What is Vitamin A
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What is Vitamin A?
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Vitamin A is a vitamin which is needed by the retina of the eye in the form of a specific
metabolite, the light-absorbing molecule retinal. This molecule is absolutely necessary for bothscotopic and color vision. Vitamin A also functions in a very different role, as an irreversibly
oxidized form retinoic acid, which is an importanthormone-like growth factor for epithelial and
other cells.
In foods of animal origin, the major form of vitamin A is an ester, primarily retinyl palmitate,
which is converted to an alcohol (retinol) in thesmall intestine. The retinol form functions as astorage form of the vitamin, and can be converted to and from its visually active aldehyde form,
retinal. The associated acid (retinoic acid), a metabolite which can be irreversibly synthesized
from vitamin A, has only partial vitamin A activity, and does not function in the retina or some
essential parts of the reproductive system.
All forms of vitamin A have a beta-ionone ring to which an isoprenoid chain is attached, called a
''retinyl group''. This structure is essential for vitamin activity. The orange pigment of carrots -beta-carotene- can be represented as two connected retinyl groups, which are used in the body to
contribute to vitamin A levels. Alpha-carotene and gamma-carotene also have a single retinyl
group which give them some vitamin activity. None of the other carotenes have vitamin activity.
The carotenoid beta-cryptoxanthin possesses an ionone group and has vitamin activity inhumans.
Vitamin A can be found in two principal forms in foods:
retinol, the form of vitamin A absorbed when eating animal food sources, is a yellow, fat-soluble substance. Since the pure alcohol form is unstable, the vitamin is found in tissues
in a form of retinyl ester. It is also commercially produced and administered as esters
such as retinyl acetate or palmitate.
The carotenes alpha-carotene, beta-carotene, gamma-carotene; and the xanthophyll beta-cryptoxanthin (all of which contain beta-ionone rings), but no other carotenoids, functionas vitamin A in herbivores and omnivore animals, which possess the enzyme required to
convert these compounds to retinal. Carnivores in general are poor converters of ionine-
containg carotenoids, and pure carnivores such as cats and ferets lack beta-carotene 15
and cannot convert any carotenoids to retinal (resulting in ''none'' of the carotenoids beingforms of vitamin A for these species).
The discovery ofvitamin Amay have stemmed from research dating back to 1906,indicating that factors other thancarbohydrates, proteins, and fats were necessary to keep
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cattle healthy. By 1917 one of these substances was independently discovered by Elmer
McCollum at the University of WisconsinMadison, and Lafayette Mendel and ThomasBurr 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). Later, a unit called retinol equivalent (RE) was introduced. 1 RE corresponded to 1
g retinol, 2 g-carotenedissolved in oil (it is only partly dissolved in most supplementpills, due to very poor solubility in any medium), 6 g -carotene in normal food
(because it is not absorbed as well as when in oils), and 12 g of either -carotene, -
carotene, or -cryptoxanthin in food (these molecules only provide 50% of the retinol as
-carotene, due to only half the molecule being convertible to usable vitamin).
Newer research has shown that the absorption of provitamin-A carotenoids is only half asmuch as previously thought, so in 2001 the US Institute of Medicine recommended a new
unit, the retinol activity equivalent (RAE). 1 g RAE corresponds to 1 g retinol, 2 g of
-carotene in oil, 12 g of "dietary"beta-carotene, or 24 g of the three other dietaryprovitamin-A carotenoids.
Substance and its chemicalenvironment
Micrograms of retinol equivalent per microgram ofthe substance
retinol 1
beta-carotene, dissolved in oil 1/2
beta-carotene, common dietary 1/12
alpha-carotene, common dietary 1/24
gamma-carotene, common dietary 1/24
beta-cryptoxanthin, common dietary 1/24
Because the production of retinol from provitamins by the human body is regulated bythe 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 theamount oflipidsingested with the provitamin; lipids increase the uptake of the
provitamin.
The conclusion that can be drawn from the newer research is that fruits and vegetablesare not as useful for obtaining vitamin A as was thought; in other words, the IU's that
these foods were reported to contain were worth much less than the same number of IU's
of fat-dissolved oils and (to some extent) supplements. This is important for vegetarians.
(Night blindness is prevalent in countries where little meat or vitamin A-fortified foodsare available.)
A sample vegan diet for one day that provides sufficientvitamin Ahas been published bythe Food and Nutrition Board (page 120:
Life Stage GroupRecommended Dietary Allowances (RDA)
Adequate Intakes (AI*)
Upper Limit
g/day
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g/day
Infants06 months712 months
400*
500*
600
600
Children13 years
48 years300400
600900
Males913 years1418 years
19 - >70 years
600
900
900
1700
2800
3000
Females913 years
1418 years19 - >70 years
600700
700
17002800
3000
Pregnancy50 years750
770
2800
3000
Lactation50 years1200
1300
2800
3000
(Note that the limit refers to synthetic and natural retinoid forms of vitamin A. Caroteneforms from dietary sources are not toxic.)
According to the Institute of Medicine of the National Academies, "RDAs are set to meetthe needs of almost all (97 to 98 percent) individuals in a group. For healthybreastfed
infants, the AI is the mean intake. The AI for other life stage and gender groups isbelieved to cover the needs of all individuals in the group, but lack of data prevent being
able to specify with confidence the percentage of individuals covered by this intake."
Vitamin A Toxicity
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Sincevitamin Ais fat-soluble, disposing of any excesses taken in through diet is much harder
than with water-soluble vitamins B and C, thus vitamin A toxicity may result. This can lead to
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nausea,jaundice, irritability, anorexia (not to be confused with anorexia nervosa, theeating
disorder),vomiting, blurry vision, headaches, hairloss, muscle andabdominal painandweakness, drowsiness and altered mental status.
Acute toxicity generally occurs at doses of 25,000 IU/kg of body weight, with chronic toxicity
occurring at 4,000 IU/kg of body weight daily for 615 months. However, liver toxicities canoccur 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 withrenal failure4000 IU can cause substantial damage.Additionally, excessive alcohol intake can increase toxicity. Children can reach toxic levels at
1,500 IU/kg of body weight.
It has been estimated that 75% of people may be ingesting more than the RDA for vitamin A on
a regular basis in developed nations. Intake of twice the RDA of preformed vitamin A
chronically may be associated withosteoporosisand hip fractures. This may be due to the fact
that an excess of vitamin A can block the expression of certain proteins that are dependent onvitamin K. This could hypothetically reduce theefficacyofvitamin D, which has a proven role
in the prevention of osteoporosis and also depends on vitamin K for proper utilization.
Highvitamin Aintake has been associated with spontaneous bone fractures in animals. Cell
culture studies have linked increased bone resorption and decreased bone formation with high
vitamin A intakes. This interaction may occur because vitamins A and D may compete for thesame receptor and then interact with parathyroidhormonewhich regulatescalcium. Indeed, a
study by Forsmo ''et al.'' shows a correlation between low bone mineral density and too high
intake of vitamin A.
Toxic effects of vitamin A have been shown to significantly affect developing fetuses.
Therapeutic doses used foracnetreatment have been shown to disrupt cephalic neural cell
activity. The fetus is particularly sensitive to vitamin A toxicity during the period oforganogenesis.
These toxicities only occur with preformed (retinoid)vitamin A(such as from liver). The
carotenoid forms (such asbeta-caroteneas 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.
Researchers have succeeded in creating water-soluble forms of vitamin A, which they believedcould reduce the potential for toxicity. However, a 2003 study found that water-soluble vitamin
A was approximately 10 times as toxic as fat-soluble vitamin.
A 2006 study found that children given water-soluble vitamin A and D, which are typically fat-
soluble, suffer fromasthmatwice as much as a control group supplemented with the fat-soluble
vitamins.
Chronically high doses of Vitamin A can produce the syndrome of "pseudotumor cerebri". This
syndrome includesheadache, blurring of vision and confusion. It is associated with increasedintracerebral pressure.
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