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      Depression and lifestyle: Focusing on nutrition, exercise, and their possible relevance to molecular mechanisms

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      Psychiatry and Clinical Neurosciences
      Wiley

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          Abstract

          Accumulating evidence has suggested the important role of lifestyle factors in depressive disorder. This paper aimed to introduce and outline recent research on epidemiological and intervention studies on lifestyle‐related factors in depressive disorder with a special focus on diet. Evidence on exercise, sleep. and related behaviors is also described. Here, findings from meta‐analytic studies are emphasized and related studies by the author's research group are introduced. Dietary factors that increase the risk of the illness include energy overload, skipping breakfast, unhealthy diet styles such as Western diet, inflammation‐prone diet, and high consumption of ultraprocessed food (UPF). Nutritional imbalances such as inadequate intake of protein, fish (Ω3 polyunsaturated fatty acids), vitamins (folate and vitamin D), and minerals (iron and zinc) increases the risk of depression. Poor oral hygiene, food allergy, addiction to alcohol, and smoking constitute risk factors. Sedentary lifestyle and increased screen time (e.g. video games and the internet) confer the risk of depression. Insomnia and disturbed sleep–wake rhythm are also involved in the pathogenesis of depression. There is accumulating evidence at the meta‐analysis level for interventions to modify these lifestyle habits in the protection and treatment of depressive disorder. Main biological mechanisms of the link between lifestyle factors and depression include monoamine imbalance, inflammation, altered stress response, oxidative stress, and dysfunction of brain‐derived neurotrophic factor, although other players such as insulin, leptin, and orexin also play a role. To increase resilience to modern stress and ameliorate depression through modification of lifestyle habits, a list of 30 recommendable interventions is presented.

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          Diagnostic and Statistical Manual of Mental Disorders

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            Vitamin D Deficiency

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              A neurotrophic model for stress-related mood disorders.

              There is a growing body of evidence demonstrating that stress decreases the expression of brain-derived neurotrophic factor (BDNF) in limbic structures that control mood and that antidepressant treatment reverses or blocks the effects of stress. Decreased levels of BDNF, as well as other neurotrophic factors, could contribute to the atrophy of certain limbic structures, including the hippocampus and prefrontal cortex that has been observed in depressed subjects. Conversely, the neurotrophic actions of antidepressants could reverse neuronal atrophy and cell loss and thereby contribute to the therapeutic actions of these treatments. This review provides a critical examination of the neurotrophic hypothesis of depression that has evolved from this work, including analysis of preclinical cellular (adult neurogenesis) and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies. Although there are some limitations, the results of these studies are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation of BDNF plays a role in the actions of antidepressant treatment.
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                Author and article information

                Contributors
                (View ORCID Profile)
                Journal
                Psychiatry and Clinical Neurosciences
                Psychiatry Clin Neurosci
                Wiley
                1323-1316
                1440-1819
                August 2023
                April 25 2023
                August 2023
                : 77
                : 8
                : 420-433
                Affiliations
                [1 ] Department of Psychiatry Teikyo University School of Medicine Tokyo Japan
                Article
                10.1111/pcn.13551
                36992617
                dd3e719e-966b-497f-8ccb-9dcbdef4c4de
                © 2023

                http://creativecommons.org/licenses/by-nc/4.0/

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