Prof. Maret Traber, Linus Pauling Institute, Oregon State University, Corvallis, USA
Prof. Gerald Rimbach, University of Kiel, Germany
Prof. Jan Frank, University of Hohenheim, Germany
Prof. Stephan Bakker, University of Groningen, The Netherlands
Prof. Veronika Somoza, University of Vienna, Austria
“Being a potent peroxyl radical scavenger, the main function of vitamin E is the protection of membranes and lipoproteins, for which it is the primary protective agent against lipid peroxidation. A number of biomarkers (e.g., malondialdehyde, F2-isoprostanes and pentane) have been used to reflect the degree of lipid peroxi- dation in vivo. Ex vivo biomarkers of cellular and intracellular membrane damage are creatine-kinase in plasma and the in vitro hemolysis test. Identification of new biomarkers is needed to evaluate/assess vitamin E status in order to more accurately define vitamin E adequacy and inadequacy. For example, dietary survey data from the US, indicated that the average dietary intake of alpha-tocopherol from food was only 7 mg/ day. At this level of intake, more than 90% of Americans did not meet the daily dietary recommendations for vitamin E (1). Recent studies demonstrated that the oxidative stability of vitamin E in commercial vegetable oils is limited and significant vitamin E losses during storage may contribute to low vitamin E intake and sta- tus (2).
Evidence from various observational human studies indicated that vitamin E has beneficial effects on the cardiovascular system. At least five studies reported that increased intakes of vitamin E are associated with decreased risk for heart attack or death from cardiovascular disease. On the other hand, results from randomized controlled trials did not detect a consistent benefit of vitamin E supplementation on cardiovas- cular health. However, recent data show that the genotype of an individual appears to be an important factor in the effect of vitamin E supplements on cardiovascular endpoints (3). The findings on the role of the geno- types related to the benefits of vitamin E are considerable and deserve further investigations. Data from previous human studies should be re-analyzed based on retrospective genotyping for apolipoprotein E (apoE), paraoxonase and haptoglobin gene variants to look into subgroups of the population that may be at risk for a reduced vitamin E status and/or increased oxidative stress (4). It is recommended conducting clinical trials on the efficacy of vitamin E intervention on cardio-vascular disease risk parameters in South- East Asia, the world region most affected by diabetes and with a high incidence of carriers of the haptoglobin 2-2 genotype. Type 2 diabetics with a haptoglobin 2-2 genotype have been reported to benefit from vitamin E supplementation (5).
Recent studies reported that vitamin E improves pathophysiological and histological status in non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) patients (6). As oxidative stress acts as a trigger to initiate cellular injury, leading to a chronic inflammatory response, vitamin E might act in NAFLD in different ways: As a chain-breaking, lipid-soluble antioxidant, quenching peroxyl radicals or as an anti- inflammatory compound, antagonizing the production of inflammatory mediators. There are also measurable differences in the profile of chemical processes involving metabolites (metabolomics) of subjects who are likely (vs. unlikely) to respond to vitamin E treatment for NASH and in those experiencing histologic impro- vement (vs. no improvement) on treatment.
Vitamin E is important for proper neurological functioning and its deficiency leads primarily to neurological dysfunction, such as spinocerebellar ataxia and dysarthria. According to recent studies, high plasma concent- rations of vitamin E at baseline and high vitamin E intake from foods was associated with decreased risk of developing Alzheimer´s disease. Moreover, cognitively normal centenarians exhibit normal plasma vitamin E concentrations. Randomized controlled trials show that intake of high doses of vitamin E delay the functional decline in Alzheimer´s disease patients (7). Reported benefits of vitamin E in Alzheimer´s disease should be further investigated by nerve physiology measurements for example.
The role of vitamin E in the cell membrane, where it protects polyunsaturated fatty acids from being oxidi- zed, has been described in detail. Emerging research suggests a crucial role of vitamin E in membrane repair. Membrane repair is an important cell response to plasma membrane disruption injury. Recently it has been shown that supplementation of muscle cells with alpha-tocopherol promotes plasma membrane repair. It has been proposed that this function is essential for maintenance of skeletal muscle homeostasis (8).”
Based on: Scientific Expert Workshop. Vitamin E – the way forward. Switzerland, April 2014.
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2. Pignitter M. et al. Cold Fluorescent Light as Major Inducer of Lipid Oxidation in Soybean Oil Stored at Household Conditions for Eight Weeks. J. Agric. Food Chem. 2014; 62:2297−2305.
3. Milman U. et al. Vitamin E supplementation reduces cardiovascular events in a subgroup of middle-aged individuals with both type 2 diabetes mellitus and the haptoglobin 2 – 2 genotype: a prospective double-blinded clinical trial. Arterioscler. Thromb. Vasc. Biol. 2008; 28:341–347.
4. Huebbe P. et al. Implications of apolipoprotein E genotype on inflammation and vitamin E status. Mol Nutr Food Res. 2010; 54(5):623–630.
5. Blum S. et al. Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype. Pharmacogenomics. 2010; 11(5):675–684.
6. Sanyal A. J. et al. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med. 2010; 362(18):1675–1685.
7. 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(1):33-44.
8. Howard A. C. Promotion of plasma membrane repair by vitamin E. Nat Commun. 2011; 2:597.