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      Metabolic disturbances connecting obesity and depression

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          Abstract

          Obesity markedly increases the odds of developing depression. Depressed mood not only impairs motivation, quality of life and overall functioning but also increases the risks of obesity complications. Abdominal obesity is a better predictor of depression and anxiety risk than overall adipose mass. A growing amount of research suggests that metabolic abnormalities stemming from central obesity that lead to metabolic disease may also be responsible for the increased incidence of depression in obesity. As reviewed here, a higher mass of dysfunctional adipose tissue is associated with several metabolic disturbances that are either directly or indirectly implicated in the control of emotions and mood. To better comprehend the development of depression in obesity, this review pulls together select findings addressing the link between adiposity, diet and negative emotional states and discusses the evidence that alterations in glucocorticoids, adipose-derived hormones, insulin and inflammatory signaling that are characteristic of central obesity may be involved.

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          The prevalence of comorbid depression in adults with diabetes: a meta-analysis.

          To estimate the odds and prevalence of clinically relevant depression in adults with type 1 or type 2 diabetes. Depression is associated with hyperglycemia and an increased risk for diabetic complications; relief of depression is associated with improved glycemic control. A more accurate estimate of depression prevalence than what is currently available is needed to gauge the potential impact of depression management in diabetes. MEDLINE and PsycINFO databases and published references were used to identify studies that reported the prevalence of depression in diabetes. Prevalence was calculated as an aggregate mean weighted by the combined number of subjects in the included studies. We used chi(2) statistics and odds ratios (ORs) to assess the rate and likelihood of depression as a function of type of diabetes, sex, subject source, depression assessment method, and study design. A total of 42 eligible studies were identified; 20 (48%) included a nondiabetic comparison group. In the controlled studies, the odds of depression in the diabetic group were twice that of the nondiabetic comparison group (OR = 2.0, 95% CI 1.8-2.2) and did not differ by sex, type of diabetes, subject source, or assessment method. The prevalence of comorbid depression was significantly higher in diabetic women (28%) than in diabetic men (18%), in uncontrolled (30%) than in controlled studies (21%), in clinical (32%) than in community (20%) samples, and when assessed by self-report questionnaires (31%) than by standardized diagnostic interviews (11%). The presence of diabetes doubles the odds of comorbid depression. Prevalence estimates are affected by several clinical and methodological variables that do not affect the stability of the ORs.
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            Depression and hypothalamic-pituitary-adrenal activation: a quantitative summary of four decades of research.

            To summarize quantitatively the literature comparing hypothalamic-pituitary-adrenal (HPA) axis function between depressed and nondepressed individuals and to describe the important sources of variability in this literature. These sources include methodological differences between studies, as well as demographic or clinical differences between depressed samples.
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              The endocannabinoid system and the brain.

              The psychoactive constituent in cannabis, Δ(9)-tetrahydrocannabinol (THC), was isolated in the mid-1960s, but the cannabinoid receptors, CB1 and CB2, and the major endogenous cannabinoids (anandamide and 2-arachidonoyl glycerol) were identified only 20 to 25 years later. The cannabinoid system affects both central nervous system (CNS) and peripheral processes. In this review, we have tried to summarize research--with an emphasis on recent publications--on the actions of the endocannabinoid system on anxiety, depression, neurogenesis, reward, cognition, learning, and memory. The effects are at times biphasic--lower doses causing effects opposite to those seen at high doses. Recently, numerous endocannabinoid-like compounds have been identified in the brain. Only a few have been investigated for their CNS activity, and future investigations on their action may throw light on a wide spectrum of brain functions.
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                Author and article information

                Journal
                Front Neurosci
                Front Neurosci
                Front. Neurosci.
                Frontiers in Neuroscience
                Frontiers Media S.A.
                1662-4548
                1662-453X
                07 October 2013
                2013
                : 7
                : 177
                Affiliations
                Department of Nutrition, Faculty of Medicine, CRCHUM and Montreal Diabetes Research Center, Université de Montréal Montreal, QC, Canada
                Author notes

                Edited by: Alfonso Abizaid, Carleton University, Canada

                Reviewed by: Matthew Hill, University of Calgary, Canada; Pietro Cottone, Boston University School of Medicine, USA

                *Correspondence: Stephanie E. Fulton, CRCHUM and Montreal Diabetes Research Center, Technopôle Angus, 2901 Rachel E., Rm-302, Montreal, QC H1W4A4, Canada e-mail: stephanie.fulton@ 123456umontreal.ca

                This article was submitted to Neuroendocrine Science, a section of the journal Frontiers in Neuroscience.

                † These authors have contributed equally to this work.

                Article
                10.3389/fnins.2013.00177
                3791387
                24109426
                e4bddd6e-40d1-449d-9bcd-629a0780a42f
                Copyright © 2013 Hryhorczuk, Sharma and Fulton.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 11 July 2013
                : 16 September 2013
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 215, Pages: 14, Words: 13865
                Categories
                Endocrinology
                Review Article

                Neurosciences
                mood disorders,abdominal obesity,saturated fatty acids,leptin,insulin,adiponectin,resistin,inflammation

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