Polyunsaturated fatty acid deficit in patients with bipolar mania

Chiu, Chih Chiang; Huang, Shih Yi; Su, Kuan‐Pin; Lu, Mong Liang; Huang, Ming; Chen, Chiao Chicy; Shen, Winston W.

doi:10.1016/s0924-977x(02)00130-x

Cited by 137 publications

(106 citation statements)

References 36 publications

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“…7,8 Epidemiological observations point to a decreased dietary n-3 polyunsaturated fatty acid (PUFA) intake being associated with an increased prevalence of bipolar disorder. 9 Blood DHA levels 10,11 and postmortem prefrontal cortex DHA levels are 16.5% lower in bipolar patients compared to normal controls. 12 Two randomized clinical trials have shown n-3 PUFA supplementation to be beneficial in treating bipolar symptoms.…”

Section: Introductionmentioning

confidence: 97%

n-3 Polyunsaturated fatty acid deprivation in rats decreases frontal cortex BDNF via a p38 MAPK-dependent mechanism

et al. 2006

Mol Psychiatry

258

151

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Decreased docosahexaenoic acid (DHA) and brain-derived neurotrophic factor (BDNF) have been implicated in bipolar disorder. It also has been reported that dietary deprivation of n-3 polyunsaturated fatty acids (PUFAs) for 15 weeks in rats, increased their depression and aggression scores. Here, we show that n-3 PUFA deprivation for 15 weeks decreased the frontal cortex DHA level and reduced frontal cortex BDNF expression, cAMP response element binding protein (CREB) transcription factor activity and p38 mitogen-activated protein kinase (MAPK) activity. Activities of other CREB activating protein kinases were not significantly changed. The addition of DHA to rat primary cortical astrocytes in vitro, induced BDNF protein expression and this was blocked by a p38 MAPK inhibitor. DHA's ability to regulate BDNF via a p38 MAPK-dependent mechanism may contribute to its therapeutic efficacy in brain diseases having disordered cell survival and neuroplasticity.

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Section: Introductionmentioning

confidence: 97%

n-3 Polyunsaturated fatty acid deprivation in rats decreases frontal cortex BDNF via a p38 MAPK-dependent mechanism

et al. 2006

Mol Psychiatry

258

151

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“…This abnormality has recently been supported by a population-based study, which produced epidemiological evidence of FA composition differences in depressed patients and which suggested that low levels of omega-3 PUFAs may have a direct effect on mood disorders [7]. In addition, a reduced DHA level was also found in a study of bipolar mania patients [8].…”

Section: Introductionmentioning

confidence: 78%

<i>Ban</i>I Polymorphism of the Cytosolic Phospholipase A<sub>2</sub> Gene and Mood Disorders in the Korean Population

Pae

Yu²,

Kim³

et al. 2004

Neuropsychobiology

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Membrane phospholipid abnormalities have been proposed to be involved in the pathogenesis of mood disorders, and in signal transduction and neurotransmitter uptake. Cytosolic phospholipase A₂ (cPLA₂) is not only an essential enzyme in the metabolism of fatty acids but also in signaling process. Therefore, we examined the association between the BanI polymorphism of the cPLA₂ gene and mood disorders. Sixty-two patients with major depressive disorder (MDD), 50 patients with bipolar I disorder (BID) and 117 healthy controls participated in this study. Genotyping was performed by using PCR-based methods. Genotype and allele distributions in MDD patients were significantly different from those of the controls. In particular, the A2 allele was associated with increased risk of MDD development (p = 0.007, odds ratio = 1.827; confidence interval = 1.141–2.927). However, the polymorphism was not different between BID patients and controls in genotype and allele distribution. This preliminary study indicates the need for further studies on the potential role of the cPLA₂ gene polymorphism in the susceptibility to mood disorders.

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“…In brief, the PUFAs and their metabolites, the eicosanoids (PGs, LTs, or TXs), might be important in modulating biological processes related to brain and physical functions. The PUFAs-PGE2 cascade hypothesis in mood disorders has been supported by a large body of evidence, including higher levels of AA [20,72] and PGE2 [73,74] in patients with mood disorders [75] , the inhibitory effect on phospholipase A2 (PLA2) activity of mood stabilizers [76,77] , and the antidepressant effect of n-3 PUFAs in mood disorders [23,33] . Chronic low-grade systemic inflammation plays a significant role in several chronic medical diseases as well as depression [78] .…”

Section: Biological Mechanism Of the Effect Of N-3 Pufas On Depressiomentioning

confidence: 99%

Biological Mechanism of Antidepressant Effect of Omega–3 Fatty Acids: How Does Fish Oil Act as a ‘Mind-Body Interface’?

Su¹

2009

Neurosignals

Self Cite

158

114

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The unsatisfactory results of monoamine-based antidepressant therapy and the high occurrence of somatic symptoms and physical illness in patients with depression imply that the serotonin hypothesis is insufficient to approach the aetiology of depression. Depressive disorders with somatic presentation are the most common form of depression. Somatization, the bodily symptoms without organic explanation, is similar to cytokine-induced sickness behaviour. Based on recent evidence, omega–3 polyunsaturated fatty acids (n–3 PUFAs, or n–3 fatty acids) are enlightening a promising path to discover the unsolved of depression, sickness behaviour and to link the connection of mind and body. The PUFAs are classified into n–3 (or omega–3) and n–6 (or omega–6) groups. Eicosapentaenoic acid and docosahexaenoic acid, the major bioactive components of n–3 PUFAs, are not efficiently synthesized in humans and should therefore be obtained directly from the diet, particularly by consuming fish. Docosahexaenoic acid deficiency is associated with dysfunctions of neuronal membrane stability and transmission of serotonin, norepinephrine and dopamine, which might connect to the aetiology of mood and cognitive dysfunction of depression. Likewise, eicosapentaenoic acid is important in balancing the immune function and physical health by reducing membrane arachidonic acid (an n–6 PUFA) and prostaglandin E₂ synthesis, which might be linked to the somatic manifestations and physical comorbidity in depression. The role of n–3 PUFAs in immunity and mood function supports the promising hypothesis of psychoneuroimmunology of depression and provides an excellent interface between ‘mind’ and ‘body’. This review is to provide an overview of the evidence about the role of n–3 PUFAs in depression and its common comorbid physical conditions and to propose mechanisms by which they may modulate molecular and cellular functions.

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Polyunsaturated fatty acid deficit in patients with bipolar mania

Cited by 137 publications

References 36 publications

n-3 Polyunsaturated fatty acid deprivation in rats decreases frontal cortex BDNF via a p38 MAPK-dependent mechanism

n-3 Polyunsaturated fatty acid deprivation in rats decreases frontal cortex BDNF via a p38 MAPK-dependent mechanism

<i>Ban</i>I Polymorphism of the Cytosolic Phospholipase A<sub>2</sub> Gene and Mood Disorders in the Korean Population

Biological Mechanism of Antidepressant Effect of Omega–3 Fatty Acids: How Does Fish Oil Act as a ‘Mind-Body Interface’?

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