterfat and cod liver oil, which they named "fat-man factor A". Their work confirmed that of Thomas Osborne and Lafayette Mendel, at Yale, which suggested a fat-soluble nutrient in butterfat, also in 1913.[1] Vitamin A was first synthesized in 1947.
Dietary intake
During the absorption process in the intestines, retinol is incorporated into chylomicrons as the ester form, and it is these particles that mediate transport to the liver. Liver cells (hepatocytes) store vitamin A as the ester, and when retinol is needed in other tissues, it is de-esterifed and released into the blood as the alcohol. Retinol then attaches to a serum carrier, retinol binding protein, for transport to target tissues. A binding protein inside cells, cellular retinoic acid binding protein, serves to store and move retinoic acid intracellularly. Carotenoid bioavailability ranges between 1/5 to 1/10 of retinol's. Carotenoids are better absorbed when ingested as part of a fatty meal. Also, the carotenoids in vegetables, especially those with tough cell walls (e.g. carrots), are better absorbed when these cell walls are broken up by cooking or mincing.
Topical use
All forms of vitamin A are used in cosmetic and medical applications applied to the skin.
Retinoic acid, retinyl palmitate, isotretinoin, tretinoin and retinol are all used medicinally as a topical treatment for acne and keratosis pilaris.
In cosmetics, vitamin A derivatives are used as so-called antiaging chemicals- vitamin A is absorbed through the skin and increases the rate of skin turnover, and gives a temporary increase in collagen giving a more youthful appearance.
Vitamin A deficiency
Vitamin A deficiency is common in developing countries but rarely seen in developed countries. Approximately 250,000 to 500,000 malnourished children in the developing world go blind each year from a deficiency of vitamin A. Night blindness is one of the first signs of vitamin A deficiency. Vitamin A deficiency contributes to blindness by making the cornea very dry and damaging the retina and cornea.
Vitamin A deficiency diminishes the ability to fight infections. In countries where children aren't immunized, infectious disease like measles have relatively higher fatality rates. Subclinical deficiency can also be a problem as it may increase children's risk of developing respiratory and diarrheal infections, decrease growth rate, slow bone development, and decrease likelihood of survival from serious illness. Iron deficiency can also affect vitamin A uptake.
Excess alcohol consumption can deplete vitamin A, however a stressed liver may be more susceptible to vitamin A toxicity. People that consume large amounts of alcohol should seek medical advice before taking vitamin A supplements.
Vitamin A overdose
Too much vitamin A can be harmful or fatal. The body converts the dimerized form, carotene, into vitamin A as it is needed, therefore high levels of carotene are not toxic compared to the ester (animal) forms. The livers of certain animals, especially those adapted to polar environments, often contain amounts of vitamin A that would be toxic to humans. The first documented death due to vitamin A poisoning was Xavier Mertz, a Swiss scientist who died in January 1913 on an Antarctic expedition that had lost its food supplies and fell to eating its sled dogs. Mertz consumed lethal amounts of vitamin A by eating the dogs' livers. The liver of the polar bear also has enough vitamin A to kill a human being, or enough to make even sled dogs very ill.
Excess vitamin A has also been suspected to be a contributor to osteoporosis. This seems to happen at much lower doses than those required to induce acute intoxication. Only preformed vitamin A can cause these problems, because the conversion of carotenoids into vitamin A is downregulated when physiological requirements are met. An excessive uptake of carotenoids can, however, cause carotenosis.
The carotenoid beta carotene was interestingly associated with an increase in lung cancer when it was studied in a lung cancer prevention trial in male smokers. In non-smokers, the opposite effect has been noted.
Although cases of vitamin A toxicity have been reported in arctic explorers and some people taking large doses of synthetic vitamin A for long periods of time, pregnant women require large amounts of vitamin A from preferably natural animal sources, such as liver, raw (non-pasteurized) butter, and cod liver oil. However excess in retinoid form must at all costs be avoided due to its well known teratological effects.
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