Vitamin E deficiency symptoms

Short answer

According to the NIH, overt vitamin E deficiency is rare, and no obvious signs of deficiency have been detected in healthy people who consume little vitamin E from food. ^[1] Deficiency is seen in diseases that impair fat absorption, in inherited transport defects, and in very-low-birth-weight infants; its main findings are neurologic, hemolytic (blood), and eye findings.

How rare is vitamin E deficiency?

The NIH reports that overt vitamin E deficiency is rare and that no obvious signs of deficiency are found in healthy people who consume little vitamin E from food. ^[1] The professional edition of the Merck Manual separates this by region: in countries with high food insecurity, the most common cause of deficiency is inadequate intake; in countries with low food insecurity, deficiency in adults is rare and mostly results from fat malabsorption. ^[2]

In surveys conducted in the US, most people’s diets were found to fall below the RDA for vitamin E; however, because fats added in cooking were not taken into account, these estimates may have been low, and these low intakes have not been associated with overt deficiency. ^[1] Deficiency takes a long time to develop in adults: according to Traber, the appearance of symptoms in adults takes more than 5 years, while in children it can appear in the first months or years. ^[3]

Who gets vitamin E deficiency?

According to the NIH, because the digestive tract needs fat to absorb vitamin E, deficiency is more likely in people with fat malabsorption. In conditions such as Crohn’s disease, cystic fibrosis, or inability to secrete bile from the liver, fatty stools or chronic diarrhea are common; these people sometimes need water-soluble forms of vitamin E (for example, tocopheryl polyethylene glycol-1000 succinate). ^[1]

The Merck Manual lists the main causes in countries with low food insecurity as diseases that impair fat absorption: abetalipoproteinemia (Bassen-Kornzweig syndrome; inherited absence of apolipoprotein B), chronic cholestatic hepatobiliary disease, pancreatitis, short bowel syndrome, and cystic fibrosis. There is also a rare genetic form resulting from a defect in liver metabolism without fat malabsorption. ^[2]

Traber’s review expands this framework as follows: α-tocopherol absorption depends on bile and pancreatic secretions, on transport with chylomicrons, and on the α-tocopherol transfer protein (α-TTP) in the liver; a condition that impairs any of these can lead to deficiency. Among the inherited groups are the following: ^[3]

• AVED (ataxia with vitamin E deficiency): arises from mutations in TTPA, the gene for α-TTP; at least 25 mutations have been reported in the review.
• Lipoprotein disorders: abetalipoproteinemia, hypobetalipoproteinemia, and chylomicron retention disease.
• Insufficient bile secretion: in cholestatic liver disease and in children with cystic fibrosis, α-tocopherol cannot be absorbed because bile is insufficiently secreted.
• Very-low-birth-weight premature infants: infants under 1,500 g are reported to be insufficient in α-tocopherol.

The same review also states that dietary deficiency may be associated with the use of damaged (peroxidized) fats and with ultra-processed foods low in micronutrients, that typical deficiency symptoms are seen in general malnutrition, and that supplementation is indicated in weight-loss programs, with medications that limit fat absorption, or after bariatric surgery. ^[3]

A single case report associated with bariatric surgery exemplifies this: in a 20-year-old woman who developed lower-extremity weakness after laparoscopic sleeve gastrectomy, vitamin E, vitamin D, and folic acid deficiencies were detected, the vitamin E deficiency was found to be associated with bilateral axonal sciatic mononeuropathy, and the picture resolved with supplementation and supportive treatment. This is a single case and gives no information about frequency. ^[5]

What symptoms does vitamin E deficiency cause?

The symptoms listed by the NIH are peripheral neuropathy, ataxia, skeletal muscle disease (myopathy), retinopathy, and impaired immune response. Vitamin E deficiency due to abetalipoproteinemia is associated with impaired nerve conduction, muscle weakness, and retinal degeneration leading to blindness. People with AVED, if they do not take very high amounts of supplements, develop nerve damage and lose the ability to walk. ^[1]

According to the Merck Manual, the main symptoms are mild hemolytic anemia and nonspecific neurologic findings; deficiency leads to fragility of red blood cells and degeneration of neurons, particularly peripheral axons and posterior column neurons. The same source states that in children cholestatic liver disease or cystic fibrosis can lead to spinocerebellar ataxia (loss of deep tendon reflexes, truncal and limb ataxia, loss of vibration and position sense, ophthalmoplegia, muscle weakness, ptosis, and dysarthria), that because adults have large vitamin E stores in fat tissue spinocerebellar ataxia develops very rarely even with fat malabsorption, and that in premature infants deficiency can contribute to retinopathy of prematurity. ^[2]

In Traber’s review, the neurologic picture is summarized as progressive sensory neuropathy: spinocerebellar ataxia, loss of motor control, and lesions in muscle and peripheral nerves; retinitis pigmentosa and macular degeneration have been reported in AVED and abetalipoproteinemia. If severe peripheral neuropathy has developed, reversing it can be difficult or even impossible. ^[3]

In a case report describing AVED, serum vitamin E was found below 0.4 mg/L in a laboratory whose normal range was 5–18 mg/L, a homozygous mutation was detected in the TTPA gene, and function improved with oral vitamin E: the patient began walking with support in the first six months and walking independently after one year. The discussion section of the case report states that AVED usually begins in the first or second decade of life with progressive ataxia and sensory loss, does not present with digestive complaints, and can mimic Friedreich ataxia. ^[4]

Are fatigue and hair loss symptoms of vitamin E deficiency?

The deficiency picture described by the NIH, the Merck Manual, and Traber consists of neurologic, hemolytic (blood), retinal, and immune-related findings; fatigue or hair loss is not counted within these descriptions. These complaints can be due to many other causes and require a separate evaluation.

How is vitamin E deficiency diagnosed?

According to the Merck Manual, vitamin E deficiency is unlikely without a predisposing condition or a history of inadequate intake; confirmation generally requires measuring the vitamin level. The most direct method is serum α-tocopherol measurement: a value below 5 mcg/mL (11.6 µmol/L) in adults suggests deficiency; the normal level of plasma α-tocopherol is given in the same source as 5–20 mcg/mL (11.6–46.4 µmol/L). ^[2]

Because the plasma tocopherol level varies with the total lipid level, in adults with high lipid levels the most accurate indicator is the ratio of serum α-tocopherol to serum lipids (below 0.8 mg/g total lipid). In children and adults with abetalipoproteinemia, the serum α-tocopherol level is generally unmeasurable. A test measuring red blood cell hemolysis in response to peroxide may suggest the diagnosis but is not specific. ^[2] Traber also states that this test is not a reliable biomarker, because red blood cell sensitivity also appears in clinical conditions other than vitamin E deficiency. ^[3]

Laboratory thresholds can vary by method and laboratory (in the AVED case above, the laboratory’s normal range was 5–18 mg/L). ^[4] The Merck Manual recommends measuring the α-tocopherol level when there are compatible findings together with inadequate intake or a predisposing condition. ^[2]

How is vitamin E deficiency treated?

Treatment is determined by a physician according to the underlying cause and the person; this page does not give a dose or schedule. The sources report these general points: the Merck Manual reports that treatment is with supplemental α-tocopherol or mixed tocopherols, but that in the early stage of nerve damage and in abetalipoproteinemia, larger amounts and injection are required to overcome the absorption and transport defect. ^[2] According to the NIH, some people with abetalipoproteinemia need very high amounts of supplements and people with AVED need large amounts; those with Crohn’s disease, cystic fibrosis, or a bile secretion problem may need water-soluble forms. ^[1] Traber reports that forms that spontaneously form micelles (TPGS) are effective in cholestatic liver disease and states that early and continuous supplementation has also been recommended in people who have a known disease leading to deficiency but no symptoms; this is presented as a researcher’s recommendation. ^[3]

In premature infants, the NIH states that supplementation may reduce some problems such as retinal complications but may increase the risk of infection. ^[1] The benefit and harm signals of supplementation in a person without deficiency are covered on the vitamin E benefits page, and the reference values and upper limit in the main guide.

Detailed guideWhat is vitamin E? Reference values, upper limit, and interactions→ Detailed guideVitamin E benefits: evidence, harm signals, and limits→ Detailed guideWhich foods contain vitamin E? Serving table and nuts→