Vitamin E: Deficiency and Hypervitaminosis
Last reviewed: 23.04.2024
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Vitamin E is a group of compounds (tocopherols and tocotrienols), which have a similar biological effect. The most biologically active is alpha-tocopherol, but beta-, gamma- and tetta-tocopherols, four tocotrienols and several stereoisomers also have important biological activity.
These substances act as antioxidants, which prevent the peroxidation of polyunsaturated fatty acids in cell membranes. Plasma levels of tocopherol vary with the total level of plasma lipids (serum) of the blood. Usually, the plasma level of a-tocopherol is 5-20 μg / ml (11.6-4.4 μmol / L). The question is whether vitamin E protects against cardiovascular diseases, Alzheimer's disease, late dyskinesias, prostate cancer in smokers. Although the amount of vitamin E in many of its enriched products and additives is estimated in ME, it is recommended that mg or μmol be used for evaluation.
Hypovitaminosis of Vitamin E
Vitamin E deficiency in diet is typical in developing countries; deficiency in adults in developed countries occurs rarely and usually due to malabsorption of lipids. The main symptoms are hemolytic anemia and neurological disorders. The diagnosis is based on measuring the ratio of plasma a-tocopherol to the total number of plasma lipids; a low ratio confirms vitamin E deficiency. Treatment consists in oral administration of vitamin E in large doses in the presence of neurological symptoms or in the case of vitamin E deficiency due to malabsorption.
Deficiency of vitamin E causes hemolysis of erythrocytes and degeneration of neurons, especially peripheral axons and posterior columnar neurons.
Causes of vitamin E deficiency
In developing countries, the most common cause is the inadequate intake of vitamin E. In developed countries, the most common causes are diseases that cause malabsorption of lipids, including abetalipoproteinemia (Bessen-Kornzweig syndrome: congenital absence of apolipoprotein B), chronic cholestatic disease, hepatobiliary disease, pancreatitis, syndrome short bowel, cystic fibrosis. A rare genetic form of vitamin E deficiency without lipid malabsorption is a consequence of impaired liver metabolism.
Symptoms of vitamin E deficiency
The main symptoms are mild hemolytic anemia and nonspecific neurologic manifestations. Abetalipoproteinemia leads to progressive neuropathy and retinopathy in the first two decades of life.
Deficiency of vitamin E promotes the development of retinopathy in prematurity (retrolental fibroplasia) and in some cases, the occurrence of intraventricular and subependemal (subdural) hemorrhages in newborns. Such premature newborns develop muscle weakness.
In children, chronic cholestatic hepatobiliary pathology or cystic fibrosis causes neurological disorders, including cerebrospinal ataxia with loss of deep tendon reflexes, ataxia of the trunk and extremities, loss of positional and vibration sensitivity, ophthalmoplegia, muscle weakness, ptosis and dysarthria.
Deficiency of vitamin E in adults with malabsorption very rarely causes cerebrospinal ataxia, because they have large reserves of vitamin E in adipose tissue.
Diagnosis of vitamin E deficiency
Vitamin E deficiency is unlikely if there is no history of insufficient intake or provoking factors in the anamnesis. To confirm the diagnosis, you usually need to determine the level of the vitamin. Measurement of the degree of hemolysis of erythrocytes in response to hydrogen peroxide may suggest a diagnosis about this diagnosis, but it is nonspecific. Hemolysis intensifies, as vitamin E deficiency weakens the stability of red blood cells.
The most direct method of diagnosis is measuring the level of a-tocopherol in the blood plasma. In adults, a vitamin E deficiency can be suspected if the tocopherol level is <5 μg / ml (<11.6 μmol / L). Since altered plasma lipid levels can affect the status of vitamin E, a low plasma to plasma lipid ratio (<0.8 mg / g total lipids) is the most accurate indicator in adults with hyperlipidemia.
The level of a-tocopherol in plasma in children and adults with abetalipoproteinemia is usually not determined.
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Prevention and treatment of vitamin E deficiency
Premature newborns may require vitamin E supplements, despite the fact that women's milk and commercial milk formulas contain a sufficient amount of vitamin E for newborns that are born on time.
In cases where malabsorption causes an obvious clinical deficit, a-tocopherol is administered at a dose of 15-25 mg / kg of body dose orally once a day. Nevertheless, higher doses in injections are used to treat neuropathy in the early stages or to overcome the effects of suction and transport defects in acanthocytosis.
Hypervitaminosis (intoxication) of vitamin E
Many adults take relatively large amounts of vitamin (a-tocopherol - 400-800 mg / day) for many months and years without explicit indications. Sometimes muscle weakness develops, fatigue, nausea and diarrhea. The most significant risk is the risk of bleeding. However, bleeding does not occur if the dose does not exceed 1000 mg / day or the patient takes orally coumarin or warfarin. 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 can increase the risk of premature death. (Miller ER 3rd, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ, Guallar E. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality, Ann Intern Med 2005; 142: 37-46. [ PubMed abstract ]).