Article

Cortisol Stress Response Is Positively Correlated with Central Obesity in Obese Women with Binge Eating Disorder (BED) before and after Cognitive-Behavioral Treatment

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  • National Institutes of Health/NIDDK
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Abstract

Stress is the most commonly reported trigger of binge eating, and high cortisol levels are positively related to both central body fat and food intake after laboratory stress. We therefore examined waist circumference (WHR) and cortisol stress responsivity after a cold pressor stress test (CPT) in 22 obese (BMI > 27) women (11 BED, 11 non-BED). BMI and WHR did not differ between groups. The BED group had higher morning basal cortisol than the non-BED group (P = .03) and greater AUC cortisol after CPT, after controlling for AUC insulin (P = .04). In the BED group, WHR was related to AUC cortisol (P = .002) and peak cortisol stress responsivity (P = .003). Twenty (10 non-BED, 10 BED) were randomized to a 6-week treatment program (CBT + Diet) or Wait-List (WL) control group. There were no BED group or treatment-group differences in WHR, morning basal cortisol, or AUC cortisol after CPT. The relationship between WHR and both AUC cortisol (P = .002) and peak cortisol stress responsivity after CPT (P = .008) remained significant in the BED group. In BED, there is a hyperactive HPA axis related to abdominal obesity that persists even after treatment, suggesting that cortisol might be a primary factor in the disorder.

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... Individuals suffering from BED have been shown to have higher morning basal cortisol levels than those without BED. (Gluck, Geliebter, & Lorence, 2004). This shows that stress plays a major role in the disorder, as well as the affiliation of BED with weight gain and obesity. ...
... Total BES scores above 27 indicate a serious binge eating problem, while scores between 18-26 indicate a moderate binge eating problem, and scores below 17 indicate the absence of a binge eating problem (Mclver et al., 2009). There are also clinical ways to assess and diagnose BED including physical exams and interviews with questions related to BED characteristics described in the DSM-5 (Gluck et al., 2004). ...
... MBIs have been studied in correlation to binge eating disorder because they aid in relieving stress, calming the mind, and cultivating acceptance of one's physical and emotional state (Sojcehr et al., 2012). With stress being the most commonly reported trigger of binge eating, and evidence correlating high cortisol levels with abdominal fat and food intake after laboratory stress, researchers are spending valuable time and resources analyzing how mindfulness interventions can effect behaviors associated with binge eating disorder (Gluck et al., 2004). Mclver, Halloran, and McGartland (2009) completed a randomized trial with ninety women measuring the effects of a 12-week yoga program on reducing binge eating severity (Mclver et al., 2009). ...
Article
This literature review examines the impact of various mindfulness-based interventions (MBIs) on the obesity-related eating behaviors of stress eating, emotional eating, and binge eating. With the inconsistency of the weight loss industry to provide long-term weight loss results, the United States is in need of alternative methods of weight loss and weight maintenance to combat the current overweight and obesity epidemic. MBIs are thought to be beneficial when targeted at behaviors of weight gain because mindfulness promotes an individual’s awareness of present physical and emotional sensations within the body, including hunger and satiety cues. Self-acceptance and stress reduction are also targeted outcomes of mindfulness and are linked to the benefits of MBIs on obesity-related eating behaviors. Results show that MBIs may be beneficial to improving the targeted eating behaviors which have been linked to weight gain. However, when weight change is the goal, MBIs have been shown to be most effective when used in conjunction with other weight loss methods such as dietary and physical activity and education modifications. To date, studies are few and contain a variety of definitions for both eating behaviors and MBIs. Future research with a narrowed scope of view and greater variation within the study populations will be beneficial. Although more research is needed, current evidence exists to support the use of MBIs to reduce the frequency and severity of stress eating, emotional eating, and binge eating.
... Furthermore, research provides evi-dence that women with BED display high stress vulnerability, with patients reporting higher acute levels of distress than healthy controls (Hilbert, Vögele, Tuschen-Caffier, & Hartmann, 2011). Gluck, Geliebter, and Lorence (2004) found some indication for a hyperactive hypothalamic-pituitary-adrenal (HPA) axis (as one of the main effector systems of stress) with exaggerated morning cortisol as well as a tendency toward greater cortisol responsivity following cold pressor stress in women with BED compared to obese nonbinge eaters. Group differences persisted even after a 6-week CBT treatment program (Gluck et al., 2004). ...
... Gluck, Geliebter, and Lorence (2004) found some indication for a hyperactive hypothalamic-pituitary-adrenal (HPA) axis (as one of the main effector systems of stress) with exaggerated morning cortisol as well as a tendency toward greater cortisol responsivity following cold pressor stress in women with BED compared to obese nonbinge eaters. Group differences persisted even after a 6-week CBT treatment program (Gluck et al., 2004). In contrast to these findings, however, another experimental study on the effects of stress in obese individuals with and without BED failed to observe group differences in baseline cortisol concentration, and even found a blunted cortisol reaction to a psychosocial stressor for subjects with BED (Rosenberg et al., 2013). ...
... Contrary to Gluck et al., (2004), we observed no significant differences between overweight/obese women with and without BED with regard to basal and stress-responsive cortisol and sAA. However, our findings are in line with recent studies also reporting no evidence of increased cortisol stress response in obese women with BED compared to obese non-BED groups (Rosenberg et al., 2013;Schulz, Laessle, & Hellhammer, 2011). ...
Article
Stress is known to be a trigger for binge eating in individuals with binge eating disorder (BED). However, the influence of stressful situations on BED patients’ body image is less understood. Our study objective was to gain insight into the effects of inducing psychosocial stress on body dissatisfaction in women with BED. Overweight women with BED (n = 29) and without an eating disorder (control group, CG; n = 38) underwent the Trier Social Stress Test for Groups (TSST-G stress) and a nonstressful control task (TSST-G no stress). Additionally, to test for the influence of body salience, participants were either exposed or not exposed to a mirror. Participants repeatedly rated their current body dissatisfaction and psychological distress. Simultaneously, biological stress reactivity was measured using salivary cortisol and alpha-amylase (sAA). Participants responded to TSST-G stress with significantly higher psychological and biological stress compared to the TSST-G control task. The psychological distress response was significantly greater in women with BED than the CG. As hypothesized, exposure to acute socioevaluative stress led to exacerbated body dissatisfaction in the BED group only. The findings of the present study suggest that acute socioevaluative stress may play an influential role in BED patients’ body dissatisfaction. Body image programs might benefit from targeting stress management or coping skills in patients with BED.
... As an example of traumatic experiences, abuse-related PTSD symptoms are associated with hyperactivation of HPA axis and with subsequent increases in peripheral cortisol, which in turn have been linked to accumulation of fat in adipose tissues and, consequently, an increase in abdominal obesity [77,78]. In line with these findings, the hyperactivation of HPA axis with an exaggerated cortisol response to stress has been observed in obese patients [79] and was also put in relation with stress-induced eating [80], with night eating syndrome (NES) [81] and with waist adiposity in binge eating disorder (BED) patients [82]. ...
... • Conditions of repeated or incontrollable chronic stress are followed by higher cortisol response and tend to activate a state of allostatic load, resulting in neural and emotional dysregulation, which contribute to maladaptive behaviors such as repeated consumption of high caloric food [96], lack of control over eating, and binge eating [82,107,108]. ...
Chapter
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The first time that terms such as food addiction and addictive eating were mentioned was in 1956, in an article by T.G. Randolph. Recently, from a psychosomatic point of view, some authors have linked obesity and food addiction. Along with the concept of food addiction (derived from the similarities between the consumption of certain foods and “substance addictions”), a couple of questions seem to arise: What if it’s not just the particular food (the substance) that we are addicted to? Could it be that we are addicted to something else that makes us eat it? Thus, the concept of eating addiction has its own set of particulars. It brings the attention back to the individual and not the external substance (the food or ingredient). The focus on confronting the obesity problem should be moved away from the food itself (the addictive substance) to the person’s act of eating (the addictive behavior). Undoubtedly, there are many links between emotions and overweight/obesity. This chapter aims to review the current state of this field of study which is the emotional basis of obesity (at least a particular case of obesity and weight-related disorders).
... Investigations into macronutrient selection following glucocorticoid administration have also yielded varying results; adrenalectomized rats have shown increases in fat intake (Bligh et al., 1993) as well as carbohydrate intake (Kumar and Leibowitz, 1988) following corticosterone administration. Stress has been associated with increased visceral adiposity in obese humans (Randrianjohany et al., 1993;Gluck et al., 2004). Complementing this work, there is evidence that corticosterone, the major stress hormone, plays an important role in energy balance. ...
... There were no differences in total body adiposity between the stressed and non-stressed rats in the present study. While the present study did not discretely measure visceral fat pads, it is known that elevations in glucocorticoids have been associated with increased visceral adiposity in humans (Randrianjohany et al., 1993, Gluck et al., 2004 and glucocorticoid administration promotes obesity in rats (Zakrzewska et al., 1999). This may suggest that a more prolonged stress exposure may be necessary before the adipogenic effects of elevated glucocorticoids become apparent. ...
... This dysregulation may persist in AN after weight gain [95,96] suggesting that the hyperactivity of the HPA axis may be involved in the pathogenesis of the disease. In BED, the results are contradictory showing higher [102] or normal [103] basal cortisol. Following stress exposure, the patients with BED showed a hyperactive [102] or hypoactive [103] response of the HPA axis. ...
... In BED, the results are contradictory showing higher [102] or normal [103] basal cortisol. Following stress exposure, the patients with BED showed a hyperactive [102] or hypoactive [103] response of the HPA axis. However, it is well-established that stress plays a major role in the initiation of binge eating episodes [33,34,36,104,105] and in the maintenance of BN [97,106]. ...
... This dysregulation may persist in AN after weight gain [95,96] suggesting that the hyperactivity of the HPA axis may be involved in the pathogenesis of the disease. In BED, the results are contradictory showing higher [102] or normal [103] basal cortisol. Following stress exposure, the patients with BED showed a hyperactive [102] or hypoactive [103] response of the HPA axis. ...
... In BED, the results are contradictory showing higher [102] or normal [103] basal cortisol. Following stress exposure, the patients with BED showed a hyperactive [102] or hypoactive [103] response of the HPA axis. However, it is well-established that stress plays a major role in the initiation of binge eating episodes [33,34,36,104,105] and in the maintenance of BN [97,106]. ...
Article
Full-text available
Eating disorders are devastating and life-threatening psychiatric diseases. Although clinical and experimental investigations have significantly progressed in discovering the neuronal causes of eating disorders, the exact neuronal and molecular mechanisms of the development and maintenance of these pathologies are not fully understood. The complexity of the neuronal substrate of eating disorders hampers progress in revealing the precise mechanisms. The present review describes the current knowledge on the implication of the neuronal systems that regulate food intake, stress, emotions, and reward in eating disorders. The current data based on clinical and experimental research strongly suggest that these systems are interconnected and a misbalance in one system leads to altered activity in other food-related regulatory networks.
... Marcus and Wing (1987) found that 20-46 per cent of obese individuals in a weight control programme reported binge eating (see also Yanovski, 2003a;2003b). More recently Gluck et al. (2004) reported that up to 46 per cent of those defined as obese, binge eat and binge eating appears to be more common in females (Freeman & Gil, 2004;Linde et al., 2004). On the basis of this evidence it looks as though getting on for half of obese people may be using food to manage difficult feelings. ...
... He suggests that persistent stress results in the release of excess cortisol which in turn promotes visceral obesity. Gluck et al. (2004) came to the same conclusion. Conversely, Heinrichs et al. (2003) discovered that social support and oxytocin suppressed cortisol production. ...
Chapter
Full-text available
The following chapter highlights the role of applied health psychology within the field of obesity management. The chapter has been written by a health psychologist who specialises in obesity management and public health approaches to obesity, and a clinical psychologist with an interest in obesity. Both authors work therapeutically with overweight and obese clients, and therefore this chapter offers a practical view on the management of obesity.
... Abuse-related PTSD symptoms are associated with hyper-activation of HPA axis and with subsequent increases in peripheral cortisol, which in turn have been linked to accumulation of fat in adipose tissues with a consequent increase in abdominal obesity (Glaser, 2000;Pasquali, Vicennati, Cacciari, & Pagotto, 2006). In line with these findings, the hyperactivation of HPA axis with an exaggerated cortisol response to stress, has been observed in obese patients (Marin et al., 1992), and were also put in relation with stress-induced eating (Vicennati, Pasqui, Cavazza, Pagotto, & Pasquali, 2009), with night eating syndrome (NES) (Birketvedt et al., 1999), and with waist adiposity in BED patients (Gluck, Geliebter, & Lorence, 2004). Another mediating factor can be the presence of dissociative symptoms. ...
... Stress-related adaptation involves the concept of allostasis, which is the ability to achieve the physiological balance through the change of the internal environment (McEwen, 2007;Seeman, Singer, Rowe, Horwitz, & McEwen, 1997;Sinha & Jastreboff, 2013). Conditions of repeated or incontrollable chronic stress are followed by higher cortisol response and tend to activate a state of allostatic load resulting in neural and emotional dysregulation, which contribute to maladaptive behaviors such as repeated consumption of high caloric food (McEwen, 2007), lack of control over eating and binge eating (Gluck, Geliebter, & Lorence, 2004;Gluck, Geliebter, Hung, & Yahav, 2004;Groesz et al., 2012). These results suggest that psychophysiological responses to stress may influence subsequent eating behavior and hence may also mediate between the trauma and eating disorder link. ...
Article
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Background and aims Several studies report a positive association between adverse life experiences and adult obesity. Despite the high comorbidity between binge eating disorder (BED) and obesity, few authors have studied the link between trauma and BED. In this review the association between exposure to adverse life experiences and a risk for the development of obesity and BED in adulthood is explored. Methods Based on a scientific literature review in Medline, PubMed and PsycInfo databases, the results of 70 studies (N = 306,583 participants) were evaluated including 53 studies on relationship between adverse life experiences and obesity, 7 studies on post-traumatic stress disorder (PTSD) symptoms in relation to obesity, and 10 studies on the association between adverse life experiences and BED. In addition, mediating factors between the association of adverse life experiences, obesity and BED were examined. Results The majority of studies (87%) report that adverse life experiences are a risk factor for developing obesity and BED. More precisely a positive association between traumatic experiences and obesity and PTSD and obesity were found, respectively, in 85% and 86% of studies. Finally, the great majority of studies (90%) between trauma and the development of BED in adulthood strongly support this association. Meanwhile, different factors mediating between the trauma and obesity link were identified. Discussion and conclusions Although research data show a strong association between life adverse experiences and the development of obesity and BED, more research is needed to explain this association.
... It is worth noting at the outset of this review that the concept "food addiction" is an ongoing area of research, with several recent reviews addressing this topic in relation to obesity and eating disorders in great detail (Hebebrand et al., 2014;Meule, 2015;Meule and Gearhardt, 2014;Potenza and Grilo, 2014). Furthermore, available evidence suggests stress and emotional regulation may play a role in BED (Corwin et al., 2011;Gianini et al., 2013;Gluck et al., 2004;Hilbert et al., 2011;Laessle and Schulz, 2009;Larsen et al., 2009;Nicholls et al., 2016;Pendleton et al., 2001;Pinaquy et al., 2003;Rosenberg et al., 2013;Schulz and Laessle, 2012). However, as these models are not the main focus of this review, they are only briefly discussed. ...
... As such, potential future research directions in this area are summarized in Table 2. In this regard, it is worth noting that while evidence indicates that stress and emotional regulation may play a role in BED (Corwin et al., 2011;Gianini et al., 2013;Gluck et al., 2004;Hilbert et al., 2011;Laessle and Schulz, 2009;Larsen et al., 2009;Nicholls et al., 2016;Pendleton Fig. 2. Schematic representations of brain circuitry implicated in BED and a proposed neurobiological model with respect to reward/motivation, inhibitory control, and habitual behavior. *Denotes data based on animal studies. ...
Article
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Relatively little is known about the neuropathophysiology of binge-eating disorder (BED). Here, the evidence from neuroimaging, neurocognitive, genetics, and animal studies are reviewed to synthesize our current understanding of the pathophysiology of BED. Binge-eating disorder may be conceptualized as an impulsive/compulsive disorder, with altered reward sensitivity and food-related attentional biases. Neuroimaging studies suggest there are corticostriatal circuitry alterations in BED similar to those observed in substance abuse, including altered function of prefrontal, insular, and orbitofrontal cortices and the striatum. Human genetics and animal studies suggest that there are changes in neurotransmitter networks, including dopaminergic and opioidergic systems, associated with binge-eating behaviors. Overall, the current evidence suggests that BED may be related to maladaptation of the corticostriatal circuitry regulating motivation and impulse control similar to that found in other impulsive/compulsive disorders. Further studies are needed to understand the genetics of BED and how neurotransmitter activity and neurocircuitry function are altered in BED and how pharmacotherapies may influence these systems to reduce BED symptoms.
... In fact, the negative mood and life stress events are the most common antecedents of binge eating episodes [7][8][9][10][11][12][13]. In addition to high sensitivity to stressful events [14,15], the individuals with binge eating disorders (BED) demonstrate abnormal reactivity of the hypothalamo-pituitary adrenal (HPA) axis. It has been reported that depending on the type of stressors, a physical stress (cold pressor stress test) led to hyperactivity [16], while a psychological stress (trier social stress test) resulted in a blunted response of the HPA axis to stress [17]. In spite of hyporeactivity of the HPA axis in response to a psychological stress in BED patients, a post-stress desire to binge and craving for sweets were significantly higher in the BED group compared to controls without BED [17]. ...
... References: [1]; [13]; [16]; [17]; [32]. ...
Article
Binge eating episodes are frequently stimulated by stress. We developed a model of binge eating proneness based on individual sensitivity of young female Sprague Dawley rats to significantly increase sucrose consumption in response to stress. The rats were subjected to unpredictable intermittent 1-h access to 10% sucrose. After the stabilization of sucrose intake, rats were assessed for consistency of higher (for binge-like eating prone, BEP) or lower (for binge-like eating resistant, BER) sucrose intake in response to unpredictable episodes of foot-shock stress. The objectives of this study included demonstrating face validity of the BEP model and determining if some of the features of this model were pre-existing before exposure to intermittent access to sucrose and repeated stress. The BEP rats consumed a larger (20% > BER) amount of sucrose in a discrete (1-h) period of time compared to the BER phenotype in non-stressful conditions and significantly increased sucrose intake (50% > BER) under stress. Conversely, stress did not affect sucrose intake in BER rats. BEP rats showed higher sucrose intake compared to BER rats at the beginning of darkness as well as during the light period when they were sated and not physically hungry. Analyses of the sucrose licking microstructure revealed that BEP rats had a high motivational drive to consume sucrose in non-stressful condition and an increased hedonic value of sucrose when they were exposed to stressful conditions. BEP rats consumed sucrose much more rapidly under stressful conditions compared to BER rats. Finally, BEP rats demonstrated compulsive-like intake of sucrose (assessed in the light-dark box) and a blunted stress-induced increase in plasma corticosterone levels. Body weight and chow intake were not different between the phenotypes. Before exposure to intermittent access to sucrose and repeated stress, the BEP rats showed no clear evidence for compulsive sucrose intake. However, from the first 1-h access to sucrose, the BEP rats exhibited sucrose overeating; and from the first exposure to stress before intermittent access to sucrose, the BEP rats showed a blunted increase in corticosterone plasma levels. Innate sucrose hyperconsumption and altered reactivity of the hypothalamo-pituitary adrenal (HPA) axis to stress may be involved in the development of binge-like eating. Increased perceived hedonic value of palatable food and an increased motivation to consume this food despite aversive conditions as well as deregulated reactivity of the HPA axis may contribute to stress-induced bingeing on sucrose in BEP rats.
... BED, the newest ED addition to the DSM-5, is characterized by recurrent binge episodes in the absence of recurrent compensatory behaviors, is the most prevalent ED with lifetime prevalence estimates between 2 and 3.5%, and is more evenly distributed between sexes than the other eating disorders (Hudson et al. 2007;Kessler et al. 2013). Binge eating disorder patients are often overweight or obese and have an elevated risk for type II diabetes, cardiovascular disease and metabolic syndrome (Dingemans et al. 2002;Gluck et al. 2004;Hudson et al. 2010). All of these conditions can lead to adverse long-term health outcomes. ...
... In laboratory settings, patients with disordered eating report an elevated desire to binge in response to verbal, interpersonal and audiovisual stressors relative to healthy controls despite no difference in autonomic and cardiovascular responses (Cattanach et al. 1988). Physiological stressors like cold stress are known to increase blood cortisol levels, hunger, and desire to eat in individuals with BED (Gluck et al. 2004). Similarly, individuals with bulimia nervosa display increased hunger and desire to binge relative to restrained eaters in an imagery task designed to provoke feelings of loneliness and rejection (Tuschen-Caffier & Vögele 1999). ...
Article
Full-text available
Eating disorders are complex brain disorders that afflict millions of individuals worldwide. The etiology of these diseases is not fully understood, but a growing body of literature suggests that stress and anxiety may play a critical role in their development. As our understanding of the genetic and environmental factors that contribute to disease in clinical populations like anorexia nervosa, bulimia nervosa, and binge eating disorder continue to grow, neuroscientists are using animal models to understand the neurobiology of stress and feeding. We hypothesize that eating disorder clinical phenotypes may result from stress-induced maladaptive alterations in neural circuits that regulate feeding, and that these circuits can be neurochemically isolated using animal model of eating disorders.
... Accordingly, a meta-analysis of 36 ecological mo- mentary assessment studies found that negative affect was greater preceding binge episodes, with a large effect size (Haedt-Matt & Keel, 2011). This may be in part due to stress increasing the reward value of food; indeed, under conditions of stress, the reinforcement value of food, desire to binge eat, and cortisol levels increase -specifically in binge eaters (Gluck, Geliebter, Hung, & Yahav, 2004;Gluck, Geliebter, & Lorence, 2004;Goldfield, Adamo, Rutherford, & Legg, 2008). Thus, heightened emotional reactivity may be linked to overeating and binge eating in individuals with BED more than in individuals with obesity. ...
... In addition, the outcomes underlie multiple pathways that may be implicated in the development and experience of BED. For example, adopting Hayes' (2009) description of the mediation process, while CM may predict the development of BED, the influence of the mediating variable (e.g., cognitive differences in impulsivity [Bartholdy et al., 2017;Hsu et al., 2002], structural differences in the mOFC [Schienle et al.,2009], or cortisol and heart rate reactivity [Gluck et al., 2004]) may partially explain the basic relationship between CM and BED. ...
Article
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The world changed overnight with the coronavirus disease (COVID-19) pandemic, which resulted in the implementation of self-isolation, quarantine, and social distancing measures by government bodies to reduce further transmission of the disease and the burden on healthcare professionals. These measures had repercussions on the mental health system, most notably by making traditional in-person therapy inaccessible for many clients. Mental health providers quickly responded by adjusting and adopting online psychotherapy in order to address the demands for services. Clinicians are learning the benefits and costs of this type of service delivery—especially early career clinicians who are in the process of learning how to implement traditional in-person therapy. The current paper describes the experiences of two early career clinicians during the pandemic as they navigated the use of online therapy to serve clients, the unforeseen lessons learned, and recommendations to other clinicians who are practicing online therapy during this unprecedented time.
... The gender distribution is more even compared to the other ED [12,13]. In accordance with over-eating and loss of control, BED patients are often overweight or obese and hold an increased risk of developing type II diabetes, cardiovascular disease and metabolic syndrome [14][15][16]. The course of BED has been the object of less research than AN and BN, but its prognosis is better. ...
Article
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Background: The mortality of Anorexia Nervosa (AN) is the highest among all psychiatric disorders, and Eating Disorders (ED) overall pose serious health threats to a significant proportion of the population. In spite of an increasing recognition of the clinical impact of ED, often, the general readiness and knowledge of the diagnostic work-up among Physicians is insufficient. Material and method: A literature search of recent national and international scientific publications on the diagnostic work-up of ED was done in November 2015. PUBMED was the major source of information, but also known publications were utilized to collate the relevant information. Result: The result is presented as essential components in the diagnostic work-up, where potential relevant clinical findings such as e.g. eating behaviours, co-morbidities, laboratory findings, medical risk and risk of suicidality, are all necessary to enable an accurate diagnosis as part of a multilayered clinical problem description, in the diagnostic work-up of ED.Discussion: Early and accurate diagnosis of ED will enable prompt initiation of relevant treatment. This is most optimally served by a multilayered clinical problem description, where the clinical diagnosis is one part, together with several other clinical aspects, of ED.
... For instance, obese individuals with BED show reduced parasympathetic cardiac control in response to mental stress [46] and elevated baseline cortisol levels compared with obese individuals without BED. [47,48] Similarly, in a 5year longitudinal study, Hudson et al. found that in those at risk for developing components of metabolic syndrome, BED confers greater risk than obesity for developing dyslipidemia (OR: 2.2) and any metabolic syndrome component (OR: 1.7). [49] Perhaps as a result of their increased likelihood of having psychiatric and medical comorbidities, obese individuals with BED have been reported to have a reduced QoL compared with obese individuals without BED. ...
Article
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Binge eating disorder (BED), now recognized as a distinct eating disorder in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, is the most prevalent eating disorder. Although nearly half of individuals with BED are obese, BED also occurs in nonobese individuals. Despite the relatively high percentage of weight loss treatment-seeking individuals meeting BED criteria, primary care physicians may not be familiar with or have ever diagnosed BED. Many providers may also have difficulty distinguishing BED as a contributory factor in obesity. This review differentiates BED from other causes of obesity by describing how obese individuals with BED differ from obese individuals without BED and from nonobese individuals with BED in areas including psychopathology, behavior, genetics, physiology, quality of life and productivity. The ways in which health-care providers can identify individuals who may have BED are also highlighted so the proper course of treatment is pursued. Overall, obese individuals with BED demonstrate a number of key characteristics that differentiate them from obese individuals without eating disorders, including increased impulsivity in response to food stimuli with loss of control over eating, resulting in the consumption of more calories. They also experience significant guilt and other negative emotions following a meal. In addition, individuals with BED patients have more psychiatric comorbidity, display more psychopathology, exhibit longer binge durations, consume more meals as snacks during the day and have less dietary restraint compared with individuals with BED who are not obese. However, the differences between individuals with BED who are obese versus not obese are not as prominent. Taken together, the evidence appears to support the conclusion that BED is a unique and treatable neurobehavioral disorder associated with distinct behavioral and psychological profiles and distinct medical and functional outcomes, and that it is not merely a subtype of obesity.
... Elevated levels of circulating cortisol lead to the development of visceral obesity (49). Gluck et al. (50) reported that in obese females with binge eating disorder, there is a positive correlation between cortisol stress response and abdominal obesity. ...
Article
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Background: Abnormal eating behavior, unhealthy weight control methods, and eating disordered symptoms have risen among college students. Objectives: The aim of this study was to examine disordered eating attitudes and their relationship with anthropometric and body composition indices in physical education students in Tabriz, the capital of East Azerbaijan province, Iran. Patients and Methods: This cross-sectional study was conducted on 210 physical education students, 105 males and 105 females aged 18 to 25, who were selected by systematic random sampling from physical education faculty of Tabriz University in Tabriz, Iran, in 2013. Eating attitude test (EAT-26) was used for the assessment of disordered eating attitudes. In addition, anthropometric and body composition indices were assessed. Results: About 10% of the studied subject had disturbed eating attitudes; significantly more males (15.4%) reported an EAT-26 ≥ 20 (disordered eating attitudes) than females (4.8%) (P < 0.05). In males, the EAT-26 score was positively correlated with weist perimeter (WP) (r = 0.21, P < 0.05) and the waist-to-hip ratio (r = 0.26, P < 0.01). In females, the EAT-26 score was positively correlated with weight (r = 0.19, P < 0.05) and the WP (r = 0.28, P < 0.01). In females, weight (P < 0.05), body mass index (BMI) (P < 0.05), WP (P < 0.01), and waist-to-hip ratio (P < 0.05) were significantly different between disordered eating attitude and healthy subjects, while in males there was no significant difference between the two groups regarding the anthropometric and body composition indices. Conclusions:Abnormal eating attitude was notable among physical education students in Tabriz, Iran. It seems that some anthropometric indices such as BMI and central obesity indices were related to the increase of disordered eating attitude. Keywords: Physical Education and Training, Eating Disorders, Body Composition, Anthropometry
... Equivocal findings may stem from co-morbid obesity, which itself is linked to HPA axis dysregulation (Nieuwenhuizen & Rutters, 2008) and altered cortisol metabolism (Morton & Seckl, 2008). During stressors, individuals with binge-type EDs may exhibit steeper cortisol increases than controls, which has been associated with increased desire to binge (Koo-Loeb et al. 1998 Gluck et al. 2004a, b). Yet, other studies find blunted cortisol response (Pirke et al. 1992; Ginty et al. 2012; Rosenberg et al. 2013) or no group differences (Tuschen-Caffier & Vogele, 1999; Monteleone et al. 2011; Schulz et al. ...
Article
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Pediatric loss-of-control (LOC) eating is a robust behavioral precursor to binge-type eating disorders. Elucidating precursors to LOC eating and binge-type eating disorders may refine developmental risk models of eating disorders and inform interventions. We review evidence within constructs of the Negative Valence Systems (NVS) domain, as specified by the Research Domain Criteria framework. Based on published studies, we propose an integrated NVS model of binge-type eating-disorder risk. Data implicate altered corticolimbic functioning, neuroendocrine dysregulation, and self-reported negative affect as possible risk factors. However, neuroimaging and physiological data in children and adolescents are sparse, and most prospective studies are limited to self-report measures. We discuss a broad NVS framework for conceptualizing early risk for binge-type eating disorders. Future neural and behavioral research on the developmental trajectory of LOC and binge-type eating disorders is required.
... Women who react to stress with high cortisol secretion were found to not only eat more while recovering from stress, but also choose sweet foods (Epel, Lapidus, McEwen, & Brownell, 2001). Stress-induced cortisol secretion is also associated with central body fat deposition (Epel et al., 2000;Gluck, Geliebter, & Lorence, 2004), a known cardiovascular risk factor (Bjorntorp, 1997). Physical responses to stress -heart rate and blood pressure -were measured after mentally challenging tests in 22 older African Americans, and researchers found that those with more central body fat had significantly greater heart rate and blood pressure increases than those with a smaller waist circumference (Waldstein, Burns, Toth, & Poehlman, 1999). ...
Article
Overweight and obesity are widespread, global health problems due in part to the relapse and weight gain that often follows weight loss treatment. Moreover, racial minorities are disproportionately affected by this chronic disorder. Empirical evidence is needed to better address the problem of poor weight maintenance after loss. This ancillary, prospective study examined weight maintenance 18 months after a behavioral weight loss trial and explored possible differences between black and white participants in percent weight change and successful weight maintenance. The relationships of psychosocial variables - experiences following a low-fat diet, barriers to healthy eating, self-efficacy for resisting eating and for exercising, social support, and stress - with weight maintenance were investigated as well as whether race moderated these relationships. Additionally, the study examined the behavioral strategies used for weight maintenance and explored dietary intake and physical activity as potential mediators of the relationship between psychosocial variables and weight maintenance. Hierarchical linear and logistic regression models were used to examine the effect of race, as well as the effect of psychosocial variables, on percent weight change and successful weight maintenance (defined as ≤ 5% weight regain), after controlling for age, gender, education, income, and marital status. Descriptive statistics and group comparative statistics (t-tests or Mann Whitney U tests) were used to examine behavioral strategies utilized for weight maintenance. Path analysis investigated possible mediation effects of lifestyle variables on percent weight change. Fifty-seven percent of the 107 participants (58% of the 81 white participants and 54% of the 26 black participants) were successful weight maintainers. No difference was found in weight maintenance between racial groups; black and white individuals gained a similar amount of weight (M = 5.0%, SD = 6.6% and M = 4.4%, SD = 5.6%, respectively). An increase in barriers to healthy eating and the impact of a stressful life event on eating affected the percent weight gained and unsuccessful weight maintenance, ps < .04. Most behavioral strategies for weight maintenance were used less than half the time. Dietary intake and physical activity did not mediate the relationship between the examined psychosocial variables and weight maintenance.A difference in weight maintenance between black and white individuals was not supported by this study. Future research should further explore the weight control barriers that individuals experience and the impact of stress on weight maintenance.
... Disorganized attachment is characterized by an irresolvable pattern of "fright without solution," where the caregivers, even if not maltreating, are and contemporary a source of protection and threat (Liotti, 2004(Liotti, , 2006(Liotti, , 2013Main & Solomon, 1990). This attachment working model can lead to an increase in Hypothalamic Pituitary Aaxis activity (Gunnar & Quevedo, 2007;Petrowski, Beetz, Schurig, Wintermann, & Buchheim, 2017), such as elevated baseline cortisol, as well as greater increase and slower decline of cortisol following stress exposure (Tarullo & Gunnar, 2006), which in turn has been put in relation with both emotional dysregulation and strong binge eating desire in response to psychological stress cues in BED patients (Gluck, Geliebter, Hung, & Yahav, 2004;Gluck, Geliebter, & Lorence, 2004;Rosenberg et al., 2013). Moreover, the activity of HPA may be attenuated by increases in endogenous opioid release caused by eating palatable food (Adam & Epel, 2007;Morris, Beilharz, Maniam, Reichelt, & Westbrook, 2015), therefore functioning as a negative reinforcement toward binge eating behaviors (Gluck, Geliebter, Hung, et al., 2004). ...
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ABSTRACT: The aim of the current study is to evaluate the presence of childhood trauma, psychological and somatoform dissociation in obese and overweight patients with and without binge eating disorder (BED). 34 patients with BED diagnosis, were compared with a sex, age and social class matched sample of 34 obese patients (OB) without diagnosis of BED and with a control sample consisting of 34 healthy people (NC) with normal weight. Traumatic experiences were assessed by means of the Traumatic Experiences Checklist (TEC). Psychoform and somatoform dissociation were assessed respectively by means of the Dissociation Questionnaire (DIS-Q) and Somatoform Dissociation Questionnaire (SDQ-20). BED patients reported significantly more childhood traumatic experiences, psychological and somatoform dissociation, compared to OB patients without BED and NC sample. Moreover, OB patients showed more traumatic experiences compared to the NC sample. BED patients showed higher levels of childhood neglect and emotional abuse compared to the OB patients and NC sample. No significant differences were shown between OB patients and NC subjects with respect to level of psychological and somatoform dissociation. Our results confirm the necessity of evaluating emotional abuse and neglect in adults with BED, and the importance of assessing psychoform and somatoform dissociation in these patients. Tailored treatment strategies based on trauma and dissociation may improve outcomes among patients with BED and a history of childhood trauma.
... Stress may induce binge-eating via HPA axis activation; indeed, acute stress has elicited significant increases in cortisol, caloric consumption and preference for high-fat/high-sugar foods in lean healthy women (Epel, Lapidus, McEwen, & Brownell, 2001;Torres & Nowson, 2007). Stress-induced cortisol responses have been positively correlated with food intake in binge-eating disorder (BED; Gluck, Geliebter, and Lorence, 2004); however, this finding has neither been replicated (Rosenberg et al., 2013) nor tested in BN or AN-BP. Moreover, reports of blunted cortisol reactivity to acute stress in both BN (Ginty, Phillips, Higgs, Heaney, & Carroll, 2012;Monteleone et al., 2011;Pirke, Platte, Laessle, Seidl, & Fichter, 1992) and a mixed sample of AN and BN (Het et al., 2015) could suggest divergent associations between stress, cortisol and eating behavior across disorders (i.e. ...
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Background Anorexia nervosa (AN) and bulimia nervosa (BN) are complex psychiatric conditions, in which both psychological and metabolic factors have been implicated. Critically, the experience of stress can precipitate loss-of-control eating in both conditions, suggesting an interplay between mental state and metabolic signaling. However, associations between psychological states, symptoms and metabolic processes in AN and BN have not been examined. Methods Eighty-five women (n = 22 AN binge/purge subtype, n = 33 BN, n = 30 controls) underwent remote salivary cortisol sampling and a 2-day, inpatient study session to examine the effect of stress on cortisol, gut hormones [acyl-ghrelin, peptide tyrosine tyrosine (PYY) and glucagon-like peptide-1] and food consumption. Participants were randomized to either an acute stress induction or control task on each day, and plasma hormones were serially measured before a naturalistic, ad libitum meal. ResultsCortisol-awakening response was augmented in AN but not in BN relative to controls, with body mass index explaining the most variance in post-awakening cortisol (36%). Acute stress increased acyl-ghrelin and PYY in AN compared to controls; however, stress did not alter gut hormone profiles in BN. Instead, a group-by-stress interaction showed nominally reduced cortisol reactivity in BN, but not in AN, compared to controls. Ad libitum consumption was lower in both patient groups and unaffected by stress. Conclusions Findings extend previous reports of metabolic dysfunction in binge-eating disorders, identifying unique associations across disorders and under stress. Moreover, we observed disrupted homeostatic signaling in AN following psychological stress, which may explain, in part, the maintenance of dysregulated eating in this serious illness.
... Indeed, dieting periods are commonly observed in the history of binge eaters, but hunger alone appears to be non-sufficient to induce a compulsive-like eating, if not accompanied by conditions of stress or negative affect [168,169]. Stress has a central role in the etiology of binge eating, considering that obese individuals with BED, compared to those without, show a higher activity of the HPA axis and cortisol/corticosterone plasma level [170][171][172][173]. Additionally, higher cortisol levels, induced by stress, are able to promote a greater consumption of sweet foods [174], and are also positively correlated with the severity of binge eating [175]. ...
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The dysfunction of melanocortin signaling has been associated with obesity, given the important role in the regulation of energy homeostasis, food intake, satiety and body weight. In the hypothalamus, the melanocortin-3 receptor (MC3R) and melanocortin-4 receptor (MC4R) contribute to the stability of these processes, but MC3R and MC4R are also localized in the mesolimbic dopamine system, the region that responds to the reinforcing properties of highly palatable food (HPF) and where these two receptors seem to affect food reward and motivation. Loss of function of the MC4R, resulting from genetic mutations, leads to overeating in humans, but to date, a clear understanding of the underlying mechanisms and behaviors that promote overconsumption of caloric foods remains unknown. Moreover, the MC4R demonstrated to be a crucial modulator of the stress response, factor that is known to be strictly related to binge eating behavior. In this review, we will explore the preclinical and clinical studies, and the controversies regarding the involvement of melanocortin system in altered eating patterns, especially binge eating behavior, food reward and motivation.
... Most studies have instead evaluated the intake of palatable food or diets high in fat or carbohydrates. [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38] This study showed that maternal separation induced changes in the selection of nutrients depending on gender. Protein intake increased in male rats and decreased in female rats, and only female rats reduced their lipid intake. ...
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This study investigated the effects of maternal separation on the feeding behavior of rats. A maternal separation model was used on postnatal day 1 (PND1), forming the following groups: in the maternal separation (MS) group, pups were separated from their mothers each day from PND1 to PND14, whereas in the control (C) group pups were kept with their mothers. Subgroups were formed to study the effects of light and darkness: control with dark and light exposure, female and male (CF and CM), and maternal separation with dark and light exposure, female and male (SDF, SDM, SLF and SLM). Female rats had higher caloric intake relative to body weight compared with male controls in the dark period only (CF=23.3±0.5 v. CM=18.2±0.7, P<0.001). Macronutrient feeding preferences were observed, with male rats exhibiting higher caloric intake from a protein diet as compared with female rats (CF=4.1±0.7, n=8 v. CM=7.0±0.5, n=8, P<0.05) and satiety development was not interrupted. Female rats had a higher adrenal weight as compared with male rats independently of experimental groups and exhibited a higher concentration of serum triglycerides (n=8, P<0.001). The study indicates possible phenotypic adjustments in the structure of feeding behavior promoted by maternal separation, especially in the dark cycle. The dissociation between the mother's presence and milk intake probably induces adjustments in feeding behavior during adulthood.
... Cortisol reactivity and the stress neurohormone corticotropin-releasing factor (CRF) effects, via HPA axis and extrahypothalamic brain site, may be a marker for vulnerability to stress, inducing binge eating and subsequent ED. Remarkably, the episode of binge eating is associated with high cortisol levels [170][171][172][173][174][175] that predict sweet food overeating [176], and CRF receptors were demonstrated to play a pivotal role in stress induced binge eating in several studies [177][178][179][180][181][182][183][184][185]. ...
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The dopamine D4 receptor (DRD4) has a predominant expression in the prefrontal cortex (PFC), brain area strictly involved in the modulation of reward processes related to both food and drug consumption. Additionally, the human DRD4 gene is characterized by a variable number of tandem repeats (VNTR) in the exon 3 and, among the polymorphic variants, the 7-repeat (7R) allele appears as a contributing factor in the neurobiological mechanisms underlying drug abuse, aberrant eating behaviors and related comorbidities. The 7R variant encodes for a receptor with a blunted intracellular response to dopamine, and carriers of this polymorphism might be more tempted to enhance dopamine levels in the brain, through the overconsumption of drugs of abuse or palatable food, considering their reinforcing properties. Moreover, the presence of this polymorphism seems to increase the susceptibility of individuals to engage maladaptive eating patterns in response to negative environmental stimuli. This review is focused on the role of DRD4 and DRD4 genetic polymorphism in these neuropsychiatric disorders in both clinical and preclinical studies. However, further research is needed to better clarify the complex DRD4 role, by using validated preclinical models and novel compounds more selective for DRD4.
... Although ED patients gained weight and reported reduced core symptoms of AN and BN after treatment, the blunted cortisol response to the TSST in ED patients observed at pretreatment persisted after treatment. This indicates that HPA axis dysfunctions in these patients may not recover along with disease symptom reduction which is in line with findings in patients with BED as well (65). ...
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Previous research has provided evidence for a reduced neuroendocrine stress response in women with eating disorders (EDs). In the present study female in-patients with Anorexia and Bulimia nervosa were compared to female healthy controls (HC) before and after completing an in-patient treatment program. Salivary cortisol, alpha-amylase (sAA), heart rate response (HR), high-frequency heart rate variability (HF-HRV) and negative affective state were measured before, during and after exposure to the Trier Social Stress Test (TSST) at pre- and post-treatment. Patients with EDs (n = 13) showed significantly less ED symptoms at post-treatment. Compared to HC (n = 22), patients displayed a blunted cortisol stress response combined with overall attenuated sAA levels at pre-treatment. At post-treatment, the blunted cortisol stress response was still observable, while the differences in sAA responses disappeared. HR was attenuated at pre-treatment in patients, also indicated by a stronger HF-HRV throughout the TSST. These cardiovascular differences disappeared at post-treatment. Patients reported in general (pre- and post-treatment) more negative affect compared to HC. This study provides further evidences of a hypo-reactive hypothalamus–pituitary–adrenal axis (HPA) in patients with EDs which persists even after symptom recovery while initial low cardiovascular stress reactivity apparently can be restored by psychotherapy. Given the small sample size the findings have to be considered preliminary.
... MDRs may be due to social stratification that operates through biological mechanisms such as those involved in responding to stress (e.g., allostatic load, weathering, metabolic syndrome) [71]. There is, however, a need for further studies to understand the role of biological and physiological pathways that may explain MDRs on BMI [72][73][74][75][76][77][78][79]. ...
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Background: Parental educational attainment is shown to be protective against health problems; the Minorities' Diminished Returns theory, however, posits that these protective effects tend to be smaller for socially marginalized groups particularly blacks than whites. Aims: To explore racial differences in the effect of parental educational attainment on body mass index (BMI) in a national sample of US adolescents. Methods: In this cross-sectional study, we used baseline data of 10,701 (8678 white and 2023 black) 12-17 years old adolescents in the Population Assessment of Tobacco and Health (PATH; 2013). Parental educational attainment was the predictor. Youth BMI (based on self-reported weight and height) was the dependent variable. Age, gender, ethnicity, and family structure were covariates. Race was the focal moderator. Results: Overall, higher parental educational attainment was associated with lower youth BMI. Race, however, moderated the effect of parental educational attainment on BMI, suggesting that the protective effect of parental educational attainment on BMI is significantly smaller for black than white youth. Conclusions: In the United States, race alters the health gains that are expected to follow parental educational attainment. While white youth who are from highly educated families are fit, black youth have high BMI at all levels of parental educational attainment. This means, while the most socially privileged group, whites, gain the most health from their parental education, blacks, the least privileged group, gain the least. Economic, social, public, and health policymakers should be aware that health disparities are not all due to lower socioeconomic status (SES) of the disadvantaged group but also diminished returns of SES resources for them. Black-white health disparities exist across all high socioeconomic status (SES) levels.
... Dysfunctions in the HPA axis are thought to play a role in eating disorder psychopathology (Lo Sauro, Ravaldi, Cabras, Faravelli, & Ricca, 2008); in particular binge eating episodes are often preceded by stress and negative affect (Laessle & Schulz, 2009;Levine & Marcus, 1997) and a growing body of research shows that cortisol released during stress might promote hunger and feeding behavior (Tataranni et al., 1996). Indeed, some studies found an augmented cortisol secretion as a result of laboratory stress in obese BED subjects compared to non-BED obese subjects (Gluck, 2006;Gluck, Geliebter, Hung, & Yahav, 2004;Gluck, Geliebter, & Lorence, 2004); in another study patients who developed weight gain after a stressful event have been found to show higher twenty-four hour urinary free cortisol (UFC/24 h) than patients who did not identify a stressful event before the onset of weight gain (Vicennati, Pasqui, Cavazza, Pagotto, & Pasquali, 2009). These data might suggest the presence of higher baseline cortisol levels in some obese BED patients. ...
... A recent meta-analysis by Adam et al. (2017) demonstrated a relationship between diurnal cortisol slope and a wide range of mental and physical health problems with the general pattern for flatter slopes to predict poorer mental and physical health. Cortisol reactivity and recovery to acute stress are also linked to physical and mental health, with flattened recovery linked to depression (Burke, Davis, Otte, & Mohr, 2005) and reactivity linked to depression and behavior problems (Susman, Dorn, Inoff-Germain, Nottel-mann, & Chrousos, 1997), health and weight (Epel, Lapidus, McEwen, & Brownell, 2001;Epel et al., 2000;Gluck, Geliebter, & Lorence, 2004), and heart disease (Hamer, O'Donnell, Lahiri, & Steptoe, 2010). These findings are not ubiquitous given that flattened cortisol reactivity has also been associated with negative physical and mental health outcomes (Phillips, Ginty, & Hughes, 2013). ...
Article
Acute reactivity of the stress hormone cortisol is reflective of early adversity and stress exposure, with some studies finding that the impact of adversity on the stress response differs by race. The objectives of the current study were to characterize cortisol reactivity to two dyadically based stress paradigms across the first year of life, to examine cortisol reactivity within Black and White infants, and to assess the impact of correlates of racial inequity including socioeconomic status, experiences of discrimination, and urban life stressors, as well as the buffering by racial socialization on cortisol patterns. Salivary cortisol reactivity was assessed at 4 months of age during the Still Face paradigm ( N = 207) and at 12 months of age across the Strange Situation procedure ( N = 129). Infants demonstrated the steepest recovery after the Still Face paradigm and steepest reactivity to the Strange Situation procedure. Race differences in cortisol were not present at 4 months but emerged at 12 months of age, with Black infants having higher cortisol. Experiences of discrimination contributed to cortisol differences within Black infants, suggesting that racial discrimination is already “under the skin” by 1 year of age. These findings suggest that race-related differences in hypothalamic–pituitary–adrenal reactivity are present in infancy, and that the first year of life is a crucial time period during which interventions and prevention efforts for maternal–infant dyads are most likely able to shape hypothalamic–pituitary–adrenal reactivity thereby mitigating health disparities early across the life course.
... We calculated the correlation between the DC values of the identified brain regions from structural connectivity analysis or brain networks from the functional connectivity analysis and EDE-Q scores. The correlation between neuroimaging findings and the behaviors of eating disorders was explored as an eating disorder that was reported to be associated with abdominal obesity (Dallman et al., 2003;Gluck et al., 2004;Daubenmier et al., 2011;Succurro et al., 2015). ...
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Abdominal obesity is important for understanding obesity, which is a worldwide medical problem. We explored structural and functional brain differences in people with abdominal and non-abdominal obesity by using multimodal neuroimaging and up-to-date analysis methods. A total of 274 overweight people, whose body mass index exceeded 25, were enrolled in this study. Participants were divided into abdominal and non-abdominal obesity groups using a waist–hip ratio threshold of 0.9 for males and 0.85 for females. Structural and functional brain differences were assessed with diffusion tensor imaging and resting-state functional magnetic resonance imaging. Centrality measures were computed from structural fiber tractography, and static and dynamic functional connectivity matrices. Significant inter-group differences in structural and functional connectivity were found using degree centrality (DC) values. The associations between the DC values of the identified regions/networks and behaviors of eating disorder scores were explored. The highest association was achieved by combining DC values of the cerebral peduncle, anterior corona radiata, posterior corona radiata (from structural connectivity), frontoparietal network (from static connectivity), and executive control network (from dynamic connectivity) compared to the use of structural or functional connectivity only. Our results demonstrated the effectiveness of multimodal imaging data and found brain regions or networks that may be responsible for behaviors of eating disorders in people with abdominal obesity.
... Our initial search generated 167 results, 14 of which met our inclusion criteria (Fig. 2). In three cases, data collected within the same cohort of participants are discussed in multiple publications (Gluck et al., 2004a(Gluck et al., ,b, 2014Rouach et al., 2007;Rosenberg et al., 2013and Klatzkin et al., 2015. With the exception of one cohort (Rouach et al., 2007;Rosenberg et al., 2013), all of the datasets included in this review featured exclusively female samples. ...
Article
Binge eating disorder (BED) is characterized by recurrent episodes of eating an excessive amount of food over a discrete time period, while feeling a loss of control over one's eating. Although stress is one of the most commonly‐reported triggers of binge eating in individuals with BED, there has been little work examining the stress response specifically in individuals with the disorder. In this review, we examine what is known about how individuals with BED respond to acute stressors. A systematic literature search identified 14 relevant articles that report on the effects of experimentally‐induced stress on objective measures. Dependent measures that have been examined include changes in the levels of hormones such as cortisol and ghrelin, cardiovascular function, ad libitum food intake, and eating rate. In this review, we describe the published findings and discuss their implications in the context of the wider literature. Overall, we found partial evidence that BED is associated with a heightened response to stress. Given the inconsistencies between studies, we suggest that reported differences between individuals with and without BED might be driven by factors that are correlated with, but not specific to, BED. We suggest that two priorities for this research area are to identify factors that modulate the stress response in individuals with BED, and to address the underrepresentation of males in this literature. This article is protected by copyright. All rights reserved.
... Participants were encouraged to keep their feet in the cold water for the entire test period, although they could withdraw their feet at any time if the pain was unbearable. Although the cold-pressor test reliably induces SAM responses, such as increased heart rate, blood pressure, norepinephrine, and epinephrine (al'Absi et al., 2002;Bolli et al., 1981;Robertson et al., 1979), HPA axis activation is only low to moderate (al'Absi et al., 2002;Gluck et al., 2004) or absent (Duncko et al., 2007;McRae et al., 2006). To improve the HPA axis response, Schwabe et al, Good Clinical Practice (ICH-GCP) and Quality Assurance. ...
Thesis
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Early life adversity (ELA) is associated with a higher risk for diseases in adulthood. Changes in the immune system have been proposed to underlie this association. Although higher levels of inflammation and immunosenescence have been reported, data on cell-specific immune effects are largely absent. In addition, stress systems and health behaviors are altered in ELA, which may contribute to the generation of the ‘ELA immune phenotype’. In this thesis, we have investigated the ELA immune phenotype on a cellular level and whether this is an indirect consequence of changes in behavior or stress reactivity. To address these questions the EpiPath cohort was established, consisting of 115 young adults with or without ELA. ELA participants had experienced separation from their parents in early childhood and were subsequently adopted, which is a standard model for ELA, whereas control participants grew up with their biological parents. At a first visit, blood samples were taken for analysis of epigenetic markers and immune parameters. A selection of the cohort underwent a standardized laboratory stress test (SLST). Endocrine, immune, and cardiovascular parameters were assessed at several time points before and after stress. At a second visit, participants underwent structural clinical interviews and filled out psychological questionnaires. We observed a higher number of activated T cells in ELA, measured by HLA-DR and CD25 expression. Neither cortisol levels nor health-risk behaviors explained the observed group differences. Besides a trend towards higher numbers of CCR4+CXCR3-CCR6+ CD4 T cells in ELA, relative numbers of immune cell subsets in circulation were similar between groups. No difference was observed in telomere length or in methylation levels of age-related CpGs in whole blood. However, we found a higher expression of senescence markers (CD57) on T cells in ELA. In addition, these cells had an increased cytolytic potential. A mediation analysis demonstrated that cytomegalovirus infection – an important driving force of immunosenescence – largely accounted for elevated CD57 expression. The psychological investigations revealed that after adoption, family conditions appeared to have been similar to the controls. However, PhD thesis MMC Elwenspoek 18 ELA participants scored higher on a depression index, chronic stress, and lower on self-esteem. Psychological, endocrine, and cardiovascular parameters significantly responded to the SLST, but were largely similar between the two groups. Only in a smaller subset of groups matched for gender, BMI, and age, the cortisol response seemed to be blunted in ELA participants. Although we found small differences in the methylation level of the GR promoter, GR sensitivity and mRNA expression levels GR as well as expression of the GR target genes FKBP5 and GILZ were similar between groups. Taken together, our data suggest an elevated state of immune activation in ELA, in which particularly T cells are affected. Furthermore, we found higher levels of T cells immunosenescence in ELA. Our data suggest that ELA may increase the risk of cytomegalovirus infection in early childhood, thereby mediating the effect of ELA on T cell specific immunosenescence. Importantly, we found no evidence of HPA dysregulation in participants exposed to ELA in the EpiPath cohort. Thus, the observed immune phenotype does not seem to be secondary to alterations in the stress system or health-risk behaviors, but rather a primary effect of early life programming on immune cells. Longitudinal studies will be necessary to further dissect cause from effect in the development of the ELA immune phenotype.
... The current study did not include any biological measures to elucidate the potential mechanism by which large central fat stores may promote LOC eating; however, previous work suggests cortisol, leptin, and insulin may be involved. For example, prior results indicate greater food intake-induced and stressinduced stimulation of cortisol among individuals with higher central fat deposition compared with individuals with peripheral obesity and among those with binge eating compared with weight-matched controls (56)(57)(58). Authors speculate that this elevated glucocorticoid release may, in turn, worsen insulin sensitivity and decrease sensitivity to leptin, an anorexigenic peptide, which may further promote overeating [e.g., Zakrzewska et al. (59)]. ...
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Background: Elevated body mass index (BMI), higher waist-to-hip ratio, and body dissatisfaction have been investigated as risk factors for the development of bulimic symptoms. Central fat deposition may be particularly relevant to eating disorders. To our knowledge, the longitudinal relations among fat distribution, body dissatisfaction, and loss-of-control (LOC) eating development and maintenance have not been studied. Objective: We examined body fat distribution, independent of BMI and depressive symptoms, as a unique correlate and predictor of body dissatisfaction and LOC eating cross-sectionally and over a 2-y follow-up. Design: Body composition was measured by using dual-energy X-ray absorptiometry in 294 adult women at risk of weight gain at baseline, 6 mo, and 24 mo. We assessed LOC eating, body dissatisfaction, and depressive symptoms at baseline, 6 wk, 6 mo, 12 mo, and 24 mo by using the Eating Disorder Diagnostic Interview, the Multidimensional Body-Self Relations Questionnaire-Appearance Scales Body Areas Satisfaction subscale, and the Center for Epidemiologic Studies-Depression Scale, respectively. Results: Independent of BMI, baseline total percentage body fat, percentage trunk fat, and percentage abdominal fat were related to greater body dissatisfaction. Total percentage body fat and trunk fat tended to be associated with greater body dissatisfaction at all subsequent time points. Women with a greater percentage trunk fat, specifically abdominal fat, were at highest risk of developing LOC eating. In the full sample, women with higher baseline percentage trunk and abdominal fat showed increases in LOC eating episode frequency over time, whereas LOC eating frequency remained stable among women with smaller percentages of fat in trunk and abdominal regions. Conclusion: These findings lend further support to the premise that increased central body fat deposition is associated with body image dissatisfaction and suggest that it may represent a risk and maintenance factor for LOC eating. This trial was registered at clinicaltrials.gov as NCT00456131.
Chapter
Preclinical models are needed to investigate the neuro- and psycho-biology of binge eating (BE) and to identify innovative pharmacotherapeutic strategies. A new model, based on the combination of cyclic caloric restriction and acute stress, has been recently developed in our laboratory to induce BE of highly palatable food (HPF) in female rats. Rats were exposed to three cycles of food restriction/refeeding and then stressed on the test day. Acute stress was elicited by exposing rats to HPF, but preventing them from accessing it for 15 min. This experimental procedure induces a marked binge-type intake of HPF. Interestingly, in this model BE does not occur during the estrus phase of the ovarian cycle; if data from female rats in estrus are not included in the statistical analysis, the variability of the BE response is very low. Topiramate, sibutramine, and fluoxetine potently inhibited HPF intake in this model, providing evidence for its predictive validity. The model has been used to investigate the effect of drugs targeting stress mechanisms. The corticotrophin-releasing factor (CRF)-1 receptor antagonist R121919 selectively inhibited BE, indicating that CRF is involved in the BE response. Its effect is likely exerted in extra-hypothalamic sites rather than in hypothalamic sites controlling the hypothalamic–pituitary–adrenal axis. In addition, orexin-1 receptor antagonists selectivity inhibit BE; studies are under way to evaluate whether their effects are related to influences on stress or on reward mechanisms. This preclinical model appears to be highly reliable and reproducible; it may represent a valid model to identify novel pharmacological treatments of BE disorder and bulimia nervosa.
Article
This study was conducted to examine if taste over load with oral capsaicin improves the adverse behavioural effects induced by partial aberration of oral sensory relays to brain with bilateral transections of the lingual and chorda tympani nerves. Male Sprague-Dawley rats received daily 1ml of 0.02% capsaicin or water drop by drop into the oral cavity following the bilateral transections of the lingual and chorda tympani nerves. Rats were subjected to ambulatory activity, elevated plus maze and forced swim tests after 11th, 14th and 17th daily administration of capsaicin or water, respectively. The basal and stress-induced plasma corticosterone levels were examined after the end of behavioural tests. Ambulatory counts, distance travelled, centre zone activities and rearing were increased, and rostral grooming decreased, during the activity test in capsaicin treated rats. Behavioural scores of capsaicin rats during elevated plus maze test did not differ from control rats. Immobility during the swim test was decreased in capsaicin rats with near significance (P=0.0547). Repeated oral capsaicin increased both the basal level and stress-induced elevation of plasma corticosterone in rats with bilateral transections of the lingual and chorda tympani nerves. It is concluded that repeated oral administration of capsaicin reduces anxiety-like behaviours in rats that received bilateral transections of the lingual and chorda tympani nerves, and that the increased corticosterone response, possibly modulating the hippocampal neural plasticity, may be implicated in the anxiolytic efficacy of oral capsaicin. Copyright © 2015 Elsevier Ltd. All rights reserved.
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We developed recently a binge-eating model in which female rats with a history of intermittent food restriction show binge-like palatable food consumption after 15 min exposure to the sight of the palatable food. This "frustration stress" manipulation also activates the hypothalamic-pituitary-adrenal stress axis. Here, we determined the role of the stress neurohormone corticotropin-releasing factor (CRF) in stress-induced binge eating in our model. We also assessed the role of CRF receptors in the bed nucleus of the stria terminalis (BNST), a brain region implicated in stress responses and stress-induced drug seeking, in stress-induced binge eating. We used four groups that were first exposed or not exposed to repeated intermittent cycles of regular chow food restriction during which they were also given intermittent access to high-caloric palatable food. On the test day, we either exposed or did not expose the rats to the sight of the palatable food for 15 min (frustration stress) before assessing food consumption for 2 h. We found that systemic injections of the CRF1 receptor antagonist R121919 (2,5-dimethyl-3-(6-dimethyl-4-methylpyridin-3-yl)-7 dipropylamino pyrazolo[1,5-a]pyrimidine) (10-20 mg/kg) and BNST (25-50 ng/side) or ventricular (1000 ng) injections of the nonselective CRF receptor antagonist d-Phe-CRF(12-41) decreased frustration stress-induced binge eating in rats with a history of food restriction. Frustration stress also increased Fos (a neuronal activity marker) expression in ventral and dorsal BNST. Results demonstrate a critical role of CRF receptors in BNST in stress-induced binge eating in our rat model. CRF1 receptor antagonists may represent a novel pharmacological treatment for bingeing-related eating disorders.
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This study was conducted to examine if γ-amino Butyric Acid (GABA)-ergic neurotransmission is implicated in the regulation of stress-induced feeding. Rats received GABAAreceptor antagonist bicuculline before each stress session during 10 days of daily restraint stress. The hypothalamic mRNA expressions of corticotropin-releasing hormone and neuropeptide Y were analyzed by in situ hybridization and the plasma corticosterone with radioimmunoassay. Bicuculline ameliorated the decrease in food intake by repeated restraints but not by a single restraint. Corticosterone increase responding to acute stress but not to repeated restraints was attenuated by bicuculline. Stress-induced expression of corticotropin-releasing hormone was blunted by bicuculline pre-treatm ent. Restraint stress did not affect neuropeptide Y expression, regardless of bicuculline pre-treatment. It is concluded that GABAAreceptors may mediate chronic but not acute, stress-induced suppression in food intake, possibly in relation with anorectic action of the hypothalamic corticotropin-releasing hormone and the hypothalamic neuropeptide Y may not be implicated in its regulatory mechanism.
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Background . Lifestyle factors like time of eating and stress exposure may impact physiology to promote excess weight gain. To understand behavioral and physiological mechanisms underlying these potential effects, we compared appetite and gut hormone responses to a series of meal and stress challenges beginning in the morning and the afternoon, in adults with normal-weight and obesity. Method . Thirty-two adults (16 with normal-weight, 16 with obesity) underwent the same test protocol on different days, each following an 8 h fast. On one day the protocol began in the morning (AM condition); on the other day it began in the late afternoon (PM condition). On each day they first received a standardized liquid meal (9:00am/4:00pm), then a stress test (Socially-Evaluated Cold Pressor Test, 11:10am/6:10pm), then an ad libitum buffet meal (11:40am/6:40pm). Appetite and stress ratings were obtained, and blood was drawn for measures of ghrelin, PYY, GLP-1, insulin, glucose, cortisol and leptin. Acetaminophen was administered as a tracer to assess gastric emptying of the liquid meal. Results . Across all three challenges, AUC cortisol was lower in the PM vs. AM condition (all p<.001), and AUC insulin and leptin were higher in the obesity vs. normal-weight group (all p<.001). For the standardized liquid meal only, AUC hunger, desire to eat and ghrelin were greater in the PM vs. AM condition (all p<0.05), and AUC ghrelin was lower in the obesity vs. normal-weight group, even when controlling for baseline values (p<0.05). AUC glucose was higher in the evening for the normal-weight group only (condition x group interaction p<0.05). Post-liquid meal gastric emptying as indexed by AUC acetaminophen was slower in the PM vs. AM (p<.01). For the stress test, AUC cortisol was lower in the PM than the AM condition even when controlling for baseline values (p<.05). AUC leptin was lower in the evening in the obesity group only (condition x group interaction p<0.01). PYY showed an acute decrease post-stressor in the normal-weight but not the obesity group (p<.05). Post-stress ad libitum buffet meal intake was similar in the evening and morning conditions, and higher in the obesity group (p<0.05). Only among the obesity group in the evening condition, higher stressor-associated stress ratings were associated with lesser fullness in relation to the buffet meal (p<0.05). Conclusions . Normal-weight individuals and those with obesity may be at risk of evening overeating as a result of differential appetite and gut hormone responses following meal intake and stress exposure.
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To examine gender-specific associations between food insecurity and insulin resistance in a representative U.S. Data on 5533 adults of 20 years of age or more (2742 men and 2791 women) without diabetes from the 2005-2010 National Health and Nutrition Examination Survey were analyzed. Respondents were categorized as having full, marginal, low, or very low food security using a validated scale. Insulin-resistant individuals were defined as those with a homeostasis model assessment of insulin resistance value 2.5 or more. Insulin resistance was higher in both normal-weight (P = .001) and overweight or obese (P < .001) women with lower food security, but no linear trend was found in men. In multiple logistic regression analyses, however, very low food security-compared with full food security-was associated with insulin resistance in normal-weight men (odds ratio, 3.99; 95% confidence interval, 1.71-9.33), and marginal food insecurity was associated with insulin resistance in overweight or obese men (odds ratio, 2.07; 95% confidence interval, 1.18-3.64) after adjusting for potential confounders. In women, the association between food insecurity and insulin resistance was no longer significant after adjustment. Food insecurity is associated with insulin resistance in adults without diabetes, and this effect varies by gender in normal-weight and overweight or obese populations. Improving food security status may help reduce insulin resistance, an underlying risk factor for diabetes and cardiovascular disease. Copyright © 2015 Elsevier Inc. All rights reserved.
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Background and purpose: Household food insecurity is defined as limited or uncertain access to nutritionally adequate and safe food or limited ability to obtain foods in socially acceptable ways. Household food insecurity is associated with weight especially in women, so, this study aimed at determining the relationship between household food security status and gestational weight gain and weight-related complications in pregnancy. Materials and methods: This cross-sectional study was conducted in 2014 in 700 mothers attending health centers in Tehran. Questionnaires of household food security US Department of Agriculture (USDA) and general information were used for data collection. Chi-square, independent sample T-test and logistic regression were also applied for statistical analysis. Results: The results showed that the prevalence of food insecurity among mothers was 34.8%. There were 25.4% of mothers who were found with food insecurity without hunger. Among the subjects food insecurity with moderate hunger was observed in 8% and 1.4% were seen with food insecurity with severe hunger. Socio-economic survey showed that mothers with household food-insecurity were young housewives with lower education who had many children and low incomes. Based on the final logistic regression model and after adjusting the confounding variables, food insecurity was found associated with gestational diabetes mellitus (OR= 2.12, CI 1.36 - 3.33) and pregnancy induced hypertension (OR= 1.64, CI 1.01 to 2.67) but not associated with risk of proteinuria (P>0.05). Conclusion: According to findings living in food insecure households may increase the risk of pregnancy complications. © 2015, Mazandaran University of Medical Sciences. All rights reserved.
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A number of studies have indicated a strong correlation between traumatic events during early life and the development of behavioral abnormalities later in life, including psychoemotional disorders such as anxiety and depression. Patients with eating disorders frequently exhibit symptoms of depression and/or anxiety, as well as reporting experiences of childhood abuse, a type of early-life trauma. Dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis is implicated in the pathophysiology not only of anxiety and depression, but also of eating disorders. Neonatal maternal separation and isolation rearing in rodents are well-known animal models of stressful experiences in early life. Many studies have demonstrated their impacts both on the activity of the HPA axis and on the development of psychoemotional disorders later in life. This chapter reviews research using animal models of eating disorders associated with stress in early life. Results suggest that neonatal maternal separation leads to the development of binge-related eating disorders when it is challenged with social or metabolic stressors later in life, in which dysfunctions in the HPA axis and the brain monoaminergic systems may play important roles. Also, social isolation in adolescence induces hyperphagia and depression-like behaviors in female rats, but not in males; a tonic increase of plasma corticosterone seems to be implicated in its underlying mechanism.
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Sibutramine, a monoamine serotonin and norepinephrine neuronal reuptake inhibitor, has been established as a safe and efficient drug not only in reduction but also in maintenance of weight loss. Both continuous and intermittent long-term treatment of sibutramine combined with diet and exercise have been demonstrated as equally effective and safe in combating obesity and co-morbidities. In the STORM study, 77% of the patients achieved weight loss and most sustained their weight loss by continuing therapy for two more years. The results of the SCOUT trial will soon be published providing valuable data regarding the impact of sibutramine together with lifestyle intervention on cardiovascular morbidity and mortality in high risk patients. Sibutramine should be considered in the treatment of abdominal obesity since it modifies body fat distribution, reduces visceral adiposity and improves the insulin resistance score. An elevation of serum adiponectin by sibutramine has been associated with these changes. Sibutramine was also shown to be effective in the treatment of adolescent obesity, either alone or combined with behavioral therapy. Based on this multiple range of action, a combination treatment with other drugs targeting obesity, eating disorders and diabetes mellitus type 2 could in concert increase efficacy while increasing tolerability by decreasing the adverse events rate. Meanwhile, variability in response to therapy with sibutramine due to genetic variation has suggested a selection of patients based on candidate genes, which will considerably amplify the response to treatment, Obesity and Metabolism 2009; 5: 145-151.
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Background: The relationship between obesity and attention-deficit-hyperactivity disorder (ADHD) is shown in recent studies. In our study, we have analyzed the relationship between childhood and adulthood (ADHD) and general psychopathological features in morbidly obese individuals who have applied for bariatric surgery. Methods: One hundred seventy-seven morbidly obese patients (body mass index ≥40) who have been referred for bariatric surgery volunteered to participate in the study. The average age of the participants is 36.60 ± 8.46, and 143 of them are female and 34 are male. All volunteers filled the Wender Utah Rating Scale short version (WURS-25), Adult ADHD Self-Report Scale (ASRS-11), and Symptom Check List (SCL-90) tests. Results: The ADHD rate in morbidly obese individuals was 19.20%. Also, we found that in morbidly obese individuals who applied for bariatric surgery, adult and childhood ADHD were highly related to psychopathological (somatization, obsessive compulsive, interpersonal sensitivity, depression, anxiety, anger, hostility, phobic anxiety, paranoid thoughts, psychoticism, and additional symptoms) features. Psychopathological features in a statement that ADHD was evaluated in the morbidly obese individuals are an active factor. Conclusions: As a result of the findings of our study, we suggest paying attention to ADHD symptoms and psychopathological factors of morbidly obese individuals.
Chapter
Prolonged or repeated exposure to stressful events has been associated with clinical depression in humans, and also produces depressive-like behaviors in rodent models. Depression has been proposed to be associated with reduced reward- motivated learning. Anhedonia is a main symptom of depression, and the concept of anhedonia refers to a reduction of the ability to experience pleasure, as reflected in a diminished interest in rewarding stimuli and pleasurable events. Many studies have suggested that anhedonia could influence life function and increase vulnerability to the development of psychic disease. A possible dysfunction in the reward and motivation systems has been lately proposed to explain the link between anhedonia and depression. It has been hypothesized that a dysregulated reward system may be associated with the development and maintenance of eating disorders. Indeed, anhedonia is considered as a feature of anorexia nervosa and the most commonly co- morbid disorder in patients with eating disorders. Dysfunctions of the hypothalamic-pituitary-adrenal (HPA) axis activity are most commonly found in patients with eating disorders. We have previously reported that rats with stress experiences in early life show depression-like behaviors including anhedonia, binge-like eating when challenged with metabolic or social stressors, and the HPA axis dysfunctions. In this chapter, neural basis of anhedonia associated with stress- induced disordered eating behaviors in animal models will be discussed.
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Recent findings suggest that acute stress can improve the execution of delayed intentions (prospective memory, PM). However, it is unclear whether this improvement can be explained by altered executive control processes or by altered associative memory functioning. To investigate this issue, we used physical-psychosocial stressors to induce acute stress in laboratory settings. Then participants completed event- and time-based PM tasks requiring the different contribution of control processes and a control task (letter fluency) frequently used to measure executive functions. According to our results, acute stress had no impact on ongoing task performance, time-based PM, and verbal fluency, whereas it enhanced event-based PM as measured by response speed for the prospective cues. Our findings indicate that, here, acute stress did not affect executive control processes. We suggest that stress affected event-based PM via associative memory processes.
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The aim of the current study is to evaluate the presence of childhood trauma, psychological and somatoform dissociation in obese (OB) and overweight patients with and without binge eating disorder (BED). In total, 34 patients with BED diagnosis were compared with a sex, age and social class matched sample of 34 OB patients without diagnosis of BED and with a control sample consisting of 34 healthy people (NC) with normal weight. Traumatic experiences were assessed by means of the Traumatic Experiences Checklist. Psychoform and somatoform dissociation were assessed respectively by means of the Dissociation Questionnaire and Somatoform Dissociation Questionnaire. BED patients reported significantly more childhood traumatic experiences, psychological and somatoform dissociation, compared to OB patients and NC sample. Moreover, OB patients showed more traumatic experiences compared to the NC sample. BED patients showed higher levels of childhood neglect and emotional abuse compared to the OB patients and NC sample. No significant differences were shown between OB patients and NC subjects with respect to level of psychological and somatoform dissociation. Our results confirm the necessity of evaluating emotional abuse and neglect in adults with BED, and the importance of assessing psychoform and somatoform dissociation in these patients. Tailored treatment strategies based on trauma and dissociation may improve outcomes among patients with BED and a history of childhood trauma. © 2018 The Author(s). This open access article is distributed under a Creative Commons Attribution (CC-BY) 4.0 license.
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Previous research has demonstrated significant associations between increased levels of ovarian hormones and increased rates of binge eating (BE) in women. However, whereas all women experience fluctuations in ovarian hormones across the menstrual cycle, not all women binge eat in response to these fluctuations, suggesting that other factors must contribute. Stress is one potential contributing factor. Specifically, it may be that hormone-BE associations are stronger in women who experience high levels of stress, particularly as stress has been shown to be a precipitant to BE episodes in women. To date, no studies have directly examined stress as a moderator of hormone-BE associations, but indirect data (that is, associations between BE and stress and between ovarian hormones and stress) could provide initial clues about moderating effects. Given the above, the purpose of this narrative review was to evaluate these indirect data and their promise for understanding the role of stress in hormone-BE associations. Studies examining associations between all three phenotypes (that is, ovarian hormones, stress, and BE) in animals and humans were reviewed to provide the most thorough and up-to-date review of the literature on the potential moderating effects of stress on ovarian hormone–BE associations. Overall, current evidence suggests that associations between hormones and BE may be stronger in women with high stress levels, possibly via altered hypothalamic–pituitary–adrenal axis response to stress and increased sensitivity to and altered effects of ovarian hormones during stress. Additional studies are necessary to directly examine stress as a moderator of ovarian hormone–BE associations and identify the mechanisms underlying these effects.
Chapter
Neuroendocrine systems seem to play a central role in both the development and the maintenance of aberrant eating behaviors, including binge eating (BE). BE occurs in several clinical conditions such as the binge-eating/purging subtype of anorexia nervosa, bulimia nervosa, and binge-eating disorder. Because of this transdiagnostic position in the spectrum of eating disorders (EDs), it has been particularly problematic to identify hormonal alterations specifically linked to BE behavior because of the direct or indirect neuroendocrine effects of the different nutritional and psychopathological aspects of the various EDs associated with BE.
Chapter
Medications, at present, play a limited role on eating disorders. Currently, only two drugs were approved by the Food and Drug Administration, fluoxetine and lisdexamfetamine dimesylate, respectively, for bulimia nervosa and binge eating disorder. Meanwhile, eating disorders are a growing public health problem, and the pharmacological management is extremely important, in support of the recommended cognitive behavioral therapy. In this context, animal models are essential to facilitate the study of human conditions and validate potential therapies. In this chapter, we will describe a preclinical model of binge-like eating, triggered by yo-yo dieting and frustration stress on palatable food. It represents a tool to investigate the underlying behavior, physiological mechanisms and the involvement of neural circuitry on binge-like eating behavior with the final aim to develop pharmacological approaches. Corticotropin-releasing factor 1 receptor antagonists, orexin receptor type 1 antagonists, and A2A adenosine receptor agonists will be discussed as promising therapeutic treatments that may have clinical implications.
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The aim of this study was to examine the influence of a 22-wk lifestyle intervention program on the cortisol response in 35 inactive, obese subjects with a body mass index >35. The subjects were randomized into a Test Group and a Control Group. The intervention program consisted of physical activity supplemented with diet and cognitive therapy seminars. Saliva was collected 3 times a day, before and after the intervention program, and 6 months later. The morning awakening and peak cortisol levels (30 min after awakening) were 67% higher in the Test Group (n = 12) than the Control Group (n = 10; P<0.05). Whereas 6 months after the intervention the cortisol awakening levels had decreased by 33% in the Test Group, the peak level was 125% higher compared with the Control Group (P<0.05). The morning cortisol increase was 90% higher 6 months after the intervention compared with the post-intervention samples in the Test Group (P<0.05). The results indicate that the 22-wk lifestyle intervention program altered cortisol levels in the inactive, obese subjects. The increased cortisol reaction may hinder efforts at weight reduction and may explain why losing weight through physical activity is difficult for obese people.
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The effects of exercise and stress on regional and whole body adiposity were examined in an established animal model of diet-induced coronary artery atherosclerosis, the cynomolgus monkey (Macaca fascicularis). A total of 79 adult male monkeys were assigned to four experimental groups after baseline stabilization and training: (i) exercise, stress, (n = 20); (ii) exercise, no stress (n = 20); (iii) sedentary, stress (n = 20); and (iv) sedentary, no stress (n = 19). The monkeys consumed an ad libitum diet containing 188 mg cholesterol per day with 43% of calories as saturated fat. Anthropometric measurements of regional and whole body adiposity were collected throughout the study. A subset (n = 40) of animals representing all four groups underwent computerized tomography (CT) scans at the end of the study to determine amounts of total abdominal, intra-abdominal and subcutaneous abdominal adipose tissue. Results indicate that, in general, stress interacted with exercise to affect anthropometric measurements of regional adiposity. In contrast, stress had independent and significant effects on the amount and distribution of abdominal fat as measured using CT. Stressed monkeys in both the exercise and sedentary groups had more intra-abdominal fat (and thus greater intra-abdominal-:subcutaneous abdominal fat ratios) than their nonstressed counterparts. There were no significant interactions between exercise and stress or exercise effects on abdominal fat distribution as measured by CT. These results support the belief that an arousal syndrome caused by chronic stress, and resulting in increased activity along the hypothalamo-adrenal axis, may play a role in the preferential deposition of fat in the abdomen.(ABSTRACT TRUNCATED AT 250 WORDS)
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Proposed binge eating disorder (BED) diagnostic criteria were investigated to provide necessary psychometric characteristics and explore their utility in assessment. One hundred four subjects (52 self-referred bingers, 52 comparison subjects) completed an initial administration of the Questionnaire of Eating and Weight Patterns (QEWP). The results supported the ability of the two core BED criteria (i.e., episodic overeating, loss of control) to discriminate between clinical and nonclinical binge eaters. Thirty-nine of the self-referred and 40 of the comparison subjects completed a second QEWP administration 3 weeks later. Results indicated that the BED diagnosis was moderately stable over the 3-week interval (kappa =.58, combined sample). Using self-monitoring data completed by the self-referred subjects, predictive efficiency analyses indicated that the QEWP was able to identify both high and low probability binge eaters. Implications of the findings for the definition, assessment, and utility of the BED diagnosis are discussed. © 1994 by John Wiley & Sons, Inc.
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Diagnostic criteria have been developed for a new eating disorder, binge eating disorder (BED), to describe the many individuals who have problems with recurrent binge eating but do not engage in the characteristic compensatory behaviors of bulimia nervosa, vomiting, or use of laxatives. The results of a multisite field trial involving 1,984 subjects indicate that the disorder is common (30.1%) among subjects attending hospital-affiliated weight control programs, but is relatively rare in the community (2.0%). The disorder is more common in females than in males and is associated with severity of obesity and a history of marked weight fluctuations. Based on these results, the DSM-IV Work Group on Eating Disorders has recommended that the disorder be considered for inclusion in DSM-IV, either as an official category or in an appendix of categories requiring further study.
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The present study investigated the association between self-esteem and free cortisol stress responses with regard to experimentally induced success or failure. 52 subjects (29 women and 23 men, mean age 22.9±2.8 years) were exposed to a computer-generated mental stressor consisting of arithmetic tasks to be calculated under time pressure. For one half of the subjects, the computer produced tasks which were easy to solve (success condition), the other half was confronted with a significantly higher level of difficulty ( failure condition). Testing was performed in groups of ten subjects at a time in the same room. After each of three sets of arithmetic tasks, individuals had to report their outcome in front of the group.Results indicate that test difficulty had a profound impact on the performance of the subjects. More important, subjects performance covaried with his/her self-esteem, i.e. persons scoring high in self-esteem achieved better results in the mental arithmetics than their counterparts in the same condition. Moreover, there was a significant negative correlation between the free cortisol response to this stress task and self-esteem in the failure condition (r=−47, p=0.01), however not in the success condition (r=−0.26; p=0.20).These results suggest that self-esteem is affecting the endocrine stress response. Furthermore, they indicate that the impact of this personality characteristic on the human cortisol stress response is also situation dependent. Inclusion of success and failure conditions turned out to be a crucial factor for revealing the role of self-esteem in endocrine stress responses. Future study designs should therefore include those variables, or assess subjective perception of success and failure, when investigating the role of personality differences in stress responses.
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Research in obesity has generally not demonstrated an association with increased rates of psychopathology compared to normal-weight comparison groups. However, studies of obese individuals from clinical samples with recurrent binge eating or binge eating disorder (BED) have generally revealed increased rates of psychiatric comorbidity compared to nonbinge eating obese individuals. Also, several studies have reported finding an association between BED and elevated rates of psychological distress, social problems, and impaired self-esteem. This report provides an overview of research findings regarding psychiatric comorbidity among individuals with BED, and it presents suggestion for future research.
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To date, there are few known predictors of stress-induced eating. The purpose of this study was to identify whether physiological and psychological variables are related to eating after stress. Specifically, we hypothesized that high cortisol reactivity in response to stress may lead to eating after stress, given the relations between cortisol with both psychological stress and mechanisms affecting hunger. To test this, we exposed fifty-nine healthy pre-menopausal women to both a stress session and a control session on different days. High cortisol reactors consumed more calories on the stress day compared to low reactors, but ate similar amounts on the control day. In terms of taste preferences, high reactors ate significantly more sweet food across days. Increases in negative mood in response to the stressors were also significantly related to greater food consumption. These results suggest that psychophysiological response to stress may influence subsequent eating behavior. Over time, these alterations could impact both weight and health.
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Urinary cortisol output and serum cortisol concentrations were measured in the steady state, under "field" conditions, and during standardized inhibitory and stimulatory tests in premenopausal, obese women, and were analyzed in relation to adipose tissue distribution. Urinary cortisol output was increased under field conditions in women with an elevated waist to hip circumference ratio (WHR) and, in particular, in women with a large abdominal sagittal diameter, indicating visceral fat accumulation. However, dexamethasone inhibition of cortisol secretion was normal. Stimulation with corticotropin analogue and with physical (cold-pressor test) or mental (color-word or mathematic) stress tests also showed elevated responses of serum cortisol, but not of prolactin or growth hormone concentrations. It is suggested that women with visceral fat accumulation have elevated cortisol secretion due to an increased sensitivity along the hypothalamic-pituitary-adrenal axis, and that this may be causing their abnormal fat depot distribution.
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The present study explored a potential mechanism for the relationship between stressors and binge eating: specifically, whether subjects with behaviors and attitudes reflecting disordered eating show distinctive psychologic or physiologic reactivity to stressors. Female undergraduates participated in a laboratory study involving four psychologically stressful tasks. Blood pressure and pulse rate were monitored, and several psychologic questionnaires were administered. Analyses revealed that the tasks provoked significant cardiovascular and affective responses in both high- and low-disordered eaters. There were no differences between groups in cardiovascular responsivity or mood state in response to diverse stressors. However, those with more disordered eating reported an increased desire to binge in response to the stressors, along with more global stress, lower self-esteem, and lower mastery than the comparison group. The results suggest that the increased desire to binge in response to stressors reported by subjects higher in disordered eating cannot be accounted for by differences in cardiovascular reactivity or negative hedonic state, relative to what subjects low in disordered eating showed in response to the same stressors.
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The present study investigated daily mood fluctuations and moods during eating in normal and overweight binge and nonbinge eaters (N = 56) and moods during binge and nonbinge episodes of individuals who binge eat (N = 29). For 2 weeks, subjects completed the Multiple Affect Adjective Checklist each morning and continuously recorded the mood during eating and the type and quantity of food eaten during each eating episode. The results indicated that bingers experience greater fluctuations of anxiety and depression than nonbingers and overweight individuals experience greater fluctuations in anxiety, hostility, and depression than normal-weight individuals. In addition, for bingers, negative mood states are experienced during a significantly greater proportion of binge episodes than nonbinge episodes, although the intensity of the negative mood state was not related to the severity of the binge-eating episode. Theoretical and clinical implications of these findings are discussed.
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The gastrointestinal motor function in patients with anorexia nervosa is poorly understood, although it may be relevant to the pathophysiology of the disorder. We have undertaken a multidisciplinary study of 8 patients with anorexia nervosa and 8 age- and sex-matched controls. We have characterized their gastrointestinal and neurohormonal function by measuring (a) gastric electrical activity, (b) antral phasic pressure activity, (c) gastric emptying of solids and liquids, and (d) hormonal and autonomic function. Patients with anorexia nervosa at the time of the initiation of therapy presented with (a) increased episodes of gastric dysrhythmia (mean percentage of dysrhythmic time: 9.75 patients vs. 0.48 controls during fasting, p less than 0.02; 7.21 patients vs. 0.18 controls postcibally, p less than 0.001), (b) impaired antral contractility (mean motility index, 12.8 patients vs. 14.2 controls, p less than 0.002), (c) delayed emptying of solids, (d) decreased postcibal blood levels of norepinephrine and neurotensin (levels of beta-endorphin, insulin, glucagon, gastric inhibitory polypeptide, gastrin, cholecystokinin, and human pancreatic polypeptide were normal), and (e) impaired autonomic function (resting diastolic blood pressure and skin conductance were decreased and the response to the cold pressor test was dampened). Differences between patient and control groups were statistically significant. We conclude that patients with anorexia nervosa present multiple gastrointestinal abnormalities involving control mechanisms as well as target organs.
Article
Proposed binge eating disorder (BED) diagnostic criteria were investigated to provide necessary psychometric characteristics and explore their utility in assessment. One hundred four subjects (52 self-referred bingers, 52 comparison subjects) completed an initial administration of the Questionnaire of Eating and Weight Patterns (QEWP). The results supported the ability of the two core BED criteria (i.e., episodic overeating, loss of control) to discriminate between clinical and nonclinical binge eaters. Thirty-nine of the self-referred and 40 of the comparison subjects completed a second QEWP administration 3 weeks later. Results indicated that the BED diagnosis was moderately stable over the 3-week interval (kappa = .58, combined sample). Using self-monitoring data completed by the self-referred subjects, predictive efficiency analyses indicated that the QEWP was able to identify both high and low probability binge eaters. Implications of the findings for the definition, assessment, and utility of the BED diagnosis are discussed.
Article
Binge eating disorder (BED) is a new eating disorder that describes the eating disturbance of a large number of individuals who suffer from recurrent binge eating but who do not regularly engage in the compensatory behaviors to avoid weight gain seen in bulimia nervosa. This multisite study of BED involved 1,785 subjects drawn from 18 weight control programs, 942 subjects from five nonpatient community samples, and 75 patients with bulimia nervosa. Approximately 29% of subjects in weight control programs met the criteria for BED. In the nonpatient community samples BED was more common than purging bulimia nervosa. The validity of BED was supported by its strong association with (1) impairment in work and social functioning, (2) overconcern with body/shape and weight, (3) general psychopathology, (4) significant amount of time in adult life on diets, (5) a history of depression, alcohol/drug abuse, and treatment for emotional problems.
Article
In this study, dexamethasone (dex) was administered in random order in doses of 0.05, 0.125, 0.25 and 0.5 mg at 10 p.m. with measurements of serum Cortisol in the morning (8 a.m.) of this and the following day. The test was performed on 22 apparently healthy men, 40 to 60 years of age, recruited from laboratory personnel, outpatient clinics or advertisements in a newspaper. Eight had a body mass index (BMI) (kg/m2) of <25 and 14 of >25. Twelve men had a waist hip ratio (WHR) of <1.0 and 10 men had a WHR of<1.0. Cortisol values at baseline were correlated inversely with WHR and were usually lower in men with a high (>1.0) rather than a low than low (<1.0) WHR after dex inhibition. There was apparently no inhibition by dex at 0.05 and 0.125 mg on average in men with a WHR of >1.0. In addition, the inhibition at 0.5 mg dex correlated negatively with the WHR and was significantly lower (p<0.05) in men with a WHR of >1.0 than in men with a WHR of <1.0. None of these differences or relationships was found to be dependent on BMI. It is concluded that men with an elevated WHR experience a decrease in the inhibition of Cortisol secretion by dex. It is suggested that this could explain or contribute to the elevated sensitivity of their HPA axis. Furthermore, lower morning Cortisol concentrations suggest a change in diurnal secretion patterns.
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The effect of glucocorticoid administration on energy metabolism and food intake was studied in 20 healthy, nondiabetic Caucasian male volunteers [27 +/- 5 (SD) yr, 72 +/- 9 kg, 20 +/- 7% body fat] randomly and blindly assigned to glucocorticoid (methylprednisolone, METH; n = 10) or placebo (PLAC; n = 10) treatment. Each subject was studied twice: during a weight maintenance diet and during ad libitum food intake. Energy metabolism was measured by indirect calorimetry and food intake by an automated food-selection system. Twenty-four-hour urinary norepinephrine excretion (24-h NE) was used as an estimate of sympathetic nervous system activity. During weight maintenance, METH intravenous infusion (125 mg/30 min) increased energy expenditure compared with PLAC, and after 4 days of oral therapy, METH (40 mg/day) decreased 24-h NE and increased energy expenditure compared with PLAC. During ad libitum food intake, after 4 days of METH (40 mg/day) or PLAC oral therapy, both groups increased their energy intake over weight maintenance, but the increase was significantly larger in the METH group compared with the PLAC group (4,554 +/- 1,857 vs. 2,867 +/- 846 kcal/day; P = 0.04). Our data suggest that therapeutic doses of glucocorticoids induce obesity mostly by increasing energy intake, an effect which may be related to the ability of glucocorticoids to act directly or indirectly on the central regulation of appetite.
Article
The purpose of this experimental investigation was to test the hypothesis that negative affective states trigger disinhibited eating in the form of binge eating in subjects with binge eating disorder (BED). BED subjects and weight-matched non-eating disordered subjects (NED) attended a laboratory experiment during which they were randomly assigned to a negative or neutral mood induction procedure prior to being served a multi-item buffet. The dependent variable of interest was postmood induction caloric intake. There were no significant differences in caloric intake between subjects in the negative and neutral mood conditions. However, negative affect was associated with eating episodes labeled binges, and associated with loss of control. Our findings suggest that mood may be an important factor that discriminates overeating and binge eating.
Article
This study examined the effects of an interpersonal stressor on subsequent calorie intake in females with (N = 20) and without (N = 20) significant bulimic symptomatology. Subjects participated in two laboratory sessions that differed according to experimental condition (stress versus no stress), completed self-report measures of mood and anxiety before and after the experimental task, and were provided with an array of snack foods after each session. Counter to the hypothesis, women with bulimic symptoms did not differentially increase their intake when exposed to stress. However, results for the intake of each macronutrient indicated that both bulimic and control women increased their consumption of carbohydrates following the stressor. Thus, stress was related to increased carbohydrate consumption by all subjects but did not differentially affect the consumption of women with bulimic symptoms. It may be that women with bulimic symptoms are not differentially vulnerable to eating in response to stress or that current laboratory paradigms are unable to detect differences in eating following a stressor.
Article
Cardiovascular and catecholamine responses to mental stressors were investigated in women with bulimia nervosa (BN) and in healthy control subjects. Fifteen women with BN and 15 control subjects completed psychosocial questionnaires before laboratory testing, where they were exposed to an interpersonally based speech stressor and a serial math task. Blood pressure, heart rate, epinephrine, norepinephrine and, via impedance cardiography, systolic time intervals, cardiac output and total peripheral resistance were measured at rest and during stress. Results indicated that BN was associated with blunted sympathetic activation in response to mental stress, indicated by increased pre-ejection period responses and blunted systolic blood pressure, heart rate and epinephrine responses. In contrast, women with BN had elevated cortisol levels when compared with control women. In addition, despite equivalent performance between groups, bulimic women reported feeling significantly more confused, frustrated, inadequate and dissatisfied with their performance during tasks. Psychosocial questionnaires also indicated that women with BN perceived more stress, had worse coping skills, lower self-esteem and sense of mastery, reported less social support, had worse mood, had greater anxiety and were more depressed when compared with control women. These results are interpreted as reflecting physiological and psychological profiles indicative of distress vs. active effort coping in BN.
Article
Immune changes may occur in patients with anorexia nervosa (AN) or bulimia nervosa (BN), and a role for proinflammatory cytokines has been proposed in the pathogenesis of both disorders. We measured plasma levels of interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha (TNF-alpha), soluble forms of the cytokine receptor proteins gp130 and leukemia inhibitory factor receptor (LIF-R), the anti-inflammatory Clara cell 16-kD protein (CC16), prolactin (PRL), cortisol and 17beta-estradiol in 21 anorexic women, 21 bulimic women and 21 healthy females. As compared to healthy subjects, anorexics exhibited significantly increased plasma levels of gp130 and LIF-R, whereas bulimics had significantly decreased blood concentrations of CC16. No significant differences emerged in the blood levels of the remaining immune parameters. Both patient groups manifested higher plasma levels of cortisol and reduced plasma concentrations of PRL and 17beta-estradiol. In anorexics, a significant negative correlation was found between plasma levels of gp130 or LIF-R and the body mass index. These findings do not support the hypothesis that proinflammatory cytokines may play a pathogenetic role in eating disorders.
Article
Cardiovascular, neuroendocrine, and psychosocial profiles were investigated in women with eating disorder tendencies, but who had never met clinical criteria for an eating disorder, and in healthy controls. Twenty-six women who scored in the highest distribution of the Eating Disorder Inventory bulimia subscale (HEDI women) and 27 women who scored in the lowest distribution (LEDI women) completed psychosocial questionnaires, underwent a speech reactivity task for measures of blood pressure and heart rate reactivity, and also underwent 24-hour ambulatory blood pressure monitoring and urinary neuroendocrine collection. The HEDI women exhibited increased blood pressure and heart rate reactivity to the speech task and increased 24-hour urinary cortisol, but decreased 24-hour urinary norepinephrine compared with LEDI women. There were no overall group differences in 24-hour ambulatory blood pressure levels, but negative mood and tension were associated with greater systolic blood pressures for all women. Finally, HEDI women reported greater depressive symptoms and anxiety, lower self-esteem and sense of mastery, less social support, poor coping skills, and greater emotional impact of daily stressors relative to LEDI women. These results indicate that the same pattern of neuroendocrine and psychosocial profiles seen in prior studies of bulimia nervosa are also present in women with eating disorder tendencies.
Article
Central obesity is the subfraction which carries most of the risks for comorbidities. In this overview we suggest that this is due to neuroendocrine perturbations, where the hypothalamic-pituitary-adrenal (HPA) axis assumes a central role. The HPA axis is stimulated by central factors, which are often called stress. This is followed by discrete, periodical elevations of cortisol secretion during every day conditions. Such observations require diurnal measurements under undisturbed conditions. Saliva cortisol is useful for such purposes. It seems likely, based on cross-sectional observations in men and longitudinal studies in animals that a prolonged period of HPA axis stimulation is followed by a continuous degradation of the regulatory mechanisms. An end stage is a rigid cortisol secretion with low morning values. In parallel with this is a diminished function of the feed-back control as well as an inhibition of growth and sex steroid hormones. Evidence also suggests that the sympathetic nervous centers become activated in parallel. The net effects of this cascade of neuroendocrine-endocrine pertubations will be insulin resistance as well as visceral accumulation of body fat. These are effects of cortisol in combination with the diminished secretion of growth and sex steroid secretions, which in normal concentrations antagonize the cortisol effects. Blood pressure will also be elevated, which might be a consequence of central stimulation of the sympathetic nervous system, with added effects of insulin. What has developed is a hypothalamic arousal with the Metabolic Syndrome as a consequence. The feed-back regulation of the HPA axis has a key position in this chain of events. This control is mediated via glucocorticoid receptors in the lower parts of the brain. The gene for this receptor has shown polymorphisms which are associated with poorly regulated cortisol secretion, central obesity, insulin resistance and hypertension.
Article
Excessive central fat puts one at greater risk of disease. In animal studies, stress-induced cortisol secretion has been shown to increase central fat. The objective of this study was to assess whether women with central fat distribution (as indicated by a high waist-to-hip ratio [WHR]), across a range of body mass indexes, display consistently heightened cortisol reactivity to repeated laboratory stressors. Fifty-nine healthy premenopausal women, 30 with a high WHR and 29 with a low WHR, were exposed to consecutive laboratory sessions over 4 days (three stress sessions and one rest session). During these sessions, cortisol and psychological responses were assessed. Women with a high WHR evaluated the laboratory challenges as more threatening, performed more poorly on them, and reported more chronic stress. These women secreted significantly more cortisol during the first stress session than women with a low WHR. Furthermore, lean women with a high WHR lacked habituation to stress in that they continued to secrete significantly more cortisol in response to now familiar challenges (days 2 and 3) than lean women with a low WHR. Central fat distribution is related to greater psychological vulnerability to stress and cortisol reactivity. This may be especially true among lean women, who did not habituate to repeated stress. The current cross-sectional findings support the hypothesis that stress-induced cortisol secretion may contribute to central fat and demonstrate a link between psychological stress and risk for disease.
Article
An abnormal regulation of the hypothalamic-pituitary-adrenal (HPA) axis is associated with risk factors for cardiovascular disease and Type 2 diabetes mellitus. The objective of this study was to examine if morning saliva cortisols show similar associations. Twenty-eight men, all 53 yr of age, delivered during an ordinary working day saliva cortisol samples immediately upon awakening and 15 min thereafter as well as at different times during the day, including after a standardized lunch. Dexamethasone (0.5 mg) suppression of cortisol was also measured. The rise of morning cortisol values was positively associated with body mass index (r: 0.45, p=0.016), waist/hip ratio (r: 0.54, p=0.003), abdominal sagittal diameter (r: 0.54, p=0.003), glucose (r: 0.54, p=0.003), insulin (r: 0.57, p=0.002) and triglycerides (r: 0.46, p=0.014). The morning rise also correlated positively with the elevation of cortisol following lunch (r: 0.45, p=0.043) but not with other cortisol measurements or dexamethasone suppression. Elevation of cortisol immediately after awakening has previously been found to provide a simple indicator of HPA axis regulation, as suggested also by the results of this study, and an elevated rise has been reported after exposure to frequent or chronic perceived stress. The rise of cortisol immediately after awakening might be an indicator of an increased risk of developing serious, prevalent diseases via the metabolic syndrome.
Article
Increased basal cortisol levels have been found in bulimia nervosa. After stress, increased cortisol levels have been associated with increased food intake in healthy women. Therefore, we assessed cortisol, hunger, and desire to binge eat after a cold pressor test (CPT) among women with binge eating disorder (BED). Twenty-two obese (body mass index [BMI] = 36.7 +/- 6.5 SD) females (11 non-BED, 11 BED) completed the Zung depression scale and underwent the CPT, hand submerged in ice water for 2 minutes. Over 60 minutes, periodic ratings of hunger and desire to binge eat were obtained, just before blood draws for cortisol, as well as insulin. On a separate day, participants had a 1-mg oral dexamethasone suppression test (DST). The BED group had higher depression scores than the non-BED (p = .04), but depression was not a significant covariate for the cortisol response or to DST. After controlling for contraceptive use (n = 3), the BED group had higher basal cortisol than the non-BED group (p = .03), but cortisol did not differ after DST (p = .40). The BED group had nearly significant greater cortisol AUC after the CPT (p = .057) after controlling for insulin AUC and contraceptive use (p = .057). The BED group also had greater AUC for hunger (p = .03) and desire to binge eat (p = .02) after the CPT. These findings support our hypothesis of a hyperactive HPA-axis in BED, which may contribute to greater hunger and binge eating.
NJ, for providing the ProCal formula Comorbidity and binge eating disorder
  • We
  • Eric Also
  • Sakeena Yahav
  • Dawn Haq
  • Hui
  • R-Kane Their Assistance
We also thank Eric Yahav, Sakeena Haq, and Dawn Hui for their assistance and R-Kane Products, Pennsauken, NJ, for providing the ProCal formula. REFERENCES 1. MITCHELL, J.E. & M.P. MUSSELL. 1995. Comorbidity and binge eating disorder. Addict. Behav. 20: 725–732.