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Cortisol response and desire to binge following psychological stress: Comparison between obese subjects with and without binge eating disorder
Psychiatry Research 208 (2013) 156–161
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Cortisol response and desire to binge following psychological stress: Comparison between obese subjects with and without binge eating disorder Noa Rosenberg 1,a,c, Miki Bloch 1,a,c,n, Irit Ben Avi a, Vanessa Rouach b, Shaul Schreiber a,c, Naftali Stern b,c, Yona Greenman b,c a b c
Department of Psychiatry, Tel Aviv Sourasky Medical Center, Tel Aviv University, Israel Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel Sackler Faculty of Medicine, Tel Aviv University, Israel
a r t i c l e i n f o
a b s t r a c t
Article history: Received 26 January 2012 Received in revised form 9 August 2012 Accepted 27 September 2012
While stress and negative affect are known to precede ‘‘emotional eating’’, this relationship is not fully understood. The objective of this study was to explore the relationship between induced psychological stress, hypothalamic-pituitary-adrenal (HPA) axis activity, and eating behavior in binge eating disorder (BED). The Trier Social Stress Test (TSST) was applied in obese participants with (n¼ 8) and without BED (n¼8), and normal weight controls (n¼8). Psychological characteristics, eating-related symptoms, and cortisol secretion were assessed. Baseline stress, anxiety and cortisol measures were similar in all groups. At baseline desire to binge was significantly higher among the BED group. While the TSST induced an increase in cortisol levels, a blunted cortisol response was observed in the BED group. In the BED group, a positive correlation was found between cortisol (area under the curve) levels during the TSST and the change in VAS scores for desire to binge. Post-TSST desire to binge and sweet craving were significantly higher in the BED group and correlated positively with stress, anxiety, and cortisol response in the BED group only. These results suggest chronic down-regulation of the HPA axis in participants with BED, and a relationship between psychological stress, the acute activation of the HPA axis, and food craving. & 2012 Elsevier Ireland Ltd. All rights reserved.
Keywords: Cortisol Psychological stress Binge eating disorder Obesity Hypothalamic-pituitary-adrenal (HPA) axis
1. 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). n Corresponding author at: Department of Psychiatry, Tel Aviv Sourasky Medical Center, Tel Aviv University, Israel. Tel.: þ 972 3 6974568; fax: þ972 3 6925774. E-mail address: [email protected] (M. Bloch). 1 These authors contributed equally to this manuscript.
0165-1781/$ - see front matter & 2012 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.psychres.2012.09.050
It is known that stress and negative affect often precede ‘‘emotional eating’’ and binge eating (Levine and Marcus, 1997; 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 a-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
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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., 1999). 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; Monteleone et al., 2003). 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 wellstandardized 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.
2. Methods 2.1. Subjects Twenty-four participants, mean age 44.2715.4 (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
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30–40 kg/m2) participants without BED (Non-BED group, n¼8); and (3) A control group consisting of normal weight individuals (lean body weight of BMI 418 kg/m2 and o25 kg/m2), without any diagnosis of eating disorder (NW group, n¼8). The diagnosis of Binge The diagnosis of binge eating disorder was made by a certified psychiatrist (NR) according to the Diagnostic and Statistical Manual of Mental Disorders, 4th Ed. (American Psychiatric Association, 2000). The sample consisted of 16 females and 8 males. There was a similar male to female ratio in the three groups. Participants diagnosed with anorexia or bulimia nervosa, those with eating disorder not otherwise specified (excluding BED), participants taking any medication affecting the central nervous system or receiving medication known to interfere with cortisol measurements such as contraceptive pills and estrogen replacement therapy were excluded from the study. Ten patients with hypertension, four with hyperlipidemia, three with type II diabetes mellitus, three with hypothyroidism and one with osteoporosis were well controlled with appropriate medical treatment. The investigation was carried out in accordance with the latest version of the Declaration of Helsinki, and it was approved by the Institutional Review Board. All subjects signed an informed consent form after the nature of the procedures had been fully explained to them. 2.2. Study design Participants were instructed to eat a light breakfast (consisting of a cup of coffee or tea and a slice of bread with cheese) round 07:00 h before arrival to the clinic. Upon arrival, information about the research was given, medical and pharmacological history was taken, and consent was signed. Patients were inquired asked about having eaten breakfast, mainly to ascertain that they were not fasting. The study procedure started at 09:00 h and took a total of 2 h to complete. At first an intravenous catheter was inserted in the subject’s forearm, and the subject was then instructed to rest in bed for 40 min before the TSST (Kirschbaum et al., 1993) began. The TSST was conducted by the same examiner (RV). The biological outcome measures included heart rate, blood pressure (systolic and diastolic) and serum cortisol levels, which were determined at 6 consecutive time points: 2 baseline time points before the TSST ( 30 min and 0) and 4 time points after it (immediately after the completion of the test at 15 min, and at the rest area every 20 min afterwards at 35, 55 and 75 min). The psychological assessment as described below was performed just before the initiation of the TSST and immediately following it. 2.3. Data collection 2.3.1. Trier Social Stress Test (TSST) The TSST is a standard psychological stress test developed for an induction of moderate psychological stress under laboratory conditions. In the test, participants are asked to deliver a speech for a job application based on personal characteristics, and to perform a mental repetitive arithmetic task in front of two clinical research members while they were under the impression of being photographed on a video camera for subsequent ‘‘behavioral analysis’’. The duration of the psychological stress is about 15 min. After the completion of the TSST, participants were taken to a rest area. 2.3.2. Psychological assessment We evaluated the participants’ subjective psychological state and eatingrelated symptoms (stress, anxiety, sweet craving and desire to binge) by using visual analog scales (VAS) with a range of 0–100 (not at all-very much, respectively). The following questions were asked: 1) To what extent do you feel at the present moment? 2) To what extent do you feel 3) To what extent do you feel 4) To what extent do you feel
an urge for uncontrolled eating (desire to binge) craving for sweet foods at the present moment? stressed at the present moment? anxiety at the present moment?
2.3.3. Laboratory measurements Cortisol was measured in serum samples by an Electrochemiluminescence Immuno Assay (‘‘Elecsys 2010’’, Roche). The within-run precision coefficient of variation (CV) was 1.4%, and the between-run CV was 2.1%. 2.4. Statistical analysis Results are given as mean7S.D. Basal cortisol levels (baseline) were calculated as the mean of measurements obtained at time points 30 and 0. The calculation of area under the curve (AUC) for cortisol levels following stress was computed as the area between the imaginary straight line between each two cortisol measurements and the baseline level. Comparisons of baseline continuous parameters (age, body-mass index, heart rate, cortisol concentrations, VAS measures) between groups (BED and Non-BED) were performed by the non-parametric Mann–Whitney U analysis. The effect of TSST on cortisol was examined by analysis of covariance (ANCOVA) with repeated measures.
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Comparison of post-stress curves of cortisol between groups was performed by the non-parametric Mann–Whitney U statistics with the Bonferroni correction due to multiple time point testing. Effect size was calculated using the Cohen’s d index. Preand post- stress changes in parameters measured by visual analog scales were compared by Wilcoxon signed rank test, and these differences were compared between groups by way of Wilcoxon rank-sum test. Associations between continuous parameters were evaluated by calculating Spearman’s correlation coefficients. P level o0.05 was considered statistically significant (two-sided). All statistical analyses were carried out using the SPSS statistical software for Windows.
3. Results 3.1. 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) ¼44.8, p o0.0001), 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) ¼4.1, p ¼0.031 (Table 1)). 3.2. Effect of TSST on cortisol levels The controlled psychological stress (TSST) induced a modest but not statistically significant elevation of cortisol levels over time in the whole sample as previously reported (Rouach et al., 2007). However, further examination of cortisol changes in each of the three groups revealed important differences. The TSST induced a significant group by time interaction for cortisol (F(10,32) ¼2.3, p¼0.039). While in the non-BED group and in the NW group a moderate elevation in cortisol levels in response to the TSST was observed, the BED group showed a blunted response at all time points (Fig. 1). Subjects were also classified as ‘‘cortisol responders’’ when the psychological stress resulted in a significant increase in cortisol levels or in sustained stable cortisol levels (n¼ 13), and as ‘‘cortisol non-responders’’ when a significant decrease in cortisol levels occurred during the test (n¼11). The proportion of responders and non-responders in our cohort is in accordance to that reported in the literature (Epel et al., 2001; Pruessner et al., 2008). There was no significant difference in the proportion of cortisol responders and nonresponders among the three groups (five responders in the NW group, five in the obese group and three in the BED group out of a total of eight subjects in each group). The between-group difference in cortisol levels (using the Mann– Whitney U test with the Bonferroni correction) was significant at the 150 time point (U¼5, N1¼ N2¼8; p¼0.015), and 750 time point (U¼7, N1¼N2¼8; p¼0.035) and at a trend level at the 350 time Table 1 Demographic, physiological and psychological parameters at baseline. Mean7 S.D.
Age, mean (years) Male female ratio BMI, mean (kg/m2) Basal serum cortisol level (mg/dl) Stressa Anxietya Sweet cravinga Uncontrolled-eatinga a
p value
NW (n ¼8)
Non-BED (n¼ 8) BED (n¼ 8)
32.6 7 3.55 3:5 21.2 7 1.9 12.4 7 6.6
50.3 75.7 3:5 35.3 7 4.2 13 74.3
49.8 7 4.9 2:6 36.8 7 4.3 9.4 7 3.2
0.026 NS o 0.0001 NS
17.5 7 14.9 5.0 77.6 6.3 7 10.6 2.5 7 7.1
23.1 7 30.1 9.4 717.0 1.9 73.7 1.9 73.7
25.0 7 34.6 15 7 20 16.3 7 19.2 21.3 7 25.3
NS NS 0.096 0.031
V.A.S. (Visual Analog Scales)
24
NW non BED
22 serum cortisol mean + sd (µg/dl)
158
Obese non BED Obese BED
20 18 16 14 12 10 8 6 4 2 0
-30
0
15 35 Time (min.)
55
75
Fig. 1. Cortisol response (mean þ S.D.) to the Trier Social Stress Test according to groups. Repeated measure analysis for group time comparison (ANOVA; p¼ 0.039). Arrow denotes TSST onset.
point (p¼0.075). The calculated effect size for the 150 and the 750 time points was large (Cohen’s d¼1.65 and 1, respectively). 3.3. Correlation between post-TSST eating and stress related parameters Stress and anxiety VAS scores increased similarly after TSST in all patient groups. Nevertheless, and similar to the observation at baseline, the ‘‘desire to binge’’ score was significantly higher in the BED group (35.0 734.2) compared to the non-BED group (5.077.6) and to the NW group (8.8717.3) subsequent to the psychological stress (F(2,23) ¼4.2, p ¼0.031), (Rouach et al., 2007). In a series of correlation analyses, we consistently found highly significant positive associations between post-TSST stress and anxiety, and the eating parameters desire to binge and sweet craving (r range: 0.72–0.91). These correlations were significant only for the BED group (Fig. 2), demonstrating that the higher the stress, the higher the feelings of sweet craving and desire to binge in this group (r¼ 0.69, p¼ 0.058; r¼0.871, p¼0.005, respectively). A similar association was found between anxiety and sweet craving and desire to binge (r¼0.72, p¼ 0.044; r¼0.91, p¼0.002, respectively). 3.4. Correlation between the cortisol and the psychological parameters response to stress There was a significant positive correlation between the cortisol AUC levels during the psychological stress test and the change in VAS scores for desire to binge (r ¼0.724, p ¼0.042) in the BED group only (Fig. 3). The correlation between cortisol AUC and sweet craving in the BED group did not reach statistical significance (r ¼0.512, p¼ 0.19). No correlation was found between VAS scores for anxiety or stress and cortisol changes in any group.
4. 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
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159
r= 0.911 p= 0.002
r= 0.871 p= 0.005
r= 0.271 p= NS
r= 0.015 p= NS
*
r=0.72 p=0.044
r=0.69 p= 0.058
r=0.688 p=0.059
r= 0.042 p= NS *
*
Fig. 2. Correlations between stress and desire to binge (A) and sweet craving (B), and between anxiety and desire to binge (C) and sweet craving (D) after the Trier Social Stress Test in the BED (n¼ 8) and non-BED group (n ¼8). VAS¼ visual analog scales were used to assess stress, anxiety and eating-related symptoms. *Full squares represent superposition of data points of non-BED (full circles) and BED (open squares) patients. Note that overlying data points from patients in the same group cannot be distinguished in the graph.
r=0.724 p=0.042
r= 0.512 p= NS
*
* r=-0.296 p= NS
r=0.234 p=NS
* Fig. 3. Correlation between cortisol area under the curve (AUC) and change in VAS scores for (A) desire to binge and (B) sweet craving (expressed as D change from baseline levels). *Full squares represent superposition of data points of non-BED (full circles) and BED (open squares) patients. Note that overlying data points from patients in the same group cannot be distinguished in the graph.
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 had a blunted cortisol response to the TSST as compared to the other groups. Second, feelings of sweet craving and desire to binge
subsequent to the TSST were highly correlated to feelings of stress and anxiety only in the BED group. And, finally, the increase in the eating parameters scores were positively correlated with the change in cortisol levels over baseline only in the BED group. Our results regarding normal basal cortisol levels in BED are not surprising in light of the contradictory results reported in past
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studies. However, having a normal weight non-BED control group strengthens the present result as we can differentiate between the effects of the eating disorder diagnosis and the possible direct effect of excess weight. This control group is also of major importance in understanding the stress-stimulated cortisol results. The blunted pattern of cortisol response to an acute stressor may reflect a compensatory down-regulation of the HPA axis secondary to the presence of chronic stress in this group of obese BED participants. In contrast to the activation of the HPA axis in acute stress, down-regulation of the HPA axis is a wellknown phenomenon during chronic stress (Checkley, 1992) and has also been reported in chronic depression (Pintor et al., 2007) and in abused women with PTSD (Bremner et al., 2003). The importance of the current finding is that such down-regulation of the HPA axis occurs also in the context of chronic stress associated with BED. Animal studies show that down-regulation of the HPA axis is associated with poorer stress regulation capacity, more prolonged stress reactions and vulnerability to allostatic load (Meaney and Szyf, 2005; Weaver et al., 2004). Thus, a hypothetical model for obesity in BED may be one of food-related stress sensitivity causing chronic stress which leads to increased glucocorticoid levels and obesity, a subsequent down-regulation of the HPA axis and a blunted biological stress response, which in turn could contribute to the stress sensitivity often observed in participants with BED (Anestis et al., 2007). The down-regulation of the HPA axis suggested by our results is in accordance with a previous report by Larsen et al. (2009) who, by repeatedly measuring cortisol throughout 2 days, found significantly lower overall cortisol secretion in obese women with BED in comparison to obese women without BED. On the other hand, our results are at odds with recent studies published by Gluck et al. (2004) showing higher basal cortisol levels and a nearly significantly greater cortisol area under the curve (AUC) following a cold stress test in obese women with BED as compared to obese women without BED. A possible explanation for this discrepancy may be the fact that we used a psychological stressor as a stimulus to the HPA axis rather than a pain stimulus used in the study by Gluck et al. While psychological stressors are central stimuli that require processing at higher brain levels, pharmacological or physical challenges act at different levels of the HPA axis (Kudielka et al., 2009; Hellhammer et al., 2009). Such discrepancies between the responses to psychological and other challenges have been reported before and suggested to imply differential activation of corticolimbic pathways (Santa Ana et al., 2006). Whereas the results of the biological markers differed between the two studies, our results replicate an increase in participants’ report of the desire to binge and sweet craving subsequent to HPA axis activation, and further show the association of this increase to perceived stress. Additional support for the distinction between a physical and a psychological challenge is the fact that Gluck et al. (2004b) found a significant correlation between cortisol area under the curve (AUC) and AUC for pain but not with hunger or desire to binge eat. In contrast, although the mean cortisol response to the psychological stress was blunted in our study, the post-stress mean cortisol AUC was positively correlated with the increase in the ‘‘desire to binge’’ scores in our BED participants. This indicates that despite the overall lower cortisol reactivity, there still remains a spectrum in the physiological response to the psychological stressor, with associated variability in the subjective feelings related to food behavior. Hence, BED patients who were ‘‘cortisol responders’’ had higher binge scores, in contrast with ‘‘cortisol non-responders’’ in whom the negative cortisol AUCs correlated with low binge scores. Our study should be repeated in a larger cohort to examine the possibility that the overall low mean cortisol response reflects a
higher percentage of ‘‘cortisol non-responders’’ in the BED population. The novelty of this report is in our data linking cortisol response with subjective feelings of eating behavior in patients with BED. In contrast with our findings linking increased binge eating scores with higher cortisol reactivity only in BED patients, Epel et al. reported higher food consumption by healthy volunteers that responded with high cortisol reactivity to the TSST in comparison with low reactors (Epel et al., 2001). They suggested that cortisol reactivity may be a marker for vulnerability to stress induced eating. We cannot rule out the possibility that had we examined a larger cohort, a correlation between cortisol reactivity and food-related thoughts would have emerged also in the healthy population. While the mean HPA axis response in our BED participants was blunted, their subjective stress response was maintained, albeit not significantly more than in the other two groups. Furthermore, in sharp difference from either the obese non-BED or NW participants, the subjective feelings of stress and anxiety were highly correlated with the urge to eat and desire to binge after the acute psychological stress. Thus, in our study, while participants with BED did not perceive psychological stress as more stressful than participants without BED, the perceived stress was correlated with binge-related thoughts. This pattern is partially indicative of the immediate role of stress in the induction of binge eating behavior and may explain the benefit of selective serotonin reuptake inhibitors in the treatment of this disorder (Leombruni et al., 2008). A major limitation of our study is its relatively small sample size. Additional studies in a larger cohort would be important to confirm our results and strengthen the suggested conclusions. This number of participants may have also limited our ability to detect additional differences among the groups. Furthermore, we did not apply mood scales, specifically depression, and thus could not control for depression scores which may have been higher in the BED group (as reported elsewhere). However, previous studies did not find a correlation between depression levels in women with BED and the HPA axis (Yanovski et al., 1993; Gluck et al., 2004). And finally, one should also take into account that measurements based on VAS are subjective, being susceptible to inaccuracies. In summary, we found that obese participants with BED, challenged with a psychological stressor, the TSST, demonstrated a blunted cortisol response compared to either obese or normal weight participants without BED. Furthermore, subsequent to the TSST, thoughts related to food cravings were highly correlated to feelings of stress and anxiety, as well as to the cortisol response in the BED group. These results imply chronic down-regulation of the HPA axis in participants with BED, and a relationship between the acute activation of the axis with subjective feelings of stress and food craving. This relationship should be further explored to enhance our understanding of the psychological and biological triggers of binge eating. Furthermore, this relationship highlights the importance of stress management, both by psychotherapy and medication, in the treatment of this disorder. References Abebe, D.S., Lien, L., Torgersen, L., von Soest, T., 2012. Binge eating, purging and non-purging compensatory behaviors decrease from adolescence to adulthood: a population-based, longitudinal study. BMC Public Health 12, 32. Adam, T.C., Epel, E.S., 2007. Stress, eating and the reward system. Physiology and Behavior 91, 449–458. American Psychiatric Association, 2000. Diagnostic and Statistical Manual of Mental Disorders, Text Revised, 4th ed. American Psychiatric Press, Washington, DC. Anestis, M.D., Selby, E.A., Fink, E.L., Joiner, T.E., 2007. The multifaceted role of distress tolerance in dysregulated eating behaviors. International Journal of Eating Disorders 40, 718–726.
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Psychiatry Research journal homepage: www.elsevier.com/locate/psychres
Cortisol response and desire to binge following psychological stress: Comparison between obese subjects with and without binge eating disorder Noa Rosenberg 1,a,c, Miki Bloch 1,a,c,n, Irit Ben Avi a, Vanessa Rouach b, Shaul Schreiber a,c, Naftali Stern b,c, Yona Greenman b,c a b c
Department of Psychiatry, Tel Aviv Sourasky Medical Center, Tel Aviv University, Israel Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel Sackler Faculty of Medicine, Tel Aviv University, Israel
a r t i c l e i n f o
a b s t r a c t
Article history: Received 26 January 2012 Received in revised form 9 August 2012 Accepted 27 September 2012
While stress and negative affect are known to precede ‘‘emotional eating’’, this relationship is not fully understood. The objective of this study was to explore the relationship between induced psychological stress, hypothalamic-pituitary-adrenal (HPA) axis activity, and eating behavior in binge eating disorder (BED). The Trier Social Stress Test (TSST) was applied in obese participants with (n¼ 8) and without BED (n¼8), and normal weight controls (n¼8). Psychological characteristics, eating-related symptoms, and cortisol secretion were assessed. Baseline stress, anxiety and cortisol measures were similar in all groups. At baseline desire to binge was significantly higher among the BED group. While the TSST induced an increase in cortisol levels, a blunted cortisol response was observed in the BED group. In the BED group, a positive correlation was found between cortisol (area under the curve) levels during the TSST and the change in VAS scores for desire to binge. Post-TSST desire to binge and sweet craving were significantly higher in the BED group and correlated positively with stress, anxiety, and cortisol response in the BED group only. These results suggest chronic down-regulation of the HPA axis in participants with BED, and a relationship between psychological stress, the acute activation of the HPA axis, and food craving. & 2012 Elsevier Ireland Ltd. All rights reserved.
Keywords: Cortisol Psychological stress Binge eating disorder Obesity Hypothalamic-pituitary-adrenal (HPA) axis
1. 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). n Corresponding author at: Department of Psychiatry, Tel Aviv Sourasky Medical Center, Tel Aviv University, Israel. Tel.: þ 972 3 6974568; fax: þ972 3 6925774. E-mail address: [email protected] (M. Bloch). 1 These authors contributed equally to this manuscript.
0165-1781/$ - see front matter & 2012 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.psychres.2012.09.050
It is known that stress and negative affect often precede ‘‘emotional eating’’ and binge eating (Levine and Marcus, 1997; 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 a-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
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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., 1999). 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; Monteleone et al., 2003). 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 wellstandardized 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.
2. Methods 2.1. Subjects Twenty-four participants, mean age 44.2715.4 (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
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30–40 kg/m2) participants without BED (Non-BED group, n¼8); and (3) A control group consisting of normal weight individuals (lean body weight of BMI 418 kg/m2 and o25 kg/m2), without any diagnosis of eating disorder (NW group, n¼8). The diagnosis of Binge The diagnosis of binge eating disorder was made by a certified psychiatrist (NR) according to the Diagnostic and Statistical Manual of Mental Disorders, 4th Ed. (American Psychiatric Association, 2000). The sample consisted of 16 females and 8 males. There was a similar male to female ratio in the three groups. Participants diagnosed with anorexia or bulimia nervosa, those with eating disorder not otherwise specified (excluding BED), participants taking any medication affecting the central nervous system or receiving medication known to interfere with cortisol measurements such as contraceptive pills and estrogen replacement therapy were excluded from the study. Ten patients with hypertension, four with hyperlipidemia, three with type II diabetes mellitus, three with hypothyroidism and one with osteoporosis were well controlled with appropriate medical treatment. The investigation was carried out in accordance with the latest version of the Declaration of Helsinki, and it was approved by the Institutional Review Board. All subjects signed an informed consent form after the nature of the procedures had been fully explained to them. 2.2. Study design Participants were instructed to eat a light breakfast (consisting of a cup of coffee or tea and a slice of bread with cheese) round 07:00 h before arrival to the clinic. Upon arrival, information about the research was given, medical and pharmacological history was taken, and consent was signed. Patients were inquired asked about having eaten breakfast, mainly to ascertain that they were not fasting. The study procedure started at 09:00 h and took a total of 2 h to complete. At first an intravenous catheter was inserted in the subject’s forearm, and the subject was then instructed to rest in bed for 40 min before the TSST (Kirschbaum et al., 1993) began. The TSST was conducted by the same examiner (RV). The biological outcome measures included heart rate, blood pressure (systolic and diastolic) and serum cortisol levels, which were determined at 6 consecutive time points: 2 baseline time points before the TSST ( 30 min and 0) and 4 time points after it (immediately after the completion of the test at 15 min, and at the rest area every 20 min afterwards at 35, 55 and 75 min). The psychological assessment as described below was performed just before the initiation of the TSST and immediately following it. 2.3. Data collection 2.3.1. Trier Social Stress Test (TSST) The TSST is a standard psychological stress test developed for an induction of moderate psychological stress under laboratory conditions. In the test, participants are asked to deliver a speech for a job application based on personal characteristics, and to perform a mental repetitive arithmetic task in front of two clinical research members while they were under the impression of being photographed on a video camera for subsequent ‘‘behavioral analysis’’. The duration of the psychological stress is about 15 min. After the completion of the TSST, participants were taken to a rest area. 2.3.2. Psychological assessment We evaluated the participants’ subjective psychological state and eatingrelated symptoms (stress, anxiety, sweet craving and desire to binge) by using visual analog scales (VAS) with a range of 0–100 (not at all-very much, respectively). The following questions were asked: 1) To what extent do you feel at the present moment? 2) To what extent do you feel 3) To what extent do you feel 4) To what extent do you feel
an urge for uncontrolled eating (desire to binge) craving for sweet foods at the present moment? stressed at the present moment? anxiety at the present moment?
2.3.3. Laboratory measurements Cortisol was measured in serum samples by an Electrochemiluminescence Immuno Assay (‘‘Elecsys 2010’’, Roche). The within-run precision coefficient of variation (CV) was 1.4%, and the between-run CV was 2.1%. 2.4. Statistical analysis Results are given as mean7S.D. Basal cortisol levels (baseline) were calculated as the mean of measurements obtained at time points 30 and 0. The calculation of area under the curve (AUC) for cortisol levels following stress was computed as the area between the imaginary straight line between each two cortisol measurements and the baseline level. Comparisons of baseline continuous parameters (age, body-mass index, heart rate, cortisol concentrations, VAS measures) between groups (BED and Non-BED) were performed by the non-parametric Mann–Whitney U analysis. The effect of TSST on cortisol was examined by analysis of covariance (ANCOVA) with repeated measures.
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Comparison of post-stress curves of cortisol between groups was performed by the non-parametric Mann–Whitney U statistics with the Bonferroni correction due to multiple time point testing. Effect size was calculated using the Cohen’s d index. Preand post- stress changes in parameters measured by visual analog scales were compared by Wilcoxon signed rank test, and these differences were compared between groups by way of Wilcoxon rank-sum test. Associations between continuous parameters were evaluated by calculating Spearman’s correlation coefficients. P level o0.05 was considered statistically significant (two-sided). All statistical analyses were carried out using the SPSS statistical software for Windows.
3. Results 3.1. 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) ¼44.8, p o0.0001), 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) ¼4.1, p ¼0.031 (Table 1)). 3.2. Effect of TSST on cortisol levels The controlled psychological stress (TSST) induced a modest but not statistically significant elevation of cortisol levels over time in the whole sample as previously reported (Rouach et al., 2007). However, further examination of cortisol changes in each of the three groups revealed important differences. The TSST induced a significant group by time interaction for cortisol (F(10,32) ¼2.3, p¼0.039). While in the non-BED group and in the NW group a moderate elevation in cortisol levels in response to the TSST was observed, the BED group showed a blunted response at all time points (Fig. 1). Subjects were also classified as ‘‘cortisol responders’’ when the psychological stress resulted in a significant increase in cortisol levels or in sustained stable cortisol levels (n¼ 13), and as ‘‘cortisol non-responders’’ when a significant decrease in cortisol levels occurred during the test (n¼11). The proportion of responders and non-responders in our cohort is in accordance to that reported in the literature (Epel et al., 2001; Pruessner et al., 2008). There was no significant difference in the proportion of cortisol responders and nonresponders among the three groups (five responders in the NW group, five in the obese group and three in the BED group out of a total of eight subjects in each group). The between-group difference in cortisol levels (using the Mann– Whitney U test with the Bonferroni correction) was significant at the 150 time point (U¼5, N1¼ N2¼8; p¼0.015), and 750 time point (U¼7, N1¼N2¼8; p¼0.035) and at a trend level at the 350 time Table 1 Demographic, physiological and psychological parameters at baseline. Mean7 S.D.
Age, mean (years) Male female ratio BMI, mean (kg/m2) Basal serum cortisol level (mg/dl) Stressa Anxietya Sweet cravinga Uncontrolled-eatinga a
p value
NW (n ¼8)
Non-BED (n¼ 8) BED (n¼ 8)
32.6 7 3.55 3:5 21.2 7 1.9 12.4 7 6.6
50.3 75.7 3:5 35.3 7 4.2 13 74.3
49.8 7 4.9 2:6 36.8 7 4.3 9.4 7 3.2
0.026 NS o 0.0001 NS
17.5 7 14.9 5.0 77.6 6.3 7 10.6 2.5 7 7.1
23.1 7 30.1 9.4 717.0 1.9 73.7 1.9 73.7
25.0 7 34.6 15 7 20 16.3 7 19.2 21.3 7 25.3
NS NS 0.096 0.031
V.A.S. (Visual Analog Scales)
24
NW non BED
22 serum cortisol mean + sd (µg/dl)
158
Obese non BED Obese BED
20 18 16 14 12 10 8 6 4 2 0
-30
0
15 35 Time (min.)
55
75
Fig. 1. Cortisol response (mean þ S.D.) to the Trier Social Stress Test according to groups. Repeated measure analysis for group time comparison (ANOVA; p¼ 0.039). Arrow denotes TSST onset.
point (p¼0.075). The calculated effect size for the 150 and the 750 time points was large (Cohen’s d¼1.65 and 1, respectively). 3.3. Correlation between post-TSST eating and stress related parameters Stress and anxiety VAS scores increased similarly after TSST in all patient groups. Nevertheless, and similar to the observation at baseline, the ‘‘desire to binge’’ score was significantly higher in the BED group (35.0 734.2) compared to the non-BED group (5.077.6) and to the NW group (8.8717.3) subsequent to the psychological stress (F(2,23) ¼4.2, p ¼0.031), (Rouach et al., 2007). In a series of correlation analyses, we consistently found highly significant positive associations between post-TSST stress and anxiety, and the eating parameters desire to binge and sweet craving (r range: 0.72–0.91). These correlations were significant only for the BED group (Fig. 2), demonstrating that the higher the stress, the higher the feelings of sweet craving and desire to binge in this group (r¼ 0.69, p¼ 0.058; r¼0.871, p¼0.005, respectively). A similar association was found between anxiety and sweet craving and desire to binge (r¼0.72, p¼ 0.044; r¼0.91, p¼0.002, respectively). 3.4. Correlation between the cortisol and the psychological parameters response to stress There was a significant positive correlation between the cortisol AUC levels during the psychological stress test and the change in VAS scores for desire to binge (r ¼0.724, p ¼0.042) in the BED group only (Fig. 3). The correlation between cortisol AUC and sweet craving in the BED group did not reach statistical significance (r ¼0.512, p¼ 0.19). No correlation was found between VAS scores for anxiety or stress and cortisol changes in any group.
4. 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
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159
r= 0.911 p= 0.002
r= 0.871 p= 0.005
r= 0.271 p= NS
r= 0.015 p= NS
*
r=0.72 p=0.044
r=0.69 p= 0.058
r=0.688 p=0.059
r= 0.042 p= NS *
*
Fig. 2. Correlations between stress and desire to binge (A) and sweet craving (B), and between anxiety and desire to binge (C) and sweet craving (D) after the Trier Social Stress Test in the BED (n¼ 8) and non-BED group (n ¼8). VAS¼ visual analog scales were used to assess stress, anxiety and eating-related symptoms. *Full squares represent superposition of data points of non-BED (full circles) and BED (open squares) patients. Note that overlying data points from patients in the same group cannot be distinguished in the graph.
r=0.724 p=0.042
r= 0.512 p= NS
*
* r=-0.296 p= NS
r=0.234 p=NS
* Fig. 3. Correlation between cortisol area under the curve (AUC) and change in VAS scores for (A) desire to binge and (B) sweet craving (expressed as D change from baseline levels). *Full squares represent superposition of data points of non-BED (full circles) and BED (open squares) patients. Note that overlying data points from patients in the same group cannot be distinguished in the graph.
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 had a blunted cortisol response to the TSST as compared to the other groups. Second, feelings of sweet craving and desire to binge
subsequent to the TSST were highly correlated to feelings of stress and anxiety only in the BED group. And, finally, the increase in the eating parameters scores were positively correlated with the change in cortisol levels over baseline only in the BED group. Our results regarding normal basal cortisol levels in BED are not surprising in light of the contradictory results reported in past
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studies. However, having a normal weight non-BED control group strengthens the present result as we can differentiate between the effects of the eating disorder diagnosis and the possible direct effect of excess weight. This control group is also of major importance in understanding the stress-stimulated cortisol results. The blunted pattern of cortisol response to an acute stressor may reflect a compensatory down-regulation of the HPA axis secondary to the presence of chronic stress in this group of obese BED participants. In contrast to the activation of the HPA axis in acute stress, down-regulation of the HPA axis is a wellknown phenomenon during chronic stress (Checkley, 1992) and has also been reported in chronic depression (Pintor et al., 2007) and in abused women with PTSD (Bremner et al., 2003). The importance of the current finding is that such down-regulation of the HPA axis occurs also in the context of chronic stress associated with BED. Animal studies show that down-regulation of the HPA axis is associated with poorer stress regulation capacity, more prolonged stress reactions and vulnerability to allostatic load (Meaney and Szyf, 2005; Weaver et al., 2004). Thus, a hypothetical model for obesity in BED may be one of food-related stress sensitivity causing chronic stress which leads to increased glucocorticoid levels and obesity, a subsequent down-regulation of the HPA axis and a blunted biological stress response, which in turn could contribute to the stress sensitivity often observed in participants with BED (Anestis et al., 2007). The down-regulation of the HPA axis suggested by our results is in accordance with a previous report by Larsen et al. (2009) who, by repeatedly measuring cortisol throughout 2 days, found significantly lower overall cortisol secretion in obese women with BED in comparison to obese women without BED. On the other hand, our results are at odds with recent studies published by Gluck et al. (2004) showing higher basal cortisol levels and a nearly significantly greater cortisol area under the curve (AUC) following a cold stress test in obese women with BED as compared to obese women without BED. A possible explanation for this discrepancy may be the fact that we used a psychological stressor as a stimulus to the HPA axis rather than a pain stimulus used in the study by Gluck et al. While psychological stressors are central stimuli that require processing at higher brain levels, pharmacological or physical challenges act at different levels of the HPA axis (Kudielka et al., 2009; Hellhammer et al., 2009). Such discrepancies between the responses to psychological and other challenges have been reported before and suggested to imply differential activation of corticolimbic pathways (Santa Ana et al., 2006). Whereas the results of the biological markers differed between the two studies, our results replicate an increase in participants’ report of the desire to binge and sweet craving subsequent to HPA axis activation, and further show the association of this increase to perceived stress. Additional support for the distinction between a physical and a psychological challenge is the fact that Gluck et al. (2004b) found a significant correlation between cortisol area under the curve (AUC) and AUC for pain but not with hunger or desire to binge eat. In contrast, although the mean cortisol response to the psychological stress was blunted in our study, the post-stress mean cortisol AUC was positively correlated with the increase in the ‘‘desire to binge’’ scores in our BED participants. This indicates that despite the overall lower cortisol reactivity, there still remains a spectrum in the physiological response to the psychological stressor, with associated variability in the subjective feelings related to food behavior. Hence, BED patients who were ‘‘cortisol responders’’ had higher binge scores, in contrast with ‘‘cortisol non-responders’’ in whom the negative cortisol AUCs correlated with low binge scores. Our study should be repeated in a larger cohort to examine the possibility that the overall low mean cortisol response reflects a
higher percentage of ‘‘cortisol non-responders’’ in the BED population. The novelty of this report is in our data linking cortisol response with subjective feelings of eating behavior in patients with BED. In contrast with our findings linking increased binge eating scores with higher cortisol reactivity only in BED patients, Epel et al. reported higher food consumption by healthy volunteers that responded with high cortisol reactivity to the TSST in comparison with low reactors (Epel et al., 2001). They suggested that cortisol reactivity may be a marker for vulnerability to stress induced eating. We cannot rule out the possibility that had we examined a larger cohort, a correlation between cortisol reactivity and food-related thoughts would have emerged also in the healthy population. While the mean HPA axis response in our BED participants was blunted, their subjective stress response was maintained, albeit not significantly more than in the other two groups. Furthermore, in sharp difference from either the obese non-BED or NW participants, the subjective feelings of stress and anxiety were highly correlated with the urge to eat and desire to binge after the acute psychological stress. Thus, in our study, while participants with BED did not perceive psychological stress as more stressful than participants without BED, the perceived stress was correlated with binge-related thoughts. This pattern is partially indicative of the immediate role of stress in the induction of binge eating behavior and may explain the benefit of selective serotonin reuptake inhibitors in the treatment of this disorder (Leombruni et al., 2008). A major limitation of our study is its relatively small sample size. Additional studies in a larger cohort would be important to confirm our results and strengthen the suggested conclusions. This number of participants may have also limited our ability to detect additional differences among the groups. Furthermore, we did not apply mood scales, specifically depression, and thus could not control for depression scores which may have been higher in the BED group (as reported elsewhere). However, previous studies did not find a correlation between depression levels in women with BED and the HPA axis (Yanovski et al., 1993; Gluck et al., 2004). And finally, one should also take into account that measurements based on VAS are subjective, being susceptible to inaccuracies. In summary, we found that obese participants with BED, challenged with a psychological stressor, the TSST, demonstrated a blunted cortisol response compared to either obese or normal weight participants without BED. Furthermore, subsequent to the TSST, thoughts related to food cravings were highly correlated to feelings of stress and anxiety, as well as to the cortisol response in the BED group. These results imply chronic down-regulation of the HPA axis in participants with BED, and a relationship between the acute activation of the axis with subjective feelings of stress and food craving. This relationship should be further explored to enhance our understanding of the psychological and biological triggers of binge eating. Furthermore, this relationship highlights the importance of stress management, both by psychotherapy and medication, in the treatment of this disorder. References Abebe, D.S., Lien, L., Torgersen, L., von Soest, T., 2012. Binge eating, purging and non-purging compensatory behaviors decrease from adolescence to adulthood: a population-based, longitudinal study. BMC Public Health 12, 32. Adam, T.C., Epel, E.S., 2007. Stress, eating and the reward system. Physiology and Behavior 91, 449–458. American Psychiatric Association, 2000. Diagnostic and Statistical Manual of Mental Disorders, Text Revised, 4th ed. American Psychiatric Press, Washington, DC. Anestis, M.D., Selby, E.A., Fink, E.L., Joiner, T.E., 2007. The multifaceted role of distress tolerance in dysregulated eating behaviors. International Journal of Eating Disorders 40, 718–726.
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