Chronic stress and obesity: A new view of "comfort food"

Chronic stress and obesity: A new view of "comfort food"

September 30, 2003 | Mary F. Dallman, Norman Pecoraro, Susan F. Akana, Susanne E. la Fleur, Francisca Gomez, Hani Houshyar, M. E. Bell, Seema Bhatnagar, Kevin D. Laugero, and Sotara Manalo
Chronic stress and obesity: A new view of "comfort food" explores how chronic stress and elevated glucocorticoid (GC) levels influence eating behavior and obesity. The study reveals that GCs have complex effects on the hypothalamic-pituitary-adrenal (HPA) axis. Acutely, GCs inhibit ACTH secretion, but chronically, they stimulate the HPA axis and increase abdominal fat. GCs also enhance the salience of pleasurable activities, such as eating high-fat or sweet foods, which can lead to increased comfort food consumption and weight gain. This behavior is thought to be a coping mechanism to reduce the activity of the chronic stress-response network, which is associated with anxiety. The study shows that chronic stress and high GC levels can lead to abdominal obesity, which in turn inhibits the expression of CRF mRNA in the hypothalamus, reducing HPA activity. In humans, chronic stress can lead to either increased comfort food intake and weight gain or decreased intake and weight loss, depending on the individual. The research also indicates that depressed individuals who overeat have lower levels of CRF, catecholamines, and HPA activity. The study suggests that eating comfort food is a way to reduce the activity of the chronic stress-response network. The findings from rat studies may explain the rise in obesity in society. GCs act on the brain to increase stimulus salience, making certain foods more appealing. This can lead to increased consumption of high-calorie foods, contributing to obesity. The study also highlights the role of abdominal energy stores in providing feedback to the brain, which can inhibit CRF activity and reduce HPA axis activity. The research indicates that chronic stress and high GC levels can lead to metabolic and neuroendocrine changes, including increased abdominal obesity and reduced HPA activity. The study also shows that GCs can increase the salience of pleasurable activities, such as eating, leading to increased consumption of comfort foods. These findings suggest that the relationship between chronic stress, GCs, and obesity is complex and involves multiple physiological mechanisms.Chronic stress and obesity: A new view of "comfort food" explores how chronic stress and elevated glucocorticoid (GC) levels influence eating behavior and obesity. The study reveals that GCs have complex effects on the hypothalamic-pituitary-adrenal (HPA) axis. Acutely, GCs inhibit ACTH secretion, but chronically, they stimulate the HPA axis and increase abdominal fat. GCs also enhance the salience of pleasurable activities, such as eating high-fat or sweet foods, which can lead to increased comfort food consumption and weight gain. This behavior is thought to be a coping mechanism to reduce the activity of the chronic stress-response network, which is associated with anxiety. The study shows that chronic stress and high GC levels can lead to abdominal obesity, which in turn inhibits the expression of CRF mRNA in the hypothalamus, reducing HPA activity. In humans, chronic stress can lead to either increased comfort food intake and weight gain or decreased intake and weight loss, depending on the individual. The research also indicates that depressed individuals who overeat have lower levels of CRF, catecholamines, and HPA activity. The study suggests that eating comfort food is a way to reduce the activity of the chronic stress-response network. The findings from rat studies may explain the rise in obesity in society. GCs act on the brain to increase stimulus salience, making certain foods more appealing. This can lead to increased consumption of high-calorie foods, contributing to obesity. The study also highlights the role of abdominal energy stores in providing feedback to the brain, which can inhibit CRF activity and reduce HPA axis activity. The research indicates that chronic stress and high GC levels can lead to metabolic and neuroendocrine changes, including increased abdominal obesity and reduced HPA activity. The study also shows that GCs can increase the salience of pleasurable activities, such as eating, leading to increased consumption of comfort foods. These findings suggest that the relationship between chronic stress, GCs, and obesity is complex and involves multiple physiological mechanisms.
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