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

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