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      Stress in obesity: Cause or consequence?

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      Medical Hypotheses

      Elsevier BV

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          Abstract

          Obesity is a global public health challenge that increases the risk of various diseases including type 2 diabetes mellitus, hypertension and cancer, and will in the future cause further increases in the incidence of chronic disease. Understanding the mechanisms of obesity is critical if we are to prevent and treat this pandemic challenge. Diet and physical activity have traditionally been the major tasks in preventing and treating obesity. However, other mechanisms are now also being considered in the quest for knowledge and understanding of obesity, including the body's stress system and cortisol release. While it seems evident that stress is a cause of obesity, whether stress is also a consequence of obesity has up to now only briefly been discussed. The aim of this article is to elucidate how stress and obesity might be linked and discuss the cause/consequence relationship between the stress response and obesity. Our hypothesis is that stress and obesity interfere by positive feedback. This may be an important issue in both our understanding and coping of obesity.

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          Most cited references 31

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          Endocrinology of the stress response.

          The stress response is subserved by the stress system, which is located both in the central nervous system and the periphery. The principal effectors of the stress system include corticotropin-releasing hormone (CRH); arginine vasopressin; the proopiomelanocortin-derived peptides alpha-melanocyte-stimulating hormone and beta-endorphin, the glucocorticoids; and the catecholamines norepinephrine and epinephrine. Appropriate responsiveness of the stress system to stressors is a crucial prerequisite for a sense of well-being, adequate performance of tasks, and positive social interactions. By contrast, inappropriate responsiveness of the stress system may impair growth and development and may account for a number of endocrine, metabolic, autoimmune, and psychiatric disorders. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors, and the timing of the stressful events, given that prenatal life, infancy, childhood, and adolescence are critical periods characterized by increased vulnerability to stressors.
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            Neuropeptide Y acts directly in the periphery on fat tissue and mediates stress-induced obesity and metabolic syndrome.

            The relationship between stress and obesity remains elusive. In response to stress, some people lose weight, whereas others gain. Here we report that stress exaggerates diet-induced obesity through a peripheral mechanism in the abdominal white adipose tissue that is mediated by neuropeptide Y (NPY). Stressors such as exposure to cold or aggression lead to the release of NPY from sympathetic nerves, which in turn upregulates NPY and its Y2 receptors (NPY2R) in a glucocorticoid-dependent manner in the abdominal fat. This positive feedback response by NPY leads to the growth of abdominal fat. Release of NPY and activation of NPY2R stimulates fat angiogenesis, macrophage infiltration, and the proliferation and differentiation of new adipocytes, resulting in abdominal obesity and a metabolic syndrome-like condition. NPY, like stress, stimulates mouse and human fat growth, whereas pharmacological inhibition or fat-targeted knockdown of NPY2R is anti-angiogenic and anti-adipogenic, while reducing abdominal obesity and metabolic abnormalities. Thus, manipulations of NPY2R activity within fat tissue offer new ways to remodel fat and treat obesity and metabolic syndrome.
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              Relationship between stress, eating behavior, and obesity.

              Stress is thought to influence human eating behavior and has been examined in animal and human studies. Our understanding of the stress-eating relation is confounded by limitations inherent in the study designs; however, we can make some tentative conclusions that support the notion that stress can influence eating patterns in humans. Stress appears to alter overall food intake in two ways, resulting in under- or overeating, which may be influenced by stressor severity. Chronic life stress seems to be associated with a greater preference for energy- and nutrient-dense foods, namely those that are high in sugar and fat. Evidence from longitudinal studies suggests that chronic life stress may be causally linked to weight gain, with a greater effect seen in men. Stress-induced eating may be one factor contributing to the development of obesity. Future studies that measure biological markers of stress will assist our understanding of the physiologic mechanism underlying the stress-eating relation and how stress might be linked to neurotransmitters and hormones that control appetite.
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                Author and article information

                Journal
                Medical Hypotheses
                Medical Hypotheses
                Elsevier BV
                03069877
                July 2011
                July 2011
                : 77
                : 1
                : 7-10
                Article
                10.1016/j.mehy.2011.03.011
                21444159
                © 2011

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