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Cortisol, Hunger, and Desire to Binge Eat Following a Cold Stress Test in Obese Women With Binge Eating Disorder
Abstract
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.
... However, subsequent studies showed that craving is heavily influenced by social and psychological triggers, implying that it is also psychological in nature (Rankin et al., 1979). Stress and NA are important triggers, as studies find that inducing stress or NA in a laboratory context can increase craving for alcohol or a BE episode, especially when the stressor includes negative self-evaluation Gluck et al., 2004;Rosenberg et al., 2013). Additionally, experiencing more craving in response to NA also predicts relapse in patients with AUD Higley et al., 2011). ...
... When it comes to food, craving is typically directed at particular kinds of food and can only be satisfied by the consumption of these items (Meule, 2020). Furthermore, patients can experience a distinct craving for a BE episode and plan these episodes well in advance (Ferriday & Brunstrom, 2011;Gluck et al., 2004;Manasse et al., 2019). Second, negative urgency is often described as a tendency to act rashly when NA is high (Sharma et al., 2014). ...
... Indeed, after inducing NA in a laboratory, studies find that NA is positively related to craving for a BE episode in individuals who binge eat, but not in healthy controls (HC) (Gluck et al., 2004). Also, studies using ESM report that average craving levels in daily life are associated with BE symptoms . ...
Alcohol use disorder (AUD) and bulimia nervosa (BN) are two psychiatric disorders that are characterized by binge behavior where large quantities of alcohol (i.e., binge drinking [BD]) or food (i.e., binge eating [BE]) are consumed within a short period of time. Furthermore, both disorders are highly prevalent, impactful, and challenging to treat. Therefore, new and improved treatments are needed for both disorders, but in order to develop them, a better understanding of what triggers binge behavior is required.
It is thought that stress and negative affect (NA) are important triggers for BD and BE. Indeed, studies in a laboratory context have shown that inducing stress and NA can lead to increased alcohol and food consumption in patients with AUD or an eating disorder respectively. Furthermore, studies conducted in daily life report that NA increases in the hours before a BE episode and that NA is higher before a BE episode than before a regular meal. However, these findings raise the question how stress and NA cause patients to experience a higher desire to binge drink or bing eat, as well as lose control, making them more likely to display binge behavior. Previous authors have hypothesized that there are several important factors such as craving, negative urgency (i.e., the tendency to act rashly under elevated stress or NA), and disturbances in reward processing including delay discounting (i.e., preferring more immediate rewards). Therefore, this thesis explores the role of these factors in how stress and NA lead to binge behavior.
First, an experience sampling method (ESM) study was performed where 76 controls, 53 patients with AUD, 51 patients with BN, and 19 patients with AUD and BN reported on their mood, behavior, and context in daily life. When it comes to BE, we found that NA was related to subsequent BE in patients with BN through rash action and craving, highlighting the importance of negative urgency and craving in the relation between NA and BE. Contrastingly, we also observed that NA was associated with subsequent not eating, indicating that NA can have competing effects on eating behaviors in patients with BN. When it comes to alcohol use, we saw that NA was non-linearly related to craving, alcohol use, and BD in patients with AUD, emphasizing that both lower and higher levels of NA can lead to alcohol consumption in patients. However, these findings raise the question whether factors such as NA, rash action, and craving can actually predict binge behavior in daily life. Therefore, we used machine learning to build person-specific and pooled prediction models for BE, alcohol use, and BD in patients with AUD and/or BN. We found that pooled models performed better at predicting BE, alcohol use, and BD, but that predictors from person-specific models might be more useful clinically. Importantly, craving and time of day were the most important predictors for all behaviors, while there were differences in how affect and social context were related to BE, alcohol use, and BD.
Second, the role of the neurobiological reward system in BE was explored by conducting a systematic review of previously published studies. We found that individuals who binge eat display a lower striatal dopamine release in rest, a change in the volume of the striatum, frontal cortex and insula as well as a lower fronto-striatal connectivity. Furthermore, there was a higher activity of the brain reward system when anticipating or receiving food, and individuals who binge eat relied more on previous experiences when making decisions and displayed more habitual behavior. These results show that individuals who binge eat display structural and functional changes in the neurobiological reward system, which could play a vital role in the onset and maintenance of BE episodes.
Third, an MRI study was performed with 50 controls, 27 patients with AUD, and 25 patients with BN. In this study, the effect of stress on alcohol and food delay discounting was investigated to see whether stress makes patients with AUD or BN prefer more immediately available alcohol or food respectively. We found that stress increased delay discounting of alcohol in patients with AUD, but not in controls, and that this was related to a lower activity of the right supplementary area. In contrast, we observed that stress increased delay discounting of food in controls, but not in patients with BN, and that this was related to a lower activity of the anterior cingulate cortex. These results suggest that acute stress could indeed make patients with AUD prefer more immediately available alcohol, while this relation might not be as straightforward in patients with BN.
Fourth, a PET/MR study was conducted in 12 controls investigating the relation between stress-induced dopamine release in the ventromedial prefrontal cortex (vmPFC), fronto-striatal functional connectivity and negative urgency in daily life. Here, stress decreased functional connectivity between the vmPFC and dorsal striatum, but increased connectivity with the contralateral ventral stiatum. However, individuals with a higher connectivity between the vmPFC and dorsal striatum showed more negative urgency in daily life. Furthermore, individuals with a higher stress-induced DA release had a higher change in fronto-striatal connectivity and displayed more daily life negative urgency. These results highlight how stress can impact dopamine signaling and fronto-striatal connectivity and how this can lead to rash action.
Taken together, this thesis shows that there is a complex relation between stress and NA on the one hand and binge behavior on the other hand. Specifically, the results indicate that stress and NA might have competing effects on eating behaviors in patients with BN, while both lower and higher levels of stress and NA might be related to alcohol use in patients with AUD. Furthermore, the findings of this thesis highlight the importance of craving, negative urgency, reward processing, and delay discounting in this relation, and demonstrate the key role of dopamine transmission and fronto-striatal connectivity. Future studies should explore how stress and NA lead to binge behavior in more depth with more diverse samples, longitudinal designs, and by combining multiple modalities.
... Low cortisol levels are associated with PTSD, but higher cortisol levels are associated with the co-occurrence of PTSD and major depressive disorder (MDD) [14]. Some researchers have reported reduced cortisol levels in abused women with bulimia nervosa [15], but other studies report higher cortisol levels in bulimia nervosa [16]. ...
... The cortisol levels in our sample ( Figure 1) were significantly higher than in typical adult normative values (i.e., adults without PTSD or bulimia). This is consistent with several existing research studies, which also found high cortisol levels in women with bulimia nervosa [16,27]. Malnutrition is also reported to impair stress response [28], and stressful events increase cortisol levels and lead to urges to binge [16]. ...
... This is consistent with several existing research studies, which also found high cortisol levels in women with bulimia nervosa [16,27]. Malnutrition is also reported to impair stress response [28], and stressful events increase cortisol levels and lead to urges to binge [16]. However, some researchers have reported low cortisol levels in abused women with bulimia nervosa [29][30]. ...
Objectives
Post-traumatic stress disorder (PTSD) symptoms are reported in over 36% of individuals with bulimia nervosa. To date, none of the clinical trials have examined nightmare reduction in this population. We evaluated the effectiveness of prazosin in bulimic females experiencing PTSD-related nightmares. We hypothesized that prazosin will decrease nightmares, normalize cortisol levels and secretory patterns, and improve sleep.
Methods
Our seven-week prospective, randomized, double-blind, placebo-controlled crossover pilot trial recruited eight adult women. Each participant received three weeks of prazosin and a placebo, separated by a one-week washout period. The order of treatment was counterbalanced across participants. Self-reports, clinician-administered scales, and salivary cortisol was collected to measure outcomes.
Results
A significant treatment effect was seen in nightmare intensity on the Clinician-Administered PTSD Scale (CAPS-I) (p=0.026) and a marginally significant effect on nightmare frequency (p=0.069). The only significant main effect of treatment on self-reported sleep parameters was on nightmares. Cortisol secretory patterns did not change, but on average, study participants had significantly higher cortisol levels compared to normative values. ANOVA showed a significant main effect of time for cortisol (F(4, 28) = 6.15, p=.001) but no within or between groups significant effects (ps>.179). Follow-up tests showed the effect of time was linear (F(1, 7) = 10.77, p=.013).
Conclusion
Prazosin significantly reduced intensity and marginally reduced the frequency of PTSD-related nightmares in bulimia nervosa but did not affect subjective sleep efficiency, quality, cortisol levels, or diurnal cortisol secretory pattern. Larger trials using objective sleep measures are warranted to replicate these findings.
... Individuals who experience heightened levels of DE (i.e., BED, emotional eating, etc.) appear more sensitive to the effects of stress, including greater levels of perceived life stress [8,[19][20][21], poorer ability to cope with stressors [22][23][24], and greater negative affect (i.e., depressed mood) when stressed [9,25]. Furthermore, relative to healthy controls, people who experience DE are more likely to engage in unrestrained food-consumption following exposure to both acute laboratory and real-life stressors [26][27][28][29][30][31][32][33]. DE episodes in themselves can also be significantly distressing [34], and in turn may perpetuate future episodes of DE if not adequately managed. ...
... To date, most research attempting to identify such mechanisms has largely focused on the role of HPA-axis, namely investigating cortisol reactivity. Indeed, several studies [26,27] have demonstrated that young people and adults who experience binge-eating demonstrate heightened basal cortisol relative to controls, which is consistent with chronic HPA-axis activation [42]. Furthermore, behavioural studies by Rouach et al. [43] and Van Strien et al. [44] identified acute laboratory stress is associated with blunted post-stress cortisol reactivity and greater ad libitum food consumption in individuals with BED and emotional eating, respectively, potentially indicating downregulation of the HPA-axis due to chronic activation [45]. ...
... Furthermore, behavioural studies by Rouach et al. [43] and Van Strien et al. [44] identified acute laboratory stress is associated with blunted post-stress cortisol reactivity and greater ad libitum food consumption in individuals with BED and emotional eating, respectively, potentially indicating downregulation of the HPA-axis due to chronic activation [45]. However, these results have not been consistently observed, with other studies identifying a non-significant, but trending increases in cortisol following acute stress induction in those with DE relative to controls [26,46]. Furthermore, several studies have failed to identify any significant differences between basal and acute post-stress cortisol levels between obese women with BED and weight-matched controls, however significant changes in post-stress ad libitum food consumption were observed in those with BED [47,48]. ...
Disinhibited eating involves overconsumption and loss of control over food intake, and underpins many health conditions, including obesity and binge-eating related disorders. Stress has been implicated in the development and maintenance of disinhibited eating behaviours, but the mechanisms underlying this relationship are unclear. In this systematic review, we examined how the impact of stress on the neurobiological substrates of food-related reward sensitivity, interoception and cognitive control explains its role in disinhibited eating behaviours. We synthesised the findings of functional magnetic resonance imaging studies including acute and/or chronic stress exposures in participants with disinhibited eating. A systematic search of existing literature conducted in alignment with the PRISMA guidelines identified seven studies investigating neural impacts of stress in people with disinhibited eating. Five studies used food-cue reactivity tasks, one study used a social evaluation task, and one used an instrumental learning task to probe reward, interoception and control circuitry. Acute stress was associated with deactivation of regions in the prefrontal cortex implicated in cognitive control and the hippocampus. However, there were mixed findings regarding differences in reward-related circuitry. In the study using a social task, acute stress associated with deactivation of prefrontal cognitive control regions in response to negative social evaluation. In contrast, chronic stress was associated with both deactivation of reward and prefrontal regions when viewing palatable food-cues. Given the small number of identified publications and notable heterogeneity in study designs, we propose several recommendations to strengthen future research in this emerging field.
... Individuals experiencing high levels of social stress may seek comfort food, leading to binge eating in an attempt to exert control over their environment (Dallman et al., 2005;Klatzkin et al., 2024;Montigny et al., 2013). Adverse environmental insults alter brain function and hormone levels, exacerbating disordered eating (Fowler et al., 2019;Gluck et al., 2004;Goldfield et al., 2008;Vega-Torres et al., 2022. Investigations in rodents, particularly rats, have revealed the impact of social isolation stress on behavior and neuronal health during adolescence (Gądek-Michalska et al., 2017;Weiss et al., 2004;Yorgason et al., 2016). ...
... Our analyses aimed to explore and validate this concept within our study context. Fluctuations in cortisol levels have been observed in women with stress disorders (Meewisse et al., 2007) and influence binge eating (Gluck et al., 2004). Blunted plasma corticosterone has also been observed in binge-like eating-prone female rats (Calvez and Timofeeva, 2016). ...
Binge eating (BE) is a highly pervasive maladaptive coping strategy in response to severe early life stress such as emotional and social neglect. BE is described as repeated episodes of uncontrolled eating and is tightly linked with comorbid mental health concerns. Despite social stressors occurring at a young age, the onset of BE typically does not occur until adulthood providing an interval for potential therapeutic intervention. Currently, our knowledge of longitudinal noninvasive digital biomarkers predictive of BE needs further development. Monitoring longitudinal impacts of adolescent social isolation stress on naturalistic behaviors in rats will enable the identification of noninvasive digital markers of disease progression to predict adult eating strategies. Recognizing adolescent naturalistic behaviors shaped by social stress informs our understanding of the underlying neurocircuits most effected. This study aimed to monitor and identify longitudinal behavioral shifts to enhance predictive capabilities in a rat model of social isolation stress-induced BE. We placed Paired (n = 12) and Socially Isolated (SI, n = 12) female rats in observational home cages weekly for seven weeks to evaluate the effect of SI on 10 naturalistic behaviors. All 10 naturalistic behaviors were simultaneously detected and tracked using Noldus Ethovision XT automated recognition software. Composite phenotypic z-scores were calculated by standardizing all 10 behaviors. When transitioning into adulthood, all rats underwent conventional emotionality testing and were exposed to a Western-like high fat diet (WD, 43% kcal from fat) to evaluate BE. Longitudinal assessments revealed SI-induced shifts in adolescent phenotypic z-scores and that sniffing, unsupported rearing, jumping, and twitching were the most susceptible to SI. SI increased emotionality compared to the Paired controls. Finally, we identified adolescent twitching as a digital biomarker of adult WD consumption. Our findings suggest that home cage monitoring can detect disrupted naturalistic behaviors associated with maladaptive coping.
... When it comes to food, craving is 39 typically directed at particular kinds of food and can only be satisfied by the consumption of these 40 items (Meule, 2020). Furthermore, patients can experience a distinct craving for a BE episode and 41 plan these episodes well in advance (Ferriday & Brunstrom, 2011;Gluck et al., 2004;Manasse et al., 42 2019). Second, negative urgency is often described as a tendency to act rashly when NA is high 43 (Sharma et al., 2014). ...
... The definition of the current study 425 has several implications as the HC group does not engage in BE. Namely, it is a reason why we have 426 hypothesized that the HC do not display a relation between NA and craving (Gluck et al., 2004). 427 ...
Studies suggest that negative affect (NA) can trigger binge eating (BE) in patients with bulimia nervosa (BN). Important factors in this relation between NA and BE could be craving (an intense desire for a BE episode) and negative urgency (the tendency to act rashly when NA is high). Therefore, this study wants to firstly explore the relations between NA, craving, rash action, and BE in daily life and secondly whether craving and rash action mediate the relationship between NA and BE. A sample of 70 female patients with BN and 76 female healthy controls (HC) took part in an experience sampling study where they reported on momentary NA, craving, rash action, and eating behaviors in daily life in a burst-measurement design over a period of 12 months. Assessments occurred eight times a day on Thursdays, Fridays, and Saturdays in seven bursts of 3 weeks, all separated by 5-week periods of no assessment. First, NA predicted subsequent rash action in the whole sample but this was more pronounced in patients with BN. Second, NA predicted subsequent craving in patients with BN, but not in HC. Third, rash action and craving predicted subsequent BE in patients with BN. Fourth, NA had competing effects on eating in patients with BN, predicting subsequent BE through rash action and craving, but also predicting subsequent not eating. These results suggest that NA can lead to BE in daily life through rash action and craving, but that NA can also lead to dietary restriction.
... Stressful events have been associated with both increased and decreased food intake [4,5], and the biological mechanism involves interactions between glucocorticoids, appetite-related hormones (e.g., ghrelin, leptin, insulin), and the brain's dopaminergic reward system [6]. Thereby, coping strategies to manage stress can lead to, on the one hand, increased food intake with a lot of sugary/fatty food or, on the other hand, avoidance of food in the context of a 'fight-or-flight reaction' [5]. ...
... Laboratory studies of the link between stress reactivity in obese individuals have yielded mixed results. Observations include heightened [4], blunted [6], or no differences [8,9] in HPA axis stress responses in obese groups compared with normal-weight individuals. These divergent results might be explained by methodological differences, especially the nature of the stressor and the lack of a control group. ...
(1) Background: In the present pilot study, we examined the response of cortisol to a digital version of the Trier Social Stress Test (TSST) and corresponding eating preferences in non-overweight and overweight adolescents. (2) Methods: The experimental study group included 35 adolescents aged 15.7 ± 0.5 years (16 boys and 19 girls). The participants were split into two groups: non-overweight (N = 24) and overweight (N = 11), according to the Body Mass Index (BMI). We induced acute stress in all participants, using a digital version of the Trier Social Stress Test (TSST), with three different digital tasks. We measured salivary cortisol before the test (T0), during the stress induction by digital tasks (T5, T10, T15), and 25 min after the stress test (T40). The Health Behavior in School-Aged Children Questionnaire (HBSC) was administered to assess the influence of stress on eating behavior: the consumption of fruit, vegetables, sweets, and soft drinks and the frequency of snacks. (3) Results: Among the entire group of adolescents, we observed a significant difference between the sexes in terms of cortisol response, girls being predominantly hyperreactive (13 girls compared to 5 boys, p = 0.03). In overweight adolescents, the cortisol reactivity was lower in boys and higher in girls (p = 0.05). The overweight hyperreactive adolescents, as compared to the hyporeactive ones, had a higher frequency of daily consumption of sweets (25% vs. 0%) and soft drink (25% vs. 0). (4) Conclusions: The individual patterns of cortisol reactivity to laboratory-induced stress could be associated with an increased risk of unhealthy eating behavior in adolescents.
... Answers regarding food consumption frequency from the survey were transformed into portions per week (0, 0.5, 1, 2, 3,7,14,21). Food groups considered in the survey were sweetened beverages, dairy, fruits, vegetables, bread, baked goods, eggs, meat, coffee/tea, alcoholic beverages, fried foods and pizza(16). ...
... Several risk factors for weight gain during con nement have been described in the literature, such as eating snacks and sugary drinks after dinner, eating in response to stress, decreasing physical activity, signi cantly increasing television and screen time, and lack of sleep (6). It has also been described that stress can lead to cortisol release, which in turn increases the feeling of hunger (21). Other authors have pointed out that con nement interrupting the work routine could result in boredom, which has been associated with increased energy intake in general and fat and carbohydrate intake in particular (2). ...
Background: SARS-CoV-2, a newly identified coronavirus responsible for the COVID-19 pandemic, has challenged health services and profoundly impacted people's lifestyle. The objective of the present study was to evaluate the effect of confinement during the COVID-19 pandemic on food consumption patterns and body weight in adults from 12 Ibero-American countries
Methods: Multicentric, cross-sectional study. Data was collected using an online survey disseminated by social networks. Sample included 10 552 people from Spain and 11 Latin American countries who were selected by snowball sampling.
Results: While 38.50% of the sample reported weight gain, 16.90% reported weight lost. Weight change was associated to sex, age, country of residence and education level. People who were not confined, more often reported having maintained their weight in comparison to people who were confined. All Latin American countries showed an increased consumption of sweetened drinks, pastry products, fried foods and alcoholic beverages during confinement. Consumption of eggs and dairy products was independent from body weigh change. People who consumed more fruits and vegetables during the confinement more often reported having lose weight. In contrast, body weight gain during confinement was associated with increased intake of sugary drinks, baked goods and pastries, pizza, fried foods and alcoholic beverages.
Conclusions: During COVID-19 confinement all the Latin American countries included in this study showed a change in their consumption patterns toward less healthy diets, which in turn was associated with an increase in the body weight of their population.
... The literature also highlights the influence of hormonal disorders on the development of the disease. Gluck et al. have pointed to an increase in cortisol secretion in response to stressors as one of the causes of BED [16]. It is postulated that endogenous estrogen and progesterone may contribute to an increased risk of binge eating [17]. ...
Background
Binge eating disorder (BED) is currently the most common form of an eating disorder. BED is characterized by the consumption of large amounts of food in a short period of time, in a manner not controlled by the sick person. Its etiology is not fully known, but it is assumed that the development of the disorder results from psychological, social, and biological factors.
Objectives
The aim of the study is to systematize information about BED and raise awareness among the public and health professionals about the issue.
Material and methods
This paper is based on a comprehensive review of scientific research conducted worldwide. Our conclusions are informed by the latest reports that explore various aspects of the daily lives of patients with BED.
Results
BED is classified into varying degrees of severity, depending on the number of bouts of eating per week. The gold standard for diagnosis is a structured psychological assessment. BED often co-exists with overweight and obesity, increasing the risk of somatic and psychosocial complications. Dietary education is the basis of therapy, and psychotherapy is the first line of treatment. Pharmacotherapy, which includes lisdexamfetamine and antidepressant, antiepileptic, psychostimulant, and anti-obesity drugs, is an important support. Forming proper eating habits is key in BED prevention.
Conclusions
The multifaceted nature of BED, which affects many aspects of patients’ lives, reduces their quality of life. Increasing social awareness, health education, and countering the stigma on those affected by this disorder are also key.
... These results suggest that stress promotes internal environments and behaviors that increase the risk of hypermetabolism, which can have serious long-term health consequences. Diseases such as obesity and diabetes are associated with systemic inflammation, increased oxidative stress, altered gene expression (such as telomere shortening), and decreased cognitive performance [144][145][146][147][148][149][150][151][152][153][154][155][156][157][158][159][160][161][162][163]. ...
The overweight status or obesity can be confirmed through classical methods such as the body mass index (BMI) and the waist-to-hip ratio (WHR). Apart from metabolic issues such as atherosclerosis, liver steatosis, or diabetes mellitus, long-term obesity or overweight status can pose a risk for cardiovascular and neurovascular complications. While some acute adverse events like coronary syndromes of strokes are well-documented to be linked to an increased body mass, there are also chronic processes that, due to their silent onset and evolution, are underdiagnosed and not as thoroughly studied. Through this review, we aimed to collect all relevant data with regard to the long-term impact of obesity on cognitive function in all ages and its correlation with an earlier onset of dementia such as Alzheimer’s disease (AD). The exact mechanisms through which a decline in cognitive functions occurs in overweight or obese persons are still being discussed. A combination of factors has been acknowledged as potential triggers, such as a sedentary lifestyle and stress, as well as a genetic predisposition, for example, the apolipoprotein E (ApoE) alleles in AD. Most research highlights the impact of vascular dysfunction and systemic inflammation on the nervous system in patients with obesity and the subsequent neurological changes. Obesity during the early to mid-ages leads to an earlier onset of cognitive dysfunction in various forms. Also, lifestyle intervention can reverse cognitive dysfunction, especially dieting, to encourage weight loss.
... Stressors can trigger binge eating [21]. During prolonged stress, our bodies release cortisol, which increases the hunger sensation [22,23]. The best recommendation for staying healthy during quarantine is to follow general health advice such as eating a balanced diet, staying hydrated, being physically active, getting enough sleep, and managing stress [24]. ...
Background: The COVID-19 pandemic caused by the coronavirus was accompanied by the emergence of various adverse conditions, as well as the deterioration of health from the point of view of chronic diseases, as well as lifestyle changes related to the preference of certain foods and changes in body weight due to the restriction of free movement.
Objective: The objective of our survey was to assess the impact of the pandemic and lockdown on selected key lifestyle elements affecting the overall health status of the Slovak population and subsequently to evaluate subjectively assessed changes in the respondents’ eating habits, daily routine, physical activity and body weight.
Material and Methods: The research group consisted of 528 participants who took part in an online distributed questionnaire survey.
Results: Respondents subjectively evaluated the change in lifestyle rather negatively. Up to 48.37% of men and 38.93% of women reported a change for the worse. Almost 59% of participants reported no change in their health, while almost a quarter reported a slight deterioration in their health. A change in eating habits for the worse was reported by 22.88% of men and 28.26% of women (p
... These divergent results could be due to different reward stimuli (i.e., food vs. money). Indeed, a small literature on eating behavior suggests acute stress is associated with increased craving/wanting for palatable foods, particularly in high stress or clinical samples (Gluck et al., 2004;Lemmens et al., 2011). Alternatively, these divergent results may indicate that stress modulates effort-based behavior differently as function of timing of learned behavior; reducing effort during early stages of learning, but increasing effort once a behavior has been instantiated. ...
Anhedonia, as evidenced by impaired pleasurable response to reward, reduced reward motivation, and/or deficits in reward-related learning, is a common feature of depression. Such deficits in reward processing are also an important clinical target as a risk factor for depression onset. Unfortunately, reward-related deficits remain difficult to treat. To address this gap and inform the development of effective prevention and treatment strategies, it is critical to understand the mechanisms that drive impairments in reward function. Stress-induced inflammation is a plausible mechanism of reward deficits. The purpose of this paper is to review evidence for two components of this psychobiological pathway: 1) the effects of stress on reward function; and 2) the effects of inflammation on reward function. Within these two areas, we draw upon preclinical and clinical models, distinguish between acute and chronic effects of stress and inflammation, and address specific domains of reward dysregulation. By addressing these contextual factors, the review reveals a nuanced literature which might be targeted for additional scientific inquiry to inform the development of precise interventions.
... For example, overvaluation of shape/weight (American Psychiatric Association, 2013;Coffino et al., 2019;Fairburn et al., 2003) may contribute to dietary restriction, which may sensitize some individuals to highly palatable foods (Hazzard et al., 2020;Polivy & Herman, 1985) and, ultimately, amplify the proposed reward processes. Further, as research suggests that a variety of contextual factors (e.g., hunger; Gluck et al., 2004;Haedt-Matt & Keel, 2011;Klatzkin et al., 2018) may influence food reward processes and behavioral responses to aversive affective states (Ma et al., 2020;Mason et al., 2020;Moyal et al., 2023), clarifying the impact of contextual factors on relationships proposed within the ARC model represents an important area of study. In addition, the basic principles of these models could be adapted to explain other transdiagnostic eating disorder symptoms, such as dietary restraint (Haynos et al., 2020) or compulsive exercise (Coniglio et al., 2022;Tabri & Wohl, 2022) in anorexia nervosa or bulimia nervosa. ...
Reward‐related processes are an increasing focus of eating disorders research. Although evidence suggests that numerous distinct reward processes may contribute to eating pathology (e.g., reward learning and delay discounting), existing etiological models of reward dysfunction tend to focus on only a limited number of reward processes, and frequently lack specificity when identifying the individual reward processes hypothesized to contribute to dysregulated eating behavior. Moreover, existing theories have been limited in their integration of reward‐related processes with other demonstrated risk and maintenance factors for eating disorders (e.g., affect and cognition), potentially contributing to underdeveloped models of eating pathology. In this article, we highlight five distinct reward processes with theorized or demonstrated relevance to eating disorders involving binge‐eating, followed by a review of two well‐established risk/maintenance factors for binge‐eating pathology. We then introduce two novel models of binge eating onset and maintenance that integrate these factors (i.e., the Affect, Reward, Cognition models), and discuss methods for testing each of the models in future research. Ultimately, we hope that the proposed models provide a springboard for the continued evolution of more precise and comprehensive theories of reward dysfunction in the eating disorders, as well as the development of novel intervention approaches.
Public Significance Statement
Eating disorders are associated with abnormalities in multiple domains of reward functioning. However, models of reward dysfunction within the eating disorders have not been well‐integrated with prominent models of affect and cognition. This article presents two novel models of onset and maintenance for binge‐eating pathology, which attempt to integrate observed reward abnormalities with other affective and cognitive processes implicated in binge‐type eating disorders.
... People with food insecurity may also need to have greater cognitive dietary restraint to spread their resources for other household members (i.e., children) or stretch food to make it last longer (Middlemass et al., 2021), which may increase their likelihood of binge eating. In addition, it has been proposed that the stress of being food insecure contributes to increased chronic activation of cortisol production pathways, an important risk factor for binge eating as well as consumption of highly palatable foods (Gluck et al., 2004;Walker et al., 2018). Numerous primary studies have similarly investigated the link between food insecurity and binge eating. ...
Objective
This review synthesized literature on the relationship between food insecurity and binge eating.
Methods
Relevant studies were identified by searching PubMed, CINAHL, PsycINFO, and gray literature from inception to October 2022. Eligible studies included primary research that assessed the relationship between food insecurity and binge eating. Data extraction was performed independently by two reviewers. Pooled odds ratios and 95% confidence intervals (CI) were obtained from random effect models with the R package meta. Analyses were stratified by binge eating versus binge‐eating disorder (BED), study type (cross‐sectional vs. longitudinal), and age (adults vs. adolescents).
Results
We included 24 articles that reported on 20 studies, and 13 articles were included in the meta‐analysis. Based on the random effects meta‐analysis, the odds of adults in the food insecure group having binge eating were 1.66 (95% CI = 1.42, 1.93) times the odds of adults in the food secure group having binge eating. The odds of adults in the food insecure group having BED were 2.70 (95% CI = 1.47, 4.96) times the odds of adults in the food secure group having BED. Insufficient data were available for a meta‐analysis on adolescents or longitudinal relationships.
Conclusions
These findings support that food insecurity is associated with binge eating in adults. There is a need for research to investigate the mechanisms underlying this relationship. Results highlight the importance of screening participants with food insecurity for disordered eating behaviors and vice versa. Future research is needed to examine whether interventions targeting food insecurity may help to mitigate disordered eating behaviors.
Public Significance
Food insecurity is a common but under‐recognized contributor to binge eating. In this article, we systematically reviewed research that has been published on the relationship between food insecurity and binge eating. We found support that food insecurity should be considered in the prevention and treatment of binge eating.
... In another study, plasma cortisol levels were found to be higher in those with glucose intolerance than in healthy subjects (23). Gluck et al found that morning cortisol levels were higher in women with binge eating disorder than in women without binge eating disorders (24). In their studies, Faulenbach et al discovered that cortisol reactivity after the postprandial period stress test in T2DM patients was lower than after the test on an empty stomach (25). ...
Background:
Stress triggers a cascade of reactions that alter the organism's dynamic steady state. There is a scarcity of interventional studies that show cortisol variability on stress over time in groups of patients with chronic noncommunicable diseases and comorbidities.
Purpose:
In this research, we aimed to examine salivary cortisol changes in the cognitive stress response of patients with Hypertension and Diabetes Mellitus (HT & DM) and patients with Hypertension (HT) and to determine the differences between them.
Methods:
The research was conducted by solving an arithmetic task as a stress test in 62 patients with HT&DM and HT that are being treated in the outpatient clinic of Medical Pharmacology and Clinical Pharmacology Department in Istanbul University, Istanbul Medical Faculty Hospital.
Results:
There was no statistically significant difference among HT&DM and HT groups on systolic and diastolic blood pressure (BP) values (p = 0.331 and p = 0.058). When measured by repeated ANOVA, salivary cortisol level [F (1.842, 60) = 8.771, p < 0.0001], systolic blood pressure [F (2.185, 60) = 12.080, p < 0.0001], diastolic blood pressure [F (2.793, 60) = 6.043, p = 0.001] and the heart rate [F (2.073, 60) = 13.259, p < 0.0001] were statistically significant for the main effect (time), while the effect of the group*time interaction factor was statistically not significant (p = 0.773; p = 0.751; p = 0.713 and p = 0.506, respectively).
Main conclusions:
In conclusion, the arithmetic problem-solving task used in the HT&DM and HT patients were found to be useful as an acute stress test in the laboratory environment. There was no statistically significant difference was found in terms of group*time interaction factor between the HT&DM and HT groups, however the salivary cortisol and BP values increased significantly after acute stress within each group.
... Some studies described higher fasting plasma insulin levels in individuals with obesity and BED compared to those with obesity without BED Succurro et al., 2015;Yagin et al., 2020). Although these findings suggest that comorbidity between obesity and BED may be associated with a higher insulin resistance, other works reported no differences neither in fasting nor satiety, regardless of the diagnosis of BED (Galmiche et al., 2020;Geliebter et al., 2005;Gluck et al., 2004;Messerli-Bürgy et al., 2010). ...
Neuroendocrine mechanisms play a key role in the regulation of eating behavior. In individuals with binge eating disorder (BED), alterations in these mechanisms signaling hunger and satiety have been observed. It has been investigated that these alterations may underlie the development and maintenance of compulsive overeating in BED. The present narrative review examined the current literature related to the neurobiological processes involved in feeding dysregulation in BED with the aim of updating the most relevant aspects with special attention to neuroendocrine signaling. Studies have shown both central and peripheral endocrine dysfunctions in hormones participating in homeostatic and hedonic pathways in BED. Most studies have been especially focused on orexigenic signals, pointing out the existence of a hyperactivated mechanism promoting hunger. Fewer studies have explored anorexigenic pathways, but the findings so far seem to suggest an abnormal satiety threshold. Despite this, to date, it is unable to identify whether these alterations are typical of the BED pathophysiology or are related to an obesogenic pattern due to most studies including patients with BED and obesity. The identification of endophenotypes in BED may provide a new approach to aberrant eating behavior, favoring the implementation of biological therapeutic targets.
... Chronic and uncontrollable stress can have detrimental effects as it can dysregulate the HPA axis, causing alterations in the release of hormones, neuropeptides and glucocorticoids (Lupien, McEwen, Gunnar, & Heim, 2009). Individuals with eating disorders, especially anorexia nervosa, have been found to have elevated cortisol levels (Gluck, Geliebter, Hung, & Yahav, 2004;Luz et al., 2019). ...
Background:
Food addiction may play a role in rising obesity rates in connection with obesogenic environments and processed food availability, however the concept of food addiction remains controversial. While animal studies show evidence for addictive processes in relation to processed foods, most human studies are psychologically focussed and there is a need to better understand evidence for biological mechanisms of food addiction in humans. Several key hormones are implicated in models of food addiction, due to their key roles in feeding, energy metabolism, stress and addictive behaviours. This systematic literature review examines evidence for relationships between food addiction, hormones and other blood biomarkers.
Methods:
A series of literature searches was performed in Scopus, PsychInfo, MedLine, ProQuest, CINAHL and Web of Science. A total of 3111 articles were found, of which 1045 were duplicates. Articles were included if they contained a psychometric measurement of food addiction, such as the Yale Food Addiction Scale, as well as addressed the association between FA and hormones or blood biomarkers in humans. Articles were assessed for eligibility by two independent reviewers.
Results:
Sixteen studies were identified that examined relationships between food addiction and blood biomarkers, published between 2015 and 2021. Significant findings were reported for leptin, ghrelin, cortisol, insulin and glucose, oxytocin, cholesterol, plasma dopamine, thyroid stimulating hormone (TSH), haemoglobin A1c (HbA1c), triglyceride (TG), amylin, tumour necrosis factor alpha (TNF- α) and cholecystokinin (CCK). Methodological issues included small sample sizes and variation in obesity status, sex and mental health-related comorbidities. Due to methodological limitations, definite connections between FA, hormones and other blood biomarkers cannot yet be determined.
Conclusion:
This systematic review identified preliminary evidence linking FA symptoms to hormones and other blood biomarkers related to feeding, addiction, and stress. However, due to the small number of studies and methodological limitations, further research is needed to evaluate biopsychosocial models of FA and to resolve controversies.
... Adults with binge eating are frequently obese [22], and have been shown to exhibit greater medial orbitofrontal cortex (OFC) activation in response to visual food stimuli [23], and greater activation in the dorsal anterior cingulate cortex (ACC) in response to high-ED food stimuli [24]. Those with binge eating often report initiating binge episodes in response to stress [25] and higher rates of stressful life events [26] and daily hassles [27], and show a greater post-stress elevation in hunger and desire to binge eat, as well as higher baseline cortisol and greater cortisol area under the curve (AUC) following stress [28]. Among obese individuals, those with binge eating may therefore be especially likely to show increased neural food cue responsiveness following stress. ...
Obesity can result from excess intake in response to environmental food cues, and stress can drive greater intake and body weight. We used a novel fMRI task to explore how obesity and stress influenced appetitive responses to relatively minimal food cues (words representing food items, presented similarly to a chalkboard menu). Twenty-nine adults (16F, 13M), 17 of whom had obesity and 12 of whom were lean, completed two fMRI scans, one following a combined social and physiological stressor and the other following a control task. A food word reactivity task assessed subjective food approach (wanting) as well as food avoidant (restraint) responses, along with neural responses, to words denoting high energy-density (ED) foods, low-ED foods, and non-foods. A multi-item ad-libitum meal followed each scan. The obese and lean groups demonstrated differences as well as similarities in activation of appetitive and attention/self-regulation systems in response to food vs. non-food, and to high-ED vs. low-ED food words. Patterns of activation were largely similar across stress and non-stress conditions, with some evidence for differences between conditions within both obese and lean groups. The obese group ate more than the lean group in both conditions. Our results suggest that neural responses to minimal food cues in stressed and non-stressed states may contribute to excess consumption and adiposity.
... Several risk factors for weight gain during confinement have been described in the literature, such as eating snacks and sugary drinks after dinner, eating in response to stress, decreasing physical activity, significantly increasing television and screen time, and lack of sleep [6]. It has also been described that stress can lead to cortisol release, which in turn increases the feeling of hunger [21]. Other authors have pointed out that confinement interrupting the work routine could result in boredom, which has been associated with increased energy intake in general and fat and carbohydrate intake in particular [2]. ...
Objectives
SARS-CoV-2, a newly identified coronavirus responsible for the COVID-19 pandemic, has challenged health services and profoundly impacted people's lifestyles. The objective of the present study was to evaluate the effect of confinement during the COVID-19 pandemic on food consumption patterns and body weight in adults from 12 Ibero-American countries.
Methods
Multicentric, cross-sectional study. Data was collected using an online survey disseminated by social networks. The sample included 10 552 people from Spain and 11 Latin American countries who were selected by snowball sampling.
Results
While 38.50% of the sample reported weight gain, 16.90% reported weight lost. Weight change was associated with sex, age, country of residence, and education level. People who were not confined more often reported having maintained their weight in comparison to people who were confined. All Latin American countries showed an increased consumption of sweetened drinks, pastry products, fried foods, and alcoholic beverages during confinement. Consumption of eggs and dairy products was independent from body weight change. People who consumed more fruits and vegetables during confinement more often reported having lost weight. In contrast, body weight gain during confinement was associated with increased intake of sugary drinks, baked goods and pastries, pizza, fried foods, and alcoholic beverages.
Conclusion
During COVID-19 confinement, the Latin American countries included in this study showed a change in their consumption patterns toward less healthy diets, which in turn was associated with an increase in the body weight of their population.
... This may present a means to 'escape' negative feelings by shifting attention to the immediate environment. Emotional eating can be aggravated by poor interoceptive hunger awareness and emotional regulation [21] and is associated with a blunted cortisol response to psychological stress [132][133][134][135][136]. Whether this is a consequence or cause of DEB and chronic palatable food intake remains to be elucidated [21], but some evidence suggests that calorically dense food may decrease the hypothalamic-pituitary-adrenal axis response to stress [97]. ...
Bariatric surgery results in long-term weight loss and an improved metabolic phenotype due to changes in the gut-brain axis regulating appetite and glycaemia. Neuroendocrine alterations associated with bariatric surgery may also influence hedonic aspects of eating by inducing changes in taste preferences and central reward reactivity towards palatable food. However, the impact of bariatric surgery on disordered eating behaviours (e.g.: binge eating, loss-of-control eating, emotional eating and ‘addictive eating’), which are commonly present in people with obesity are not well understood. Increasing evidence suggests gut-derived signals, such as appetitive hormones, bile acid profiles, microbiota concentrations and associated neuromodulatory metabolites, can influence pathways in the brain implicated in food intake, including brain areas involved in sensorimotor, reward-motivational, emotional-arousal and executive control components of food intake. As disordered eating prevalence is a key mediator of weight-loss success and patient well-being after bariatric surgery, understanding how changes in the gut-brain axis contribute to disordered eating incidence and severity after bariatric surgery is crucial to better improve treatment outcomes in people with obesity.
... In this way, using food to control or relieve discomfort [7] can increase or decrease the quantity of eaten food [1,8] and trigger risky eating behaviors, such as restrictive eating, binge eating, and disordered eating [1,[9][10][11]. These changes can impact people's physical [2,5] and mental [11] health and could result in the development of eating disorders [8,12,13]. Thus, exploring how individuals use food to cope with emotions and stress is an important step for the development of efficient health protocols and diet interventions. ...
Purposes
To develop a Brazilian Portuguese version of the Eating and Appraisal due to Emotions and Stress (EADES) Questionnaire and estimate the psychometric properties of the EADES factorial model for young Brazilian adults and also to assess the association between EADES factors and age, body mass index (BMI), and economic level.
Methods
The cross-cultural adaptation was performed using a standardized protocol. The psychometric properties were assessed separately for each sex. A structural model for each sex was developed to investigate the influence of age, economic level, and BMI on the EADES factors.
Results
A total of 1240 participants completed the study [65.8% female, mean age 23.91 (SD = 5.03) years]. The EADES original factorial model did not present good psychometric properties. Then, a factorial model proposed for a Mexican sample was tested and a different model was fitted for each sex. The results showed that younger women have lower self-efficacy and self-confidence and poorer assessment of resources and coping skills. Women with a higher economic level have lower self-efficacy. Higher BMI was associated with lower self-efficacy and self-confidence in both sexes. Younger men have lower self-efficacy and poorer assessment of resources and coping skills.
Conclusions
The Brazilian Portuguese version of the EADES provided valid and reliable data after refinement, and a different model was fitted for each sex. Sex, age, BMI, and economic level were significantly associated with the EADES factors.
Level of evidence
Level V, descriptive cross-sectional study.
... These females had elevated levels of plasma corticosterone and reduced corticotrophin-releasing factor mRNA expression in the paraventricular nucleus of the hypothalamus (Lenglos et al., 2013), raising the possibility that these female rats comfort-eat to relieve stress, leading to a decrease in HPA axis activity. In humans, experimental induction of stress (cold pressor test) leads to an increase in cortisol levels and consequent feelings of hunger and desire to binge eat in women with obesity and binge eating disorder when compared to women with obesity that are non-binge eaters (Gluck et al., 2004). Other stressors, such as social stress or seeing unpleasant images/videos, are also associated with an increase in food consumption and cravings in both men and women (Christensen and Pettijohn, 2001;Chua et al., 2004;Laessle and Schulz, 2009;Waters et al., 2001). ...
Disordered eating is often associated with marked psychological and emotional distress, and severe adverse impact on quality of life. Several factors can influence eating behavior and drive food consumption in excess of energy requirements for homeostasis. It is well established that stress and negative affect contribute to the aetiology of eating disorders and weight gain, and there is substantial evidence suggesting sex differences in sub-clinical and clinical types of overeating. This review will examine how negative affect and stress shape eating behaviors, and how the relationship between the physiological, endocrine, and neural responses to stress and eating behaviors differs between men and women. We will examine several drivers of overeating and explore possible mechanisms underlying sex differences in eating behavior.
... Interestingly, the consumption of the more rewarding food in the free-choice paradigm and the CPP for the HPF are both significantly suppressed by genetic ablation and pharmacological blockade of GHSR1a [34,36,57,61], and the GHSR1a knockout (KO) mice also failed to present the accumbal dopamine release elicited by exposure to the HPF [34]. The absence of GHSR1a also revealed to be protective against stress-induced hedonic eating, since mice lacking this receptor failed to exhibit CPP and increased intake of HFD, after being exposed to a stressful procedure [62], a factor that is known to promote the overconsumption of HPF in both humans and rodents [63][64][65][66][67][68]. ...
The peripheral peptide hormone ghrelin is a powerful stimulator of food intake, which leads to body weight gain and adiposity in both rodents and humans. The hormone, thus, increases the vulnerability to obesity and binge eating behavior. Several studies have revealed that ghrelin’s functions are due to its interaction with the growth hormone secretagogue receptor type 1a (GHSR1a) in the hypothalamic area; besides, ghrelin also promotes the reinforcing properties of hedonic food, acting at extra-hypothalamic sites and interacting with dopaminergic, cannabinoid, opioid, and orexin signalling. The hormone is primarily present in two forms in the plasma and the enzyme ghrelin O-acyltransferase (GOAT) allows the acylation reaction which causes the transformation of des-acyl-ghrelin (DAG) to the active form acyl-ghrelin (AG). DAG has been demonstrated to show antagonist properties; it is metabolically active, and counteracts the effects of AG on glucose metabolism and lipolysis, and reduces food consumption, body weight, and hedonic feeding response. Both peptides seem to influence the hypothalamic–pituitary–adrenal (HPA) axis and the corticosterone/cortisol level that drive the urge to eat under stressful conditions. These findings suggest that DAG and inhibition of GOAT may be targets for obesity and bingeing-related eating disorders and that AG/DAG ratio may be an important potential biomarker to assess the risk of developing maladaptive eating behaviors.
... In other words, unlike emotion-congruent consumption, negative emotions increase consumption. This strategy is prevalent among healthy, normal weight (Macht 1999;Macht et al. 2005;Macht and Simons 2000), as well as obese (Agras and Telch 1998;Gluck et al. 2004) people. Food is used to reduce arousal (Cantor 1981), to improve negative mood (Booth 1994;Thayer 2001), to escape from unwanted self-awareness (Heatherton and Baumeister 1991), or to reduce stress (Polivy and Herman 1999). ...
Adolescence is a transitional phase that spans from childhood to adulthood, during which physical and psychological mutations transform the individual. In this life stage, young consumers become more independent and start to take the first autonomous consumption decisions as a way of escaping from parental control. As a result, parents lose their primary influence on adolescents, who devote their attention to peers. Friends, then, become a source of inspiration in the consumption process, especially for those products that are publicly consumed or characterized by a strong symbolic meaning, including food (Story et al. 2002; Stanford University 2020). For these reasons, adolescence is an interesting context in which to explore how individuals build their future relationships with goods, services, and brands.
... In other words, unlike emotion-congruent consumption, negative emotions increase consumption. This strategy is prevalent among healthy, normal weight (Macht 1999;Macht et al. 2005;Macht and Simons 2000), as well as obese (Agras and Telch 1998;Gluck et al. 2004) people. Food is used to reduce arousal (Cantor 1981), to improve negative mood (Booth 1994;Thayer 2001), to escape from unwanted self-awareness (Heatherton and Baumeister 1991), or to reduce stress (Polivy and Herman 1999). ...
A great designer is able to understand and satisfy both our material and emotional needs. “Abundance has satisfied, and even over-satisfied, the material needs of millions—boosting the significance of beauty and emotion” (Pink 2006). As our fundamental needs are met, we are increasingly looking for emotionally satisfying experiences (Brown 2008). In order to fulfill consumer needs and produce innovative food experiences that enhance consumers’ well-being, designers should bear in mind that consumers are not only cognitive but also emotional beings and food is an extremely emotion-laden experience due to its symbolic nature.
... This relationship between BED and metabolic disease may be due to very high intake of fat and calories during binge episodes, leading to insulin resistance, hyperinsulinemia and impaired glycemic control (17). Elevated cortisol levels have been found in obese women with binge eating disorder, and hypercortisolism can lead to acutely increased insulin resistance and gluconeogenesis (18,19). BED appears to be an independent risk factor for developing T2DM, as studies have shown that those with BED are at a 13 times greater risk for developing T2DM compared to those without BED. ...
Objective
To familiarize health care providers with the diagnosis and treatment of binge eating disorder (BED), a common comorbidity of type 2 diabetes (T2DM).
Methods
Literature review of binge eating and type 2 diabetes. Key words used in search include: binge eating disorder, type 2 diabetes, obesity, and treatment.
Results
The prevalence of binge eating disorder in patients with type 2 diabetes appears to be much higher than the 2 to 3.5% prevalence of BED in the general public. Studies suggest that up to 20% of patients with T2DM have an underlying eating disorder, the most common of which is binge eating. BED is likely underdiagnosed, though there are multiple simple tools that providers can use to improve screening for the disorder. Though the relationship between BED and A1c control can vary, it appears that binge eating behaviors can worsen metabolic markers, including glycemic control. Various medications used by patients with diabetes have been associated with new-onset BED, and treatment may be as simple as removing or replacing these agents. There are several medications that have been found to significantly reduce binge eating frequency and potentially weight. Patients with BED generally benefit from psychotherapy, including cognitive behavioral therapy.
Conclusion
Binge eating disorder, a diagnosis just recently added to the ICD-10 diagnostic list, is very common in patients with obesity and T2DM. The diagnosis is important to establish, as treatment—or referral for treatment—could potentially improve many of the comorbidities and metrics of T2DM.
... However, one critical limitation of the CPT is that it does not incorporate social evaluative stress, which (as noted earlier) is the key factor associated with activation of the HPA axis. In line with this limitation, findings of studies assessing the influence of the CPT on HPA axis activation are somewhat mixed: some studies have found that the CPT does not elicit increases in salivary cortisol (Duncko et al., 2007;McRae et al. 2006); other studies have reported small increases (al'Absi, et al. 2002;Gluck et al., 2004); and yet other studies have found evidence of a moderate cortisol response (e.g., McCullough et al. 2015;Schoofs, Wolf, & Smeets, 2009;Shields et al. 2019), though still notably smaller than that elicited by the TSST (see Shields et al. 2017, for a metaanalysis in the context of studies examining the effect of stress on memory). ...
Laboratory stress-induction procedures have been critical in illuminating the effects of stress on human health, cognition, and functioning. Here, we present a novel stress induction procedure, the Simple Singing Stress Procedure (SSSP), that overcomes some of the practical challenges and conceptual limitations of existing procedures in measuring the causal influence of stress on psychological variables. In the stress condition of the SSSP, participants were instructed to sing a song in front of the experimenter while being video- and audio-recorded. Participants were also informed that they would have to sing again at the end of the experiment, and that this second performance would later be assessed by a panel of experimenters. Participants in a no-stress condition instead read lyrics in each phase. Our findings revealed that participants in the stress condition showed significantly higher blood pressure immediately following the initial singing session, as well as heightened salivary cortisol at a latency consistent with the initial singing session, than those in the no-stress condition. Our stress procedure also generated elevations in self-reported stress ratings immediately after the first singing session and subsequently in anticipation of the second singing session, relative to the no-stress condition. Collectively, these findings suggest that the SSSP is a simple and effective stress induction procedure that may be a promising alternative to existing protocols.
... 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]. ...
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.
The Behavioral Susceptibility Theory posits that food approach/avoidance traits are key genetic contributors to obesity and disordered eating. The genetic tendency to approach/avoid food may manifest with emotional eating (i.e., over or under-eating in response to emotional cues). Research indicates that emotional eating (EE) affects long-term success after bariatric surgery, but findings focus mainly on the tendency to overeat in response to negative emotions. The current study examined the role of both emotional over- and under-eating within a pre-bariatric sample, and their association with psychosocial outcomes. Using Latent Class Analysis, responses from 446 participants (74.3% female; 71.5% White, 12.1% African American, 10.3% Hispanic, 4.1% multiracial, 1.1% Other/Unreported; MAge = 42.38, MBMI = 49.15 kg/m2) on the emotional eating subscales of the Adult Eating Behavior Questionnaire were analyzed to identify EE patterns. Participants also responded to measures of emotional distress, quality of life, and disordered eating (e.g., night eating, binge eating, and avoidant/restrictive food intake disorder). A four-class solution emerged: (a) emotional over- and undereating (EOE-EUE; 14.4%), (b) emotional overeating (EOE; 25.3%), (c) emotional undereating (EUE; 26.0%), and (d) non-emotional eating (non-EE; 34.3%). Consistent with previous research, the EOE-EUE class exhibited high levels of psychosocial impairment, and emotional eating classes exhibited higher levels of disordered eating compared to the non-emotional eating class. These findings provide a more nuanced understanding of EE within a pre-bariatric population by identifying patterns of both over- and under-eating within individuals and differentially identifying risk factors associated with such patterns. Limitations include the lack of a non-surgery-seeking comparison group, the potential for response biases, and the reliance on cross-sectional data.
O comportamento alimentar é um dos fatores centrais subjacentes à obesidade, por isso, o objetivo da presente revisão de literatura é revisar a relação entre comer emocional e desenvolvimento de sobrepeso e obesidade, bem como o papel do mindful eating e comer intuitivo na mudança desse comportamento alimentar. Para a revisão bibliográfica foi realizada busca de documentos, artigos e livros nas bases de dados PubMed, Science Direct e SciELO e sites oficiais de órgãos públicos, no período de fevereiro a novembro de 2022. Constatou-se que o comer emocional é um comportamento alimentar disfuncional associado ao ganho de peso, maior IMC, sintomas depressivos e curta duração de sono. Programas convencionais de emagrecimento não lidam com o comer emocional. Mindful eating e comer intuitivo mostram-se como estratégias eficazes para atender as necessidades de comedores emocionais. Dessa forma, programas direcionados para perda de peso devem levar em consideração o comportamento alimentar individual e adotar abordagens comportamentais que ensinem habilidade de regulação emocional.
Tıkınırcasına Yeme Bozukluğunun (TYB) en önemli belirtilerinden biri gıda
alımına ilişkin yaşanan kontrol kaybıdır. TYB belirtileri yaşayan bireylerin yeme
atakları sonrası suçluluk, üzüntü ve iğrenme duyguları (olumsuz duygular)
yaşadıkları bilinmektedir. Bu olumsuz duyguların ortaya çıkma ve sürdürülme
sebeplerinin bilişsel çarpıtmalar olabileceği ve bu durumlarla baş etme
stratejilerinin eksik olmasının, duygu düzenleme güçlüğü yaşamaları ile ilişkili
olabileceği düşünülmektedir. Gıda tüketiminin kısa süreli bile olsa hafifletme ve
rahatlama etkisi sebebi ile bireyler gıda tüketimini ödül olarak algılamakta ve
dürtüsel davranışlar sergilemektedirler. İnsan ödül sistemi, teşvik edici belirgin
kuramı bağlamında “isteme” ve “beğenme” olarak bilinen iki ana bileşenden
oluşmaktadır. Bu bileşenler birbirleri ile yakından ilişkili olsa da nörobiyolojik ve
psikolojik olarak birbirlerinden belirli koşullarda ayrılmaktadırlar. Bu bağlamda,
TYB belirtilerini ortaya çıkarabileceği düşünülen bu değişkenlerin bir arada
değerlendirilmesinin önemli olduğu düşünülmüştür. Bu çalışmanın amacı, TYB
düzeyinin stres altında tercihleri ne şekilde etkilediğini ve bu etkide duygu
düzenleme, dürtüsellik ve temel inançların rolünün incelenmesidir.
The relationship between neuroinflammation and binge eating is a complex interplay involving the central nervous system. Neuroinflammatory processes, often triggered by various factors, can influence neural circuits related to appetite regulation. Elevated levels of inflammatory markers in the brain have been observed in individuals with binge eating tendencies, suggesting a potential connection between inflammation and dysregulated eating behaviors. Exploring these mechanisms can contribute to a deeper understanding of the neural basis of binge eating, offering avenues for targeted interventions and therapeutic strategies. This review delves into the connection between neuroinflammation and binge eating, its neurobiological implications, insights, and therapeutic interventions. Also, insights into potential personalized treatment approaches based on neurinflammatory markers were considered. The review concludes by stating future directions and suggesting recommendations.
Objective:
Loss of control (LOC) eating is prevalent but understudied among young men. Affect regulation models propose that LOC eating functions as a maladaptive effort to escape from distressing affective states. As such, negative affect is thought to increase before and decrease after LOC eating. However, examinations with young men are lacking and it remains unclear whether specific emotional experiences are differentially implicated in their LOC eating.
Methods:
The current study examined the temporal roles of affect in LOC eating in 31 young men (18-35 years; Mage = 25.74 ± 5.61y; 46.7 % White; 30 % Black/African American; 10 % Hispanic/Latino, 10 % South Asian) who reported engaging in recurrent LOC eating. Participants completed a 14-day ecological momentary assessment protocol and recorded all eating episodes each day and their state affect five times per day. Generalized linear mixed models were conducted to examine the trajectories of global and item-level negative and positive affect pre- and post-LOC eating episodes.
Results:
Negative affect did not change significantly before or after LOC eating (ps > .05). Positive affect did not change significantly before LOC eating (ps > .05). Global positive affect, excitement, and happiness decreased significantly after LOC eating (ps ≤ .001).
Discussion:
Study findings contradict extant theory and empirical data largely from female samples. Negative affect did not increase risk for LOC eating, nor did LOC eating function to improve participants' mood; rather, positive mood slightly decreased after LOC eating. Further investigation around the observed decline in positive affect after LOC eating will clarify if this is a relevant intervention point in this population.
The hypothalamic-pituitary-adrenal (HPA) axis is the main component of the endogenous stress response system which regulates the bodily response to real or perceived environmental stressors threatening homeostasis. Several theoretical models have been developed to conceptualize the link between stress and eating behavior, so the HPA axis activity has been widely investigated in people with eating disorders. In patients with eating disorders, both increased and decreased HPA axis activity has been reported. The contradictory findings can be due in part to the heterogeneity of methodologies used across studies. Reduced caloric intake and weight loss, as well as binge-purging behaviors, are associated with an increased activity of HPA axis. However, when considering the occurrence of early adverse experiences, which are associated with impairment of HPA axis functioning, the findings are less clear-cut. Thus, it is important to remember that the mechanisms connecting stress and eating disorders are complex and multi-layered. It is important to recognize the variables that can contribute to these results in order to build formulations and develop precise and targeted treatments.
Background
Stress is associated with binge eating and emotional eating (EE) cross-sectionally. However, few studies have examined stress longitudinally, limiting understanding of how within-person fluctuations in stress influence EE over time and whether stress is a risk factor or consequence of EE. Additionally, little is known regarding how the biological stress response relates to EE.
Methods
We used an intensive, longitudinal design to examine between-person and within-person effects of major life stress, daily stress, and cortisol on EE in a population-based sample of women ( N = 477; ages 15–30; M = 21.8; s.d. = 3.0) from the Michigan State University Twin Registry. Participants reported past year major life stress, then provided daily ratings of EE and stress for 49 consecutive days. Hair cortisol concentration (HCC) was collected as a longitudinal biological stress measure.
Results
Women reported greater EE when they experienced greater mean stress across days (between-person effects) or greater stress relative to their own average on a given day (within-person effects). Daily stress was more strongly associated with EE than major life stress. However, the impact of daily stress on EE was amplified in women with greater past year major life stress. Finally, participants with lower HCC had increased EE.
Conclusions
Findings confirm longitudinal associations between stress and EE in women, and highlight the importance of within-person shifts in stress in EE risk. Results also highlight HCC as a novel biological stress measure that is significantly associated with EE and may overcome limitations of prior physiological stress response indicators.
Introducción:
En 2020, la Organización Mundial de la Salud (OMS) declaró la emergencia de salud pública por SARS-CoV-2¹; el 11 de marzo de 2020 se notificó la pandemia global por COVID-19 y el gobierno colombiano decretó para todas las ciudades el aislamiento preventivo obligatorio². Para el mes de mayo, Cali reportó 1635 casos de COVID confirmados y 85 fallecidos por un virus con un 4,95% de letalidad³. Lo anterior influenció de forma importante las rutinas alimentarias de las familias durante el primer trimestre del periodo de confinamiento. Considerando que esta situación era atípica en el país, era necesario describir la percepción del comportamiento alimentario durante este primer trimestre de aislamiento preventivo obligatorio en la ciudad de Cali, considerando las normas de bioseguridad establecidas para el periodo mencionado.
Objetivo:
Describir el comportamiento alimentario de 1814 familias en Cali durante el primer trimestre de aislamiento preventivo obligatorio.
Metodología:
Estudio cuantitativo, descriptivo transversal, con técnica de encuesta. Se aplicó un instrumento virtual compuesto por 28 ítems, que indagó el comportamiento alimentario de las familias.
Discusión:
Se encontró que el 95,1% de los hogares percibió escasez y aumento de precios en alimentos que componen la canasta alimentaria familiar, y el 67,2% de las familias estuvieron preocupadas por la alimentación. Hubo un aumento en el consumo de alimentos y se modificó el número de tiempos de comida/día. Los hábitos alimentarios, ingesta de refrescos y consumo de alcohol también se modificaron durante confinamiento.
Conclusiones:
Se puede afirmar que durante el primer trimestre de cuarentena por COVID-19 en Cali se modificó el comportamiento alimentario de las familias encuestadas, una de las razones estuvo relacionada con un cambio en los ingresos económicos, que afectó la cantidad de dinero disponible para alimentos. Durante este periodo se modificaron también los tiempos de comida y la variedad en la ingesta de alimentos. En general, se describieron aspectos que afectaron la seguridad alimentaria de las familias.
p>Lacey and Evans' (1986) Multi-Impulsivist Theory suggests that impulsivity is a key factor underlying the propensity to binge eat, and it may be equally or more closely associated with the core features of binge eating psychopathology such as negative affect and cognitive restraint. Theoretical perspectives are discussed and the literature review examines the relationship between binge eating and impulsivity by discussing the co-morbid symptomatologies mat exist between binge eating and other impulse dysregulated disorders. A specific focus addresses the multi-dimensional nature of impulsivity and its inherent methodological and theoretical considerations. The literature review suggests that the use of a behavioural delay discounting procedure to measure impulsivity would elucidate the relationship between binge eating and impulsivity. The empirical study used a behavioural delay-discounting task to measure levels of impulsivity in a group of binge eaters and a group of controls. It also investigated the utility of using a delay discounting procedure to understand the 'loss of control' phenomenon in binge eating behaviour. In line with previous research, both self-report and delay-discounting measures evidenced significantly higher levels of impulsivity in binge-eaters, although a lack of correlations between behavioural and self-report measures were identified. The study provides preliminary evidence suggesting that the delay-discounting model may be a useful utility to predict the 'loss of control' phenomenon inherent in binge eaters, although future research is required to consolidate and support this utility. These findings have implications for clinical interventions, which may lead to the development of more effective treatments.</p
Çalışmanın amacı, Covid-19 salgını sebebiyle evde karantina altında kalmanın gıda tüketim sıklığı ve fiziksel aktivite sıklığı üzerindeki etkilerini araştırmaktır. Araştırmanın ana kütlesi, Türkiye’de farklı bölgelerde bulunan 18 yaş ve üstü bireylerden oluşmaktadır. Ana kütleyi oluşturan bireyler arasından kolayda örnekleme yöntemiyle 411 kişiye ulaşılmış, 7 katılımcı araştırma kriterlerini karşılamamasından dolayı çıkartılmış ve 404 kişi araştırmaya dâhil edilmiştir. Araştırmada online anket ile ulaşılan verilere SPSS paket programıyla Wilcoxon Signed-Rank testi, tek yönlü varyans analizi Kruskal-Wallis testi ve Mann-Whitney U testi yapılmıştır. Analiz sonuçlarına göre, fiziksel aktivite sıklıklarından; hareketsiz davranışlarda medeni durum ve yaş arasında, hafif aktif davranışlarda çalışma durumları arasında, çok aktif davranışlarında cinsiyet arasında istatistiksel olarak anlamlı bir farklılık bulunmuştur. Ancak, orta derecede aktif fiziksel aktiviteler ile hiçbir grup arasında anlamlı farklılıklar bulunamamıştır. Ayrıca, tüm gruplar için Covid-19 öncesi ve sırasında hareketsiz davranışta yüksek düzeyde artışlar, fiziksel aktivite sıklıklarının tüm derecelerinde (hafif aktif, orta derecede aktif ve çok aktif) ise, yarı yarıya düşüşler gözlemlenmiştir. Son olarak, katılımcıların yaşları ve çalışma durumları itibariyle beslenme alışkanlıkları arasında istatistiki açıdan anlamlı farklılıklar tespit edilmiştir.
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.
Purpose
This research aims to introduce an anxious product-shaking effect, whereby consumers regulate the emotion of anxiety (i.e. anxious, nervous and jittery) elicited through product packaging design by shaking a product, which decreases eating intentions and behavior. Shaking product interaction as a result of anxiety-inducing product packaging design is introduced as a strategy to counter emotional eating, as an effective preventive measure of obesity.
Design/methodology/approach
Three laboratory studies (Studies 1–3) and one online study (Study 4) are conducted. Study 1 examines the effect of anxiety-inducing product packaging design on product interaction (i.e. shaking vs pouring). Study 2 investigates whether product shaking is a form of emotional regulation to anxiety-inducing product packaging design. Study 3 explores the effect of emotional regulation suppression (i.e. pouring) and facilitation (i.e. shaking) on eating behavior. Study 4 examines the moderating role of phobia severity on the effect of anxiety-inducing product packaging on emotional regulation and the downstream consequences on eating intentions.
Findings
Results demonstrate that the presence of anxiety-eliciting product packaging design results in shaking of the product (Study 1) as a form of emotional regulation (Study 2). Results from Study 3 find that emotional regulation facilitation (i.e. shaking) decreases eating, while emotion regulation suppression (i.e. pouring) increases eating. Results of Study 4 show that when exposed to anxiety-inducing product packing design, those with low phobia severity are less likely to regulate their emotions, which subsequently increases their eating intentions.
Research limitations/implications
This research is limited as it focuses only on product interaction and consumption of food products.
Practical implications
This research has important implications for marketers and product managers, as well as public policymakers, in encouraging responsible consumption behaviors in consumers. Marketing, product managers and policymakers should consider packaging design to introduce anxiety-inducing imagery on the packaging itself as a way to encourage shaking emotional regulation and to reduce eating, especially of unhealthy foods such as confectionary.
Originality/value
This research introduces and provides evidence of an anxious product-shaking effect that can reduce consumption of unhealthy food products. Anxiety-inducing packaging design strategy results in the emotional regulation of product shaking, which can reduce eating intentions and behavior.
Background:
Emotional eating has emerged as a contributing factor to overeating, potentially leading to obesity or disordered eating behaviors. However, the underlying biological mechanisms related to emotional eating remain unclear. The present study examined emotional, hormonal, and neural alterations elicited by an acute laboratory stressor in individuals with and without emotional eating.
Methods:
Emotional (n = 13) and non-emotional eaters (n = 15) completed two main study visits, one week apart: one visit included a Stress version and the other a No-stress version of the Maastricht Acute Stress Task (MAST). Immediately pre- and post-MAST, blood was drawn for serum cortisol and participants rated their anxiety level. After the MAST, participants completed a Food Incentive Delay (FID) task during functional magnetic resonance imaging (fMRI), followed by an ad libitum snack period.
Results:
Emotional eaters exhibited elevated anxiety (p = 0.037) and cortisol (p = 0.001) in response to the Stress MAST. There were no changes in anxiety or cortisol among non-emotional eaters in response to the Stress MAST or in either group in response to the No-stress MAST. In response to the Stress MAST, emotional eaters exhibited reduced activation during anticipation of food reward in mesolimbic reward regions (caudate: p < 0.014, nucleus accumbens: p = 0.022, putamen: p = 0.013), compared to non-emotional eaters. Groups did not differ in snack consumption.
Conclusions:
These data indicate disrupted neuroendocrine and neural responsivity to psychosocial stress amongst otherwise-healthy emotional eaters, who demonstrated hyperactive HPA-axis response coupled with hypoactivation in reward circuitry. Differential responsivity to stress may represent a risk factor in the development of maladaptive eating behaviors.
Simple Summary
Bone represents the most common site of metastasis for breast cancer and the establishment and growth of metastatic cancer cells within the skeleton significantly reduces the quality of life of patients and their survival. The interplay between sympathetic nerves and bone cells, and its influence on the process of breast cancer bone metastasis is increasingly being recognized. Several mechanisms, all dependent on β-adrenergic receptor signaling in stromal bone cells, were shown to promote the establishment of disseminated cancer cells into the skeleton. This review provides a summary of these mechanisms in support of the therapeutic potential of β-blockers for the early management of breast cancer metastasis.
Abstract
The skeleton is heavily innervated by sympathetic nerves and represents a common site for breast cancer metastases, the latter being the main cause of morbidity and mortality in breast cancer patients. Progression and recurrence of breast cancer, as well as decreased overall survival in breast cancer patients, are associated with chronic stress, a condition known to stimulate sympathetic nerve outflow. Preclinical studies have demonstrated that sympathetic stimulation of β-adrenergic receptors in osteoblasts increases bone vascular density, adhesion of metastatic cancer cells to blood vessels, and their colonization of the bone microenvironment, whereas β-blockade prevented these events in mice with high endogenous sympathetic activity. These findings in preclinical models, along with clinical data from breast cancer patients receiving β-blockers, support the pathophysiological role of excess sympathetic nervous system activity in the formation of bone metastases, and the potential of commonly used, safe, and low-cost β-blockers as adjuvant therapy to improve the prognosis of bone metastases.
The COVID-19 pandemic is known to influence the dietary habits of adults, but results
for adolescents in studies are ambiguous. The present work aimed to analyze the differences in the
scores of the Adolescents’ Food Habits Checklist (AFHC) before and during the pandemic in the
Polish Adolescents’ COVID-19 Experience (PLACE-19) Study population. The PLACE-19 Study was
conducted during the pandemic among a population of 2448 students recruited from secondary
schools in all regions of Poland using a random quota sampling. The participants were required to
complete an AFHC consisting of 23 items pertaining to food purchase, preparation, and consumption
habits. Current habits (during the pandemic) and previous habits were assessed and scored separately.
The total (p = 0.001), purchase (p < 0.001), and consumption scores (p = 0.014) indicated that the
AFHC scores during the pandemic were higher than before. For questions on purchase habits, a
lower number of respondents reported eating in a restaurant, eating takeaway meals, having lunch
away from home, or buying pastries, cakes or crisps. For questions on preparation habits, an greater
number of respondents reported that they usually avoided eating fried food and tried to keep their
overall sugar intake down, but fewer respondents said they tried to have low-fat desserts. For
questions on consumption habits, a lower number of respondents reported that they usually ate a
dessert or pudding if one were available and a larger number said they made sure to eat at least
one serving of vegetables or salad a day and at least three servings of fruit most days. Based on the
obtained results, it may be stated that although there was an increase in the AFHC scores during the
pandemic, a similar share of respondents showed improved or worsened food habits, and a similar
share changed their food habits from healthy to unhealthy and from unhealthy to healthy. At the
same time, a majority of changes were associated with purchase habits, which were probably forced
by lockdowns and the resultant restrictions in eating out or grocery shopping
The COVID-19 outbreak has affected billions of people worldwide. We are facing a critical situation with various challenges. Many countries have imposed restrictions in daily life activities to control the spread of virus. This caused change in working patterns and living conditions like staying indoors 1. This forced staying indoors for long time can cause stress conditions that directly affect eating habits. Prolonged stress triggers the release of cortisol that produce hunger sensation 2. In some people it also leads to binge eating disorder (BED). In BED there is regular and frequent intake of large quantities of food and no control over eating. Studies indicate that stress induces changes in our food preferences from low fat diet to high fat diet 3. Thus stress causes unhealthy food addiction that leads to obesity. Obesity boost the production of adipokines and other cytokines that eventually cause low grade inflammation, and affect the development of other metabolic conditions like diabetes and arterial hypertension 4. Data from different studies have shown high intake of food during quarantine in adults. A study was conducted in Poland to evaluate nutritional habits in adult during quarantine. About 50% people reported more eating and 43% stated weight gain. Weight loss was observed only in 18% of individuals. An increase in body mass index (BMI) was associated with high intake of fast-food, dairy and meat and, relatively less consumption of fruits, vegetables, and legumes during quarantine. This weight gain tendency was observed in older, overweight and obese subjects while underweight subjects showed a tendency towards weight loss 1. So, this study highlights a change in eating habits during quarantine and, obese and overweight people are more vulnerable. Thus, staying healthy during this period of confinement is challenging. Healthy eating habits during this time is important to enhance our immune system as virus is continuously spreading. It is important to remain physical active to control weight and eat balanced diet containing all essential nutrients. It is recommended to avoid high glycemic index carbohydrates like sweets, sugar or bread. Instead low glycemic index carbohydrates like brown rice, whole grain, legumes, vegetables and fruits should be used. Proteins are an important part of diet, so food rich in protein but with low percentage of fat should be included in diet 5. A balanced diet also helps in normal functioning of immune system.
Purpose
Emerging work indicates divergence in the neurobiologies of binge-eating disorder (BED) and obesity despite their frequent co-occurrence. This review highlights specific distinguishing aspects of BED, including elevated impulsivity and compulsivity possibly involving the mesocorticolimbic dopamine system, and discusses implications for differential therapeutics for BED.
Methods
This narrative review describes epidemiologic, clinical, genetic, and preclinical differences between BED and obesity. Subsequently, this review discusses human neuroimaging work reporting differences in executive functioning, reward processing, and emotion reactivity in BED compared with obesity. Finally, on the basis of the neurobiology of BED, this review identifies existing and new therapeutic agents that may be most promising given their specific targets based on putative mechanisms of action relevant specifically to BED.
Findings
BED is characterized by elevated impulsivity and compulsivity compared with obesity, which is reflected in divergent neurobiological characteristics and effective pharmacotherapies. Therapeutic agents that influence both reward and executive function systems may be especially effective for BED.
Implications
Greater attention to impulsivity/compulsivity-related, reward-related, and emotion reactivity–related processes may enhance conceptualization and treatment approaches for patients with BED. Consideration of these distinguishing characteristics and processes could have implications for more targeted pharmacologic treatment research and interventions.
Context The prevalence of obesity and overweight increased in the United States
between 1978 and 1991. More recent reports have suggested continued increases
but are based on self-reported data.Objective To examine trends and prevalences of overweight (body mass index [BMI]
≥25) and obesity (BMI ≥30), using measured height and weight data.Design, Setting, and Participants Survey of 4115 adult men and women conducted in 1999 and 2000 as part
of the National Health and Nutrition Examination Survey (NHANES), a nationally
representative sample of the US population.Main Outcome Measure Age-adjusted prevalence of overweight, obesity, and extreme obesity
compared with prior surveys, and sex-, age-, and race/ethnicity–specific
estimates.Results The age-adjusted prevalence of obesity was 30.5% in 1999-2000 compared
with 22.9% in NHANES III (1988-1994; P<.001).
The prevalence of overweight also increased during this period from 55.9%
to 64.5% (P<.001). Extreme obesity (BMI ≥40)
also increased significantly in the population, from 2.9% to 4.7% (P = .002). Although not all changes were statistically significant,
increases occurred for both men and women in all age groups and for non-Hispanic
whites, non-Hispanic blacks, and Mexican Americans. Racial/ethnic groups did
not differ significantly in the prevalence of obesity or overweight for men.
Among women, obesity and overweight prevalences were highest among non-Hispanic
black women. More than half of non-Hispanic black women aged 40 years or older
were obese and more than 80% were overweight.Conclusions The increases in the prevalences of obesity and overweight previously
observed continued in 1999-2000. The potential health benefits from reduction
in overweight and obesity are of considerable public health importance.
Compared the validities of 3 widely used self-report depression measures: the Beck Depression Inventory (BDI), the MMPI Depression scale, and the Self-Rating Depression Scale (SRDS). Each inventory was administered to 101 inpatient psychiatric ward patients and to 99 chemical dependency ward patients. All of the Ss were male and less than 60 yrs of age. The 3 scales were correlated with clinicians' global ratings of depression, with scores on 5 DSM-III-based factor-analytic depression scales, and with an overall depression score based on the DSM-III criteria. In general, the SRDS produced better validity coefficients than the BDI, which in turn yielded higher correlations with these criteria than did the MMPI Depression Scale. (5 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Stress is widely thought to lead to overeating. Studies of stress-induced eating have tested two models. One has tested whether stress increases eating in all exposed organisms and has been tested primarily with animals and physical stressors. The other has tested individual differences in vulnerability to stress-induced eating and has tested only human subjects and psychological stressors. The most consistent set of findings shows that "restrained" eating predicts vulnerability among women; we conclude that for the stressors studied to date, the individual-difference model has received stronger support. Because the question motivating much of this research is whether stress-induced eating causes obesity, future research should assess the effect of stress on weight-change more directly.
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)
This study evaluated the effectiveness of group cognitive-behavioral treatment (CBT) and group interpersonal psychotherapy (IPT) for binge eating. Fifty-six women with nonpurging bulimia were randomly assigned to 1 of 3 groups: CBT, IPT, or a wait-list control (WL). Treatment was administered in small groups that met for 16 weekly sessions. At posttreatment, both group CBT and group IPT treatment conditions showed significant improvement in reducing binge eating, whereas the WL condition did not. Binge eating remained significantly below baseline levels for both treatment conditions at 6-month and 1-year follow-ups. These data support the central role of both eating behavior and interpersonal factors in the understanding and treatment of bulimia.
Natural or experimental starvation is frequently associated with hypercortisolism, reflected as incomplete suppression of serum cortisol after dexamethasone. To determine whether rapid weight loss per se or some other aspect of starvation induces disruption of the hypothalamic-pituitary-adrenal (HPA) axis, we evaluated 2 categories of obese women (body mass index > 30 kg/m2) undergoing rapid weight loss: binge eaters (n = 12) and nonbinge eaters (n = 8). We performed psychometric evaluation and 1 mg overnight dexamethasone suppression tests in the obese subjects, as well as in 12 race- and age-matched normal-weight women. The obese women were tested before and after 12 weeks of a 3349 kJ/day (800 kcal/day) liquid formula diet, and lost an average of 19.3 kg, which represented 17.3% of their total body weight. Binge eaters, who were initially more depressed than either nonbinge eaters or normal-weight controls, had a significant amelioration of their symptoms with weight loss. Neither group had evidence of...
• A 1-mg dexamethasone suppression test (DST) was carried out in 66 women with bulimia and in 26 age- and sexmatched controls. Blood samples were obtained at 4 PM on the day following dexamethasone ingestion, and levels of cortisol and of dexamethasone in the plasma were measured. Thirtytwo percent of the patients vs only 7% of the controls had plasma cortisol levels of 140 nmol/L (5 μ/dL) or greater following the DST (a positive DST). The plasma levels of dexamethasone varied substantially, and there was a significant inverse relationship between the plasma level of cortisol and that of dexamethasone. Patients with positive DST results had lower levels of plasma dexamethasone than did those with negative DST results, and the mean plasma level of dexamethasone was lower in the bulimic group than in the control group. These results suggest that factors other than a disturbance of hypothalamic-pituitary-adrenal activity may contribute to positive DST results in bulimia.
RECENT development and use of the Self-Rating Depression Scale (SDS) has Proven to be a valuable tool in the assessment of depressive disorders in a group of hospitalized inpatients.1 There is a similar need in outpatient clinics to quantitate the amount of depressive symptomatology present or absent in the patients seen for treatment. Depressive symptoms may be present in any of the psychiatric disturbances seen in such a clinic, and a diagnosis of depressive disorder must still be made on a clinical basis. However, the use of such a scale is valuable in documenting and quantitating initial symptoms and complaints, and following changes in the patient's clinical course subsequent to treatment, using any of the modalities available.
The purpose of a self-rating depression scale to be used in such an outpatient clinic setting would be similar to the ones stated previously with respect to its
Binge eating disorder (BED) is a newly characterized eating disorder that encompasses individuals who have severe distress and dysfunction due to binge eating, but who do not regularly engage in inappropriate compensatory behaviors. While relatively uncommon in the general community, BED becomes more prevalent with increasing severity of obesity. BED is associated with early onset of obesity, frequent weight cycling, body shape disparagement, and psychiatric disorders. These associations occur independent of the degree of obesity. Although many individuals with BED have good short-term weight loss regardless of treatment modality, as a group they may be prone to greater attrition during weight-loss treatment and more rapid regain of lost weight. Current treatments geared toward binge eating behaviors include antidepressant medications, cognitive behavioral psychotherapy, and interpersonal psychotherapy; however, these treatments have little efficacy in promoting weight loss, and only modest success in long-term reduction of binge eating. As a significant proportion of obese individuals entering weight-loss treatment and research programs are likely to meet criteria for BED, those conducting clinical research should be aware of this distinct subgroup and determine the contribution of BED to outcome measures. (OBESITY RESEARCH 1993; 1:306–324)
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.
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.
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.
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.
Among the more consistent observations in patients with major depression is dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis presenting as elevation of basal cortisol, dexamethasone-mediated negative feedback resistance, increased cerebrospinal fluid levels of corticotropin-releasing factor (CRF), and a blunted adrenocorticotropic hormone (ACTH) response to challenge with exogenous CRF. These features appear to be state, rather than trait markers, and are normalized upon successful treatment. These pathophysiologic adaptations may arise from defects in central drive to the neuroendocrine hypothalamus, disruption of normal adrenocortical hormone receptor function or a modification of HPA axis function at any level. Functional assessment of the HPA axis is thought to provide a window into central nervous system operation that may be of diagnostic value in this and other affective disorders regardless of whether CRF and glucocorticoids are directly involved in the origin of major depression or merely exacerbate the consequences of other primary defects.
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.
Seventy-two psychoanalysts collected information on 84 obese patients and on a control sample of 63 of their patients of normal weight. Despite the fact that obesity was the chief complaint of only 6% of the obese patients, weight losses at 42 months of psychoanalytic treatment compared favorably with those after traditional medical efforts: 47% of the obese psychoanalytic patients lost more than 9 kg, and 19% lost more than 18 kg. There was also a striking decrease in the percentage of obese patients suffering from body image disparagement--from 44% to 12%, an unexpectedly good result for this chronic and intractable disorder.
Adrenocortical activity was studied in 19 emaciated women with anorexia nervosa. Relative to body size the patients' mean cortisol production rates of 0.591 mg/kg/day and 16.4 mg m2/day were significantly elevated compared to those of 0.322 mg/kg/day and 11.4 mg/m2/day for age and sex matched normal controls (p less than 0.001 and 0.02, respectively). The 24-hr mean plasma cortisol concentration in 18 patients was 10.6 microgram/dl and was significantly higher than that of the controls (6.8 microgram/dl, p less than 0.001). The average excretion of urinary free cortisol in nine patients was 205 microgram/day, significantly greater than that of 65 microgram/day in the controls (less than 0.01). Three patients underwent overnight suppression with 1 mg of dexamethasone and had inadequate responses. These data suggest that cortisol production is excessive in emaciated patients with anorexia nervosa due to a disturbance of the hypothalamic-pituitary mechanisms regulating adrenocortical function. The excessive adrenal activity may reflect certain psychobiological disturbances as well as the effects of malnutrition.
This study describes 84 obese patients compared with 63 matched, normal-weight patients, all treated by psychoanalysis or psychoanalytic therapy. Information about the characteristics of the 2 samples was contributed by 72 psychoanalysts, members of the American Academy of Psychoanalysis. The study had 3 goals: to test the feasibility of a large-scale research project using data contributed by psychoanalysts with disparate theoretical orientations working in various parts of the country; to assess in a systematic way, on the basis of psychoanalytic data, personality characteristics of obese as compared with non-obese patients; and to ascertain the effectiveness of psychoanalysis in treating 2 problems specific to obesity: overweight and disparagement of body image.
Earlier, the authors reported on the association of nicotine dependence with major depression and anxiety disorders in a group of young adults. This report describes the occurrence of withdrawal symptoms and their sociodemographic and psychiatric correlates in persons in that group who tried unsuccessfully to abstain from smoking.
A random sample of 1,007 members of a health maintenance organization, 21-30 years old, were interviewed with a revised version of the NIMH Diagnostic Interview Schedule. Data on nicotine withdrawal came from a subset of 239 smokers who had tried unsuccessfully to quit or cut down on smoking.
With two exceptions, each of the DSM-III-R nicotine withdrawal symptoms was reported by more than one-half of these smokers. Withdrawal symptoms were more severe in white than in black smokers but were unrelated to sex, educational level, or marital status. Persons with histories of major depression or any anxiety disorder reported more severe withdrawal symptoms than persons with neither of these disorders. Severity of withdrawal, or any specific symptom, did not account for the association between major depression and continued smoking. Furthermore, severity of withdrawal was unrelated to continued smoking.
While the long-term clinical significance of nicotine withdrawal is unclear, the evidence indicates that in the general population, abstinence from smoking is associated with a variety of disturbances, including a craving for cigarettes, dysphoria, and symptoms of irritability or nervousness. In this study disturbances were more severe in persons with histories of major depression or anxiety disorders.
Recent prospective, epidemiological research has demonstrated the power of an increased waist/hip circumference ratio (WHR) to predict both cardiovascular disease (CVD) and non-insulin dependent diabetes mellitus (NIDDM) in men and women. Obesity, defined as an increased total body fat mass, seems to interact synergistically in the development of NIDDM, but not of CVD. Increased WHR with obesity (abdominal obesity) seems to be associated with a cluster of metabolic risk factors, as well as hypertension. This metabolic syndrome is closely linked to visceral fat mass. Increased WHR without obesity may instead be associated with lift style factors such as smoking, alcohol intake, physical inactivity, coagulation abnormalities, psychosocial, psychological and psychiatric factors. Direct observations show, and the risk factor associations further strengthen the assumption, that abdominal (visceral) obesity is more closely associated to NIDDM than CVD, while an increased WHR without obesity may be more closely linked to CVD than NIDDM. It remains to be established to what extent, if any, an increased WHR in lean men, and particularly in lean women, indicates fat distribution. Other components of the WHR measurement might be of more importance in this connection.
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.
The aim of this study was to determine the ability of transcranial Doppler ultrasonography when used to assess cerebral vasoreactivity. The results of this method were compared with regional cerebral blood flow measurements.
Forty-three patients with symptoms suggesting cerebrovascular disease took part. Transcranial Doppler findings in the middle cerebral arteries were compared with regional cerebral blood flow in the corresponding perfusion territories before and after acetazolamide administration.
There was a significant positive correlation between the absolute increase in cerebral blood flow in milliliters per 100 g per minute and the percent increase in velocity (r = 0.63). The right-left, side-to-side difference of the acetazolamide response obtained by the two methods also showed a positive correlation (r = 0.80). Control limits obtained from healthy subjects were used for both the blood flow increase (absolute values and asymmetry in absolute values) and the velocity increase (percent increase and asymmetry in percent increase). The two methods then agreed in their evaluation of vasoreactivity in 74 (86%) of the 86 middle cerebral artery perfusion territories; 20 (23%) were assessed by both methods as having a reduced vasodilatory reserve. Eleven hemispheres with a slightly reduced regional cerebral blood flow response to acetazolamide were not detected by transcranial Doppler, whereas all territories with a marked reduction were identified by Doppler. Only one hemisphere with a normal cerebral blood flow increase after acetazolamide administration was assessed by Doppler as having reduced vasoreactivity.
Transcranial Doppler and the acetazolamide test may be used in clinical situations to assess cerebral vasoreactivity.
Disturbances in the hypothalamo-pituitary-adrenal (HPA) and other endocrine axes were assessed in 24 women with bulimia and healthy controls. Overnight blood samples for measuring nocturnal plasma cortisol, prolactin (PRL), growth hormone (GH), luteinizing hormone (LH), and follicle stimulating hormone (FSH) were obtained at 30-min intervals. A 1.5 mg dexamethasone suppression test (DST) and a TRH-test were performed. Patients were monitored closely while their nutritional intake was recorded over 21 days. Compared with healthy controls, nocturnal cortisol plasma levels were not elevated in the bulimics. There was a trend toward insufficient cortisol suppression in the DST in patients with bulimia, which was most pronounced in patients with signs of restricted caloric intake. Plasma dexamethasone levels were significantly reduced in bulimics compared with healthy controls. There was a trend for blunted thyrotropin stimulating hormone (TSH) responses to thyrotropin releasing hormone (TRH) in bulimia. The prolactin response to TRH was significantly reduced in bulimics with a history of anorexia nervosa. Plasma LH and plasma FSH were significantly reduced in bulimics with signs of reduced caloric intake [low T3, high levels of beta-hydroxy-butyric acid (BHBA), reduced daily caloric intake, high number of fasting days] as compared with healthy controls. Bulimics with high BHBA levels had significantly reduced nocturnal prolactin plasma levels. Results show that multiple neuroendocrine disturbances exist in bulimia in a milder form than in anorexia nervosa. Evidence for the impact of caloric intake on endocrine functions is presented. Endocrine dysfunctions in our bulimic sample did not show a positive association with the presence of depressive symptoms.
We studied hypothalamic-pituitary-adrenal-cortical (HPA) activity in nine underweight women with anorexia nervosa, 12 women of normal body weight with bulimia, and nine control subjects. The measures of HPA activity were the pattern of plasma cortisol secretion over 24 hr and the responses of plasma cortisol to dexamethasone suppression and to low dose ACTH stimulation. The patients with anorexia nervosa had significantly elevated 24 hr concentrations of plasma cortisol compared to the controls and showed significantly less cortisol suppression following dexamethasone. There was no difference between patients with anorexia nervosa and controls in the rise in plasma cortisol following ACTH. On most measures of HPA activity, the normal weight patients with bulimia were indistinguishable from the controls. These results suggest that HPA activity is normal in most patients of normal body weight with bulimia and that the psychological and behavioral disturbances common to both anorexia nervosa and bulimia are, in the absence of significant weight loss, insufficient to produce major alterations in HPA activity.
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.
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.
A 1-mg dexamethasone suppression test (DST) was carried out in 66 women with bulimia and in 26 age- and sex-matched controls. Blood samples were obtained at 4 PM on the day following dexamethasone ingestion, and levels of cortisol and of dexamethasone in the plasma were measured. Thirty-two percent of the patients vs only 7% of the controls had plasma cortisol levels of 140 nmol/L (5 micrograms/dL) or greater following the DST (a positive DST). The plasma levels of dexamethasone varied substantially, and there was a significant inverse relationship between the plasma level of cortisol and that of dexamethasone. Patients with positive DST results had lower levels of plasma dexamethasone than did those with negative DST results, and the mean plasma level of dexamethasone was lower in the bulimic group than in the control group. These results suggest that factors other than a disturbance of hypothalamic-pituitary-adrenal activity may contribute to positive DST results in bulimia.
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.
The relationship of the endogenous opioid system and the hypothalamic-pituitary-adrenal axis to obesity was studied. Morning levels of plasma cortisol and beta-endorphin immunoreactivity in obese patients before diet treatment were found to be no different from those in matched family members of normal weight. In 32 untreated obese patients, no relationship between weight or body mass index (a measurement of obesity) and plasma levels of beta-endorphin immunoreactivity or cortisol was found. However, plasma cortisol levels were significantly correlated with obese patient ratings on the depression subscale of the General Health Questionnaire. Dexamethasone administration failed to suppress plasma beta-endorphin levels in untreated obese patients, but this finding has been reported in normal subjects in whom a similar assay methodology was used; it suppressed plasma cortisol levels in 29 of 32. The three patients resistant to suppression also suffered from benign essential hypertension. Plasma beta-endorphin immunoreactivity was unchanged, but cortisol levels significantly decreased as weight was lost on a 400-calorie/day modified protein fast. Patients who failed to complete the 6-month diet program had significantly increased plasma beta-endorphin levels compared to those who successfully completed the program.
The authors studied postdexamethasone cortisol secretion in 18 depression-free, healthy, obese subjects before and after weight loss. Although all subjects suppressed cortisol normally before weight loss, 5 of 18 (27.5%) failed to suppress cortisol after an average loss of 13.5 kg. This failure to suppress cortisol was not associated with any change in depression ratings.
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.
The authors determined the prevalence of binge eating disorder in a self-referred study group of moderately and severely obese subjects and investigated whether binge eating disorder was associated with psychiatric disorders, a history of psychotherapy, a family history of psychiatric illness, or a history of sexual abuse.
They interviewed 89 obese women and 39 obese men (body mass index > 30 kg/m2) who were not currently in weight loss treatment, using the Binge Eating Disorder Clinical Interview, the Structured Clinical Interview for DSM-III-R, and the Structured Clinical Interview for DSM-III-R Personality Disorders.
Forty-three (34%) of the subjects met criteria for binge eating disorder--33 women and 10 men. Black and white subjects had similar rates of binge eating disorder. Subjects with binge eating disorder were significantly more likely than those without the disorder to have a lifetime prevalence of a DSM-III-R axis I or axis II diagnosis and to have undergone psychotherapy or counseling. The lifetime rates of major depression, panic disorder, bulimia nervosa, borderline personality disorder, and avoidant personality disorder were all significantly higher in subjects with binge eating disorder. The rate of reported sexual abuse was not higher among subjects with binge eating disorder; however, they were significantly more likely to have a family history of substance abuse. The relative risks for psychiatric disorders were higher in both moderately and severely obese subjects with binge eating disorder than in those without the disorder.
Among both moderately and severely obese subjects, binge eating disorder is associated with higher rates of axis I and axis II psychiatric disorders.
Immunological and neuroendocrine parameters were examined in 11 women with anorexia nervosa, 6 restricted and 5 bulimic-anorectics, 17-43 years old with 2-15 years duration of the disease, and in 11 age- and sex-matched psychophysically healthy controls. The T lymphocyte proliferative response to phytohemagglutinin (PHA), plasma adrenocorticotropic hormone (ACTH), cortisol and beta-endorphin (beta-EP) levels was examined in basal conditions and after corticotropin-releasing hormone (CRH) stimulation. Cortisol inhibition by dexamethasone (DST), and basal growth hormone (GH) and prolactin (PRL) levels were also examined. The immune study did not reveal significant differences between patients and controls. ACTH and cortisol basal levels were significantly higher in anorectics, while beta-EP, GH and PRL concentrations did not differ in the two groups. ACTH, beta-EP and cortisol responses to CRH were blunted in anorectics and the DST impaired in 55% of the patients. No correlations were observed between neuroendocrine impairments and the T lymphocyte response to PHA, or between the immunological neuroendocrine parameters and the body mass index of either patients or controls.
Natural or experimental starvation is frequently associated with hypercortisolism, reflected as incomplete suppression of serum cortisol after dexamethasone. To determine whether rapid weight loss per se or some other aspect of starvation induces disruption of the hypothalamic-pituitary-adrenal (HPA) axis, we evaluated 2 categories of obese women (body mass index > 30 kg/m2) undergoing rapid weight loss: binge eaters (n = 12) and nonbinge eaters (n = 8). We performed psychometric evaluation and 1 mg overnight dexamethasone suppression tests in the obese subjects, as well as in 12 race- and age-matched normal-weight women. The obese women were tested before and after 12 weeks of a 3349 kJ/day (800 kcal/day) liquid formula diet, and lost an average of 19.3 kg, which represented 17.3% of their total body weight. Binge eaters, who were initially more depressed than either nonbinge eaters or normal-weight controls, had a significant amelioration of their symptoms with weight loss. Neither group had evidence of disruption of the HPA axis before or after weight loss. Thus, the rate of failure to suppress cortisol after dexamethasone was approximately 10% in each of the obese and control groups, and did not differ between the pre- and postweight loss condition or between binge eaters and nonbinge eaters. Serum free T4 was unchanged, whereas T3 fell significantly with weight loss. We conclude that weight loss may improve affect in the obese without altering HPA axis activity, and postulate that one of the concomitants of restricted energy intake, perhaps in combination with a threshold body weight, may be of greater importance in causing abnormalities of dexamethasone suppression testing than rapid weight loss per se.
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.
A new device based on the plethysmographic measurement of body volume has been developed for the purpose of estimating human body composition. The device, the BOD POD Body Composition System, uses the relationship between pressure and volume to derive the body volume of a subject seated inside a fiberglass chamber. Derivation of body volume, together with measurement of body mass, permits calculation of body density and subsequent estimation of percent fat and fat-free mass. Critical issues which have hampered prior plethysmographic approaches are discussed. The present system's ability to measure the volume of inanimate objects was evaluated for accuracy, reliability, and linearity. Twenty successive tests of a known volume (50,039 ml) on two separate days produced values of 50,037 +/- 12.7 ml and 50,030 +/- 13.5 ml (mean +/- SD) for each day, respectively. The CV for these series were 0.025% and 0.027%. Further testing across a wide range of volumes approximating human size (25-150 1) produced the following regression equation where y = measured volume (1) and x = actual volume (1): y = 0.9998x - 0.0274, r2 = 1.0, SEE = 0.004 1. The resultant device is likely to enhance opportunities for the quick, simple and noninvasive measurement of body composition for both research and clinical applications.
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.
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.
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.
The early preclinical detection of cerebrovascular complications in individuals with diabetes is one of the goals of care described in the St. Vincent Declaration. In accordance with this goal, the aim of the present work was to investigate whether altered cerebral microvascular function in patients suffering from type 1 diabetes can be detected with a transcranial Doppler probe after the administration of acetazolamide. A total of 72 type 1 diabetic patients and 40 healthy control subjects entered the study. Patients were divided into two groups: those with long-term diabetes (disease duration of >10 years, n = 37) and those with short-term diabetes (disease duration of < or =10 years, n = 35). Mean blood-flow velocity in the middle cerebral artery (MCAV) was measured at rest and at 5, 10, 15, and 20 min after intravenous administration of 1 g acetazolamide with a transcranial Doppler probe and expressed as the percentage change from the pretest measurement. The percentage increase in MCAV (cerebrovascular reactivity) was calculated at each time point and compared between the groups. Cerebrovascular reserve capacity (CRC), expressed as the maximal percentage increase of the MCAV, was compared between the groups. Additionally, a reproducibility study of CRC was performed in 10 patients, using intraclass correlations. Cerebrovascular reactivity in the long-term diabetes group was lower (means +/- SD: 5 min, 23.4 +/- 15.4%; 10 min, 28.8 +/- 17.0%; 15 min, 30.0 +/- 15.6%; 20 min, 24.2 +/- 17.8%) than that of the control subjects (5 min, 43.5 +/- 23.9%; 10 min, 55.3 +/- 24.0%; 15 min, 56.7 +/- 23.8%; 20 min, 54.8 +/- 25.9%) and the short-term diabetic patients (5 min, 43.6 +/- 25.9%; 10 min, 52.2 +/- 27.7%; 15 min, 55.3 +/- 32.2%; 20 min, 45.8 +/- 35.8%). CRC was lower in the long-term diabetes group than in the control group or the short-term diabetes group. Impairment of cerebrovascular reactivity was associated with retino- and nephropathy and increased levels of fibrinogen. In contrast, CRC was independent from actual glucose, insulin, glycosylated hemoglobin, von Willebrand factor antigen, and alpha-2 macroglobulin levels. Transcranial Doppler measurements of the changes in MCAV after stimulation with acetazolamide can detect altered cerebral microvascular function in patients with diabetes. Cerebrovascular reactivity and reserve capacity are reduced in patients with long-term diabetes. Further prospective studies should delineate the clinical significance of our results.
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.
Among the more consistent observations in patients with major depression is dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis presenting as elevation of basal cortisol, dexamethasone-mediated negative feedback resistance, increased cerebrospinal fluid levels of corticotropin-releasing factor (CRF), and a blunted adrenocorticotropic hormone (ACTH) response to challenge with exogenous CRF. These features appear to be state, rather than trait markers, and are normalized upon successful treatment. These pathophysiologic adaptations may arise from defects in central drive to the neuroendocrine hypothalamus, disruption of normal adrenocortical hormone receptor function or a modification of HPA axis function at any level. Functional assessment of the HPA axis is thought to provide a window into central nervous system operation that may be of diagnostic value in this and other affective disorders regardless of whether CRF and glucocorticoids are directly involved in the origin of major depression or merely exacerbate the consequences of other primary defects.
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.
Noradrenergic systems have been shown to be disordered in depressive illness. The plasma norepinephrine response to a cold pressor test was used to investigate norepinephrine activity in subtypes of depressive illness. Patients with melancholic or psychotic depression, non-melancholic depression, general anxiety disorder and normal control subjects had a cold pressor test carried out under standard conditions. Blood samples were taken to measure plasma norepinephrine during the test. The plasma norepinephrine response to a cold pressor test was reduced in the melancholic/psychotic depressed patients compared to control subjects. No other intergroup comparisons were statistically significant. These results suggest noradrenergic systems are disturbed and subresponsive to stress in melancholic/psychotic depressed patients. This does not appear related to other clinical or biochemical factors.