Omega-3 polyunsaturated fatty acids and reduction of depressive symptoms in older adults: A systematic review and meta-analysis

Zhang, Bai; Bo, Ai; Wu, Sijie; Gai, Qiong-Yan; Chi, Iris

doi:10.1016/j.jad.2018.07.057

Cited by 50 publications

(23 citation statements)

References 51 publications

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“…Our findings about n-3 fatty acids intake are consistent with other studies, including cross-sectional [18,23,24], prospective cohort [17,[25][26][27], meta-analysis [19,28] and experimental studies [20]. The results from a cross-sectional study [23] indicated that higher n-3 fatty acids intake was inversely associated with the risk of evaluated depressive symptoms.…”

Section: Discussionsupporting

confidence: 90%

“…As essential nutrients for human body, polyunsaturated fatty acids (mainly n-3 and n-6 fatty acids) have also been reported to be associated with depression [15][16][17][18]. Observational and experimental studies have indicated that a higher consumption of n-3 fatty acids is associated with lower risk of depression [17][18][19][20][21][22][23][24][25][26][27][28], suggesting that n-3 fatty acids have a protective effect on depression. However, few studies have explored the association between n-6 fatty acids and depression, and the results are inconsistent [16][17][18]29].…”

Section: Introductionmentioning

confidence: 99%

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Associations of n-3, n-6 Fatty Acids Intakes and n-6:n-3 Ratio with the Risk of Depressive Symptoms: NHANES 2009–2016

Zhang

Sun

et al. 2020

Nutrients

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Many studies have explored the association between n-3 fatty acids and depression, but research on the associations of n-6 fatty acids and n-6:n-3 ratio with depression is more scarce, and the results are controversial. Therefore, we conducted this cross-sectional study to explore the associations of n-3 and n-6 fatty acid intakes and n-6:n-3 ratio with the risk of depressive symptoms using data from National Health and Nutrition Examination Survey (NHANES) 2009–2016. Dietary data on n-3 and n-6 fatty acids were obtained through two 24-h dietary recall interviews, and were adjusted by energy. Depressive symptoms were measured by PHQ-9 (nine-item Patient Health Questionnaire). We applied logistic regression and restricted cubic spline models to assess the relationships of n-3 and n-6 fatty acids intake and n-6:n-3 ratio with the risk of depressive symptoms. A total of 17,431 individuals over 18 years old were enrolled in this study. In the multivariate-adjusted model 2, compared with the lowest category, the highest odd ratios (ORs) with 95% confidence intervals (CIs) for n-3 fatty acid intake and n-6:n-3 ratio were 0.71 (0.55–0.92) and 1.66 (1.10–2.50), and middle OR (95% CI) for n-6 fatty acid intake was 0.72 (0.56–0.92), respectively. Our study suggests that n-3 and n-6 fatty acids intake were inversely associated with the risk of depressive symptoms, while the n-6:n-3 ratio was positively associated with the risk of depressive symptoms.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Associations of n-3, n-6 Fatty Acids Intakes and n-6:n-3 Ratio with the Risk of Depressive Symptoms: NHANES 2009–2016

Zhang

Sun

et al. 2020

Nutrients

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“…It is worthy to mention that many (but not all) of these studies show greater efficacy of EPA than DHA, while our studies suggest equal potency and efficacy for the two compounds [14, 52, 56–58]. Note, however, that 1) the EPA- or DHA-“enriched” preparations used in clinical studies are 80:20 mixtures of the two n-3 PUFA species and 2) orally-ingested preparations are metabolized, something that does not occur in cell-culture medium…”

Section: Discussionmentioning

confidence: 85%

N-3 polyunsaturated fatty acids promote astrocyte differentiation and neurotrophin production independent of cAMP in patient-derived neural stem cells

Wang

Sheridan

et al. 2020

Preprint

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30Evidence from epidemiological and laboratory studies, as well as randomized placebo-controlled 31 trials, suggests supplementation with n-3 polyunsaturated fatty acids (PUFAs) may be efficacious 32 for treatment of major depressive disorder (MDD). The mechanisms underlying n-3 PUFAs 33 potential therapeutic properties remain unknown. There are suggestions in the literature that glial 34 hypofunction is associated with depressive symptoms and that antidepressants may normalize 35 glial function. In this study, iPSC-derived neuronal stem cell lines were generated from 36 individuals with MDD. Astrocytes differentiated from patient-derived neuronal stem cells 37 (iNSCs) were verified by GFAP. Cells were treated with eicosapentaenoic acid (EPA), 38 docosahexaenoic acid (DHA) and stearic acid (SA). During astrocyte differentiation, we found 39 that n-3 PUFAs increased GFAP expression and GFAP positive cell formation. BDNF and 40 GDNF production were increased in the astrocytes derived from patients subsequent to n-3 41 PUFA treatment. Stearic Acid (SA) treatment did not have this effect. CREB activity 42 (phosphorylated CREB) was also increased by DHA and EPA but not by SA. Furthermore, when 43 these astrocytes were treated with n-3 PUFAs, the cAMP antagonist, RP-cAMPs did not block n-44 3 PUFA CREB activation. However, the CREB specific inhibitor (666-15) diminished BDNF 45 and GDNF production induced by n-3 PUFA, suggesting CREB dependence. Together, these 46 results suggested that n-3 PUFAs facilitate astrocyte differentiation, and may mimic effects of 47 some antidepressants by increasing production of neurotrophic factors. The CREB-dependence 48 and cAMP independence of this process suggests a manner in which n-3 PUFA could augment 49 antidepressant effects. These data also suggest a role for astrocytes in both MDD and 50 antidepressant action. 51 52 53Major depressive disorder (MDD) is the most common psychiatric disorder, with almost 54 one in six individuals experiencing at least one depressive episode at some point in their lifetime. 55It is currently the leading cause of disability worldwide [1, 2]. While effective treatments exist, 56 about one third of patients treated with antidepressants do not reach symptomatic remission [3, 57 4]. While some of these non-remitters may respond to ketamine or other rescue strategies, 58 additional therapeutic options are needed. 59Brain regions and even cell-types contributing to MDD are not well established [4]. 60Evidence from clinical, preclinical and post-mortem studies suggests that dysfunction and 61 degeneration of astrocytes may be one of potential candidates, and astrocytes may also represent 62 a potential therapeutic target for MDD [5][6][7][8]. Antidepressants, including SSRIs and ketamine, 63 increase brain-derived neurotrophic factor (BDNF) and glial cell-derived neurotrophic factor 64 (GDNF) expression in primary cultured animal astrocytes [9][10][11]. Substantial evidence suggested 65 that astrocytes might be the main resource of antidepressant...

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“…Several reports using meta-analysis demonstrated that ω-3 PUFAs could reduce depressive symptoms beyond placebo (Lin et al, 2010, 2017; Sublette et al, 2011; Mello et al, 2014; Grosso et al, 2016; Hallahan et al, 2016; Mocking et al, 2016; Sarris et al, 2016; Bai et al, 2018; Hsu et al, 2018). Dietary intake of ω-3 PUFAs is known to be associated with lower risk of depression.…”

Section: Inflammation In Depression and Sehmentioning

confidence: 99%

Role of Soluble Epoxide Hydrolase in Metabolism of PUFAs in Psychiatric and Neurological Disorders

Hashimoto

2019

Front. Pharmacol.

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Inflammation plays a key role in the pathogenesis of a number of psychiatric and neurological disorders. Soluble epoxide hydrolases (sEH), enzymes present in all living organisms, metabolize epoxy fatty acids (EpFAs) to corresponding 1,2-diols by the addition of a molecule of water. Accumulating evidence suggests that sEH in the metabolism of polyunsaturated fatty acids (PUFAs) plays a key role in inflammation. Preclinical studies demonstrated that protein expression of sEH in the prefrontal cortex, striatum, and hippocampus from mice with depression-like phenotype was higher than control mice. Furthermore, protein expression of sEH in the parietal cortex from patients with major depressive disorder was higher than controls. Interestingly, Ephx2 knock-out (KO) mice exhibit stress resilience after chronic social defeat stress. Furthermore, the sEH inhibitors have antidepressant effects in animal models of depression. In addition, pharmacological inhibition or gene KO of sEH protected against dopaminergic neurotoxicity in the striatum after repeated administration of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) in an animal model of Parkinson’s disease (PD). Protein expression of sEH in the striatum from MPTP-treated mice was higher than control mice. A number of studies using postmortem brain samples showed that the deposition of protein aggregates of α-synuclein, termed Lewy bodies, is evident in multiple brain regions of patients from PD and dementia with Lewy bodies (DLB). Moreover, the expression of the sEH protein in the striatum from patients with DLB was significantly higher compared with controls. Interestingly, there was a positive correlation between sEH expression and the ratio of phosphorylated α-synuclein to α-synuclein in the striatum. In the review, the author discusses the role of sEH in the metabolism of PUFAs in inflammation-related psychiatric and neurological disorders.

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Omega-3 polyunsaturated fatty acids and reduction of depressive symptoms in older adults: A systematic review and meta-analysis

Cited by 50 publications

References 51 publications

Associations of n-3, n-6 Fatty Acids Intakes and n-6:n-3 Ratio with the Risk of Depressive Symptoms: NHANES 2009–2016

Associations of n-3, n-6 Fatty Acids Intakes and n-6:n-3 Ratio with the Risk of Depressive Symptoms: NHANES 2009–2016

N-3 polyunsaturated fatty acids promote astrocyte differentiation and neurotrophin production independent of cAMP in patient-derived neural stem cells

Role of Soluble Epoxide Hydrolase in Metabolism of PUFAs in Psychiatric and Neurological Disorders

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