Depression and Obesity: Integrating the Role of Stress, Neuroendocrine Dysfunction and Inflammatory Pathways

Abstract

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.

WITHDRAWN: Identification of Non-coding RNA Biomarkers in Stress-induced Depression via Comprehensive Analysis of Competing Endogenous RNA Network

“…The MAPK signaling pathway plays an important role in many important cellular physiological/pathological processes, such as environmental stress adaptation and in ammatory response [37]. As we known, depression is an affective disorder that occurs in response to prolonged external stressors and involves a range of pathophysiological processes including an in ammatory response [38]. Therefore, MAPK signaling pathway was thought to be associated with depression.…”

Psychosocial Stress and Overweight and Obesity: Findings From the Chicago Community Adult Health Study

“…Other factors, such as physical inactivity and poor dietary behaviors, interact together to increase risk of obesity. Mounting evidence suggests that stress increases the risk of overweight and obesity, and this may occur via psychological and/or behavioral pathways [9,10]. For example, stressful life events are associated with increased depressive symptoms [11] and people with depression are at a greater risk of developing obesity compared to people without depression [12].…”

Neuroinflammatory and behavioral susceptibility profile of mice exposed to social stress towards cocaine effects

“…We face demanding situations on a daily basis, such as conflicts between work and family life, arguments with children and partner, or constant deadlines that can have a negative impact on our global welfare (Almeida, 2005). Numerous studies link this chronic exposure to stress to some epidemic diseases, such as obesity, depression (Ouakinin et al, 2018) and drug addiction (Koob and Schulkin, 2019;Ruisoto and Contador, 2019). In fact, social stress is considered to be a risk factor that influences all stages of the addictive process, from initiation, maintenance and escalation of intake to relapse into drug taking (Koob, 2008;Koob and Schulkin, 2019).…”