Pathways linking depression, adiposity, and inflammatory markers in healthy young adults (original) (raw)
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Is Chronic Inflammation a Possible Cause of Obesity-Related Depression?
Mediators of Inflammation, 2009
Adult obesity has been associated with depression, especially in women. Whether depression leads to obesity or obesity causes depression is unclear. Chronic inflammation is observed in obesity and depression. In 63 obese women without additional diseases depression level was assessed with the Beck's questionnaire. After evaluation of depression level study group was divided into groups according to the mood status (A-without depression, B-mild depression, and C-severe depression), and serum concentration of TNF-α, sTNFs, leptin, and IL-6 were measured by ELISA. No differences in age, body mass, BMI, and body composition were observed in study groups. We did not observe differences of serum concentrations of TNF-α, sTNFRs, leptin, and IL-6 between subgroup A and subgroups B and C. It seems that circulating adipokines did not exert influence on depression levels in obese women.
Acta Biochimica Polonica, 2016
Background. During the last few decades, adiposity has become a relatively common phenomenon worldwide. The available data on the effects of pro-inflammatory factors in both depression and adiposity has been attracting great attention. Aim. We sought to assess the prevalence of-889C>T IL-1α,-31T>C and-511C>T IL-1β,-330T>G IL-2 and-174G>C IL-6 genes and their association with adiposity and depression in Polish subjects. Methods. A cohort study was conducted in 2013/2014, covering a sample of 297 individuals (217 female and 80 male). Anthropometric data was handled using the BIA analysis method, while for genotyping PCR-RFLP techniques were used. Results. A positive correlation between depression and anthropometric parameters: adipose tissue (in kg) and adipose tissue (in %) (R=0.135 and p=0.02, R=0.114 and p<0.05, respectively) was found. No association between studied polymorphisms and depression was observed. Conclusion. Although it was not possible to demonstrate any influence of the studied polymorphisms as the genetic modulator of depression, authors believe that the presented data are noticeable and may provide the basis for future studies on larger groups.
Acta Biochimica Polonica, 2016
During the last few decades, adiposity has become a relatively common phenomenon worldwide. The available data on the effects of pro-inflammatory factors in both depression and adiposity has been attracting great attention. We sought to assess the prevalence of -889C>T IL-1α, -31T>C and -511C>T IL-1β, -330T>G IL-2 and -174G>C IL-6 genes and their association with adiposity and depression in Polish subjects. A cohort study was conducted in 2013/2014, covering a sample of 297 individuals (217 female and 80 male). Anthropometric data was handled using the BIA analysis method, while for genotyping PCR-RFLP techniques were used. A positive correlation between depression and anthropometric parameters: adipose tissue (in kg) and adipose tissue (in %) (R=0.135 and p=0.02, R=0.114 and p
Cytokine levels in depressed and non-depressed subjects, and masking effects of obesity
Journal of Psychiatric Research, 2014
In major depressive disorder, changes in cytokine levels have been reported to play a role in pathogenesis. Therefore, we sought to investigate a broad range of cytokines in depression. We compared serum levels of interleukin (IL)-2, IL-4, IL-5, IL-10, IL-12, IL-13, granulocyte macrophage colonystimulating factor (GM-CSF), interferon (INF-g) and tumor necrosis factor (TNF)-a in 64 subjects with current depression and 206 non-depressed subjects.
Frontiers in Endocrinology
Literature on depression and obesity describes the relevance of the hypothalamic pituitary adrenal axis dysfunction, sympathetic nervous system (SNS) activation, and inflammatory processes as well as the interaction of genetic and environmental factors. Recent investigation in obesity highlights the involvement of several regulation systems, particularly in white adipose tissue. The hypothalamic pituitary adrenal axis, gonadal, growth hormone, leptin, sympathetic nervous system and adrenergic, dopaminergic, and serotoninergic central pathways, all seem interconnected and involved in obesity. From another perspective, the role of psychosocial chronic stressors, determining poor mental and physical health, is well documented. Empirical data can support biologically conceivable theories describing how perceptions of the external social environment are transduced into cellular inflammation and depression. Although in neurobiological models of depression, stress responses are associated with neuroendocrine and neuro-inflammatory processes, concerning similar pathways to those described in obesity, an integrating model is still lacking. The aim of this mini-review is to offer a reflexion on the interplay between the neuroendocrine dysfunctions related to chronic stress and the nature of the shared biologic mechanisms in the pathophysiology of both clinical entities, depression and obesity. We highlight dysfunctional answers of mind body systems that are usually activated to promote regulation and adaptation. Stress response, as a mediator between different level phenomena, may undertake the role of a plausible link between psychological and biological determinants of disease. Depression and obesity are major public health issues, urging for new insights and novel interventions and this discussion points to the need of a more in-depth approach.
Metabolic disturbances connecting obesity and depression
Frontiers in Neuroscience, 2013
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.
Brain, behavior, and immunity, 2018
Obesity is a major public health burden associated with neuropsychiatric comorbidities leading to social and occupational impairment. Given the growing prevalence of both obesity and mental disorders worldwide, understanding the risk factors of obesity-related neuropsychiatric comorbidities is crucial to develop preventive strategies and individualized treatments. Recent findings suggest that adiposity-driven inflammation contributes to neuropsychiatric comorbidities in obesity. However, not all obese subjects afflicted with chronic inflammation develop neuropsychiatric symptoms, suggesting additional risk factors. The aim of this study was to investigate the impact of personal history of major depressive disorder (MDD) on obesity-related inflammation and neuropsychiatric symptoms, and their relationship. A case-control study was conducted comparing 66 obese patients (body mass index > 35 kg/m) and 22 healthy non-obese participants, free of any current neuropsychiatric diseases i...