Contributions
Abstract: EP1341
Type: ePoster
Abstract Category: Clinical aspects of MS - 5 Epidemiology
Background: The omega-3 fatty acid α-Linolenic acid (ALA) has anti-inflammatory properties, and consumption of food rich in ALA has been associated with a decreased risk of developing multiple sclerosis (MS) (1). It is, however, not known if serum levels of ALA affect disease activity in MS- patients.
Objective: To study whether disease activity is associated with ALA serum levels in patients with relapsing-remitting MS.
Methods: We conducted a prospective cohort study of 87 patients with relapsing-remitting MS, originally included in a randomized placebo-controlled trial (RCT) of omega-3 fatty acids in MS (the OFAMS Study), and followed them for two years with repeated MRI- and serum measures. The patients received no immunomodulatory treatment during the first six months, and all patients were initiated on subcutaneous interferon β-1a (IFNB) after month 6 and throughout the follow-up period.
MRI and serum ALA measurements were performed at baseline and at months 6, 12 and 24. We used random-intercept logistic regression to estimate the effect of ALA on disease activity adjusting for age and EDSS at baseline, treatment allocation in the RCT and IFNB-status. In a second multivariable model, we additionally adjusted for vitamin D, cotinine, HLA-DRB1*15, vitamin A and BMI.
Results: Higher serum levels were inversely correlated with MRI disease activity. Each weight percent increase in ALA of total serum phospholipid fatty acid levels were associated with a subsequent reduced risk of new MRI-activity: OR 0.52 (95% CI: 0.29-0.95) for new T2-lesions, OR 0.68 (95% CI: 0.40-1.17) for new T1Gd+ lesions and OR 0.53 (95% CI: 0.28-0.97) for combined unique activity (the sum of T1Gd+ and new or enlarging T2 lesions). Similar Associations were found after further adjusting for HLA-DRB1*15 status, vitamin D, cotinine, vitamin A and BMI.
Conclusions: We detected an inverse association between serum levels of ALA and MRI-disease activity. The association remained similar after adjusting for all several known cofounders. This indicates that ALA could have unique anti-inflammatory properties relevant for the pathogenesis of MS.
References: 1 K Bjornevik, T Chitnis, A Ascherio, KL Munger. Polyunsatturated fatty acids and the risk of multiple sclerosis. Multiple Sclerosis Journal. 2015. 21, 53-54.
Disclosure:
Ø. Torkildsen served on the scientific advisory board for Biogen, Sanofi-Aventis, Merck.
K.-M. Myhr has received research support, speaker honoraria or served on the scientific advisory board for Almirall, Biogen, Genzyme, Novartis Norway, Roche or Teva.
A.G. Beiske has received research support, travel funding or served on scientific advisory board for Genzyme and Teva and Novartis.
H. Hovdal report no disclosures.
R. Midgard received speaker honoraria, travel funding or served on the scientific advisory board for Novartis Norway.
T Riise reports no disclosures.
S. Wergeland has received speaker honoraria from Biogen, Novartis.
K Bjørnevik reports no disclosures.
Abstract: EP1341
Type: ePoster
Abstract Category: Clinical aspects of MS - 5 Epidemiology
Background: The omega-3 fatty acid α-Linolenic acid (ALA) has anti-inflammatory properties, and consumption of food rich in ALA has been associated with a decreased risk of developing multiple sclerosis (MS) (1). It is, however, not known if serum levels of ALA affect disease activity in MS- patients.
Objective: To study whether disease activity is associated with ALA serum levels in patients with relapsing-remitting MS.
Methods: We conducted a prospective cohort study of 87 patients with relapsing-remitting MS, originally included in a randomized placebo-controlled trial (RCT) of omega-3 fatty acids in MS (the OFAMS Study), and followed them for two years with repeated MRI- and serum measures. The patients received no immunomodulatory treatment during the first six months, and all patients were initiated on subcutaneous interferon β-1a (IFNB) after month 6 and throughout the follow-up period.
MRI and serum ALA measurements were performed at baseline and at months 6, 12 and 24. We used random-intercept logistic regression to estimate the effect of ALA on disease activity adjusting for age and EDSS at baseline, treatment allocation in the RCT and IFNB-status. In a second multivariable model, we additionally adjusted for vitamin D, cotinine, HLA-DRB1*15, vitamin A and BMI.
Results: Higher serum levels were inversely correlated with MRI disease activity. Each weight percent increase in ALA of total serum phospholipid fatty acid levels were associated with a subsequent reduced risk of new MRI-activity: OR 0.52 (95% CI: 0.29-0.95) for new T2-lesions, OR 0.68 (95% CI: 0.40-1.17) for new T1Gd+ lesions and OR 0.53 (95% CI: 0.28-0.97) for combined unique activity (the sum of T1Gd+ and new or enlarging T2 lesions). Similar Associations were found after further adjusting for HLA-DRB1*15 status, vitamin D, cotinine, vitamin A and BMI.
Conclusions: We detected an inverse association between serum levels of ALA and MRI-disease activity. The association remained similar after adjusting for all several known cofounders. This indicates that ALA could have unique anti-inflammatory properties relevant for the pathogenesis of MS.
References: 1 K Bjornevik, T Chitnis, A Ascherio, KL Munger. Polyunsatturated fatty acids and the risk of multiple sclerosis. Multiple Sclerosis Journal. 2015. 21, 53-54.
Disclosure:
Ø. Torkildsen served on the scientific advisory board for Biogen, Sanofi-Aventis, Merck.
K.-M. Myhr has received research support, speaker honoraria or served on the scientific advisory board for Almirall, Biogen, Genzyme, Novartis Norway, Roche or Teva.
A.G. Beiske has received research support, travel funding or served on scientific advisory board for Genzyme and Teva and Novartis.
H. Hovdal report no disclosures.
R. Midgard received speaker honoraria, travel funding or served on the scientific advisory board for Novartis Norway.
T Riise reports no disclosures.
S. Wergeland has received speaker honoraria from Biogen, Novartis.
K Bjørnevik reports no disclosures.