#MSBlog: Blood vitamin E level rises with suppression of inflammation by interferon-beta. Chicken or Egg?
Løken-Amsrud et al. Alpha-tocopherol and MRI Outcomes in Multiple Sclerosis - Association and Prediction. PLoS One. 2013;8(1):e54417. doi: 10.1371/journal.pone.0054417.
OBJECTIVE: Alpha-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 MSers.
METHODS: Prospective cohort study in 88 relapsing-remitting MSers (RRMSers), originally included in a randomised placebo-controlled trial of omega-3 fatty acids (the OFAMS study), before and during treatment with interferon beta. The MSers were followed for two years with repeated 12 magnetic resonance imaging (MRI) scans and nine serum measurements of alpha-tocopherol.
RESULTS: During 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.
CONCLUSION: During treatment with IFNB, increasing serum concentrations of alpha-tocopherol were associated with reduced odds for simultaneous and subsequent MRI disease activity in RRMS patients.
"These results will need confirmation, but are interesting in that they indicate that blood alpha-tocopherol levels, a form of vE, are associated with a positive treatment response to IFNbeta. This does not mean that alpha-tocopherol is necessarily affecting MS disease activity in itself, but rather that alpha-tocopherol levels are reduced as part of the inflammatory response. In other words inflammation consumes alpha-tocopherol and that when you suppress inflammation you stop consuming alpha-tocopherol and your blood levels rise."
"This is a typical example of the chicken-or-egg or causal-association conundrum that scientists face all the time. Clearly more research is needed to dissect this problem."
"This study does not support MSers taking alpha-tocopherol supplements; further data would be required from properly conducted randomised trials before this recommendation could be made."