Do Docosahexaenoic and Eicosapentaenoic Acids Have Similar Effects on Inflammation Markers? Pairwise and Network Meta-Analyses of Randomized Controlled Trials

Abstract Objectives The aim of this study was to compare the effect of DHA and EPA on several markers of systemic inflammation by pairwise and network meta-analyses of randomized controlled trials (RCTs). Methods MEDLINE, EMBASE and The Cochrane Library were searched through September 2019. We included RCTs of ≥ 7 days that directly compared the effects of DHA with EPA and RCTs of indirect comparisons, in which the effects of DHA or EPA were assessed individually compared with a control fatty acid. Differences in circulating concentrations of CRP, IL-6, TNF-α and adiponectin were the primary outcome. Data were pooled by pairwise and network meta-analysis and expressed as mean differences (MDs) with 95% confidence intervals (CIs). Heterogeneity was assessed (Cochran Q statistic) and quantified (I2 statistic) in the pairwise meta-analysis. Inconsistency and transitivity were evaluated in the network meta-analysis. The certainty of evidence was assessed using GRADE (Grading of Recommendations Assessment, Development, and Evaluation). Results Eligibility criteria were met by 5 RCTs (N = 411) for the pairwise meta-analysis and 20 RCTs (N = 1231) for the network meta-analysis. In the pairwise meta-analysis, DHA and EPA had similar effects on plasma CRP (MDDHA vs. EPA = 0.14 mg/L [95% CI −0.57, 0.85]; I2 = 61%), IL-6 (MDDHA vs. EPA = 0.10 pg/mL [−0.15, 0.34]; I2 = 40%) and TNF-α (MDDHA vs. EPA = −0.10 pg/mL [−0.37, 0.18]; I2 = 40%). The effects of DHA and EPA on plasma CRP (MDDHA vs. EPA = −0.33 mg/L [−0.75, 0.10]), IL-6 (MDDHA vs. EPA = 0.09 pg/mL [−0.12, 0.30]) and TNF-α (MDDHA vs. EPA = −0.02 pg/mL [−0.25, 0.20]) were also similar according to the network meta-analysis. DHA and EPA had similar effects on plasma adiponectin in the network meta-analysis. Conclusions The present pairwise and network meta-analyses comparing EPA to DHA suggest that DHA and EPA do not differentially modify systemic markers of subclinical inflammation. Funding Sources The authors have no funding to report.