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vitamin A

 
Dictionary: vitamin A
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n.
A fat-soluble vitamin or a mixture of vitamins, especially vitamin A1 or a mixture of vitamins A1 and A2, occurring principally in fish-liver oils, milk, and some yellow and dark green vegetables, and functioning in normal cell growth and development. Its deficiency causes hardening and roughening of the skin, night blindness, and degeneration of mucous membranes. Also called retinol.


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Britannica Concise Encyclopedia: vitamin A
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Fat-soluble alcohol, most abundant in fatty fish and especially in fish-liver oils. It is not found in plants, but many vegetables and fruits contain beta-carotene (see carotene), which is readily converted in the body to vitamin A. It functions directly in vision, especially night vision. A derivative, retinaldehyde, is a component of the visual pigments, including rhodopsin, in the retina. Humans require vitamin A in very small amounts. Unlike carotenes, it is toxic in large amounts and is readily destroyed by exposure to heat, light, or air.

For more information on vitamin A, visit Britannica.com.

Sci-Tech Encyclopedia: Vitamin A
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A pale-yellow alcohol, soluble in fat but not in water. In pure form, it is readily destroyed by oxidation and light, which may cause losses during storage. Vitamin A is found in all animal tissues, although it is particularly concentrated in the liver. There are two different dietary sources for the vitamin: animal sources which contain vitamin A itself, mostly in the form of retinyl esters, and plant sources which contain carotenoids that are converted to vitamin A in animal tissues such as the absorptive cells in the intestine. The most vitamin A–enriched animal food source is fish liver oil. Plant carotenoids are found in green and yellow fruits and vegetables such as carrots, apricots, asparagus, broccoli, and green leafy vegetables. See also Carotenoid.

In vitamin A deficiency, the epithelial tissues of many organs are affected. Growth failure occurs, and young animals can suffer from neurological symptoms resulting from pressures on the central nervous system. Vitamin A deficiency is also strongly associated with depressed immune function and higher morbidity and mortality due to infectious diseases such as diarrhea, measles, and respiratory infections. A severe manifestation of vitamin A deficiency is night blindness and inflammation of the eyes (xerophthalmia), followed by irreversible blindness.

The symptoms seen in vitamin A deficiency reflect the multiple roles of this compound in animals. These roles are fulfilled by two compounds that are synthesized from vitamin A in the body: vitamin A aldehyde (retinaldehyde), which is critical for vision, and vitamin A acid (retinoic acid), which controls many physiological functions in both the embryo and the adult. See also Vision.

Studies of many mammalian species suggested that approximately 20 IU (6 μg) of vitamin A per kilogram of body weight will support growth and prevent symptoms of deficiency. The current intake recommendations of vitamin A in the United States is 3 mg/day and about 1 mg/day in the European Union. See also Vitamin.

Food and Nutrition: vitamin A
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Essential in the diet either as the preformed vitamin (retinol) found in animal foods or as a precursor, carotene, found in plant foods (usually both are present in the diet). Required for control of growth, cell turnover and fetal development, maintenance of fertility, and maintenance of the epithelial tissues lining the mouth and respiratory and urinary tracts; essential in vision.

Deficiency leads to slow adaptation to see in dim light (poor dark adaptation), an early sign of deficiency, and later to night blindness; then drying of the tear ducts (xerophthalmia) and ulceration of the cornea (keratomalacia) resulting in blindness.  Retinol occurs in animal products, especially liver, kidney, fish liver oils, milk, and butter. Carotene is found in green- and orange-coloured vegetables and fruits; especially rich in red palm oil and carrots.

The vitamin A content of foods is expressed as retinol equivalents, i.e. retinol plus carotene; 1 μg retinol = 6 μg β-carotene = 12 μg other active carotenoids = 3.33 international units.

Food and Fitness: vitamin A
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retinol; carotene

A fat-soluble vitamin which helps with normal functioning of the mucus membranes of the eye and respiratory tract, and the formation of visual pigments in the eye. It is also essential for normal tissue growth and differentiation. Vitamin A can be manufactured in the body from beta-carotene, found in a variety of foods, particularly green vegetables and carrots. Vitamin A deficiency increases the risk of all infections, especially those of the respiratory, digestive, and urinogenital tracts, and causes a number eye disorders, including night blindness. It is the most prevalent vitamin deficiency, affecting more than 200 million people worldwide. It is the commonest preventable cause of blindness in the world. However, in economically developed countries, most people can acquire adequate amounts from a well-balanced diet. There is little evidence to support the use of vitamin A supplements, even for athletes whose demands would be expected to be considerably higher than normal. Excessive intakes of vitamin A can lead to nausea, vomiting, anorexia, headaches, hairlessness, bone and joint pain, and bone fragility. (This toxicity applies only to preformed retinol; carotene is not toxic in excess.) Women who are, or might become, pregnant are advised not to take vitamin A supplements, unless advised to do so by their doctor. The safe upper limit in pregnancy (3300 micrograms per day) is considerably lower than for non-pregnant women (7500 micrograms per day) because there may be a risk to the developing baby.

The US Recommended Daily Allowance is 5000 IU or 750 microgram retinol equivalents (the UK adult Reference Nutrient Intake is 700 micrograms for males and 600 micrograms for females). A footballer, acting on the premise that more is better, attempted to improve his performance by consuming 100 000 IU of vitamin A a day in cod liver oil, liver, milk, and vitamin supplements. The huge amounts of vitamin A taken over a period of more than two months resulted in the footballer's legs swelling and becoming stiff, and his bones changing structure. Fortunately, the changes were reversed within a month of the diet being discontinued.

Dental Dictionary: vitamin A
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n

(retinal, retinol, retinoic acid), a fatsoluble substance, occurring in several chemical forms in food and function: retinal, an aldehyde; retinol, an alcohol; and retinoic acid, an acid. All three function in calcified and epithelial tissue growth. The aldehyde-alcohol (retinal-retinol) interconversion allows regeneration of rhodopsin (visual purple) in the rod cells of the retina. A deficiency results in hyperkeratinization of non-secretory protective epithelium, deranged secretory function of the mucous membrane, dark dysadaptation (night blindness), and possibly, enamel hypoplasia. Dietary sources include liver, kidney, and lung as well as carotenes (provitamins A) from the plant kingdom.

Drug Info: Vitamin A
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Brand names: Aquasol A®, Unilife-A™



Vitamin A capsules

What are vitamin A capsules?

VITAMIN A (Aquasol A®) is a naturally occurring vitamin. There are two natural sources of vitamin A. Eggs, butter, milk, meat, and oily fish contain retinol, the primary retinoid of animal origin. Green and yellow fruits and vegetables contain beta-carotene, a carotenoid of plant origin, that is converted into vitamin A in the body. Vitamin A is necessary for normal health and growth, especially of the eyes and skin. A deficiency of vitamin A can cause night blindness, dry eyes, eye infections, skin problems, and slowed growth. A normal balanced diet contains a sufficient amount of vitamin A for good health. Only take vitamin A under your prescriber's supervision. Large amounts of vitamin A taken over a long time can cause serious, unwanted effects. Generic vitamin A capsules are available.

What should I tell my health care provider before I take this medicine?

They need to know if you have any of the following conditions:
• an alcohol problem
• kidney disease
• liver disease
• vitamin A toxicity
• an unusual or allergic reaction to vitamin A, other medicines, foods, dyes, or preservatives
• pregnant or trying to get pregnant

How should I take this medicine?

Take vitamin A capsules by mouth. Follow the directions on the prescription label. To reduce upset stomach take vitamin A with food. To make it easier for children to swallow you can open the capsule and mix the contents with jam, applesauce or other foods. Take your doses at regular intervals. Do not take your medicine more often than directed.

What if I miss a dose?

If you miss a dose, skip that dose. Continue with your next scheduled dose. Do not double or take extra doses.

What drug(s) may interact with vitamin A?

• cholestyramine
• etretinate
• female hormones, including contraceptive or birth control pills
• isotretinoin
• mineral oil
• orlistat
• porfimer PDT
• warfarin

Tell your prescriber or health care professional about all other medicines you are taking, including non-prescription medicines, nutritional supplements, or herbal products. Also tell your prescriber or health care professional if you are a frequent user of drinks with caffeine or alcohol, if you smoke, or if you use illegal drugs. These may affect the way your medicine works. Check with your health care professional before stopping or starting any of your medicines.

What should I watch for while taking vitamin A?

Make sure you have a proper diet. Taking supplemental vitamin A does not replace the need for a balanced diet.

Do not take vitamin A supplements if you are pregnant or trying to get pregnant. Too much vitamin A can cause birth defects.

What side effects may I notice from taking vitamin A?

The recommended daily allowance of vitamin A does not cause any side effects.
Side effects related to overdose include:
• dark yellow or brown urine
• bleeding from gums, sore lips and mouth
• bulging soft spot on the head of babies
• confusion, irritability, unusual excitement
• diarrhea
• dizziness, drowsiness
• dry, cracked or peeling of skin
• double vision
• headache (severe)
• joint pains
• nausea, vomiting
• sweating
• unusual tiredness
• yellowing of the eyes or skin
Call your prescriber or health care professional as soon as you can if you think you have taken an overdose and have any of these side effects.

Where can I keep my medicine?

Keep out of the reach of children in a container that small children cannot open.

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F); do not freeze. Protect from light. Keep container tightly closed. Throw away any unused medicine after the expiration date.


Last updated: 7/1/2002

Important Disclaimer: The drug information provided here is for educational purposes only. It is intended to supplement, not substitute for, the diagnosis, treatment and advice of a medical professional. This drug information does not cover all possible uses, precautions, side effects and interactions. It should not be construed to indicate that this or any drug is safe for you. Consult your medical professional for guidance before using any prescription or over the counter drugs.

Alternative Medicine Encyclopedia: Vitamin A
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Description

Vitamin A is one of four fat-soluble vitamins necessary for good health. It serves an important role as an antioxidant by helping to prevent free radicals from causing cellular damage. Adequate levels are important for good eyesight, and poor night vision may be one of the first symptoms of a deficiency. It is also necessary for proper function of the immune, skeletal, respiratory, reproductive, and integumentary (skin) systems.

General Use

An adequate level of vitamin A unquestionably contributes to good health. It is essential for the proper function of the retina, where it can act to prevent night blindness, as well as lower the odds of getting age-related macular degeneration (AMD), which is the most common cause of blindness in the elderly. There is also evidence that good levels of vitamin A in the form of carotenoids may decrease the risk of certain cancers, heart attacks, and strokes. The immune system is also strengthened. It is unclear, however, if supplemental forms of vitamin A have the same benefit as consuming the nutrient in natural foods in the case of a person without deficiency. Taking high levels of vitamin A in any supplemental form is not advisable without the counsel of a healthcare professional.

Preparations

Natural Sources

There are two basic forms of vitamin A. Retinoids, the active types, are contained in animal sources, including meat, whole milk, and eggs. Liver is particularly rich in vitamin A, since it is one of the storage sites for excess. Precursor forms of the vitamin (carotenoids) are found in orange and leafy green produce such as sweet potatoes, carrots, collard greens, spinach, winter squash, kale, and turnip greens. Very fresh foods have the highest levels, followed by frozen foods. Typically, canned produce has little vitamin A. Preparing vegetables by steaming, baking, or grilling helps them to release the carotenes they contain. Alpha and beta carotene, as well as some of the other lesser-known carotenoids, can be converted to vitamin A in the small intestine. This is done by the body on an as-needed basis, so there is no risk of overdose as there is with the active form.

Supplemental Sources

Supplements may contain either the active or precursor forms of vitamin A. The active form may be more desirable for those who may have some difficulty in converting the carotenoids into the active vitamin. This is more often true in those over age 55 or who have a condition that impairs the absorption of fat. There is a water-soluble form of the vitamin, retinyl palmitate, which may be better utilized in the latter case. Carotenes are also available either as oil-based or natural water-based formulas. Be sure to store both away from light and heat, which will destroy them.

Units

There are several units that can express the amount of vitamin A activity in a product. Many supplements are still labeled with the old International Unit (IU), although the more current and most accurate unit is the Retinol Equivalent (RE). The new measurement distinguishes between the differences in absorption of retinol and beta carotene. One RE is equal to one microgram (MICROg) of retinol, or six MICROg of beta carotene.

Dose Limits

Adults should take no more than 25,000 IU (5,000 RE) per day of vitamin A in its active form, except in the case of women who are pregnant or may become pregnant. The latter group should not exceed 10,000 IU (2,000 RE) per day in order to avoid potential toxic effects to the fetus. The best way to get vitamins is in the natural food form, as the complexities are not always either known or reproducible in a supplement. A diet rich in foods containing carotenoids is optimal, but in the event of nutritional deficiencies, supplements may be needed. Mixed carotenoids are preferable to either large doses of vitamin A or pure beta carotene supplements to avoid toxicity and maximize healthful benefits. Some of the minor carotenoids appear to have beneficial effects that are still being explored. A good mixture will contain alpha and beta carotene, as well as lycopene and xanthophylls. Eating foods high in many carotenoids may confer some benefits—such as a lower risk of cancer, heart attacks, and strokes—which a supplement may not.

Deficiency

Levels of vitamin A low enough to cause symptomatic deficiency are uncommon in people of normal health in industrialized nations. Symptoms of deficiency may include, but are not limited to, loss of appetite, poor immune function causing frequent infections (especially respiratory), hair loss, rashes, dry skin and eyes, visual difficulties including night blindness, poor growth, and fatigue. Generally symptoms are not manifested unless the deficiency has existed for a period of months. Deficiencies are more likely in people who are malnourished, including alcoholics, the chronically ill, and those with impaired fat absorption. Another group at increased risk of vitamin A deficiency are persons with type 1 diabetes whose disorder is poorly controlled. People with normal health and nutritional status have a considerable vitamin A reserve.

In countries where nutritional status tends to be poor and deficiency is more common, vitamin A has been found to reduce the mortality rate of children suffering from a number of different viral infections.

Experts in plant genetics have been working on a strain of rice that contains beta carotene, hoping to help people in developing countries avoid the risk of vitamin A deficiency. Known as Golden Rice, the new strain is being sent to research institutes in developing countries for further study.

Risk Factors for Deficiency

Taking the RDA level of a nutrient will prevent a deficiency in most people, but under certain circumstances, an individual may require higher doses of vitamin A. Those who consume alcoholic beverages may be more prone to vitamin A deficiency. People taking some medications, including birth control pills, methotrexate, cholestyramine, colestipol, and drugs that act to sequester bile will also need larger amounts. Those who are malnourished, chronically ill, or recovering from surgery or other injuries may also benefit from a higher than average dose. Patients undergoing treatments for cancer, including radiation and chemotherapy, typically have compromised immune systems that may be boosted by judicious supplementation with vitamin A. Other conditions that may impair vitamin A balance include chronic diarrhea, cystic fibrosis, and kidney or liver disease. Diabetics are often deficient in vitamin A, but may also be more susceptible to toxicity. Any supplementation for these conditions should be discussed with a healthcare provider. Supplements are best taken in the form of carotenoids to avoid any potential for toxicity. There is not an established RDA for beta carotene. Recommendations for how much to take vary between 6 and 30 mg a day, but the middle range—around 15 mg—is a reasonable average.

Precautions

Overdose can occur when taking megadoses of the active form of this vitamin. Amounts above what is being utilized by the body accumulate in the liver and fatty tissues. Symptoms may include dry lips and skin, bone and joint pain, liver and spleen enlargement, diarrhea, vomiting, headaches, blurry or double vision, confusion, irritability, fatigue, and bulging fontanel (soft spot on the head) in infants; these are most often reversible, but a doctor should be contacted if a known overdose occurs. Very high levels of vitamin A may also create deficiencies of vitamins C, E, and K. Symptoms will generally appear within six hours following an acute overdose, and take a few weeks to resolve after ceasing the supplement. Children are more sensitive to high levels of vitamin A than adults are, so instructions on products designed for children should be followed with particular care. Vitamin supplements should always be kept out of reach of children.

It is especially important to avoid overdoses in pregnancy, as it may cause miscarriage or fetal malformations. Using supplements that provide carotenoids will avoid the potential of overdose. Those with kidney disease are also at higher risk for toxicity due to either vitamin A or beta carotene, and should not take these supplements without professional healthcare advice.

There is some evidence that taking beta carotene supplements puts smokers at a higher risk of lung cancers. The CARET (Beta Carotene and Retinol Efficacy Trial) study is one that demonstrated this effect. Clarification through more study is needed, as evidence also exists showing that beta carotene, along with other antioxidants, can be a factor in cancer prevention. For example, a team of American researchers has recently reviewed evidence that vitamin A protects against bladder cancer, and a group in Germany is testing an aerosol form of vitamin A to prevent lung cancer. Some of the lesser-known carotenoids may be key factors in the relationship between vitamin intake and cancer. Whole sources of vitamin A are better obtained from foods than from supplements. Smokers should consult with a healthcare provider before taking supplemental beta carotene.

Side Effects

Very high levels of carotenoids (carotenemia) may cause an orange discoloration of the skin, which is harmless and transient.

Interactions

Vitamin A supplements should not be taken in conjunction with any retinoid medications, including isotretinoin (Accutane), a drug used to treat acne. There is a higher risk of toxicity.

A very low fat diet or use of fat substitutes impairs absorption of all the fat-soluble vitamins, including A. Mineral oil and aluminum-containing antacids may also inhibit absorption, as do the cholesterol-lowering drugs cholestyramine and colestipol. Vitamin A reserves of the body are depleted by a number of substances, including alcohol, barbiturates, caffeine, cortisone, tobacco, and very high levels of vitamin E. Overuse of alcohol and vitamin A together may increase the possibility of liver damage.

Taking appropriate doses of vitamin C, vitamin E, zinc, and selenium optimizes absorption and use of vitamin A and carotenoids. As vitamin A is fat-soluble, a small amount of dietary fat is also helpful.

Studies of both children and pregnant women with iron deficiency anemia show that this condition is better treated with a combination of iron supplements and vitamin A than with iron alone.

Resources

Books

Bratman, Steven, and David Kroll. Natural Health Bible. Prima Publishing, 1999.

Feinstein, Alice. Prevention's Healing with Vitamins. Rodale Press, 1996.

Griffith, H. Winter. Vitamins, Herbs, Minerals & Supplements: The Complete Guide. Fisher Books, 1998.

Jellin, Jeff, Forrest Batz, and Kathy Hitchens. Pharmacist's letter/Prescriber's Letter Natural Medicines Comprehensive Database. Therapeutic Research Faculty, 1999.

Periodicals

Baena, R. M., C. Campoy, R. Bayes, et al. "Vitamin A, Retinol-Binding Protein and Lipids in Type 1 Diabetes Mellitus." European Journal of Clinical Nutrition 56 (January 2002): 44–50.

Beyer, P., S. Al-Babili, X. Ye, et al. "Golden Rice: Introducing the Beta-Carotene Biosynthesis Pathway Into Rice Endosperm by Genetic Engineering to Defeat Vitamin A Deficiency." Journal of Nutrition 132 (March 2002): 506S–510S.

Kamat, A. M., and D. L. Lamm. "Chemoprevention of Bladder Cancer." Urology Clinics of North America 29 (February 2002): 157–168.

Kohlhaufl, M., K. Haussinger, F. Stanzel, et al. "Inhalation of Aerosolized Vitamin A: Reversibility of Metaplasia and Dysplasia of Human Respiratory Epithelia—A Prospective Pilot Study." European Journal of Medical Research 7 (February 21, 2002): 72–78.

Miksad, R., V. de Ledinghen, C. McDougall, et al. "Hepatic Hydrothorax Associated with Vitamin A Toxicity." Journal of Clinical Gastroenterology 34 (March 2002): 275–279.

van den Berg, H., M. van der Gaag, and H. Hendriks. "Influence of Lifestyle on Vitamin Bioavailability." International Journal of Vitamin and Nutrition Research 72 (January 2002): 53–59.

Yeum, K. J., and R. M. Russell. "Carotenoid Bioavailability and Bioconversion." Annual Review of Nutrition 22 (2002): 483–504.

[Article by: Judith Turner; Rebecca J. Frey, PhD]

Sports Science and Medicine: vitamin A
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retinol

A fat-soluble vitamin which helps with normal functioning of the mucous membranes of the eye and respiratory tract, and the formation of visual pigments in the eye. Vitamin A can be manufactured in the body from beta carotene, found in a variety of foods particularly green vegetables and carrots. Vitamin A deficiency increases the risk of infections of the respiratory, digestive, and urinogenital tracts, and causes a number eye disorders, including night blindness. Although it is the most prevalent vitamin deficiency in the world, most people can acquire adequate amounts from a well-balanced diet. There is little evidence to support the use of vitamin A supplements, even for athletes whose demands would be expected to be considerably higher than normal. Excessive intakes of vitamin A can lead to nausea, vomiting, anorexia, headaches, hairlessness, bone and joint pain, and bone fragility.

Veterinary Dictionary: vitamin A
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A fat-soluble, organic alcohol formed in animal tissues from carotenoids found in plants. Called also retinol. It is formed from carotenoids, principally carotene, in the intestinal epithelium, except by cats, and stored in the liver. It is essential for the proper growth and maintenance of surface epithelium, for the accurate sculpting and proper growth of bones, and for the maintenance of light-sensitive pigments in the eye.
Nutritional deficiency due to lack of carotene in the diet in herbivores and to lack of carotene and preformed vitamin A in the diet in omnivores and carnivores causes hypovitaminosis A. The resulting clinical syndrome varies with species and age. In young animals there is compression of the brain and spinal cord caused by faulty bone growth and characterized by convulsions, blindness and posterior paralysis. In other animals there is night blindness, corneal keratinization, pityriasis, hoof defects, infertility and possibly congenital defects.
Hypovitaminosis in birds is manifested by poor egg production, ocular discharge at first watery then thick and caseous, a nasal discharge and pustular lesions and accumulations of caseous material in the mouth, pharynx, esophagus and trachea.

  • v. A2 — called also dehydroretinol and found in fish livers. Has the same effects and efficiency as retinol; it is absorbed unchanged and is immediately metabolically active.
  • v. A excess — see hypervitaminosis A.
  • v. A poisoning — see hypervitaminosis A.
  • v. A-responsive dermatosis — seborrhea, particularly in Cocker spaniels, is sometimes found to be responsive to vitamin A.
  • teratogenic v. A — causes abnormalities in closure of the neural tube in the developing fetus causing defects in the brain, eye and heart.
Wikipedia: Vitamin A
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The structure of retinol, the most common dietary form of vitamin A

Vitamin A is linked to a family of similarly shaped molecules, the retinoids, which complete the remainder of the vitamin sequence. Its important part is the retinyl group, which can be found in several forms. 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 the small intestine. Vitamin A can also exist as an aldehyde (retinal). The acid (retinoic acid), a metabolite, has only partial vitamin A activity, and does not function in the retina. Precursors to the vitamin (provitamins) are present in foods of plant origin as three 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] 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 in humans.

The retinyl group, when attached to a specific protein, is the only primary light absorber in visual perception, and the compound name is related to the retina of the eye. The retinyl group also functions in retinoic acid, which exhibits hormone-like activities in other parts of the body.

Vitamin A can be found in various forms:

  • retinol, the form of vitamin A absorbed when eating animal food sources, is a yellow, fat-soluble, vitamin with importance in vision and bone growth. Since the alcohol form is unstable, the vitamin is usually produced and administered in a form of retinyl acetate or palmitate.
  • other retinoids, a class of chemical compounds that are related chemically to vitamin A, are used in medicine.[2]
  • The carotenes alpha-carotene, beta-carotene, gamma-carotene; and the xanthophyll beta-cryptoxanthin (all of which contain beta-ionone rings), but no other carotenoids, function as 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 15,15'-monooxygenase and cannot convert any carotenoids to retinals (resulting in no carotenoids being forms of vitamin A for these species).

Contents

Discovery of vitamin A

The discovery of vitamin A may have 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 Burr 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] Vitamin A was first synthesized in 1947 by two Dutch chemists, David Adriaan van Dorp and Jozef Ferdinand Arens.

Equivalencies of retinoids and carotenoids (IU)

As some carotenoids can be converted into vitamin A, attempts have been made to determine how much of them in the diet is equivalent to a particular amount of retinol, so that comparisons can be made of the benefit of different foods. Unfortunately the situation is confusing because the accepted equivalences have changed. For many years, a system of equivalencies was used in which an international unit (IU) was equal to 0.3 μg of retinol, 0.6 μg of β-carotene, or 1.2 μg of other provitamin-A carotenoids.[4] Later, a unit called retinol equivalent (RE) was introduced. 1 RE corresponded to 1 μg retinol, 2 μg β-carotene dissolved in oil (it is only partly dissolved in most supplement pills, due to very poor solubility in any medium), 6 μg β-carotene in normal food (because it is not absorbed as well as when in oils), and 12 μg of either α-carotene, γ-carotene, or β-cryptoxanthin in food (these molecules only provide 50% of the retinol as β-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 as much as previously thought, so in 2001 the US Institute of Medicine recommended a new unit, the retinol activity equivalent (RAE). 1 μg RAE corresponds to 1 μg retinol, 2 μg of β-carotene in oil, 12 μg of "dietary" beta-carotene, or 24 μg of the three other dietary provitamin-A carotenoids.[5]

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
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 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.[6]

The conclusion that can be drawn from the newer research is that fruits and vegetables are 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 foods are available.)

A sample vegan diet for one day that provides sufficient vitamin A has been published by the Food and Nutrition Board (page 120[5]). On the other hand, reference values for retinol or its equivalents, provided by the National Academy of Sciences, have decreased. The RDA (for men) of 1968 was 5000 IU (1500 μg retinol). In 1974, the RDA was set to 1000 RE (1000 μg retinol), whereas now the Dietary Reference Intake is 900 RAE (900 μg or 3000 IU retinol). This is equivalent to 1800 μg of β-carotene supplement (3000 IU) or 10800 μg of β-carotene in food (18000 IU).

Recommended daily intake

Vitamin A
Dietary Reference Intake[7]:

Life Stage Group RDA/AI*

μg/day

 UL

μg/day
Infants

0–6 months
7–12 months
400*
500*
600
600
Children

1–3 years
4–8 years
300
400
600
900
Males

9–13 years
14–18 years
19 - >70 years
600
900
900
1700
2800
3000
Females

9–13 years
14–18 years
19 - >70 years
600
700
700
1700
2800
3000
Pregnancy

<19 years
19 - >50 years
750
770
2800
3000
Lactation

<19 years
19 - >50 years
1200
1300
2800
3000

RDA = Recommended Dietary Allowances
AI* = Adequate Intakes
UL = Upper Limit

(Note that the limit refers to synthetic and natural retinoid forms of vitamin A. Carotene forms from dietary sources are not toxic.[8][9])

According to the Institute of Medicine of the National Academies, "RDAs are set to meet the needs of almost all (97 to 98 percent) individuals in a group. For healthy breastfed infants, the AI is the mean intake. The AI for other life stage and gender groups is believed 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."[10]

Sources of vitamin A

Egg.

Vitamin A is found naturally in many foods:

Note: data taken from USDA database bracketed values are retinol equivalences and percentage of the adult male RDA per 100g.

Conversion of carotene to retinol varies from person to person and bioavailability of carotene in food varies.[12][13]

Metabolic functions of vitamin A

Vitamin A plays a role in a variety of functions throughout the body, such as:

  • Vision
  • Gene transcription
  • Immune function
  • Embryonic development and reproduction
  • Bone metabolism
  • Haematopoiesis
  • Skin health
  • Antioxidant Activity

Vision

The role of vitamin A in the vision cycle is specifically related to the retinal form. Within the eye, 11-cis-retinal is bound to rhodopsin (rods) and iodopsin (cones) at conserved lysine residues. As light enters the eye the 11-cis-retinal is isomerized to the all-"trans" form. The all-"trans" retinal dissociates from the opsin in a series of steps called bleaching. This isomerization induces a nervous signal along the optic nerve to the visual center of the brain. Upon completion of this cycle, the all-"trans"-retinal can be recycled and converted back to the 11-"cis"-retinal form via a series of enzymatic reactions. Additionally, some of the all-"trans" retinal may be converted to all-"trans" retinol form and then transported with an interphotoreceptor retinol-binding protein (IRBP) to the pigment epithelial cells. Further esterification into all-"trans" retinyl esters allow this final form to be stored within the pigment epithelial cells to be reused when needed.[14] The final conversion of 11-cis-retinal will rebind to opsin to reform rhodopsin in the retina. Rhodopsin is needed to see black and white as well as see at night. It is for this reason that a deficiency in vitamin A will inhibit the reformation of rhodopsin and lead to night blindness.[15]

Gene transcription

Vitamin A, in the retinoic acid form, plays an important role in gene transcription. Once retinol has been taken up by a cell, it can be oxidized to retinal (by retinol dehydrogenases) and then retinal can be oxidized to retinoic acid (by retinal oxidase). The conversion of retinal to retinoic acid is an irreversible step, meaning that the production of retinoic acid is tightly regulated, due to its activity as a ligand for nuclear receptors.[14] Retinoic acid can bind to two different nuclear receptors to initiate (or inhibit) gene transcription: the retinoic acid receptors (RARs) or the retinoid "X" receptors (RXRs). RAR and RXR must dimerize before they can bind to the DNA. RAR will form a heterodimer with RXR (RAR-RXR), but it does not readily form a homodimer (RAR-RAR). RXR, on the other hand, readily forms a homodimer (RXR-RXR) and will form heterodimers with many other nuclear receptors as well, including the thyroid hormone receptor (RXR-TR), the Vitamin D3 receptor (RXR-VDR), the peroxisome proliferator-activated receptor (RXR-PPAR) and the liver "X" receptor (RXR-LXR).[16] The RAR-RXR heterodimer recognizes retinoid acid response elements (RAREs) on the DNA whereas the RXR-RXR homodimer recognizes retinoid "X" response elements (RXREs) on the DNA. The other RXR heterodimers will bind to various other response elements on the DNA.[14] Once the retinoic acid binds to the receptors and dimerization has occurred, the receptors undergo a conformational change that causes co-repressors to dissociate from the receptors. Coactivators can then bind to the receptor complex, which may help to loosen the chromatin structure from the histones or may interact with the transcriptional machinery.[16] The receptors can then bind to the response elements on the DNA and upregulate (or downregulate) the expression of target genes, such as cellular retinol-binding protein (CRBP) as well as the genes that encode for the receptors themselves.[14]

Dermatology

Vitamin A appears to function in maintaining normal skin health. The mechanisms behind retinoid's therapeutic agents in the treatment of dermatological diseases are being researched. For the treatment of acne, the most effective drug is 13-cis retinoic acid (isotretinoin). Although its mechanism of action remains unknown, it is the only retinoid that dramatically reduces the size and secretion of the sebaceous glands.[citation needed] Isotretinoin reduces bacterial numbers in both the ducts and skin surface. This is thought to be a result of the reduction in sebum, a nutrient source for the bacteria. Isotretinoin reduces inflammation via inhibition of chemotatic responses of monocytes and neutrophils.[14] Isotretinoin also has been shown to initiate remodeling of the sebaceous glands; triggering changes in gene expression that selectively induces apoptosis.[17] Isotretinoin is a teratogen and its use is confined to medical supervision.

Retinal/retinol versus retinoic acid

Vitamin A deprived rats can be kept in good general health with supplementation of retinoic acid. This reverses the growth-stunting effects of vitamin A deficiency, as well as xerophthalmia. However, such rats show infertility (in both male and females) and continued degeneration of the retina, showing that these functions require retinal or retinol, which are intraconvertable but which cannot be recovered from the oxidized retinoic acid.[18]

Deficiency

Vitamin A deficiency is estimated to affect millions of children around the world. Approximately 250,000-500,000 children in developing countries become blind each year owing to vitamin A deficiency, with the highest prevalence in Southeast Asia and Africa.[19] According to the World Health Organization (WHO), vitamin A deficiency is under control in the United States, but in developing countries vitamin A deficiency is a significant concern. With the high prevalence of vitamin A deficiency, the WHO has implemented several initiatives for supplementation of vitamin A in developing countries. Some of these strategies include intake of vitamin A through a combination of breast feeding, dietary intake, food fortification, and supplementation. Through the efforts of WHO and its partners, an estimated 1.25 million deaths since 1998 in 40 countries due to vitamin A deficiency have been averted.[20]

Vitamin A deficiency can occur as either a primary or secondary deficiency. A primary vitamin A deficiency occurs among children and adults who do not consume an adequate intake of yellow and green vegetables, fruits and liver. Early weaning can also increase the risk of vitamin A deficiency. Secondary vitamin A deficiency is associated with chronic malabsorption of lipids, impaired bile production and release, low fat diets, and chronic exposure to oxidants, such as cigarette smoke. Vitamin A is a fat soluble vitamin and depends on micellar solubilization for dispersion into the small intestine, which results in poor utilization of vitamin A from low-fat diets. Zinc deficiency can also impair absorption, transport, and metabolism of vitamin A because it is essential for the synthesis of the vitamin A transport proteins and the oxidation of retinol to retinal. In malnourished populations, common low intakes of vitamin A and zinc increase the risk of vitamin A deficiency and lead to several physiological events.[14] A study in Burkina Faso showed major reduction of malaria morbidity with combined vitamin A and zinc supplementation in young children.[21]

Since the unique function of retinyl group is the light absorption in retinylidene protein, one of the earliest and specific 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. Some other 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.[22] 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.[23][24].

Toxicity

Main article: Hypervitaminosis A

Since vitamin A is 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 nausea, jaundice, irritability, anorexia (not to be confused with anorexia nervosa, the eating disorder), vomiting, blurry vision, headaches, hairloss, muscle and abdominal pain and weakness, 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 6–15 months.[25] 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. Children can reach toxic levels at 1500IU/kg of body weight.[26]

In chronic cases, hair loss, dry skin, 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.[27]

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 with osteoporosis and 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 on vitamin K. This could hypothetically reduce the efficacy of vitamin D, which has a proven role in the prevention of osteoporosis and also depends on vitamin K for proper utilization[28].

High vitamin A intake 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 the same receptor and then interact with parathyroid hormone which regulates calcium.[26] Indeed, a study by Forsmo et al. shows a correlation between low bone mineral density and too high intake of vitamin A.[29]

Toxic effects of vitamin A have been shown to significantly affect developing fetuses. Therapeutic doses used for acne treatment have been shown to disrupt cephalic neural cell activity. The fetus is particularly sensitive to vitamin A toxicity during the period of organogenesis.[14]

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.[30][31][32]

Researchers have succeeded in creating water-soluble forms of vitamin A, which they believed could reduce the potential for toxicity.[33] However, a 2003 study found that water-soluble vitamin A was approximately 10 times as toxic as fat-soluble vitamin.[34] A 2006 study found that children given water-soluble vitamin A and D, which are typically fat-soluble, suffer from asthma twice as much as a control group supplemented with the fat-soluble vitamins.[35]

Chronically high doses of Vitamin A can produce the syndrome of "pseudotumor cerebri".[36] This syndrome includes headache, blurring of vision and confusion. It is associated with increased intracerebral pressure.[37]

See also

References

  1. ^ a b Carolyn Berdanier. 1997. Advanced Nutrition Micronutrients. pp 22-39
  2. ^ American Cancer Society: Retinoid Therapy
  3. ^ a b Wolf, George (2001-04-19). "Discovery of Vitamin A". Encyclopedia of Life Sciences. doi:10.1038/npg.els.0003419. http://www.mrw.interscience.wiley.com/emrw/9780470015902/els/article/a0003419/current/html. Retrieved 2007-07-21. 
  4. ^ Composition of Foods Raw, Processed, Prepared USDA National Nutrient Database for Standard Reference, Release 20 USDA, Feb. 2008
  5. ^ a b Chapter 4, Vitamin A of Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, hickel, Silicon, Vanadium, and Zinc, Food and Nutrition Board of the Institute of Medicine, 2001
  6. ^ NW Solomons, M Orozco. Alleviation of Vitamin A deficiency with palm fruit and its products. Asia Pac J Clin Nutr, 2003
  7. ^ Dietary Reference Intakes: Vitamins
  8. ^ "Sources of vitamin A". http://www.vitamins-supplements.org/vitamin-A-sources.php. Retrieved 2007-08-27. 
  9. ^ "Linus Pauling Institute at Oregon State University: Vitamin A Safety". http://lpi.oregonstate.edu/infocenter/vitamins/vitaminA#safety. Retrieved 2007-09-02. 
  10. ^ Food and Nutrition Board. Institute of Medicine. National Academies. (2001) "Dietary Reference Intakes"
  11. ^ The RAE value in the USDA data for broccoli leaves is similar to the IU value for broccoli florets, which implies that the leaves have about 20 times as much beta-carotene.
  12. ^ Borel P, Drai J, Faure H, et al. (2005). "[Recent knowledge about intestinal absorption and cleavage of carotenoids]" (in French). Ann. Biol. Clin. (Paris) 63 (2): 165–77. PMID 15771974. 
  13. ^ Tang G, Qin J, Dolnikowski GG, Russell RM, Grusak MA (2005). "Spinach or carrots can supply significant amounts of vitamin A as assessed by feeding with intrinsically deuterated vegetables". Am. J. Clin. Nutr. 82 (4): 821–8. PMID 16210712. 
  14. ^ a b c d e f g Combs, Gerald F. (2008). The Vitamins: Fundamental Aspects in Nutrition and Health (3rd ed.). Burlington: Elsevier Academic Press. ISBN 9780121834937. 
  15. ^ McGuire, Michelle; Beerman, Kathy A. (2007). Nutritional sciences: from fundamentals to food. Belmont, CA: Thomson/Wadsworth. ISBN 0534537170. 
  16. ^ a b Stipanuk, Martha H. (2006). Biochemical, Physiological and Molecular Aspects of Human Nutrition (2nd ed.). Philadelphia: Saunders. ISBN 978116002093. 
  17. ^ Nelson, A. M.; et al. (2008). "Neutrophil gelatinase-associated lipocalin mediates 13-cis retinoic acid-induced apoptosis of human sebaceous gland cells". Journal of Clinical Investigation 118 (4): 1468–1478. doi:10.1172/JCI33869. 
  18. ^ http://la.rsmjournals.com/cgi/content/abstract/5/2/239 Lab Anim 1971;5:239-250. The production of experimental vitamin A deficiency in rats and mice. T. Moore and P. D. Holmes. doi:10.1258/002367771781006492.
  19. ^ "Office of Dietary Supplements. Vitamin A". National Institute of Health. http://www.dietary-supplements.info.nih.gov/factsheets/vitamina.asp. Retrieved 2008-04-08. 
  20. ^ "Micronutrient Deficiencies-Vitamin A". World Health Organization. http://www.who.int/nutrition/topics/vad/en/index.html. Retrieved 2008-04-09. 
  21. ^ Zeba AN, Sorgho H, Rouamba N, et al. (2008). "Major reduction of malaria morbidity with combined vitamin A and zinc supplementation in young children in Burkina Faso: a randomized double blind trial". Nutr J 7: 7. doi:10.1186/1475-2891-7-7. PMID 18237394. http://www.nutritionj.com/content/7/1/7. 
  22. ^ Roncone DP (2006). "Xerophthalmia secondary to alcohol-induced malnutrition". Optometry (St. Louis, Mo.) 77 (3): 124–33. doi:10.1016/j.optm.2006.01.005. PMID 16513513. 
  23. ^ Strobel M, Tinz J, Biesalski HK (2007). "The importance of beta-carotene as a source of vitamin A with special regard to pregnant and breastfeeding women". Eur J Nutr 46 Suppl 1: I1–20. doi:10.1007/s00394-007-1001-z. PMID 17665093. 
  24. ^ Schulz C, Engel U, Kreienberg R, Biesalski HK (2007). "Vitamin A and beta-carotene supply of women with gemini or short birth intervals: a pilot study". Eur J Nutr 46 (1): 12–20. doi:10.1007/s00394-006-0624-9. PMID 17103079. 
  25. ^ Rosenbloom, Mark. "Toxicity, Vitamin". eMedicine. http://www.emedicine.com/emerg/topic638.htm. 
  26. ^ a b Penniston, Kristina L.; Tanumihardjo, Sherry A. (01 Feb 2006). "The acute and chronic toxic effects of vitamin A". Am. J. Clin. Nutr. 83 (2): 191–201. PMID 16469975. http://www.ajcn.org/cgi/content/abstract/83/2/191. 
  27. ^ Eledrisi, Mohsen S.. "Vitamin A Toxicity". eMedicine. http://www.emedicine.com/med/topic2382.htm. 
  28. ^ Masterjohn, C (December 4, 2006). "Vitamin D toxicity redefined: vitamin K and the molecular mechanism.". http://www.ncbi.nlm.nih.gov/pubmed/17145139. 
  29. ^ Forsmo, Siri; Fjeldbo,Sigurd Kjørstad; Langhammer, Arnulf (2008). "Childhood Cod Liver Oil Consumption and Bone Mineral Density in a Population-based Cohort of Peri- and Postmenopausal Women: The Nord-Trøndelag Health Study". Am. J. Epidemiol. 167 (4): 406–411. doi:10.1093/aje/kwm320. PMID 18033763. 
  30. ^ Sale TA, Stratman E (2004). "Carotenemia associated with green bean ingestion". Pediatr Dermatol 21 (6): 657–9. doi:10.1111/j.0736-8046.2004.21609.x. PMID 15575851. 
  31. ^ Nishimura Y, Ishii N, Sugita Y, Nakajima H (1998). "A case of carotenodermia caused by a diet of the dried seaweed called Nori". J. Dermatol. 25 (10): 685–7. PMID 9830271. 
  32. ^ Takita Y, Ichimiya M, Hamamoto Y, Muto M (2006). "A case of carotenemia associated with ingestion of nutrient supplements". J. Dermatol. 33 (2): 132–4. doi:10.1111/j.1346-8138.2006.00028.x. PMID 16556283. 
  33. ^ Science News. Water-soluble vitamin A shows promise.
  34. ^ Myhre AM, Carlsen MH, Bøhn SK, Wold HL, Laake P, Blomhoff R (December 2003). "Water-miscible, emulsified, and solid forms of retinol supplements are more toxic than oil-based preparations". Am. J. Clin. Nutr. 78 (6): 1152–9. PMID 14668278. http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=14668278. 
  35. ^ Kull I, Bergström A, Melén E, et al. (December 2006). "Early-life supplementation of vitamins A and D, in water-soluble form or in peanut oil, and allergic diseases during childhood". J. Allergy Clin. Immunol. 118 (6): 1299–304. doi:10.1016/j.jaci.2006.08.022. PMID 17157660. http://www.jacionline.org/article/S0091-6749(06)01775-1/abstract. 
  36. ^ Brazis PW (March 2004). "Pseudotumor cerebri". Current neurology and neuroscience reports 4 (2): 111–6. doi:10.1007/s11910-004-0024-6. PMID 14984682. 
  37. ^ AJ Giannini, RL Gilliland. The Neurologic, Neurogenic and Neuropsychiatric Disorders Handbook. New Hyde Park, NY. Medical Examination Publishing Co., 1982,pp. 182-183.

Further reading

  • Litwack, Gerald (2007). Vitamin A. Vitamins and Hormones. 75. San Diego, CA: Elsevier Academic Press. ISBN 9780127098753. 

External links

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Vitamins (A11)
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A
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