Omega-3 fatty acids for inflamed depression - A match/mismatch study.

Inflammation Major depressive disorder N-3 PUFAs

Journal

Brain, behavior, and immunity
ISSN: 1090-2139
Titre abrégé: Brain Behav Immun
Pays: Netherlands
ID NLM: 8800478

Informations de publication

Date de publication:
01 Mar 2024
Historique:
received: 30 09 2023
revised: 31 01 2024
accepted: 27 02 2024
medline: 4 3 2024
pubmed: 4 3 2024
entrez: 3 3 2024
Statut: aheadofprint

Résumé

Despite decades of research on the pathophysiology of depression, the development of new therapeutic interventions has been slow, and no biomarkers of treatment response have been clinically implemented. Several lines of evidence suggest that the clinical and biological heterogeneity among patients with major depressive disorder (MDD) has hampered progress in the field. MDD with low-grade inflammation - "inflamed depression" - is a subtype of depression that may be associated with a superior antidepressant treatment response to anti-inflammatory compounds. Omega-3 fatty acid eicosapentaenoic acid (EPA) has anti-inflammatory properties, and preliminary data suggest that it may be particularly efficacious in inflamed depression. In this study we tested the hypothesis that add-on EPA has greater antidepressant efficacy in MDD patients with high baseline high-sensitivity C-reactive protein (hs-CRP) compared to MDD patients with low hs-CRP. All subjects received 2.2 g EPA, 400 mg docosahexaenoic acid and 800 mg of other fatty acids/day for 8 weeks, added to stable ongoing antidepressant treatment. The primary outcome was change in the 17-item Hamilton Depression Rating Scale (HAMD-17). Patients and raters were blind to baseline hs-CRP status. In an intention-to-treat analysis including all subjects with at least one post baseline visit (n = 101), ahs-CRPcut-off of ≥1 mg/L, but not ≥3 mg/L, was associated with a greater improvement in HAMD-17 total score. In addition to a general antidepressant effect among patients with hs-CRP ≥ 1 mg/L, adjuvant EPA treatment improved symptoms putatively related to inflamed depression such as fatigue and sleep difficulties. This adds to the mounting evidence that delineation of MDD-subgroups based on inflammation may be clinically relevant to predict treatment response to anti-inflammatory interventions.

Identifiants

pubmed: 38432599
pii: S0889-1591(24)00273-3
doi: 10.1016/j.bbi.2024.02.029
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Klara Suneson (K)

Unit for Biological and Precision Psychiatry, Department of Clinical Sciences Lund, Lund University; Office for Psychiatry and Habilitation, Psychiatric Clinic Malmö, Region Skåne, Malmö, Sweden.

Gustav Söderberg Veibäck (GS)

Unit for Biological and Precision Psychiatry, Department of Clinical Sciences Lund, Lund University; Department of Gastroenterology and Nutrition, Department of Clinical Sciences, Skåne University Hospital, Malmö, Sweden.

Jesper Lindahl (J)

Unit for Biological and Precision Psychiatry, Department of Clinical Sciences Lund, Lund University; Office for Psychiatry and Habilitation, Psychiatric Clinic Lund, Region Skåne, Lund, Sweden.

Johanna Tjernberg (J)

Unit for Biological and Precision Psychiatry, Department of Clinical Sciences Lund, Lund University; Office for Psychiatry and Habilitation, Psychiatry Research Skåne, Region Skåne, Lund, Sweden.

Darya Ståhl (D)

Unit for Biological and Precision Psychiatry, Department of Clinical Sciences Lund, Lund University.

Simon Ventorp (S)

Unit for Biological and Precision Psychiatry, Department of Clinical Sciences Lund, Lund University.

Filip Ängeby (F)

Unit for Biological and Precision Psychiatry, Department of Clinical Sciences Lund, Lund University; Office for Psychiatry and Habilitation, Psychiatric Clinic Lund, Region Skåne, Lund, Sweden.

Karl Lundblad (K)

Office for Psychiatry and Habilitation, Psychiatric Clinic Lund, Region Skåne, Lund, Sweden; Office for Psychiatry, Norra Stockholm Psykiatri, Region Stockholm, Sweden.

Owen M Wolkowitz (OM)

Department of Psychiatry and Behavioral Sciences and Weill Institute for Neurosciences, University of California, San Francisco, CA, USA.

Daniel Lindqvist (D)

Unit for Biological and Precision Psychiatry, Department of Clinical Sciences Lund, Lund University; Office for Psychiatry and Habilitation, Psychiatry Research Skåne, Region Skåne, Lund, Sweden. Electronic address: Daniel.lindqvist@med.lu.se.

Classifications MeSH