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Vitamin E


by Larry E. Johnson, MD, PhD

Vitamin E is a group of compounds (including tocopherols and tocotrienols) that have similar biologic activities. The most biologically active is α-tocopherol, but β-, γ-, and δ-tocopherols, 4 tocotrienols, and several stereoisomers may also have important biologic activity. These compounds act as antioxidants, which prevent lipid peroxidation of polyunsaturated fatty acids in cellular membranes. Plasma tocopherol levels vary with total plasma lipid levels. Normally, the plasma α-tocopherol level is 5 to 20 μg/mL (11.6 to 46.4 µmol/L). High-dose vitamin E supplements do not protect against cardiovascular disorders; whether supplements can protect against tardive dyskinesia or increase or decrease the risk of prostate cancer is controversial. There is no convincing evidence that doses of up to 2000 IU/day slow the progression of Alzheimer disease.

Although the amount of vitamin E in many fortified foods and supplements is given in IU, current recommendations are to use mg.

Vitamin E Deficiency

Dietary vitamin E deficiency is common in developing countries; deficiency among adults in developed countries is uncommon and usually due to fat malabsorption. The main symptoms are hemolytic anemia and neurologic deficits. Diagnosis is based on measuring the ratio of plasma α-tocopherol to total plasma lipids; a low ratio suggests vitamin E deficiency. Treatment consists of oral vitamin E, given in high doses if there are neurologic deficits or if deficiency results from malabsorption.

Vitamin E deficiency causes fragility of RBCs and degeneration of neurons, particularly peripheral axons and posterior column neurons.


In developing countries, the most common cause is

  • Inadequate intake of vitamin E

In developed countries, the most common causes are

  • Disorders that cause fat malabsorption, including abetalipoproteinemia (Bassen-Kornzweig syndrome, due to genetic absence of apolipoprotein B), chronic cholestatic hepatobiliary disease, pancreatitis, short bowel syndrome, and cystic fibrosis

A rare genetic form of vitamin E deficiency without fat malabsorption results from defective liver metabolism.

Symptoms and Signs

The main symptoms are mild hemolytic anemia and nonspecific neurologic deficits. Abetalipoproteinemia results in progressive neuropathy and retinopathy in the first 2 decades of life (see Lipid Disorders:Abetalipoproteinemia (Bassen-Kornzweig syndrome)).

Vitamin E deficiency may contribute to retinopathy of prematurity (also called retrolental fibroplasia) in premature infants and to some cases of intraventricular and subependymal hemorrhage in neonates. Affected premature neonates have muscle weakness.

In children, chronic cholestatic hepatobiliary disease or cystic fibrosis causes neurologic deficits, including spinocerebellar ataxia with loss of deep tendon reflexes, truncal and limb ataxia, loss of vibration and position senses, ophthalmoplegia, muscle weakness, ptosis, and dysarthria.

In adults with malabsorption, vitamin E deficiency very rarely causes spinocerebellar ataxia because adults have large vitamin E stores in adipose tissue.


  • Low α-tocopherol level or low ratio of serum α-tocopherol to serum lipids

Without a history of inadequate intake or a predisposing condition, vitamin E deficiency is unlikely. Confirmation usually requires measuring the vitamin level. Measuring RBC hemolysis in response to peroxide can suggest the diagnosis but is nonspecific. Hemolysis increases as vitamin E deficiency impairs RBC stability.

Measuring the serum α-tocopherol level is the most direct method of diagnosis. In adults, vitamin E deficiency is suggested if the α-tocopherol level is < 5 μg/mL (< 11.6 µmol/L). Because abnormal lipid levels can affect vitamin E status, a low ratio of serum α-tocopherol to lipids (< 0.8 mg/g total lipid) is the most accurate indicator in adults with hyperlipidemia.

In children and adults with abetalipoproteinemia, serum α-tocopherol levels are usually undetectable.


  • Supplemental α-tocopherol or mixed tocopherols (α-, β-, and γ-tocopherols)

If malabsorption causes clinically evident deficiency, α-tocopherol 15 to 25 mg/kg po once/day should be given. Or mixed tocopherols (200 to 400 IU) can be given. However, larger doses of α-tocopherol given by injection are required to treat neuropathy during its early stages or to overcome the defect of absorption and transport in abetalipoproteinemia.


Although premature neonates may require supplementation, human milk and commercial formulas have enough vitamin E for full-term neonates.

Key Points

  • Vitamin E deficiency is usually caused by inadequate dietary intake in developing countries or by a disorder causing fat malabsorption in developed countries.

  • The deficiency causes mainly mild hemolytic anemia and nonspecific neurologic deficits.

  • In patients with inadequate intake or a predisposing condition plus compatible findings, measure the tocopherol level to confirm the diagnosis.

  • Treat with supplemental tocopherol.

Vitamin E Toxicity

Many adults take relatively large amounts of vitamin E (α-tocopherol 400 to 800 mg/day) for months to years without any apparent harm. Occasionally, muscle weakness, fatigue, nausea, and diarrhea occur. The most significant risk is bleeding. However, bleeding is uncommon unless the dose is > 1000 mg/day or the patient takes oral coumarin or warfarin. Thus, the upper limit for adults aged ≥ 19 yr is 1000 mg for any form of α-tocopherol.

Recent analyses of previous studies report that high vitamin E intakes may increase the risk of hemorrhagic stroke and premature death.

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