Omega-3 polyunsaturated fatty acids and depression: a review of the evidence.
ABSTRACT Brain lipids contain a high proportion of polyunsaturated fatty acids (PUFA), which are a main component of cell membranes. Omega-3 (omega-3) PUFA eicosapentaeoic acid (EPA) and docosahexaenoic acid (DHA) are the most common PUFA in the brain. The physiological roles of omega-3 PUFA in the brain include regulation of cell membrane fluidity, dopaminergic and serotoninergic transmission, membrane-bound enzymes and cellular signal transduction. They are also thought to play a role in brain glucose metabolism, eicosanoid synthesis, gene expression, cell growth and protection from apoptosis. Increasing evidence from animal and human research shows omega-3 PUFA depletion may play an etiological role in several inflammatory, autoimmune and neuropsychiatric disorders. In particular, an association between omega-3 PUFA and depression was repeatedly suggested in observational and experimental studies on populations affected by major depression, depressed mood or post-partum depression. Consistently, the potential therapeutic role of omega-3 PUFA dietary supplementation was tested in clinical trials on depression. The current review identifies and evaluates available epidemiological evidence of a negative relationship between omega-3 PUFA and depression and examines its biological plausibility. Although current evidence increasingly supports an inverse association between omega-3 PUFA and depression, the validity of findings from observational and experimental research is limited by several methodological issues. Further studies with larger sample sizes and more sophisticated design are required to provide convincing evidence of a causal relationship between omega-3 PUFA and depression.
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ABSTRACT: The role of cholesterol in psychiatric diseases has aroused the interest of the medical community, particularly in association with violent and suicidal behavior. Herein, we discuss some aspects of brain cholesterol metabolism, exploring possible mechanisms underlying the findings and reviewing the available literature on the possible neurochemical link between suicide and low or reduced levels of serum cholesterol. Most of the current hypotheses suggest a decreased serotonergic activity due to a decrease in cholesterol in the lipid rafts of synaptic membranes. Some aspects and limitations of this assumption are emphasized. In addition to serotonin hypofunction, other mechanisms have been proposed to explain increased impulsivity in suicidal individuals, including steroid modulation and brain-derived neurotrophic factor decrease, which could also be related to changes in lipid rafts. Other putative markers of suicidal behavior (e.g. protein S100B) are discussed in connection with cholesterol metabolism in the brain tissue. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.Psychiatry Research 10/2014; 220(3):745-751. · 2.68 Impact Factor
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