Stress response and binge eating disorder

doi:10.1016/j.appet.2005.05.004

Appetite

Volume 46, Issue 1, January 2006, Pages 26-30

https://doi.org/10.1016/j.appet.2005.05.004 Get rights and content

Abstract

In clinical practice, obese patients report stress as a primary trigger for binge eating. However, the biological mechanism underlying this relationship is poorly understood. This paper presents, a theoretical overview of how cortisol secretion, a major component of the stress response, could play a role in binge eating, given that exogenous glucocorticoids can lead to obesity by increasing food intake. I will discuss findings from recent studies demonstrating links between laboratory stress, cortisol, food intake and abdominal fat in humans. Cortisol is elevated following laboratory stressors in women with anorexia nervosa (AN), bulimia nervosa (BN), and obesity, but has not been widely studied in women with binge eating disorder (BED). Additionally, I will review recent findings demonstrating a greater cortisol response to stress in obese women with BED compared to non-BED.

Section snippets

Background

Obesity, defined as a body mass index [BMI, in kg/m²] >30, has become a medical epidemic in the US (Caballero, 2001). There is a subset of obese individuals who have binge eating disorder (BED) (Mitchell & Mussell, 1995). These individuals exhibit greater psychopathology, often do less well in weight loss treatment and relapse more quickly than non-BED (Yanovski, Nelson, Dubbert, & Spitzer, 1993a). BED is characterized by the consumption of objectively large amounts of food and a sense of loss

Cortisol and appetitive behavior

Cortisol is involved in appetite regulation (Wolkowitz, Epel, & Rues, 2001) and energy balance by increasing available energy through gluconeogenesis and lipolysis (Epel, Lapidus, McEwen, & Brownell, 2001). In animals, glucocorticoid administration (Bray, 1985) and corticosterone replacement (Castonguay, 1991) led to hyperphagia and weight gain. Corticosterone also increased fat intake in a dose-dependent fashion in rats (Castonguay, 1991). Dallman and colleagues recently described a ‘chronic

Cortisol stress response in eating disorders

The key hormonal pathway that governs the endocrine response to stress is the hypothalamic-pituitary-adrenal (HPA) axis. The dexamethasone suppression test (DST) is widely used in clinical settings to test for hypercortisolemia and diminished sensitivity to HPA negative feedback (Walsh, Gladis, & Roose, 1987a). Oral dexamethasone characteristically suppresses the morning rise in cortisol. DST non-suppression and hypercortisolemia have been reported in anorexia nervosa (AN) (Brambilla et al.,

Chronic hypercortisolemia and stress responsivity

Although acute elevation of cortisol plays a protective role during stress, persistently elevated levels promote insulin resistance and abdominal obesity (Bjorntorp and Rosmond, 2000, Jayo et al., 1993). Most studies have observed that chronic stress over-activates the hypothalamic-pituitary-adrenal (HPA) axis and fuels insulin release, in turn activating abdominal fat storage (Dallman, Akana, Strack, Hanson, & Sebastian, 1995). However, the literature is mixed, in that some studies show a

Emotional stress responses and food intake

The majority of studies have measured food intake following laboratory stressors without measuring biological correlates. Surprisingly, many have failed to observe differences in overall levels of consumption, but rather differences in macronutrient content. For example, Levine and Marcus found no differences between women with bulimic symptoms versus control women following an interpersonal speech task (Levine & Marcus, 1997). However, both bulimic and control women increased their consumption

Research limitations and future directions

There are several limitations to the stress and eating studies to date. Researchers use a variety of methods by which to induce stress in the laboratory and it is therefore difficult to compare results from study to study. None of the approaches used to date are naturalistic and therefore they reveal nothing about factors that might actually lead to binge eating in real life. Moreover, these laboratory stressors last for various durations, ranging in length from 2 to 45 min. The psychological

Acknowledgements

Presented at Society for the Study of Ingestive Behavior (SSIB) Satellite Symposium, Hueston Woods Resort, Ohio, July 18–20, 2004. Chaired by Allan Geliebter and Harry R. Kissileff. The satellite was supported in part by the New York Obesity Research Center, SSIB, General Mills Foods, McNeil Nutritionals, Ortho-McNeil Pharmaceuticals, Procter & Gamble. The author would like to thank Allan Geliebter, PhD for his support and guidance and Kelly Allison, PhD and Elissa Epel, PhD for their helpful

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Short CommunicationStress response and binge eating disorder

Abstract

Section snippets

Background

Cortisol and appetitive behavior

Cortisol stress response in eating disorders

Chronic hypercortisolemia and stress responsivity

Emotional stress responses and food intake

Research limitations and future directions

Acknowledgements

Gastroenterology

Neuroscience

Brain Research Bulletin

The Journal of Nutrition

Brain Research Bulletin

Physiology and Behavior

Physiology and Behavior

Appetite

Appetite

Metabolism

Addictive Behaviors

Biological Psychiatry

Comprehensive Psychiatry

Appetite

Serum leptin concentration in obese patients with binge eating disorder

International Journal of Obesity Related Metabolic Disorders

Behavioral and neuroendocrine characteristics of the night-eating syndrome

The Journal of the American Medical Association

Neuroendocrine abnormalities in visceral obesity

International Journal of Obesity and Related Metabolic Disorders

Psychoimmunoendocrine investigation in anorexia nervosa

Neuropsychobiology

Binge eating as a major phenotype of melanocortin 4 receptor gene mutations

The New England Journal of Medicine

Genetic and environmental contributions to obesity and binge eating

The International Journal of Eating Disorders

Psychologic and physiologic reactivity to stressors in eating disordered individuals

Psychosomatic Medicine

The neural network that regulates energy balance is responsive to glucocorticoids and insulin and also regulates HPA axis responsivity at a site proximal to CRF neurons

Annals of the New York Academy of Sciences

Chronic stress and obesity: a new view of ‘comfort food’

Proceedings of the National Academy of Sciences of the United States of America

Binge eating disorder: Clinical features and treatment of a new diagnosis

Harvard Review of Psychiatry

Stress may add bite to appetite in women: A laboratory study of stress-induced cortisol and eating behavior

Psychoneuroendocrinology

Stress and body shape: stress-induced cortisol secretion is consistently greater among women with central fat

Psychosomatic Medicine

Short Communication
Stress response and binge eating disorder