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Many people may not have sufficient vitamin E intakes

September 18, 2014

According to a new US review big portions of the populations do not meet the estimated required intakes of vitamin E, which is particularly important for all children through about age two, for women who are pregnant and for the elderly.

The review evaluated the information available on the adverse consequences of inadequate vitamin E (alpha-tocopherol) supply status (1). More than 90% of Americans do not consume sufficient dietary vitamin E (2) to meet estimated average requirements (EARs). Many of the consequences of this inadequate intake are less obvious, such as its impact on things like nervous system and brain development, or general resistance to infection. However, current research has shown that plasma alpha-tocopherol concentrations below 12 mmol/L are associated with increased infection, anemia, stunting of growth, and poor outcomes during pregnancy for both the infant and the mother (3). Hypothetically, these low intakes of antioxidant alpha-tocopherol lead first to anemia because of a damage of erythrocytes by oxygen. Experimental data indicate that vitamin E is critically important to the early development of the nervous system in embryos, in part because it protects the function of omega-3 fatty acids, especially docosahexaenoic acid (DHA), which is important for brain health. In the elderly, severe or chronic vitamin E depletion may lead to cognitive impairment while increased intakes seem to slow the progression of Alzheimer's disease (4). The protection of DHA by vitamin E is thought to be important throughout life: a study showed that people with high plasma DHA concentrations had a 47% reduction in the risk of developing all-cause dementia (5).

Measures of circulating vitamin E levels in the blood often rise with age as lipid levels also increase, but do not prove an adequate delivery of vitamin E to tissues and organs. There seem to be efficient regulatory controls governing circulating vitamin E concentrations: an increase and normalization of blood vitamin E concentrations at the expense of depletion of (liver) tissue alpha-tocopherol. These processes serve to protect circulating lipids, which are readily oxidized and potentially exposed to higher concentrations of oxygen and reactive oxygen species. Here the case of nonalcoholic fatty liver disease, related to obesity and type 2 diabetes, is of interest because the progression of this disorder to more serious forms of the disease is dependent on oxidative damage to lipids, suggesting that inadequate vitamin E intakes may promote disease progression and a vitamin E supplementation may improve the disease (6). The researchers concluded that these data emphasize the importance of adequate vitamin E status in obese individuals to maintain healthy liver function and potentially prevent the progression of fatty liver to more serious forms of the disease.

Supplements providing vitamin E intakes in excess of 100-fold dietary intakes increase plasma concentra-tions only by about 2- to 4-fold above baseline values (7). The limitation on plasma concentrations and prevention of toxic tissue concentrations appear to be a result of increased hepatic vitamin E metabolism and excretion (8). Intakes of 12–15 mg alpha-tocopherol per day are sufficient in normal healthy individuals to provide adequate vitamin E status on the basis of the health benefits associated with these intakes (9).

References

  1. Traber M. G. Vitamin E Inadequacy in Humans: Causes and Consequences. Adv. Nutr. 2014; 5:1–12.
  2. Moshfegh A. et al. What we eat in America, NHANES 2001–2002: usual nutrient intakes from food compared to dietary reference intakes. USDA, Agricultural Research Service. http://www.ars.usda.gov/SP2User-Files/Place/12355000/pdf/0102/usualintaketables2001–02.pdf.
  3. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for vitamin C, vitamin E, selenium, and carotenoids. Washington: National Academies Press; 2000.
  4. Dysken M. W. et al. Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial. JAMA. 2014; 311:33–44.
  5. Schaefer E. J. et al. Plasma phosphatidylcholine docosahexaenoic acid content and risk of dementia and Alzheimer disease: the Framingham Heart Study. Arch Neurol. 2006; 63:1545–1550.
  6. Sanyal A. J. et al. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med. 2010; 362:1675–1685.
  7. Roberts L. J. Jr. et al. The relationship between dose of vitamin E and suppression of oxidative stress in humans. Free Radic Biol Med. 2007; 43:1388–1393.
  8. Traber M. G. Mechanisms for the prevention of vitamin E excess. J Lipid Res. 2013; 54:2295–2306.
  9. Wright M. E. et al. Higher baseline serum vitamin E concentrations are associated with lower total and cause-specific mortality in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Clin Nutr. 2006; 84:1200–1207.