The structure of retinol, the most common dietary form of vitamin A
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.[1] All forms of vitamin A have a Beta-ionone ring to which an isoprenoid chain is attached. This structure is essential for vitamin activity.[1]
Discovery of vitamin A
The discovery of vitamin A stemmed from research dating back to 1906, indicating that factors other than carbohydrates, proteins, and fats were necessary to keep cattle healthy.[3] 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).[3]
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.[4]
Substance and its chemical environment |
Micrograms of retinol equivalent per microgram of the substance |
retinol |
1 |
beta-carotene, dissolved in oil |
1/2 |
beta-carotene, common dietary |
1/12 |
alpha-carotene, common dietary |
1/24 |
beta-cryptoxanthin, common dietary |
1/24 |
Vitamin A US Dietary Reference Intake:
(Note that the limit refers to retinoid forms of vitamin A. Carotene forms from dietary sources are not toxic.[5])
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.
Conversion of carotene to retinol varies from person to person and bioavailability of carotene in food varies.[7][8]
One of the earliest manifestations of vitamin A deficiency is 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[9]. 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. With relations to dentistry, a deficiency in Vitamin A leads to enamel hypoplasia.
Adequate supply of Vitamin A is especially important for pregnant and breastfeeding women, since deficiencies cannot be compensated by postnatal supplementation.[10][11]
Main article: Hypervitaminosis A
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.[12] 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, anemia, and diarrhea can all be evident on top of the symptoms associated with less serious toxicity.[13]
These toxicities only occur with preformed (retinoid) vitamin A (such as from liver). The carotenoid forms (such as beta-carotene as found in carrots), give no such symptoms, but excessive dietary intake of beta-carotene can lead to carotenodermia, which causes orange-yellow discoloration of the skin.[14] [15][16]
A new study shows a correlation between low bone mineral density and too high intake of vitamin A.[17]
fat soluble |
A (Retinol, Beta-carotene, Tretinoin, Alpha-carotene) |
water soluble: B vitamins |
B1 (Thiamine, Sulbutiamine, Benfotiamine) |
water soluble: other |
C (Ascorbic acid) - Choline |
Retrieved from "http://en.wikipedia.org/wiki/Vitamin_A"Categories: Vitamins
Vitamin A
