Cortisol response and desire to binge following psychological stress: Comparison between obese subjects with and without binge eating disorder
Introduction
The obesity pandemic in the Western world with its associated increased morbidity and overall mortality has become a major public health hazard (Flegal et al., 2007). The magnitude of this problem has resulted in substantial research, thus increasing our understanding of the biological factors involved in appetite and eating behavior. A specific area in this field, the relationship between stress regulatory systems and eating behavior, has also received much recent attention.There is increasing evidence that central components of the reward system also play a role in the regulation of the stress response (Ueta et al., 2003). A subset of people who are obese suffer from binge eating disorder (BED), an eating disorder characterized by bouts of uncontrolled binges without the compensatory behaviors that characterize bulimic patients. About 30% of obese people are diagnosed with BED (Yanovski et al., 1993), while the prevalence within the general population ranges from 2 to 3% (Smink et al., 2012) to about 6% (Abebe et al., 2012).
It is known that stress and negative affect often precede “emotional eating” and binge eating (Mastorakos and Zapanti, 2004, Pike et al., 2006), but this relationship is not fully understood (Kaye, 2008). Negative emotions have been associated with both increased and decreased food intake (Geliebter and Aversa, 2003), and while this may be related to individual stress reactivity (Cattanach et al., 1988), the mechanisms underlying such opposed behaviors have not been elucidated (Cizza and Rother, 2011). Under conditions of high emotional load, restrained and emotional eaters usually eat more food, specifically sweet and fat foods (Lattimore and Caswell, 2004), perhaps suggesting a lack of responsiveness to satiety signals while under stress (Gibson, 2006).
Neuronal networks that interconnect the hypothalamus and the limbic system suggest the existence of a neural circuit in which mood states strongly influence eating behavior. It is commonly observed that acute stress can induce food restriction. This may be a result of a number of mechanisms, including anorexic signals through the effect of increased central corticotropin-releasing hormone (CRH) secretion with consequent stimulation of α-melanocyte-stimulating hormone (Mastorakos and Zapanti, 2004). Conversely, under conditions of chronic stress and sustained increase in circulating cortisol levels, carbohydrate and fat intake are enhanced (Adam and Epel, 2007), CRH is suppressed and neuropeptide Y (NPY) hypothalamic secretion is stimulated (Kyrou and Tsigos, 2007). Hence, It may be hypothesized that contrary to acute stress in which the activation of the hypothalamic–pituitary–adrenal (HPA) axis results in an inhibition of food consumption, under conditions of chronic stress, the activation of the HPA axis may prolong the actions of glucocorticoids in appetite centers, thus causing an orexigenic effect (Kyrou and Tsigos, 2007).
The hypothesis that activation of the HPA axis is involved in the onset of binge eating attacks relies on several lines of evidence: (1) Stress plays a definite role in the initiation of binge eating episodes (Pike et al., 2006, Telch and Agras, 1996); (2) cortisol is a mediator of increased caloric intake (Drapeau et al., 2003), as indicated by the response to infusions of glucocorticoids in both humans and rats (Tataranni et al., 1996, Dallman, 2010); and (3) high cortisol levels are positively related to food intake after laboratory stress stimuli (Gluck, 2006).
In eating disorders such as anorexia nervosa (AN), bulimia nervosa (BN), and night eating syndrome, there is evidence of a hyperactive HPA axis with higher basal cortisol levels (Birketvedt et al., 2002, Pirke et al., 1992) and impaired cortisol suppression by exogenous corticosteroids (Brambilla et al., 1993, Monteleone et al., 2003).
Very few studies have examined the HPA axis in participants with BED. Cortisol suppression after dexamethasone administration has been shown to be normal in this population (Yanovski et al., 1993, Gluck et al., 2004). Single measurement evening cortisol levels (Coutinho et al., 2007), as well as morning cortisol levels, have been reported to be normal in both obese and as well as in non-obese women with BED (Monteleone et al., 2000, Pintor et al., 2007). In contrast, overall cortisol secretion as reflected by repeated cortisol measurements during the day for two consecutive days was found to be significantly lower in obese women with BED in comparison to obese women without BED (Larsen et al., 2009). Finally, Gluck and colleagues found higher basal cortisol levels in obese women with BED, and a nearly significantly higher cortisol secretion following a cold stress test in comparison to the control group (Gluck et al., 2004). In view of the contradictory results reported in these studies, no conclusions can be drawn as to the HPA axis function in BED subjects. An extensive review of HPA axis and stress involvement in eating disorders was published by Lo Sauro et al. (2008). This review concludes that different HPA axis abnormalities have been observed in BED and obese subjects, but these alterations are considered to be mainly due to excess weight. Thus, the specific association between BED and the HPA axis that is not secondary to obesity still merits study.
To further investigate the involvement of the HPA axis in the eating response to negative emotions, we chose to use a well-standardized psychological stress test, the Trier Social Stress Test (TSST). Cortisol secretion and cognitions related to eating were measured before and immediately after the psychological stress in obese participants with and without BED and a control group of normal weight participants (Rouach et al., 2007). Our hypothesis was that the cortisol response to acute stress in obese BED patients would be higher than in obese non-BED patients, and would be positively correlated with psychological stress and with food craving.
Section snippets
Subjects
Twenty-four participants, mean age 44.2±15.4 (range 23–70) were recruited from the Obesity Clinic and through advertising among personnel from the Tel Aviv Sourasky Medical Center. The study population comprised the following three groups: (1) Obese (body mass index (BMI) between 30 and 40 kg/m2) participants with a diagnosis of binge eating disorder (BED group, n=8); (2) Obese (BMI between 30–40 kg/m2) participants without BED (Non-BED group, n=8); and (3) A control group consisting of normal
Baseline physiological and psychological parameters
By definition, body-mass index (BMI) was significantly lower in the NW group than in both obese groups (F(2,21)=44.8, p<0.0001), but BMI was similar in the obese groups with or without binge eating. Baseline BMI, cortisol and subjective measurements of stress, anxiety and eating parameters are summarized in Table 1. The only difference of note was the higher “desire to binge” score in the BED group compared with the other two groups (F(2,21)=4.1, p=0.031 (Table 1)).
Effect of TSST on cortisol levels
The controlled psychological
Discussion
In this study we examined the cortisol response to a standard psychological stress test (TSST) in a group of obese volunteers with and without BED and a group of normal weight controls. We also assessed the subjective eating behavior related cognitions in these three groups in correlation to their perception of levels of anxiety and stress following the TSST. Our results indicate a number of important findings. First, basal cortisol levels were similar in the three groups, but BED participants
References (47)
- et al.
Stress, eating and the reward system
Physiology and Behavior
(2007) - et al.
Assessment of the hypothalamic-pituitary-adrenal axis over a 24-hour diurnal period and in response to neuroendocrine challenges in women with and without childhood sexual abuse and posttraumatic stress disorder
Biological Psychiatry
(2003) - et al.
Does binge eating disorder alter cortisol secretion in obese women?
Eating Behaviors
(2007) - et al.
Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior
Psychoneuroendocrinology
(2001) - et al.
Emotional eating in overweight, normal weight, and underweight individuals
Eating Behaviors
(2003) Stress response and binge eating disorder
Appetite
(2006)- et al.
Salivary cortisol as a biomarker in stress research
Psychoneuroendocrinology
(2009) Neurobiology of anorexia and bulimia nervosa purdue ingestive behavior research center symposium influences on eating and body weight over the lifespan: children and adolescents
Physiology and Behavior
(2008)- et al.
Why do we respond so differently? Reviewing determinants of human salivary cortisol responses to challenge
Psychoneuroendocrinology
(2009) - et al.
Differential effects of active and passive stress on food intake in restrained and unrestrained eaters
Appetite
(2004)
Randomized, double-blind trial comparing sertraline and fluoxetine 6-month treatment in obese patients with Binge Eating Disorder
Progress in Neuropsychopharmacology and Biological Psychiatry
Circultaing leptin in patients with anorexia nervosa, bulimia nervosa or binge-eating disorder: relationship to body weight, eating patterns, psychopathology and endocrine changes
Psychiatry Research
Antecedent life events of binge-eating disorder
Psychiatry Research
Corticotropin-releasing factor test in melancholic patients in depressed state versus recovery: a comparative study
Progress in Neuropsychopharmacology and Biological Psychiatry
The effect of a mental challenge test of plasma norepinephrine and cortisol in bulimia nervosa and in controls
Biological Psychiatry
Deactivation of the limbic system during acute psychosocial stress: evidence from positron emission tomography and functional magnetic resonance imaging studies
Biological Psychiatry
The acute ghrelin response to a psychological stress challenge does not predict the post-stress urge to eat
Psychoneuroendocrinology
PTSD and the HPA axis: differences in response to the cold pressor task among individuals with child vs. adult trauma
Psychoneuroendocrinology
Binge eating, purging and non-purging compensatory behaviors decrease from adolescence to adulthood: a population-based, longitudinal study
BMC Public Health
Diagnostic and Statistical Manual of Mental Disorders
Text Revised
The multifaceted role of distress tolerance in dysregulated eating behaviors
International Journal of Eating Disorders
Hypothalamic-pituitary-adrenal axis in the night eating syndrome
American Journal of Physiology Endocrinology and Metabolism
Psychoimmunoendocrine investigation in anorexia nervosa
Neuropsychobiology
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These authors contributed equally to this manuscript.