Vitamin E is vital for health, but reports that more than three-quarters of the population in developed countries do not meet dietary intake recommendations raise important questions.
Despite the proven biological function of vitamin E as a powerful antioxidant, global intake is declining likely as a result of increased consumption of highly processed foods rather than whole grains, nuts and seeds. The impact of such a downward trend in both the developing and developed worlds is a serious public health concern. A key element in cell membranes, vitamin E helps to protect polyunsaturated fatty acids (PUFAs) from rancidity and offers numerous benefits to brain, eye, cardiovascular, maternal and infant health.
However, new research to fully investigate the role of vitamin E and the consequences of inadequate status in the body has been limited until very recently. Studies published earlier this year sparked renewed interest in this important and under-consumed vitamin. This is driving a review of long-held methods of assessing daily intake requirements, as well as innovative research designed to gain a better understanding of vitamin E’s biological functions.
Intake and Biomarkers
Changes to modern eating habits make it difficult to obtain sufficient quantities of vitamin E from the diet alone. This means supplementation or food fortification is necessary to boost intake, but opinion on just how much vitamin E is needed to deliver the recognized functional benefits is undergoing a radical shift. In terms of measuring vitamin E intake, the alpha-tocopherol (a-TE)form is the most biologically active and of utmost importance. a-TE, one of eight forms of vitamin E, is the most abundant in the human body and the only form that is preferentially maintained in plasma and tissues.
Current guidelines on adequate intakes of vitamin E vary according to age, gender, individual country and are largely based on historic data. In Europe, for example, the Recommended Daily Intake (RDI) is 4 to 25 mg alpha-tocopherol equivalent (a-TE/d for men and between 3 to 12 mg a-TE/d for women, while in the United States, the RDA is generally slightly higher at 15 mg alpha-tocopherol/d. There are a number of problems with the use of a-TE in dietary recommendations, mostly related to the fact that gamma-tocopherol is high in vegetable oils.
Recommendations of alpha-tocopherol use were based on expectations that alpha-tocopherol would be the predominant form of vitamin E consumed and approximately 10 percent of the tocopherol intake would be gamma-tocopherol. In actuality, the predominance of soy and corn oils has dramatically shifted tocopherol intakes from alpha-tocopherol toward gamma-tocopherol.
Spurred on by new research linking higher doses of vitamin E to a number of health benefitsincluding the beneficial effect in neurodegenerative conditions such as Alzheimer’s disease or fatty liver diseasethere is a growing body of evidence supporting an increase of RDI levels to 30 mg a-TE/d.1
Several meta-analyses reported by the media claimed a high intake of vitamin E (at levels of 400 IU or more) may not be beneficial to health,2 but such claims have been strongly countered by the findings of a recent comprehensive review.3 This paper, published in the Journal of Lipid Research in March 2013, concluded that biological mechanisms exist to routinely eliminate excess levels of the vitamin and so make it almost impossible to consume a harmful amount. These findings are in line with a recent meta-analysis on vitamin E and all-cause mortality, which concluded supplementation with vitamin E appears to have no effect on all-cause mortality at doses up to 5,500 IU/d.4
Alongside calls to stimulate the intake of vitamin E and to increase the RDI of vitamin E is the push to establish biomarkers to assess inadequate status within the body. The fact that over 90 percent of Americans do not currently consume sufficient dietary vitamin E,5 yet the current method of measuring circulating alpha-tocopherol concentrations shows no obvious deficiencies, suggests additional biomarkers that change with nutrient intake are needed. Indeed, according to Maret Traber, Ph.D., principal investigator and principal at the Linus Pauling Institute, “Circulating alpha-tocopherol concentrations are very difficult to interpret because as a person ages plasma lipid concentrations also increase and this causes a rise in plasma carriers for alpha-tocopherol, leading to higher circulating alpha-tocopherol concentrations. However, abnormal lipoprotein metabolism does not necessarily increase alpha-tocopherol delivery to tissues."
Traber continued, “Attention is now moving to look at an alternative biomarker, the urinary excretion of the vitamin E metabolite alpha-carboxy-ethyl-hydroxychromanol (α-CEHC).6 This line of thinking is based on the assumption that as dietary or supplemental alpha-tocopherol intake increases, ultimately plasma alpha-tocopherol concentrations reach a plateau and the liver metabolizes the ‘extra’ vitamin E, leading to increases in the urinary excretion of vitamin E metabolites." She noted research is ongoing in this area.7
Building on Positive Findings
Perhaps one of the main challenges involved in getting vitamin E back on the public health agenda is the notorious difficulty in showing adverse consequences of deficiency, even in experimental animals fed deficient diets. Traber explained, “In general, plasma alpha-tocopherol concentrations of less than 12 μmol/L are defined as deficient and are associated with increased infection, anaemia, stunting of growth and poor outcomes during pregnancy for both the infant and mother. While initial findings support the use of vitamin E supplements in situations where low plasma alpha-tocopherol concentrations were documented, the available information on plasma levels is currently limited. A clearly structured approach is now required in order to measure adequacy of status during pregnancy, as well as to evaluate improved outcomes as a result of vitamin E supplementation."8
Given the importance of vitamin E in the developing nervous system and the protection of peripheral nervesas supported by a number of studiesits role in age-related diseases such as Alzheimer’s disease and macular degeneration is a relatively new and exciting line of research. Central to initial investigations is the overall finding that vitamin E may protect essential fatty acids (EFAs) in the brain from lipid peroxidation and that improved brain vitamin E status is protective for cognitive function.9,
While much is known about vitamin E, there remain crucial gaps and inconsistencies in existing knowledge which promising researchsuch as that outlined in this reviewtry to address. What is clear is this essential micronutrient has significant potential that has yet to be fully realized. This is why collaboration and investment in new research is vital to advance current understanding and support sustained, consistent and effective communication.
For more on this essential micronutrient, visit INSIDER’s “Vitamin E" topic page.
1. Péter S et al. “The challenge of setting appropriate intake recommendations for vitamin E: Considerations on status and functionality to define nutrient requirements." Int J Vitam Nutr Res. 83 (2/13) (2013)
2. Miller ER et al. “Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality." Ann Intern Med. 2005 Jan 4;142(1):37-46. Epub 2004 Nov 10
3. Traber MG. “Mechanisms for the prevention of vitamin E excess." J Lipid Res. 2013 Sep;54(9):2295-306.
4. Abner EL et al. “E and all-cause mortality: A meta-analysis." Current Aging Science. 2011, 4, 1-13
5. Fulgoni V L 3rd et al: ‘Foods, fortificants and supplements: where do Americans get their nutrients?’ J Nutr. 2011;141:1847-1854.
6. Lebold KM, Ang A, Traber MG, Arab L: Urinary alpha-carboxyethyl hydroxychroman can be used as a predictor of alpha-tocopherol adequacy, as demonstrated in the Energetics Study. Am J Clin Nutr. 2012;96:801-9
7. Traber, M: ‘Vitamin E inadequacy in humans: causes and consequences’. Adv. Nutr. 5: 1–12, 2014.
8. Traber M. Ibid.
9. Dysken MW et al. “Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial." JAMA. 2014;311(1):33-44
10. Schaefer EJ et al. “Plasma phosphatidylcholine docosahexaenoic acid content and risk of dementia and Alzheimer disease: the Framingham Heart Study." Arch Neurol. 2006;63:1545-50