Obesity Induced by Chronic Psychological Stress: A Review of Neuroendocrine Mechanisms and Metabolic Effects

Abstract

In modern society, the frequency of chronic stress states such as stress and anxiety in individuals is increasing, and the number of obese people is increasing. Multiple studies have clearly pointed out that chronic stress is positively correlated with body weight. Its core mechanism is that the prolonged activation of the HPA axis results in a long-term increase in cortisol, which interferes with the function of the hypothalamic feeding center through neuroendocrine. This review focuses on the neuroendocrine mechanism of the "cortisol-NPY" pathway in stress-induced obesity, and sorts out the signal transduction mechanism from HAP axis activation to arcuate nucleus NPY/AgRP upregulation, POMC/CART downregulation, and then to imbalanced eating behavior. At the same time, the positive feedback in the short-term relief of anxiety by high-fat and high-sugar intake is analyzed, and how this mechanism promotes the vicious cycle of stress eating. Further experiments such as TSST illustrate the individual differences in cortisol reactivity and its value in predicting metabolic risks. At the intervention level, this article explores the application prospects of drug strategies targeting NPY signals and psychological regulation programs represented by CBT. The central regulatory mechanism mediated by cortisol helps to more accurately identify susceptible individuals and formulate personalized prevention and treatment strategies for stress-induced obesity.