Vitamin E requirement

Vegetable oils are rich sources of vitamin E, whereas liver and eggs contain moderate amounts. The RDA for a-tocopherol is 10 mg for men and 8 mg for women. Vitamin E requirement increases as the intake of polyunsaturated fatty acid increases. 

To some extent the vitamin E requirement may be lessened by the presence in the diet of synthetic antioxidants and by selenium. Much evidence supports a relationship between the nutritional need for selenium and that for vitamin E. Lack of either causes muscular dystrophy in many animals as well as severe edema (exudative diathesis) in chicks. Since vitamin E-deficient rats have a low selenide (Se2 ) content, it has been suggested that vitamin E protects reduced selenium from oxidation.) Vitamin C (ascorbic acid), in turn, protects vitamin E. 

Horwitt (2001) has criticized this high reference intake, noting that it was based on reinterpretation of the same data as had been provided to the committee in 1998, which set a lower RDA. Data were from studies that he had performed (Horwitt, 1960), andhe notes that to provide a diet rich in polyunsaturated fatty acids and low in vitamin E, the oils had been oxidized to remove vitamin E, and therefore contained large amounts of oxidized lipids that would increase apparent vitamin E requirements. 

Valk EE and Hornstra G (2000) Relationship between vitamin E requirement and polyunsaturated fatty acid intake in man a review. International Journal of Vitamin and Nutrition Research 70, 31-42. 

Since vitamin E requirements depend on dietary polyunsaturated fatty acids, which vary considerably between individuals, it has not been seen as expedient to establish a single Population Reference Intake value. 

Dutta-Roy, A.K., Gordon, M.J., Campbell, F.M., Duthie, G.G., and James, W.P. 1994. Vitamin E Requirements, Transport and Metabolism Role of CX-Tocopherol Binding Proteins. J. Nutr. Biochem. 5 562-570. 

Dietary vitamin E requirements frequently are expressed as milligram a-tocopherol equivalents, but food and supplement labels typically use lU to express vitamin E activity, and 1.0 lU is equivalent to l.Omg of all-racemic-a-tocopherol acetate. The relative activity of all racemic-a-tocopherol is set at 74% that of RRR-a-tocopherol, considered to have the highest bioavailability, and thus as the standard against which all the others mnst be compared. ... 

For these reasons alone, a vitamin E symposium will not be short of problems and material for discussion. Many more unanswered questions come to light, however, when the biochemical and physiological properties of vitamin E are considered. The program of this meeting includes papers on the metabolism of vitamin E interrelations among vitamin E, metals, and ubi( uinones vitamin E and nucleic acid metabolism interrelations between vitamin E and polyunsaturated fatty acids vitamin E requirements of human infants vitamin E in health and disease of poultry, sheep, cattle, and pigs and so on. Everywhere, alongside established facts, there are unanswered questions and unsolved problems. 

The interrelations between vitamin E and selenium in cattle and sheep are undoubtedly as complex as they are in other species. It seems reasonable to state that vitamin E, in combatting the toxicity of unsaturated fat, acts as an antioxidant, for its effect can be duplicated by many other antioxidants and redox dyestuffs. Similarly it is indisputable that selenium is a dietar essential for ruminants and that its absence from their diet results in muscular disease. Both unsaturated fat excess and selenium deficiency must produce primary disturbances in the muscle cells. These disturbances need not be common to both, for muscle reacts similarly to a variety of biochemical insult. In the presence of selenium and the absence of unsaturated fat, vitamin E requirements of ruminants appear to be extremely small. The failure to produce reproductive disorders in ruminants by experimental vitamin E deficiency, and the failure to produce muscular disease on fat-free diets deficient in vitamin E but likely to have been adequate in selenium content is evidence of this contention. How vitamin E acts in preventing muscular disease due to selenium deficiency, however, is not known, and this aspect needs elucidation. 

Vitamin E is the name given to a number of structurally related compounds the most important of which is a-tocopherol. The vitamin is needed for mitochondrial electron-transport function and prevents oxidation of various compounds including polyunsaturated fatty acids and vitamin A. The dependence of vitamin E requirement on the amount of dietary polyunsaturated fatty acids has been fully discussed by Jager (1975). Traditionally, vitamin E has been known as the fertility vitamin. However, deficiency leads to serious changes in skeletal muscle, the blood system and other tissues before reproduction is impaired. The effects on different animals are described by Jager (1975). The topic of vitamin E is also covered by Scott (1978). 

Horwitt [125] has investigated vitamin E requirements in humans by administering a vitamin E-defi-cient diet supplemented with unsaturated fats for the purpose of removing vitamin E. He found that the amount of tocopherol in tissue is inversely related to the amount of unsaturated fat that has been administered. A significant observation was that 30% of the individuals receiving the unsaturated fats also developed duodenal ulcers. Hemorrhagic endarteritis similar to that observed in vitamin E-deficient chicks has been described in a child who, for therapeutic purposes, was fed a diet rich in milk and unsaturated fat, but devoid of vitamin E. 

It is difficult to establish vitamin E requirements, partly because deficiency is more or less unknown but also because the requirement depends on the intake of polyunsaturated fatty acids. It is generally accepted, albeit with little experimental evidence, that an acceptable intake of vitamin E is 0.4 mg a-tocopherol equivalent per gram of dietary polyunsaturated fatty acid. This does not present any problem as the plant oils that are rich sources of polyunsaturated fatty acids are also rich sources of vitamin E. 

It is noteworthy that when fat is added to the diet it will destroy the vitamin E in both the diet and the digestive tract if rancidity occurs. For this reason, the quantitative relationship between vitamin E and the amount and kind of dietary fat is of practical importance the higher the consumption of polyunsaturated fats, the higher the vitamin E requirement. 

Vitamin E is added to whole milk powder and cereals to supplement dietary requirements. The vitamin E requirement increases with an increased intake of polyunsaturated fatty acid and several types of margarines are enriched with vitamin E. The acetate ester of a-tocopherol is used as a supplement on account of its greater stability (Ottaway, 2008). 

The amount of vitamin E required by the body depends upon its size and the amount of polyunsaturated fats in the diet, as vitamin E is needed to protect these fats from oxidation. The requirement for vitamin E depends upon intake of refined oils, fried foods, or rancid oils. Supplemental estrogen or estrogen imbalance in women increases the need for vitamin E, as does air pollution. The recommended dietary allowance (RDA) for vitamin E is really quite low, many people do not consume this in their diet alone. Table 19.1 lists the RDAs and tolerable upper intake levels (ULs) for vitamin E. The new recommendations for vitamin E are expressed as milligrams of RRR-a-tocopherol equivalents. Dietary supplements of vitamin E are labeled in terms of international units (lU). 1 mg of synthetic vitamin E (a//-rac-a-tocopheryl acetate is equivalent to 1 lU vitamin E, but only 0.45 mg RRR-a-tocopherol. 1 mg of natural vitamin E (RRR-a-tocopherol) provides 1.5 lU. For the LIE, the Food and Nutrition Board recommended 1000 mg of any a-tocopherol form, which is equivalent to 1500 lU RRR- or 100 lEI all-rac-a-tocopherol (Food and Nutrition Board, 2000 Hathcock et al., 2005 Combs, 2008). 

In 2000, the Food and Nutrition Board (FNB) [86] defined a-tocopherol as the only form that meets human vitamin E requirements, because only a-tocopherol has been shown to reverse human vitamin E deficiency symptoms. 

Wiss and co-workers (1964) (44) as well as Weber and Weiser (1967) (45) clarified the relationship between vitamin E requirement and intake of linoleic acid by the hemolysis test. According to these authors man needs 0.5 to 1.0 mg vitamin E per gram linoleic acid to compensate for the increased requirement of vitamin E due to higher polyenic acid content in such diets. Only therefore and not for ailing and healthy hearts" can a daily intake of 10-15 mg vitamin E be recommended. 

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