VITAMIN E IN FOODS
Good food sources of Vitamin E include plant oils (e.g., cottonseed, canola, safflower, and sunflower oils), wheat germ, asparagus, almonds, peanuts, and sunflower seeds. Animal fats and dairy products contain little vitamin E.
The vitamin E contents of a food depends on the harvesting, processing, storage, and cooking because vitamin E is highly susceptible to destruction by oxygen, metals, light, and deep-frying. Thus, foods that are highly processed and/or deep fried are usually poor sources of vitamin E.
Vitamin E Needs
The RDA for vitamin E is 15 mg/day of alpha -tocopherol for both men and women. The recommendation is based on the amount of vitamin E needed to prevent breakdown if red blood cell membranes, a process called hemolysis. The 15-mg allotment is equivalent to 22 IU of a natural source and 33 IU of a synthetic source of vitamin E.
Food and supplement labels often report itamin E activity in IUs. When converting IUs of vitamin E in synthetic form to milligrams, 1 IU equals about 0.45 mg. If the vitamin E is from a natural source, 1 IU equals 0.67 mg because the natural form of vitamin E is more potent than the synthetic form. The Daily Value of vitamin E used on food and supplement labels is 30 IU.
FUNCTIONS OF VITAMIN E
Vitamin E is an important part of the body’s antioxidant network. It funtions as an antioxidanr that stops chain reactions caused by free radicals that can potentially damage cells. Free radicals are very unstable compounds that have an unpaired electron. Normally, atoms left with an unpaired electron after oxidation reactions immediately pair with another, creating more stable compounds. However, when this does not occur, free radicals remain and act as strong oxidizing (electron-seeking) agents. These can be very destructive to electron-dense cell components, such as cell membranes and DNA.
Vitamin E is one of the most effective mechanism for stopping lipid peroxidation chain reactions in the body. By donating a hydrogen to lipid radicals, vitamin E stops the cain of oxidation reactions. which protects the lipids in the body.
VITAMIN E DEFICIENCY
Vitamin E deficiency is rare in humans. Individuals with fat malabsorption conditions, such as cystic fibrosis and Crohn’s disease, smokers, and preterm infants are at greater risk. Preterm infants are particularly susceptible because they are born with limited stored of vitamin E and have insufficient intestinal absorption of this vitamin. Smokers are at increased risk of deficiency because of oxidative stress cause by smoke.
Vitamin E deficiency is characterized by the premature breakdown of red blood cells (hemolsys) and the development of hemolytic anemia. Because of the serious risk of this, preterm infants are given supplemental vitamin E and specialized formulas containing vitamin E early in life.
Vitamin E deficiency can also impair immune functions and cause neurological changes in the spinal cord and peripheral nervous system. These symptoms have been noted in individuals who developed vitamin E deficiency as a resuls of a genetic abnormality in lipoproyein synthesis, which decreases vitamin E transport and distribution in the body.
VITAMIN E TOXICITY
Although vitamin E is relatively non-toxic, excessive amounts can interfere with the role of vitamin K in blood clotting. This causes insufficient clotting and the risk of hemorrhaging. These risks are of particular concern in individuals taking daily aspirin or anticoagulation medications. Megadoses of vitamin E can result in hemorraging in these individuals. To prevent toxicity-related problems, the Upper Level for vitamin E is set at 1000 mg (1500 IU) of alpha-tocopherol from natural sources and 1100 IU from synthetic sources.
