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      Obesity moderates the complex relationships between inflammation, oxidative stress, sleep quality and depressive symptoms

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          Abstract

          Background

          The relationship between obesity and depression is complex. This study assessed the impact of body mass index (BMI) on the link between BMI, inflammation, oxidative stress, sleep quality and self-reported depressive symptoms.

          Methods

          We used data from the U.S. National Health and Nutritional Examination Survey 2005–2008 cycles ( n = 9133; ≥20y). Depressive symptoms and sleep quality were determined from questionnaires. C-reactive Protein (CRP) was used as a biomarker of inflammation and γ-glutamyltransferase was used to assess oxidative stress. The relationship between depressive symptoms, sleep quality, and biomarkers were assessed with regression models. The moderating effects of BMI and sex were tested.

          Results

          BMI was a significant moderator of the relationship between γ-glutamyltransferase and depressive symptoms ( p = 0.02), but not CRP or sleep quality. Higher BMI increased odds of depressive symptoms in women (OR (95% CI): 3.92 (1.85–8.30) for BMI ≥25 to < 30 kg/m 2; 3.17 (1.53–6.58) for BMI ≥30 to < 35 kg/m 2; and 7.38 (2.11–25.76) for BMI ≥35 kg/m 2). BMI was also a significant moderator of γ-glutamyltransferase levels in those with vs without depressive symptoms. Those with depressive symptoms had 24% poorer sleep quality compared to those without depressive symptoms after adjusting for inflammation, oxidative stress and other confounders.

          Conclusions

          The link between oxidative stress and depressive symptoms may be particularly relevant for females and people living with obesity. People with depressive symptoms also have a substantial reduction in sleep quality. Thus, research should examine these relationships prospectively to inform and improve the mental health of the adult population in developed countries.

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          Most cited references44

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          Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk.

          We sought to investigate the effects of sleep loss on high-sensitivity C-reactive protein (CRP) levels. Concentrations of high-sensitivity CRP are predictive of future cardiovascular morbidity. In epidemiologic studies, short sleep duration and sleep complaints have also been associated with increased cardiovascular morbidity. Two studies were undertaken to examine the effect of acute total and short-term partial sleep deprivation on concentrations of high-sensitivity CRP in healthy human subjects. In Experiment 1, 10 healthy adult subjects stayed awake for 88 continuous hours. Samples of high-sensitivity CRP were collected every 90 min for 5 consecutive days, encompassing the vigil. In Experiment 2, 10 subjects were randomly assigned to either 8.2 h (control) or 4.2 h (partial sleep deprivation) of nighttime sleep for 10 consecutive days. Hourly samples of high-sensitivity CRP were taken during a baseline night and on day 10 of the study protocol. The CRP concentrations increased during both total and partial sleep deprivation conditions, but remained stable in the control condition. Systolic blood pressure increased across deprivation in Experiment 1, and heart rate increased in Experiment 2. Both acute total and short-term partial sleep deprivation resulted in elevated high-sensitivity CRP concentrations, a stable marker of inflammation that has been shown to be predictive of cardiovascular morbidity. We propose that sleep loss may be one of the ways that inflammatory processes are activated and contribute to the association of sleep complaints, short sleep duration, and cardiovascular morbidity observed in epidemiologic surveys.
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            Adverse effects of modest sleep restriction on sleepiness, performance, and inflammatory cytokines.

            Total sleep restriction in humans is associated with increased daytime sleepiness, decreased performance, and hormonal/metabolic disturbances. The effects of mild chronic sleep restriction that mimic real life are not known. To assess the effects of modest sleep restriction from 8 to 6 h/night for 1 wk, 25 young, healthy, normal sleepers (12 men and 13 women) were studied for 12 consecutive nights in the sleep laboratory. After 1 wk of sleep restriction, although subjects' nighttime sleep was deeper, subjects were significantly sleepier (multiple sleep latency test) and performed worse in four primary variables of psychomotor vigilance test (both P < 0.01). Furthermore, 24-h secretion of IL-6 was increased by 0.8 +/- 0.3 pg/ml (P < 0.05) in both sexes, whereas TNFalpha was increased only in men. Also, the peak cortisol secretion was lower after sleep restriction than at baseline, and this difference was stronger in men (55.18 +/- 24.83 nmol/liter; P < 0.05) than in women (35.87 +/- 24.83 nmol/liter; P < 0.16). We conclude that in young men and women, modest sleep loss is associated with significant sleepiness, impairment of psychomotor performance, and increased secretion of proinflammatory cytokines. Given the potential association of these behavioral and physical alterations with health, well-being, and public safety, the idea that sleep or parts of it are optional should be regarded with caution.
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              When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders.

              Previous theories have emphasized the role of excessive glucocorticoid activity in the pathology of chronic stress. Nevertheless, insufficient glucocorticoid signaling (resulting from decreased hormone bioavailability or reduced hormone sensitivity) may have equally devastating effects on bodily function. Such effects may be related in part to the role of glucocorticoids in restraining activation of the immune system and other components of the stress response, including the sympathetic nervous system (SNS) and corticotropin-releasing hormone (CRH). The literature on neuroendocrine function and glucocorticoid-relevant pathologies in stress-related neuropsychiatric disorders, including posttraumatic stress disorder and major depression, was reviewed. Although not occurring together, both hypocortisolism and reduced responsiveness to glucocorticoids (as determined by dexamethasone challenge tests) were reliably found. Stress-related neuropsychiatric disorders were also associated with immune system activation/inflammation, high SNS tone, and CRH hypersecretion, which are all consistent with insufficient glucocorticoid-mediated regulation of stress hyperresponsiveness. Finally, antidepressants, a mainstay in the treatment of stress-related disorders, were regularly associated with evidence of enhanced glucocorticoid signaling. Neuroendocrine data provide evidence of insufficient glucocorticoid signaling in stress-related neuropsychiatric disorders. Impaired feedback regulation of relevant stress responses, especially immune activation/inflammation, may, in turn, contribute to stress-related pathology, including alterations in behavior, insulin sensitivity, bone metabolism, and acquired immune responses. From an evolutionary perspective, reduced glucocorticoid signaling, whether achieved at the level of the hormone or its receptor, may foster immune readiness and increase arousal. Emphasis on insufficient glucocorticoid signaling in stress-related pathology encourages development of therapeutic strategies to enhance glucocorticoid signaling pathways.
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                Author and article information

                Contributors
                alanna.rigobon@mail.utoronto.ca
                thirumagal.kanagasabai@mcgill.ca
                416 323-6400 , valerie.taylor@wchospital.ca
                Journal
                BMC Obes
                BMC Obes
                BMC Obesity
                BioMed Central (London )
                2052-9538
                3 December 2018
                3 December 2018
                2018
                : 5
                : 32
                Affiliations
                [1 ]ISNI 0000 0001 2157 2938, GRID grid.17063.33, Faculty of Medicine, , University of Toronto, ; Toronto, Canada
                [2 ]ISNI 0000 0004 1936 8649, GRID grid.14709.3b, Department of Epidemiology, Biostatistics, and Occupational Health, , McGill University, ; Montreal, Canada
                [3 ]ISNI 0000 0001 2157 2938, GRID grid.17063.33, Women’s College Research Institute, , University of Toronto, ; Toronto, Canada
                [4 ]ISNI 0000 0004 0474 0188, GRID grid.417199.3, Women’s College Hospital, ; 76 Grenville Street Room E947, Toronto, ON M5S 1B2 Canada
                Article
                208
                10.1186/s40608-018-0208-2
                6276225
                57e1f7a3-1df5-4e81-8da1-770c6aa83f32
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 13 March 2018
                : 21 August 2018
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2018

                body mass index (bmi),obesity,sleep,inflammation,oxidative stress,depression

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