Abstract

ObjectiveAlpha-tocopherol is the main vitamin E compound in humans, and has important antioxidative and immunomodulatory properties. The aim of this study was to study alpha-tocopherol concentrations and their relationship to disease activity in Norwegian multiple sclerosis (MS) patients.MethodsProspective cohort study in 88 relapsing-remitting MS (RRMS) patients, originally included in a randomised placebo-controlled trial of omega-3 fatty acids (the OFAMS study), before and during treatment with interferon beta. The patients were followed for two years with repeated 12 magnetic resonance imaging (MRI) scans and nine serum measurements of alpha-tocopherol.ResultsDuring interferon beta (IFNB) treatment, each 10 µmol/L increase in alpha-tocopherol reduced the odds (CI 95%) for simultaneous new T2 lesions by 36.8 (0.5–59.8) %, p = 0.048, and for combined unique activity by 35.4 (1.6–57.7) %, p = 0.042, in a hierarchical regression model. These associations were not significant prior to IFNB treatment, and were not noticeably changed by gender, age, body mass index, HLA-DRB1*15, treatment group, compliance, or the concentrations of 25-hydroxyvitamin D, retinol, neutralising antibodies against IFNB, or the omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid. The corresponding odds for having new T1 gadolinium enhancing lesions two months later was reduced by 65.4 (16.5–85.7) %, p = 0.019, and for new T2 lesions by 61.0 (12.4–82.6) %, p = 0.023.ConclusionDuring treatment with IFNB, increasing serum concentrations of alpha-tocopherol were associated with reduced odds for simultaneous and subsequent MRI disease activity in RRMS patients.

Highlights

  • Vitamin E is an essential nutritional factor found in vegetable oils and margarines, vegetables, fruits, nuts and to some extent fish [1]

  • Eighty-eight relapsing-remitting MS (RRMS) patients, 57 (65%) women and 31 (35%) men, 58 (66%) HLA-DRB1*15 positive, age 38.9 (8.3) years, body mass index (BMI) 25.7 (4.3), disease duration 1.9 (3.1) years, and EDSS score at baseline of 1.9 (0.8) were included in the study

  • The mean difference between concentrations at baseline and through the rest of the study period was 2.0 (3.9) mmol/L for the patients treated with omega-3 fatty acids (n = 46) and 4.5 (3.8) mmol/L for the placebo group (n = 41) (p = 0.003 for difference)

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Summary

Introduction

Vitamin E is an essential nutritional factor found in vegetable oils and margarines, vegetables, fruits, nuts and to some extent fish [1]. Vitamin E has antioxidative and immunomodulatory properties and is considered one of the most important antioxidative factors against reactive oxygen species (ROS) overload and damages from oxidative stress [3]. Vitamin E is shown to affect different immune cells. Vitamin E enhanced naıve T cell function by increasing division and interleukin-2 production, and by reducing T cell suppressive prostaglandin E2 from macrophages [3]. Vitamin E has been shown to induce morphological changes and down regulate different adhesions molecules, both associated with deactivation [6]. Treatment with vitamin E inhibited demyelination caused by ethidium bromide [7], increased subsequent remyelination (7), and has been shown to exert dosedependent effects in a murine lupus model [8]

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