About this item:

293 Views | 366 Downloads

Author Notes:

Corresponding Author: Mark Hyman Rapaport, MD, Suite 4000 WMB, 101 Woodruff Circle, Atlanta, GA 30322, Tele: 404-727-8382, Fax: 404-727-3233, ; Email: mrapapo@emory.edu.

For the disclosure of conflicts of interest, view the full article.

Subjects:

Research Funding:

The study was funded by grant 5R01MH74085 from the National Institutes of Health to Drs. Mischoulon and Rapaport. EPA-enriched and DHA-enriched preparations and matching placebos were provided by Nordic Naturals (Watsonville, CA).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Biochemistry & Molecular Biology
  • Neurosciences
  • Psychiatry
  • Neurosciences & Neurology
  • RANDOMIZED CONTROLLED-TRIAL
  • C-REACTIVE PROTEIN
  • EICOSAPENTAENOIC ACID
  • CLINICAL-TRIALS
  • DOUBLE-BLIND
  • DOCOSAHEXAENOIC ACID
  • METABOLIC SYNDROME
  • INTERFERON-ALPHA
  • METAANALYSIS
  • ASSOCIATION

Inflammation as a predictive biomarker for response to omega-3 fatty acids in major depressive disorder: a proof-of-concept study

Tools:

Journal Title:

Molecular Psychiatry

Volume:

Volume 21, Number 1

Publisher:

, Pages 71-79

Type of Work:

Article | Post-print: After Peer Review

Abstract:

This study explores whether inflammatory biomarkers act as moderators of clinical response to omega-3 (n-3) fatty acids in subjects with Major Depressive Disorder (MDD). 155 subjects with DSM-IV MDD, a baseline 17-item Hamilton Depression Rating Scale (HAM-D-17) score ≥ 15 and baseline biomarker data (IL-1ra, IL-6, hs-CRP, leptin, adiponectin), were randomized between 05/18/06 and 06/30/11, to 8 weeks of double-blind treatment with eicosapentaenoic acid (EPA)-enriched n-3 1060 mg/day, docosahexaenoic acid (DHA)-enriched n-3 900 mg/day, or placebo. Outcomes were determined using mixed model repeated measures (MMRM) analysis for “high” and “low” inflammation groups based on individual and combined biomarkers. Results are presented in terms of standardized treatment effect size (ES) for change in HAM-D-17 from baseline to treatment week 8. While overall treatment group differences were negligible (ES=−0.13 to +0.04), subjects with any “high” inflammation improved more on EPA than placebo (ES=−0.39) or DHA (ES=−0.60) and less on DHA than placebo (ES=+0.21); furthermore, EPA-placebo separation increased with increasing numbers of markers of high inflammation. Subjects randomized to EPA with “high” IL-1ra or hs-CRP or low adiponectin (“high” inflammation) had medium ES decreases in HAM-D-17 scores versus subjects “low” on these biomarkers. Subjects with “high” hs-CRP, IL-6 or leptin were less placebo-responsive than subjects with low levels of these biomarkers (medium to large ES differences). Employing multiple markers of inflammation facilitated identification of a more homogeneous cohort of subjects with MDD responding to EPA versus placebo in our cohort. Studies are needed to replicate and extend this proof of concept work.

Copyright information:

© 2015, Rights Managed by Nature Publishing Group

Export to EndNote