Vitamin E is a fat-soluble nutrient that is actually eight compounds—four tocopherols and four tocotrienols. The synthetic dl-alpha-tocopherol (all-rac-alpha tocopherol) is also referred to as vitamin E and is found in dietary supplements and fortified foods. Tocopherols are considered to be the most active of the vitamin E compounds and are found throughout the food chain in both plant and animal sources.

The primary function of vitamin E in the body is as an antioxidant. Because it is fat-soluble, it is important for preventing oxidation of fats in places like cell membranes and mitochondria, as well as preventing the oxidation of low-density lipoproteins (LDLs) circulating in the blood. Vitamin E also plays a small role in cell signaling, affecting the expression of some immune cells. It also has a role in circulation being somewhat vasodilatory, inducing nitric oxide and having some antithrombic function. 

In its antioxidant role, vitamin E is called a “chain-breaking” antioxidant due to its ability to block the destructive free-radical cascade in the phospholipid membrane of human cells. Once it has done its job, such as donating an electron to neutralize something like a dangerous peroxyl radical, vitamin E becomes a free radical itself (the tocopherol radical). It then must contact another antioxidant (such as vitamin C or coenzyme Q10) in order to be recycled back to a harmless form.

Accordingly, vitamin C must also be recycled by glutathione or lipoic acid, which must in turn be restored by nicotinamide adenine dinucleotide (NADH) or nicotinamide adenine dinucleotide phosphate (NADPH). This is important to understand since it shows that while vitamin E is a very important antioxidant, it is really at the top of a cascade. In studies examining therapeutic doses of vitamin E, it has been suggested that the rest of the cascade cannot bear the burden of tocopherol radical generated (and so on down the line). Thus, it is important that while we recognize the importance of vitamin E as an independent nutrient, we must see its overall larger place as well.

Only plants, not animals, make vitamin E. Oily plants are richest in vitamin E and provide the most bioavailable sources. Animal fats also concentrate vitamin E, and it is present in animal sources only to the degree it was present in the diet of the animal. Most vitamin E is absorbed in micellar form by passive diffusion in the jejunum. This process is dependent on bile and pancreatic enzymes, which are involved in the formation of the micelles. As there are cases of vitamin E deficiency reported in the clear absence of fat malabsorption, it is also suspected that another unidentified factor plays a role in uptake. Percent absorption of vitamin E is variable and generally decreases as dose increases. Like most fatty nutrients, vitamin E is transported in lymph. In the case of vitamin E, LDL is the carrier molecule. LDL is also responsible for the transport of vitamin E into target cells via the LDL receptor.


Vitamin E deficiency is generally considered to be quite rare. Findings are primarily neuromuscular and resemble spinocerebellar ataxia. Early findings may include memory changes, distal muscular weakness, loss of proprioception and balance, decreased vibratory sensation, night blindness, changes in visual fields, and diminished deep-tendon reflexes. As disease progresses, there can be frank dementia, nystagmus, blindness, retinal disease (pigmented retinopathy), ptosis, areflexia, progressive neuropathy and myelopathy, arrhythmia, and dysphagia. While early stages are reversible, late stages are not. Many clinical texts note that the symptoms can be identical to any ataxia, while eye disease can mimic retinitis pigmentosa; thus, these conditions should be part of the differential diagnosis. 

Known risk factors for vitamin E deficiency are short-bowel syndrome, abetalipoproteinemia, cystic fibrosis, cholestatic liver disease, and malabsorption.


Some references list vitamin E in milligrams, others in international units (IU). To dose vitamin E products, it is important to understand the difference. Most vitamin E that is supplemented is alpha-tocopherol. The synthetic and natural forms are used interchangeably, but are not equivalent in their activity level. Natural vitamin E, which will be listed on a product label as d-alpha-tocopherol or tocopheryl (or as RRR-alpha-tocopherol) has a much higher vitamin E activity than the synthetic form (seen on a label as dl-alpha-tocopherol or allrac-alpha-tocopherol). Margaret Traber, PhD, the esteemed vitamin E researcher, gives the equivalents as follows:1

  • RRR-alpha-tocopherol (natural or d-alpha-tocopherol): IU x 0.67 = mg RRR-alpha-tocopherol (100IU=67mg) 
  • all-rac-alpha-tocopherol (synthetic or dl-alpha-tocopherol): IU x 0.45 = mg RRR-alpha-tocopherol (100IU=45mg)


Large ranges are often cited for replacement of vitamin E in deficiency states. The Merck Manual cites a range of 15 to 25mg/kg/day for malabsorption syndromes. For a 150lb person, this would be a range of 680IU to about 1,150IU of natural vitamin E. Some references cite a larger range of 200IU to 3,600IU.2 Doses for neuropathy start at 100mg/kg/day (this is 6,800IU for a 150lb adult). This should be given in divided doses, with doses tapering when symptoms begin to subside. Alternately, injections of vitamin E can be given. The water miscible forms are preferred in malabsorption, as they have demonstrated better uptake. Many sources state that recovery from neuropathy is often incomplete despite recovery of laboratory values. 

Prevention and Maintenance 

The recommended daily allowance (RDA) for vitamin E is 15mg (22.5IU) of natural vitamin E for people aged 14 years or older.2 One thousand milligrams (1,500IU of natural vitamin E, 1,100IU of synthetic vitamin E) is considered by the Institute of Medicine to be the tolerable upper limit (UL) for vitamin E. This is based on the level least likely to cause red cell hemolysis and bleeding. Levels over 1,600IU/day may inhibit vitamin K-dependant clotting. One study found that a daily supplementation of 2,000IU or higher was associated with an increased risk of death.3 Research has not observed any adverse effects related to consumption of vitamin E in foods.2

Vitamin E is well distributed throughout the human diet. The best sources include oils, such as sunflower (5.6mg/Tbsp), safflower (4.6mg/Tbsp), and soybean (1.1mg/Tbsp) oils; nuts and seeds, particularly sunflower seeds (7.4mg/oz), hazelnuts (4.3mg/oz), peanut butter (2.9mg/2 Tbsp), and peanuts (2.2mg/oz);2 and avocado (3.1mg/cup).4 Mangos (1.48mg/cup), cooked sweet potatoes (1.42mg/cup), and cooked asparagus (1.32mg/0.5cup)4 are also high in vitamin E, but virtually all fruits, vegetables, grains, and seeds have some vitamin E. Research has suggested that the bioavailability of vitamin E is greater in foods than supplements.5 It may thus make sense to counsel at-risk patients to look for vitamin E-fortified foods in addition to supplemental sources.

Interactions and Reactions

Vitamin E does have drug interactions. Because of the potential for increased bleeding, concurrent use of blood thinners or aspirin therapy should be closely monitored. The higher the vitamin E level, the greater the risk. For this reason, patients on vitamin E therapy are also generally asked to discontinue taking products containing vitamin E at levels higher than the RDA two or more weeks prior to a surgical procedure. There is some evidence that vitamin E inhibits the uptake in the brain of tricyclic antidepressants, antipsychotics in the phenothiazine class, and propranolol. The fat-blocking drugs orlistat and olestra can decrease absorption of vitamin E. Since orlistat has been approved for over-the-counter use, patients who take it should be monitored for vitamin E deficiency.


Vitamin E is an important antioxidant that plays a vital role in human health. While deficiency seems to be rare, there is a risk with significant malabsorptive procedures. In terms of testing, regular evaluations of vitamin E levels likely make sense only in those patients who are at greatest risk. Alternately, patients who present with symptoms of neuropathy that is not due to other causes should be evaluated for vitamin E status.

This article was adapted with permission from: Jacques J. Vitamin E. In: Micronutrition for the Weight Loss Surgery Patient. Edgmont, PA: Matrix Medical Communications; 2005:79–84.

Additional Sources
  1. Kaplan GE. Vitamin E deficiency. Accessed Mar 2004.
  2. National Institutes of Health Office of Dietary Supplements. Vitamin E – fact sheet for health professionals. Updated 26 Mar 2021. Accessed 17 Apr 2024.
  3. Miller ER, Pastor-Barriuso R, Dalal D. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med. 2005;142(1):37–46.
  4. United States Department of Agriculture. USDA National Nutrient Database for Standard Reference Release 28. Nutrients: vitamin E (alpha-tocopherol) (mg). 10 Nov 2015. Accessed 17 Apr 2024.
  5. Leonard SW, Good CK, Gugger ET, Traber MG. Vitamin E bioavailability from fortified breakfast cereal is greater than that from encapsulated supplements. Am J Clin Nutr. 2004;79(1):86–92.   

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