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      Omega-3 fatty acid deficiencies in neurodevelopment, aggression and autonomic dysregulation: Opportunities for intervention

      , ,
      International Review of Psychiatry
      Informa UK Limited

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          Abstract

          Mechanisms by which aggressive and depressive disorders may be exacerbated by nutritional deficiencies in omega-3 fatty acids are considered. Early developmental deficiencies in docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) may lower serotonin levels at critical periods of neurodevelopment and may result in a cascade of suboptimal development of neurotransmitter systems limiting regulation of the limbic system by the frontal cortex. Residual developmental deficits may be manifest as dysregulation of sympathetic responses to stress including decreased heart rate variability and hypertension, which in turn have been linked to behavioral dysregulation. Little direct data are available to disentangle residual neurodevelopmental effects from reversible adult pathologies. Ensuring optimal intakes of omega-3 fatty acids during early development and adulthood shows considerable promise in preventing aggression and hostility.

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          Most cited references97

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          The initial Global Burden of Disease study found that depression was the fourth leading cause of disease burden, accounting for 3.7% of total disability adjusted life years (DALYs) in the world in 1990. To present the new estimates of depression burden for the year 2000. DALYs for depressive disorders in each world region were calculated, based on new estimates of mortality, prevalence, incidence, average age at onset, duration and disability severity. Depression is the fourth leading cause of disease burden, accounting for 4.4% of total DALYs in the year 2000, and it causes the largest amount of non-fatal burden, accounting for almost 12% of all total years lived with disability worldwide. These data on the burden of depression worldwide represent a major public health problem that affects patients and society.
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            Emotion, Decision Making and the Orbitofrontal Cortex

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              Dietary omega-3 fatty acids normalize BDNF levels, reduce oxidative damage, and counteract learning disability after traumatic brain injury in rats.

              Omega-3 fatty acids (i.e., docosahexaenoic acid; DHA) regulate signal transduction and gene expression, and protect neurons from death. In this study we examined the capacity of dietary omega3 fatty acids supplementation to help the brain to cope with the effects of traumatic injury. Rats were fed a regular diet or an experimental diet supplemented with omega-3 fatty acids, for 4 weeks before a mild fluid percussion injury (FPI) was performed. FPI increased oxidative stress, and impaired learning ability in the Morris water maze. This type of lesion also reduced levels of brain-derived neurotrophic factor (BDNF), synapsin I, and cAMP responsive element-binding protein (CREB). It is known that BDNF facilitates synaptic transmission and learning ability by modulating synapsin I and CREB. Supplementation of omega-3 fatty acids in the diet counteracted all of the studied effects of FPI, that is, normalized levels of BDNF and associated synapsin I and CREB, reduced oxidative damage, and counteracted learning disability. The reduction of oxidative stress indicates a benevolent effect of this diet on mechanisms that maintain neuronal function and plasticity. These results imply that omega-3 enriched dietary supplements can provide protection against reduced plasticity and impaired learning ability after traumatic brain injury.
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                Author and article information

                Journal
                International Review of Psychiatry
                International Review of Psychiatry
                Informa UK Limited
                0954-0261
                1369-1627
                July 11 2009
                January 2006
                July 11 2009
                January 2006
                : 18
                : 2
                : 107-118
                Article
                10.1080/09540260600582967
                16777665
                0edc7828-c1e5-4113-87a1-b8334367a149
                © 2006
                History

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