3,7-Dimethyl-9-(2,6,6-trimethyl-1-cyclohexenyl)-2,4,6,8-nonatetraen-1-ol, Axerophthol, Retinol solution, Vitamin A alcohol solution, Vitamin A1, all-trans-Retinol, Retinol solution
NHU / China
BASF / German
DSM / Nederland
ADISSEO / France
ZMC / China
KINGDOMWAY / China
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Retinol, also known as Vitamin A1, is a vitamin found in food and used as a dietary supplement. As a supplement it is used to treat and prevent vitamin A deficiency, especially that which results in xerophthalmia. In areas where deficiency is common a single large dose is recommended to those at high risk a couple of times a year. It is also used to prevent further issues in those who have measles. It is used by mouth or injection into a muscle.
Retinol at normal doses is well tolerated. High doses may result in an enlarged liver, dry skin, or hypervitaminosis A. High doses during pregnancy may result in harm to the baby. Retinol is in the vitamin A family. It or other forms of vitamin A are needed for eyesight, maintenance of the skin, and human development. It is converted in the body to retinal and retinoic acid through which it acts. Dietary sources include fish, dairy products, and meat.
Retinol was discovered in 1909, isolated in 1931, and first made in 1947. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system. Retinol is available as a generic medication and over the counter. The wholesale cost in the developing world is about 0.02 to 0.30 USD per 50,000 units. In the United States it is not very expensive.
Retinol is used to treat vitamin A deficiency.
Three approaches may be used when populations have low vitamin A levels :(A) through dietary modification involving the adjustment of menu choices of affected persons from available food sources to optimize vitamin A content, (B) enriching commonly eaten and affordable foods with vitamin A, a process called fortification. It involves addition of synthetic vitamin A to staple foods like margarine, bread, flours, cereals and other infant formulae during processing and (C) giving high-doses of vitamin A to the targeted deficient population, a method known as supplementation.
See also: Hypervitaminosis A
The Tolerable Upper Intake Level (UL) for vitamin A, for a 25-year-old male, is 3,000 micrograms/day, or about 10,000 IU.
Too much vitamin A in retinoid form can be harmful or fatal, resulting in what is known as hypervitaminosis A. 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 such as polar bears and seals, often contain amounts of vitamin A that would be toxic to humans. Thus, vitamin A toxicity is typically reported in Arctic explorers and people taking large doses of synthetic vitamin A. The first documented death possibly caused by 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 may have consumed lethal amounts of vitamin A by eating the dogs' livers.
Vitamin A acute toxicity occurs when an individual ingests vitamin A in large amounts more than the daily recommended value in the threshold of 25,000 IU/kg or more. Often, the individual consumes about 3–4 times the RDA's specification. Toxicity of vitamin A is believed to be associated with the intervention methods used to upgrade vitamin A levels in the body such as food modification, fortification and supplementation, all of which are employed to combat vitamin A deficiency Toxicity is classified into two categories: acute and chronic toxicities. The former occurs few hours or days after ingestion of large amounts of vitamin A accidentally or via inappropriate therapy. The later toxicity (Chronic) takes place when about 4,000 IU/kg or more of vitamin A is consumed for a prolonged period of time. Symptoms associated with both toxicities include nausea, blurred vision, fatigue, weight-loss, menstrual abnormalities etc.
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.
Dietary supplementation with β-carotene was 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.
Excess preformed vitamin A during early pregnancy has also been associated with a significant increase in birth defects. These defects may be severe, even life-threatening. Even twice the daily recommended amount can cause severe birth defects. The FDA currently recommends that pregnant women get their vitamin A from foods containing β-carotene and that they should ensure that they consume no more than 5,000 IU of preformed vitamin A (if any) per day. Although vitamin A is necessary for fetal development, most women carry stores of vitamin A in their fat cells, so over-supplementation should be strictly avoided.
A review of all randomized controlled trials in the scientific literature by the Cochrane Collaboration published in JAMA in 2007 found that supplementation with β-carotene or vitamin A increased mortality by 5% and 16%, respectively.
Contrary to earlier observations, recent studies emerging from some developing countries (India, Bangladesh and Indonesia) have strongly suggested that in populations in which vitamin A deficiency is common and maternal mortality is high, dosing expectant mothers can greatly reduce the maternal mortality rate. Similarly, dosing newborn infants with 50,000 IU (15 mg) of vitamin A within two days of birth, can significantly reduce neonatal mortality.
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