Vitamin E and Tocopherols and Tocotrienols + Food Sources of Vitamin E + Role in the Body
What is vitamin E?
Similar to many other vitamins, vitamin E is not necessarily a single molecule but a class of similar molecules accomplishing related activities. There are about eight or so vitamin E molecules that can be subdivided into two major classes, tocopherols and tocotrienols, which themselves can be subdivided and given Greek descriptors (i.e.,α, β, δ, γ).
What foods are good sources of vitamin E?
Good food sources of vitamin E include plant oils, margarine, and some fruits and vegetables, such as peaches and asparagus (see ). The average adult intake of vitamin E approximates the RDA, which is 15 alpha-tocopherol equivalents (TE) daily. More common supplement forms of vitamin E include α-tocopherol succinate and α-tocopherol acetate. In addition,α-tocopherol phosphate, which has the same nutritional value of the succinate and acetate forms, is also available as are mixed tocopherols and gamma tocopherol versions. Furthermore, alpha-tocopherol supplements from natural sources (often labeled dl-α-tocopherol) will have more of the usable form of vitamin E than synthetic vitamin E, which can contain forms of alpha-tocopherol that our body can’t use.
How is vitamin E handled in the body?
Vitamin E shows a fair absorption (25 to 50 percent) from the small intestine. Factors such as an increased need or low stores of vitamin E may certainly increase the absorption percentage. Like other fat-soluble vitamins, vitamin E needs the assistance of lipid digestive and absorptive processes (e.g., chylomicrons). Much of the absorbed vitamin E will end up in the liver as chylomicron remnants are removed from the blood. The liver can then add vitamin E to VLDLs, which are then released into circulation where they can be delivered to most cells. By and large this is vitamin E in the form of alpha-tocopherol which means that it is the most significant form found in the blood as well as throughout our body.
Because vitamin E is not very water soluble, very little is lost in urine; however, large intakes of vitamin E will result in a proportionate increase in urinary losses. The primary means for vitamin E loss from the body appears to be through the feces. The liver incorporates vitamin E into bile, which is dumped into the digestive tract. Some of this vitamin E, along with vitamin E from dietary sources, is not absorbed and becomes part of feces.
What does vitamin E do in the body?
By and large vitamin E functions as an antioxidant protecting cells from free radicals and most of its activity is attributable to α-tocopherol. As vitamin E is a lipid-soluble molecule it is logical to think that vitamin E would be most active in lipid-rich areas of our cells. This appears to be the case, as vitamin E’s antioxidant activities are recognized mostly in regard to protecting the lipid-rich cell membranes. Cell membranes contain a tremendous amount of phospholipids, each of which contain two fatty acids. Furthermore, double bonds within some of these fatty acids appear to be very vulnerable to free-radical attack. Vitamin E appears to protect fatty acids by donating one of its own electrons to a free radical. This pacifies the free radical and also spares the fatty acids in cell membranes.
Since lipoproteins provide a primary means of shuttling vitamin E throughout the body, researchers have speculated that vitamin E may be involved in the prevention of heart disease. Some evidence suggests that vitamin E helps protect LDL from oxidation. Oxidized LDL is believed to be a strong risk factor for atherosclerosis.
How much vitamin E do we need daily?
The RDA for men and women of all ages is 15 mg (or 22.5 IU) of vitamin E daily. This is also the recommended level during pregnancy while the RDA is increased to 19 mg during lactation. Like other vitamins, the RDA is viewed as a minimum recommendation.
What are alpha-tocopherol equivalents?
Among the vitamin E molecules, alpha-tocopherol is the most prevalent, popular, and probably potent in the body. For this reason the RDA for vitamin E is provided in alpha-tocopherol equivalents (α-TE). Here, 1 alpha-TE unit has the activity of 1 mg of alpha-tocopherol. Since other forms of vitamin E are not as potent, the alpha-TE unit amount bestowed to a food is based on the amount of alpha-tocopherol as well as the potential vitamin E activity contributions made by the other forms. For example, if a food contained 25 mg of alpha-tocopherol and 50 mg of another form of vitamin E which is only 50 percent as potent as alpha-tocopherol, the food is said to contain 50 alpha-TE (25 mg of alpha-tocopherol + 25 mg [50 percent of 50 mg] of other vitamin E form).
What happens if too little vitamin E is consumed?
Vitamin E deficiency is somewhat rare in adults with the exception of those who have medical problems that impact the normal digestion of lipids. Any situation in which normal fat digestion and absorption are hindered can ultimately reduce the amount of vitamin E absorbed from the digestive tract. A deficiency may take many months or years to show itself through medical symptoms such as red blood cell fragility and neurological abnormalities. Usually the medical problem is treated long before vitamin E deficiency signs are recognized. However, children with cystic fibrosis are a special concern, as the pancreas produces inadequate amounts of digestive enzymes in those with this disease.
Can vitamin E become toxic?
Compared to the fat-soluble vitamins discussed so far, vitamin E is relatively nontoxic. However, studies on people eating fifty to one hundred times the RDA have demonstrated that these amounts can result in nausea, diarrhea, and headaches, while some individuals complained of general weakness and fatigue. It should be recognized that excessive vitamin E supplementation may interfere with vitamin K’s activity in blood clotting.
Do we need more vitamin E if we eat more unsaturated fat sources?
As unsaturated fatty acids are more prone to free-radical attack, many researchers contend that diets containing more unsaturated fatty acids will increase the need for vitamin E. One fate of diet-derived fatty acids is to become part of phospholipids in cell membranes. In fact, the more unsaturated fatty acids found in the diet, the more unsaturated fatty acids found in cell membrane phospholipids. They argue that as we shift our fatty acid intake to more unsaturated fatty acids, such as the polyunsaturated omega-3 and omega-6 fatty acids, we may need to provide these fatty acids with adequate antioxidant escorts (e.g., vitamin E). Other antioxidants such as vitamin C are not as impressive in directly protecting unsaturated fatty acids. This is because their water solubility keeps them more involved in the watery intracellular fluid rather than the lipid portion of cell membranes.
The choice of unsaturated fatty acid sources, such as plant oils or fish (oil in fish), differs in regard to vitamin E contribution. Plant oils contain vitamin E while fish oils do not. Some researchers believe that if we derive most of our unsaturated fatty acids from fish sources those foods should be complemented with foods higher in vitamin E or a supplement containing vitamin E. The idea is intriguing and awaits research validation.
Does vitamin E work with other antioxidants in a team-like manner?
It should be recognized that other antioxidant-like compounds such as vitamin C and selenium can support vitamin E’s efforts. After vitamin E concedes an electron to a free radical it can be restocked with another electron from vitamin C. Thus vitamin C helps keep vitamin E equipped in its battle against free radicals. This helps to recycle vitamin E. The mineral selenium, as part of the enzyme glutathione peroxidase, seems to have a beneficial effect upon vitamin E status. It has been suggested that like vitamin C, glutathione peroxidase also helps to recycle vitamin E by restocking it with an electron. Also, glutathione peroxidase helps inactivate free radicals such as peroxides, which ultimately reduces the workload of vitamin E. One important consideration is that supplementation can often counterbalance internal efforts to strengthen antioxidant capacity. Based on this, higher supplementation doses of antioxidant nutrients may not provide additional support under normal conditions.