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Vitamin A is an essential human nutrient. It exists not as a single compound, but in several forms. In foods of animal origin, the major form of vitamin A is an alcohol (retinol), but can also exist as an aldehyde (retinal), or as an acid (retinoic acid). Precursors to the vitamin (a provitamin) are present in foods of plant origin as some of the members of the carotenoid family of compounds.
Additional recommended knowledge
Discovery of vitamin A
The discovery of vitamin A stemmed from research dating back to 1908, indicating that factors other than carbohydrates, proteins, and fats were necessary to keep cattle healthy. By 1917 one of these substances was independently discovered by Elmer McCollum at the University of Wisconsin-Madison, and Lafayette Mendel and Thomas Osborne at Yale University. Since "water-soluble factor B" (Vitamin B) had recently been discovered, the researchers chose the name "fat-soluble factor A" (vitamin A).
Equivalencies of retinoids and carotenoids (IU)
Vitamin A intake is often expressed in international units (IU) or as retinol equivalents (RE), with 1 IU = 0.3 micrograms retinol. Because the production of retinol from provitamins by the human body is regulated by the amount of retinol available to the body, the conversions apply strictly only for vitamin A deficient humans. The absorption of provitamins also depends greatly on the amount of lipids ingested with the provitamin; lipids increase the uptake of the provitamin.
Recommended daily intake
Vitamin A US Dietary Reference Intake:
Vitamin A is found naturally in many foods. Each of the following contains at least 0.15 mg (which is equal to 150 micrograms -500 IU). See Recommended Daily Intake.) of Vitamin A or beta carotene per 1.75-7 oz. (50-200 g):
note: bracketed values are retinol equivalences and percentage of RDI per 100g.
One of the earliest manifestations of vitamin A deficiency is acne problems, and impaired vision, particularly in reduced light Night blindness. Persistent deficiency gives rise to a series of changes, the most devastating of which occur in the eyes. Collectively, the ocular changes are referred to as (xerophthalmia). First there is dryness of the conjunctiva (xerosis) as the normal lacrimal and mucus secreting epithelium is replaced by a keratinized epithelium. This is followed by the build-up of keratin debris in small opaque plaques (Bitot's spots) and, eventually, erosion of the roughened corneal surface with softening and destruction of the cornea (keratomalacia) and total blindness. Other changes include impaired immunity, hypokeratosis (white lumps at hair follicles), keratosis pilaris and squamous metaplasia of the epithelium lining the upper respiratory passages and urinary bladder to a keratinized epithelium.
As vitamin A is fat-soluble, disposing of any excesses taken in through diet is much harder than with water-soluble vitamins B and C. As such, vitamin A toxicity can result. This can lead to nausea, jaundice, irritability, anorexia (not to be confused with anorexia nervosa, the eating disorder), vomiting, blurry vision, headaches, muscle and abdominal pain and weakness, drowsiness and altered mental status.
Acute toxicity generally occurs at doses of 25,000 IU/kg, with chronic toxicity occurring at 4,000 IU/kg daily for 6-15 months. However, liver toxicities can occur at levels as low as 15,000 IU per day to 1.4 million IU per day, with an average daily toxic dose of 120,000 IU per day. In people with renal failure 4000 IU can cause substantial damage. Additionally excessive alcohol intake can increase toxicity.
In chronic cases, hair loss, drying of the mucous membranes, fever, insomnia, fatigue, weight loss, bone fractures, anaemia, and diarrhoea can all be evident on top of the symptoms associated with less serious toxicity.
These toxicities only occur with preformed (retinoid) vitamin A (such as from liver), the caretonoid forms (such as beta carotene as found in carrots) give no such symptoms.
A new study shows a correlation between low bone mineral density and too high intake of vitamin A.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Vitamin_A". A list of authors is available in Wikipedia.|