Adrenaline stress and Obesity

Adrenaline stress and Obesity have their solution in healthy living
Adrenaline stress and Obesity: All you need to know
The prevalence of obesity has increased dramatically in the last several decades. Obesity, particularly upper body obesity (UBO), is associated with type 2 diabetes (T2DM), dyslipidemia, and hypertension. These associations describe the metabolic syndrome, a clustering of symptoms with insulin resistance as a core cause. Currently, adrenaline stress and the prevalence of obesity and metabolic syndrome is above average deeming both conditions important public health issues, requiring immediate efforts to understand these diseases and reduce their occurrences. And therefore, as we progress into the discussion, doctor Dalal Akoury MD President and founder of AWAREmed health and wellness resource center will be helping us to some of these to perspective.
Adrenaline stress and obesity: Stress response
Stress is a challenge to the natural homeostasis of an organism. Animals react to stress by producing a physiological stress response to regain equilibrium lost by the stressor. The stress response is characterized by acute behavioral and physical adaptations, including increased cognition, analgesia, gluconeogenesis, lipolysis, and inhibition of reproduction. There are two major components of the stress response: the autonomic nervous system (ANS), which encompasses the sympathetic and parasympathetic nervous system, and the HPA axis. These systems work centrally and peripherally to produce several responses. The ‘fight or flight response’ is an active reaction to either confront the stressor or escape confrontation. The ‘defeat response’ is when the individual does not engage in either the fight or flight response and ultimately ‘loses’ the confrontation; this is the primary stress response in modern society and is associated with HPA axis changes. Although the ANS is a key element of the stress response, the purpose of this review is to discuss the role of the HPA axis in obesity and metabolic disease.
Stress can be caused by external stressors such as employment or social strains or by intrinsic stressors such as sleep deprivation. Although an acute short-term stress response is necessary for homeostasis recovery, chronic or prolonged stress responses can be harmful and may cause several disease states. A study on women reported that history of depression was associated with hyperactivity of the HPA axis and decreased bone mineral density. In the past three decades, numerous studies has shown that obesity and other metabolic risk factors are associated with lower socioeconomic status, job strain, sleep deprivation, and depression
Hypothalamic–pituitary–adrenal axis
The HPA axis is one of two major neuroendocrine systems associated with the stress response. Corticotrophin-releasing hormone (CRH), secreted from the Para-ventricular nucleus (PVN) of the hypothalamus, stimulates the synthesis of adrenocorticotropic (ACTH) from the anterior pituitary gland. Physical stressors such as hypoglycemia, hemorrhage, and immune stimuli activate PVN neurons expressing arginine vasopressin and CRH. ACTH stimulates cortisol production from the adrenal cortex.
The first evidence that cortisol levels may be related to obesity and metabolic disease was based on clinical observations of Cushing’s syndrome; the pathological hypercortisolemia in Cushing’s syndrome is associated with UBO, glucose intolerance [impaired glucose tolerance (IGT)], and hypertension. Adrenalectomy in Cushing’s syndrome patients reverses IGT and obesity.Studies in the field of obesity research in the past 10 years have demonstrated that obesity and metabolic syndrome are characterized by chronic inflammation. This may sound technical, but you can schedule an appointment with doctor Akoury for more professional clarity.
Adrenaline stress and obesity: All you need to know
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