Sub-Clinical Vitamin E Deficiency and Brain Health: An Emerging Area of Nutrition Research
The existence of vitamin E was first discovered back in 1922 when Evans and Bishop reported on a fat-soluble compound in butter fat and wheat germ that restored fertility to rats raised on a restricted diet. Fast-forward nearly one hundred years and the functions of vitamin E and its role in human health is still being researched, according to Ulatowski and Manor in the 2013 edition of Annual Review of Nutrition, published this month.
The main functions of vitamin E are generally listed as being a fat-soluble antioxidant, and contributing to the immune system (see review by the US Office of Dietary Supplements). However, vitamin E is also known to regulate gene expression and affect cell signaling, calling into question whether it has other important functions in the body outside these two classic areas. In particular, some studies have linked higher vitamin E levels with reduced risk of cognitive impairment (Morris et al.), calling to question whether vitamin E has additional neurological functions.
Vitamin E deficiency is relatively uncommon in humans, and primary deficiency is found in people with inherited mutations in the gene that codes for the alpha-tocopherol transporter protein (aTTP), the protein that selectively binds alpha-tocopherol and transports it between membranes. People with two copies of the defective gene develop a condition called spinocerebellar ataxia, which characterized by a progressive loss of speech, poor reflexes, gait problems, return of Babinski reflex and others that are indicative of a poorly functioning neurological system. Secondary vitamin E deficiency arises mainly from other conditions that affect lipid absorption, such as cystic fibrosis. Large doses of vitamin E are effective in preventing neurological symptoms that are associated with primary of secondary vitamin E deficiency.
Some other indicators that vitamin E is important for the brain include the preference that the brain has alpha-tocopherol (the most biologically important form, and the basis of recommendations,see Bourre,Clement, and Ingold), the expression of the alpha-tocopherol transporter protein in the brain (Copp and associates) , and the brain appears protected somewhat from vitamin E depletion.
Overall, there is a paucity of data on the role of vitamin E in brain health. This is partly due to the lack of distinct deficiency disease and little biochemical testing for vitamin E levels. The effect of sub-clinical deficiency has been identified as an area urgently needing further research, especially given that intakes are well below recommendations, even in well-nourished populations (conduct searches on vitamin E intakes in the US population via www.micronutrientcalculator.org). A further avenue of research is the effect of common polymorphisms within the gene coding for aTTP, which may profoundly affect individual recommendations (for example, Zanon-Moreno and co-workers look at the effect of SNPs on circulating levels of vitamin E and risk of glaucoma). This review fits in with a recent “wake-up call” regarding the state of vitamin E research. -jb-
Lynn Ulatowski and Danny Manor. Vitamin E Trafficking in Neurologic Health and Disease. Annual Review of Nutrition. Vol. 33: 87-103 (Volume publication date July 2013). First published online as a Review in Advance on April 29, 2013. DOI: 10.1146/annurev-nutr-071812-161252