Vitamin
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A vitamin is an organic compound required as a nutrient in tiny amounts by an organism.[1] A compound is called a vitamin when it cannot be synthesized in sufficient quantities by an organism, and must be obtained from the diet. Thus, the term is conditional both on the circumstances and the particular organism. For example, ascorbic acid functions as vitamin C for some animals but not others, and vitamins D and K are required in the human diet only in certain circumstances.[1] Vitamins are defined by their biological activity, not their structure. Thus, each "vitamin" actually refers to a number of vitamer compounds, which form a set of distinct chemical compounds that show the biological activity of a particular vitamin. Such a set of chemicals are grouped under an alphabetized vitamin "generic descriptor" title, such as "vitamin A," which (for example) includes retinal, retinol, and many carotenoids. [1] Vitamers are often inter-convertible in the body. The term vitamin does not include other essential nutrients such as dietary minerals, essential fatty acids, or essential amino acids, nor does it encompass the large number of other nutrients that promote health but that are not essential for life.
Vitamins have diverse biochemical functions, including function as hormones (e.g. vitamin D), antioxidants (e.g. vitamin E), and mediators of cell signaling and regulators of cell and tissue growth and differentiation (e.g. vitamin A) [1]. The largest number of vitamins (e.g. B complex vitamins) function as precursors for enzyme cofactor bio-molecules (coenzymes), that help act as catalysts and substrates in metabolism. When acting as part of a catalyst, vitamins are bound to enzymes and are called prosthetic groups. For example, biotin is part of enzymes involved in making fatty acids. Vitamins also act as coenzymes to carry chemical groups between enzymes. For example, folic acid carries various forms of carbon group – methyl, formyl and methylene - in the cell. Although these roles in assisting enzyme reactions are vitamins' best-known function, the other vitamin functions are equally important.[1]
Until the 1800s, vitamins were obtained solely through food intake, and changes in diet (which, for example, could occur during a particular growing season) can alter the types and amounts of vitamins ingested. Vitamins have been produced as commodity chemicals and made widely available as inexpensive pills for several decades,[1] allowing supplementation of the dietary intake.
History
The value of eating certain foods to maintain health was recognized long before vitamins were identified. The ancient Egyptians knew that feeding a patient liver would help cure night blindness, an illness now known to be caused by a vitamin A deficiency. The advancement of ocean voyage during the Renaissance resulted in prolonged periods without access to fresh fruits and vegetables, and made illnesses from vitamin deficiency common among ship's crew.
In 1749, the Scottish surgeon James Lind discovered that citrus foods helped prevent scurvy, a particularly deadly disease in which collagen is not properly formed, causing poor wound healing, bleeding of the gums, severe pain, and death.[1] In 1753, Lind published his Treatise on the Scurvy, which recommended using lemons and limes to avoid scurvy, which was adopted by the British Royal Navy. This led to the nickname Limey for sailors of that organization. Lind's discovery, however, was not widely accepted by individuals in the Royal Navy's Arctic expeditions in the 19th century, where it was widely believed that scurvy could be prevented by practicing good hygiene, regular exercise, and by maintaining the morale of the crew while on board, rather than by a diet of fresh food.[1] As a result, Arctic expeditions continued to be plagued by scurvy and other deficiency diseases. In the early 20th century, when Robert Falcon Scott made his two expeditions to the Antarctic, the prevailing medical theory was that scurvy was caused by "tainted" canned food.[1]
In 1881, Russian surgeon Nikolai Lunin studied the effects of scurvy while at the University of Tartu in present-day Estonia.[1] He fed mice an artificial mixture of all the separate constituents of milk known at that time, namely the proteins, fats, carbohydrates, and salts. The mice that received only the individual constituents died, while the mice fed by milk itself developed normally. He made a conclusion that "a natural food such as milk must therefore contain, besides these known principal ingredients, small quantities of unknown substances essential to life".[1] However, his conclusions were rejected by other researchers when they were unable to reproduce his results. One difference was that he had used table sugar (sucrose), while other researchers had used milk sugar (lactose) that still contained small amounts of vitamin B.
In the Orient where polished white rice was the common staple food of the middle class, beriberi resulting from lack of vitamin B was endemic. In 1884, Takaki Kanehiro, a British trained medical doctor of the Japanese Navy observed that beriberi was endemic among low ranking crew who often ate nothing but rice but not among crews of Western navies and officers who were entitled to a Western-style diet. Kanehiro initially believed that lack of protein was the chief cause of beriberi. With the support of Japanese navy, he experimented using crews of two battleships, one crew was fed only white rice, while the other was fed a diet of meat, fish, barley, rice, and beans. The group that ate only white rice documented 161 crew with beriberi and 25 deaths, while the latter group had only 14 cases of beriberi and no deaths. This convinced Kanehiro and the Japanese Navy that diet was the cause of beriberi. This was confirmed in 1897, when Christiaan Eijkman discovered that feeding unpolished rice instead of the polished variety to chickens helped to prevent beriberi in the chickens. The following year, Frederick Hopkins postulated that some foods contained "accessory factors"—in addition to proteins, carbohydrates, fats, et cetera—that were necessary for the functions of the human body.[1] Hopkins was awarded the 1929 Nobel Prize for Physiology or Medicine with Christiaan Eijkman for their discovery of several vitamins.
In 1910, Japanese scientist Umetaro Suzuki succeeded in extracting a water-soluble complex of micronutrients from rice bran and named it aberic acid. He published this discovery in a Japanese scientific journal.[1] When the article was translated into German, the translation failed to state that it was a newly discovered nutrient, a claim made in the original Japanese article, and hence his discovery failed to gain publicity. Polish biochemist Kazimierz Funk isolated the same complex of micronutrients and proposed the complex be named "Vitamine" (a portmanteau of "vital amine") in 1912.[1] The name soon became synonymous with Hopkins' "accessory factors", and by the time it was shown that not all vitamins were amines, the word was already ubiquitous. In 1920, Jack Cecil Drummond proposed that the final "e" be dropped to deemphasize the "amine" reference after the discovery that vitamin C had no amine component.
Throughout the early 1900s, the use of deprivation studies allowed scientists to isolate and identify a number of vitamins. Initially, lipid from fish oil was used to cure rickets in rats, and the fat-soluble nutrient was called "antirachitic A". The irony here is that the first "vitamin" bioactivity ever isolated, which cured rickets, was initially called "vitamin A", the bioactivity of which is now called vitamin D.[1] What we now call "vitamin A" was identified in fish oil because it was inactivated by ultraviolet light. In 1931, Albert Szent-Györgyi and a fellow researcher Joseph Svirbely determined that "hexuronic acid" was actually vitamin C and noted its anti-scorbutic activity. In 1937, Szent-Györgyi was awarded the Nobel Prize for his discovery. In 1943 Edward Adelbert Doisy and Henrik Dam were awarded the Nobel Prize for their discovery of vitamin K and its chemical structure.
In humans
Vitamins are classified as either water-soluble, meaning that they dissolve easily in water or fat-soluble vitamins, which are absorbed through the intestinal tract with the help of lipids (fats). In general, water-soluble vitamins are readily excreted from the body. Each vitamin is typically used in multiple reactions and, therefore, most have multiple functions.[1]
In humans there are 13 vitamins: 4 fat-soluble (A, D, E and K) and 9 water-soluble (8 B vitamins and vitamin C).
| Vitamin generic descriptor name | Vitamer chemical name(s) | Solubility | Recommended dietary allowances (male, age 19–70)[1] | Deficiency disease | Upper Intake Level (UL/day)[1] | Overdose disease |
|---|---|---|---|---|---|---|
| Vitamin A | Retinoids (retinol, retinoids and carotenoids) | Fat | 900 µg | Night-blindness and Keratomalacia[1] | 3,000 µg | Hypervitaminosis A |
| Vitamin B1 | Thiamine | Water | 1.2 mg | Beriberi | N/D[1] | ? |
| Vitamin B2 | Riboflavin | Water | 1.3 mg | Ariboflavinosis | N/D | ? |
| Vitamin B3 | Niacin, niacinamide | Water | 16.0 mg | Pellagra | 35.0 mg | |
| Vitamin B5 | Pantothenic acid | Water | 5.0 mg[1] | Paresthesia | N/D | ? |
| Vitamin B6 | Pyridoxine, pyridoxamine, pyridoxal | Water | 1.3-1.7 mg | Anaemia[1] | 100 mg | Impairment of proprioception, nerve damage |
| Vitamin B7 | Biotin | Water | 30.0 µg | Dermatitis, enteritis | N/D | ? |
| Vitamin B9 | Folic acid, folinic acid | Water | 400 µg | Deficiency during pregnancy is associated with birth defects, such as neural tube defects | 1,000 µg | Refer to deficiency of Vitamin B6 |
| Vitamin B12 | Cyanocobalamin, hydroxycobalamin, methylcobalamin | Water | 2.4 µg | Megaloblastic anaemia[1] | N/D | ? |
| Vitamin C | Ascorbic acid | Water | 90.0 mg | Scurvy | 2,000 mg | Refer to Vitamin C megadosage |
| Vitamin D | Ergocalciferol, cholecalciferol | Fat | 5.0 µg-10 µg[1] | Rickets and Osteomalacia | 50 µg | Hypervitaminosis D |
| Vitamin E | Tocopherols, tocotrienols | Fat | 15.0 mg | Deficiency is very rare; mild hemolytic anemia in newborn infants.[1] | 1,000 mg | ? |
| Vitamin K | phylloquinone, menaquinones | Fat | 120 µg | Bleeding diathesis | N/D | ? |
In nutrition and diseases
Vitamins are essential for the normal growth and development of a multicellular organism. Using the genetic blueprint inherited from its parents, a fetus begins to develop, at the moment of conception, from the nutrients it absorbs. It requires certain vitamins and minerals to be present at certain times. These nutrients facilitate the chemical reactions that produce among other things, skin, bone, and muscle. If there is serious deficiency in one or more of these nutrients, a child may develop a deficiency disease. Even minor deficiencies may cause permanent damage.[1]
For the most part, vitamins are obtained with food, but a few are obtained by other means. For example, microorganisms in the intestine—commonly known as "gut flora"—produce vitamin K and biotin, while one form of vitamin D is synthesized in the skin with the help of natural ultraviolet in sunlight. Humans can produce some vitamins from precursors they consume. Examples include vitamin A, produced from beta carotene, and niacin, from the amino acid tryptophan.[1]
Once growth and development are completed, vitamins remain essential nutrients for the healthy maintenance of the cells, tissues, and organs that make up a multicellular organism; they also enable a multicellular life form to efficiently use chemical energy provided by food it eats, and to help process the proteins, carbohydrates, and fats required for respiration.
Deficiencies
Deficiencies of vitamins are classified as either primary or secondary. A primary deficiency occurs when an organism does not get enough of the vitamin in its food. A secondary deficiency may be due to an underlying disorder that prevents or limits the absorption or use of the vitamin, due to a “lifestyle factor”, such as smoking, excessive alcohol consumption, or the use of medications that interfere with the absorption or use of the vitamin.[1] People who eat a varied diet are unlikely to develop a severe primary vitamin deficiency. In contrast, restrictive diets have the potential to cause prolonged vitamin deficits, which may result in often painful and potentially deadly diseases.
Because human bodies do not store most vitamins, humans must consume them regularly to avoid deficiency. Human bodily stores for different vitamins vary widely; vitamins A, D, and B12 are stored in significant amounts in the human body, mainly in the liver,[1] and an adult human's diet may be deficient in vitamins A and B12 for many months before developing a deficiency condition. Vitamin B3 is not stored in the human body in significant amounts, so stores may only last a couple of weeks.[1][1]
Well-known human vitamin deficiencies involve thiamine (beriberi), niacin (pellagra), vitamin C (scurvy) and vitamin D (rickets). In much of the developed world, such deficiencies are rare; this is due to (1) an adequate supply of food; and (2) the addition of vitamins and minerals to common foods, often called fortification.[1][1]
Side effects and overdose
In large doses, some vitamins have documented side effects that tend to be more severe with a larger dosage. The likelihood of consuming too much of any vitamin from food is remote, but overdosing from vitamin supplementation does occur. At high enough dosages some vitamins cause side effects such as nausea, diarrhea, and vomiting.[1][1] When side effects emerge, recovery is often accomplished by reducing the dosage. The concentrations of vitamins an individual can tolerate vary widely, and appear to be related to age and state of health.[1] In the United States, overdose exposure to all formulations of vitamins was reported by 62,562 individuals in 2004 (nearly 80% of these exposures were in children under the age of 6), leading to 53 "major" life-threatening outcomes and 3 deaths[1]—a small number in comparison to the 19,250 people who died of unintentional poisoning of all kinds in the U.S. in the same year (2004).[1]
Supplements
Dietary supplements, often containing vitamins, are used to ensure that adequate amounts of nutrients are obtained on a daily basis, if optimal amounts of the nutrients cannot be obtained through a varied diet. Scientific evidence supporting the benefits of some dietary supplements is well established for certain health conditions, but others need further study.[1]
In the United States, advertising for dietary supplements is required to include a disclaimer that the product is not intended to treat, diagnose, mitigate, prevent, or cure disease, and that any health claims have not been evaluated by the Food and Drug Administration.[1] In some cases, dietary supplements may have unwanted effects, especially if taken before surgery, with other dietary supplements or medicines, or if the person taking them has certain health conditions.[1] Vitamin supplements may also contain levels of vitamins many times higher, and in different forms, than one may ingest through food.[1]
Intake of excessive quantities can cause vitamin poisoning, most commonly for Vitamin A and Vitamin D. For this reason, most common vitamins have recommended upper daily intake amounts.
Governmental regulation of vitamin supplements
Most countries place dietary supplements in a special category under the general umbrella of foods, not drugs. This necessitates that the manufacturer, and not the government, be responsible for ensuring that its dietary supplement products are safe before they are marketed. Unlike drug products, that must explicitly be proven safe and effective for their intended use before marketing, there are often no provisions to "approve" dietary supplements for safety or effectiveness before they reach the consumer. Also unlike drug products, manufacturers and distributors of dietary supplements are not generally required to report any claims of injuries or illnesses that may be related to the use of their products.[1] [1]
Names in current and previous nomenclatures
The reason the set of vitamins seems to skip directly from E to K is that the vitamins corresponding to "letters" F-J were either reclassified over time, discarded as false leads, or renamed because of their relationship to "vitamin B", which became a "complex" of vitamins. The German-speaking scientists who isolated and described vitamin K (in addition to naming it as such) did so because the vitamin is intimately involved in the Koagulation of blood following wounding. At the time, most (but not all) of the letters from F through J were already designated, so the use of the letter K was considered quite reasonable.
The following table lists chemicals that had previously been classified as vitamins, as well as the earlier names of vitamins that later became part of the B-complex:
| Previous name[1][1] | Chemical name[1][1] | Reason for name change[1] |
|---|---|---|
| Vitamin B4 | Adenine | DNA metabolite |
| Vitamin B8 | Adenylic acid | DNA metabolite |
| Vitamin F | Essential fatty acids | Needed in large quantities (does not fit the definition of a vitamin). |
| Vitamin G | Riboflavin | Reclassified as Vitamin B2 |
| Vitamin H | Biotin | Reclassified as Vitamin B7 |
| Vitamin J | Catechol, Flavin | Protein metabolite |
| Vitamin L1[1] | Anthranilic acid | Protein metabolite |
| Vitamin L2[1] | Adenylthiomethylpentose | RNA metabolite |
| Vitamin M | Folic acid | Reclassified as Vitamin B9 |
| Vitamin O | Carnitine | Protein metabolite |
| Vitamin P | Flavonoids | No longer classified as a vitamin |
| Vitamin PP | Niacin | Reclassified as Vitamin B3 |
| Vitamin U | S-Methylmethionine | Protein metabolite |
See also
References
General References Include:
- Stedman's Medical Dictionary. Ed. Maureen Barlow Pugh et.al. 27th ed. Baltimore: Lippincott Williams & Wilkins, 2000.
- Donatelle, Rebecca J. Health: The Basics. 6th ed. San Francisco: Pearson Education, Inc. 2005.
External links
- USDA RDA chart in PDF format
- Health Canada Dietary Reference Intakes Reference Chart for Vitamins
- NIH Office of Dietary Supplements: Fact Sheets
- NIH Office of Dietary Supplements. Dietary Supplements: Background Information
Vitamins (A11) | |
|---|---|
| Fat soluble | A: Retinol - Beta-carotene - Tretinoin - Alpha-carotene
D: 7-Dehydrocholesterol → Previtamin D3 → Cholecalciferol (D3) → Calcidiol → Calcitriol (active form) → Calcitroic acid; Ergosterol → Ergocalciferol (D2); (analogues: Dihydrotachysterol, Calcipotriol, Tacalcitol) E: Tocopherol - Tocotrienol K: Naphthoquinone - Phylloquinone/K1 - Menatetrenone/K2 |
| Water soluble: B vitamins | B1 (Thiamine, Sulbutiamine, Benfotiamine) - B2 (Riboflavin) - B3 (Niacin, Nicotinamide) - B5 (Pantothenic acid, Dexpanthenol, Pantethine) - B6 (Pyridoxine, Pyridoxal phosphate) - B7 (Biotin) - B9 (Folic acid) - B12 (Cyanocobalamin, Hydroxocobalamin, Methylcobalamin, Cobamamide) |
| Water soluble: other | C (Ascorbic acid) - Choline |
| see also enzyme cofactors | |
Food chemistry |
|---|
| Carbohydrates • Colors • Enzymes • Flavors • Food additives • Lipids • Minerals • Proteins • Vitamins • Water |
Nutritional pathology (E40-68, 260-269) | |
|---|---|
| Malnutrition | Kwashiorkor - Marasmus - Catabolysis |
| Avitaminosis | B vitamins: B1: Beriberi/Wernicke's encephalopathy, B2: Ariboflavinosis, B3: Pellagra, B6: Pyridoxine deficiency, B7: Biotin deficiency, B9: Folate deficiency, B12: Vitamin B12 deficiency other vitamins: A: Vitamin A deficiency/Bitot's spots, C: Scurvy, D: Rickets/Osteomalacia |
| Mineral deficiency | Zinc deficiency - Iron deficiency - Magnesium deficiency - Chromium deficiency |
| Hyperalimentation | Obesity - Vitamin poisoning (Hypervitaminosis A, Hypervitaminosis D, Hypervitaminosis E) |
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Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .