Eating behavior and stress: a pathway to obesity

Abstract

Stress causes or contributes to a huge variety of diseases and disorders. Recent evidence suggests obesity and other eating-related disorders may be among these. Immediately after a stressful event is experienced, there is a corticotropin-releasing-hormone (CRH)-mediated suppression of food intake. This diverts the body’s resources away from the less pressing need to find and consume food, prioritizing fight, flight, or withdrawal behaviors so the stressful event can be dealt with. In the hours following this, however, there is a glucocorticoid-mediated stimulation of hunger and eating behavior. In the case of an acute stress that requires a physical response, such as a predator-prey interaction, this hypothalamic-pituitary-adrenal (HPA) axis modulation of food intake allows the stressful event to be dealt with and the energy used to be replaced afterward. In the case of ongoing psychological stress, however, chronically elevated glucocorticoids can lead to chronically stimulated eating behavior and excessive weight gain. In particular, stress can enhance the propensity to eat high calorie “palatable” food via its interaction with central reward pathways. Activation of this circuitry can also interact with the HPA axis to suppress its further activation, meaning not only can stress encourage eating behavior, but eating can suppress the HPA axis and the feeling of stress. In this review we will explore the theme of eating behavior and stress and how these can modulate one another. We will address the interactions between the HPA axis and eating, introducing a potential integrative role for the orexigenic hormone, ghrelin. We will also examine early life and epigenetic modulation of the HPA axis and how this can influence eating behavior. Finally, we will investigate the clinical implications of changes to HPA axis function and how this may be contributing to obesity in our society.

Maternal Separation Induced Visceral Hypersensitivity from Childhood to Adulthood

“…7,25,26 Early life stress can influence development of the HPA axis, as well as regulation of satiety-related hormones, leptin, insulin, and ghrelin, again influencing appetite, feeding behavior, and metabolism, which results in the development of obesity. 27 The weight of MS rats can gradually return to normal level on PND56, suggesting that the harmful effect of MS on weight can be improved in rat adulthood after normal feeding.…”

A Conceptual Framework for the Expansion of Behavioral Interventions for Youth Obesity: A Family-Based Mindful Eating Approach

“…The first is through chronically elevated glucocorticoid levels resulting from hypothalamic-pituitary-adrenal axis activation. 17,48 Elevated glucocorticoids stimulate appetite while conserving energy expenditure, thereby leading to weight gain. Glucocorticoids also enhance the preference for calorically dense ''comfort foods.''…”

“…Glucocorticoids also enhance the preference for calorically dense ''comfort foods.'' 48 Also hypothesized is that psychosocial stressors can influence obesity risk through use of maladaptive coping behaviors, such as lack of exercise and overeating. 20,49 Thus, the need for obesity treatment programs that teach youth how to build resources to cope effectively with stressors is being increasingly acknowledged.…”

Assessment of Obesity, Presumed and Proven Causes and Prevention Strategies: A Review

“…These are documented in several studies listed in Table 8 and include the following: a. Sedentary life style [92][93][94]96] b. Eating out frequently in traditional and non-traditional restaurants instead of cooking at home [97,98] c. Frequent vacations involving sumptuous dining and wining [99] d. Insufficient sleep or lack of sleep [100] e. Staying home watching television and movies all day [101,102] f. Shift work, night shift and unusual work schedules [103] g. Eating patterns and eating behaviours [104,105] h. Too much sitting instead of moving [94] i. Sudden discontinuation of smoking [106][107][108]111].…”