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Vitamin E: deficiency and hypervitaminosis

Medical expert of the article

Obstetrician-gynecologist, reproductive specialist
, medical expert
Last reviewed: 04.07.2025

Vitamin E is a group of compounds (tocopherols and tocotrienols) that have similar biological effects. The most biologically active is alpha-tocopherol, but beta-, gamma-, and theta-tocopherols, four tocotrienols, and several stereoisomers also have important biological activity.

These substances act as antioxidants that prevent peroxidation of polyunsaturated fatty acids in cell membranes. Plasma levels of tocopherol vary with total plasma (serum) lipid levels. Typically, plasma levels of a-tocopherol are 5-20 μg/mL (11.6-46.4 μmol/L). It is controversial whether vitamin E protects against cardiovascular disease, Alzheimer's disease, tardive dyskinesia, and prostate cancer in smokers. Although the amount of vitamin E in many fortified foods and supplements is estimated in IU, it is recommended to use mg or μmol for estimation.

Vitamin E hypovitaminosis

Dietary deficiency of vitamin E is common in developing countries; deficiency in adults in developed countries is rare and usually due to lipid malabsorption. The main symptoms are hemolytic anemia and neurological deficits. Diagnosis is by measuring the ratio of plasma a-tocopherol to total plasma lipids; a low ratio confirms vitamin E deficiency. Treatment is with high-dose oral vitamin E if neurological deficits are present or if vitamin E deficiency develops due to malabsorption.

Vitamin E deficiency causes hemolysis of red blood cells and degeneration of neurons, especially peripheral axons and posterior column neurons.

Causes of Vitamin E Deficiency

In developing countries, the most common cause is inadequate vitamin E intake. In developed countries, the most common causes are diseases that cause lipid malabsorption, including abetalipoproteinemia (Bessen-Kornzweig syndrome: congenital absence of apolipoprotein B), chronic cholestatic disease, hepatobiliary disease, pancreatitis, short bowel syndrome, and cystic fibrosis. A rare genetic form of vitamin E deficiency without lipid malabsorption is a consequence of impaired liver metabolism.

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Symptoms of Vitamin E Deficiency

The main symptoms are mild hemolytic anemia and nonspecific neurological manifestations. Abetalipoproteinemia leads to progressive neuropathy and retinopathy in the first two decades of life.

Vitamin E deficiency contributes to the development of retinopathy of prematurity (retrolental fibroplasia) and, in some cases, intraventricular and subependymal (subdural) hemorrhages in neonates. Such premature infants develop muscle weakness.

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

Vitamin E deficiency in adults with malabsorption very rarely causes cerebrospinal ataxia because they have large stores of vitamin E in adipose tissue.

Diagnosis of vitamin E deficiency

Vitamin E deficiency is unlikely unless there is a history of inadequate intake or precipitating factors (conditions). Determination of vitamin levels is usually required to confirm the diagnosis. Measuring the degree of red blood cell hemolysis in response to hydrogen peroxide may suggest the diagnosis but is nonspecific. Hemolysis is increased because vitamin E deficiency impairs red blood cell stability.

The most direct method of diagnosis is measurement of plasma alpha-tocopherol levels. In adults, vitamin E deficiency can be suspected if the tocopherol level is < 5 μg/mL (< 11.6 μmol/L). Because altered plasma lipid levels can affect vitamin E status, a low plasma alpha-tocopherol to plasma lipid ratio (< 0.8 mg/g total lipid) is the most accurate indicator in adults with hyperlipidemia.

Plasma alpha-tocopherol levels are usually undetectable in children and adults with abetalipoproteinemia.

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Prevention and treatment of vitamin E deficiency

Premature infants may require vitamin E supplements, although human milk and commercial formulas contain sufficient vitamin E for full-term infants.

In cases where malabsorption causes obvious clinical deficiency, α-tocopherol is given orally at a dose of 15-25 mg/kg body weight once daily. However, higher doses are used by injection to treat early neuropathy or to overcome the effects of absorption and transport defects in acanthocytosis.

Hypervitaminosis (intoxication) of vitamin E

Many adults take relatively large amounts of the vitamin (α-tocopherol - 400-800 mg/day) for many months and years without clear indications. Muscle weakness, fatigue, nausea and diarrhea sometimes develop. The most significant risk is the risk of bleeding. However, bleeding does not occur unless the dose exceeds 1000 mg/day or the patient takes coumarin or warfarin orally. Thus, the upper limit for adults over 19 years is 1000 mg (2326 μmol) for any form of α-tocopherol. Recent reviews of previous studies have reported that taking high doses of vitamin E may increase the risk of premature death.


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