title: Mitigation of Inflammation-Induced Mood Dysregulation by Long-Chain Omega-3 Fatty Acids.
abstract: Although evidence suggests that chronic elevations in immune-inflammatory signaling can precipitate mood symptoms in a subset of individuals, associated risk and resilience mechanisms remain poorly understood. Long-chain omega-3 (LCn-3) fatty acids, including eicosapentaenic acid (EPA) and docosahexaenoic acid (DHA), have anti-inflammatory and inflammation-resolving properties that maintain immune-inflammatory signaling homeostasis. Cross-sectional evidence suggests that the mood disorders major depressive disorder and bipolar disorder are associated with low EPA and/or DHA biostatus, elevations in the LCn-6:LCn-3 fatty acid ratio, and elevated levels of pro-inflammatory eicosanoids, cytokines, and acute-phase proteins. Medications that are effective for reducing depressive symptoms or stabilizing manic depressive oscillations may act in part by downregulating immune-inflammatory signaling and are augmented by anti-inflammatory medications. Recent prospective longitudinal evidence suggests that elevations in the LCn-6:LCn-3 fatty acid ratio are a modifiable risk factor for the development of mood symptoms, including depression and irritability, in response to immune-inflammatory signaling. Together these data suggest that increasing LCn-3 fatty acid intake and biostatus represents a feasible strategy to mitigate the negative impact of elevated immune-inflammatory signaling on mood stability. Key teaching points: • Long-chain omega-3 (LCn-3) fatty acids have anti-inflammatory and inflammation-resolving properties. • Major mood disorders are associated with both LCn-3 fatty acids deficiency and elevated immune-inflammatory signaling. • Prospective evidence suggests that low LCn-3 fatty acid biostatus increases risk for developing inflammation-induced mood dysregulation. • Taken collectively, this evidence suggests that increasing LCn-3 fatty acid intake and biostatus represents a promising strategy to mitigate the detrimental effects of elevated immune-inflammatory signaling on mood.
authors.affiliation: a Department of Psychiatry and Behavioral Neuroscience , Division of Bipolar Disorders Research, University of Cincinnati College of Medicine , Cincinnati , Ohio.
authors.forename: Robert K
authors.initials: RK
authors.lastname: McNamara
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism; D000339:Affect; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000378:metabolism; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000276:immunology; D019964:Mood Disorders / Q000188:drug therapy* / Q000209:etiology / Q000276:immunology; D011446:Prospective Studies; D012307:Risk Factors; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000209:Acute-Phase Proteins; D000893:Anti-Inflammatory Agents; D016207:Cytokines; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid
keywords: arachidonic acid; bipolar disorder; cytokines; depression; docosahexaenoic acid (DHA); inflammation; mood; omega-3 fatty acids