a Department of Psychosomatic Medicine and Psychotherapy, University Medical Hospital Tübingen, Tübingen , b Department of General Internal Medicine and Psychosomatics, Heidelberg University Hospital, Heidelberg , c Department of Psychosomatic Medicine and Psychotherapy, University Hospital Giessen and Marburg, Giessen and Marburg , and d Department of Psychosomatic Medicine and Psychotherapy, Klinikum rechts der Isar, Technical University of Munich, Munich , Germany

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Psychosomatic Medicine in Germany: More Timely than Ever

Emotion regulation model in binge eating disorder and obesity--a systematic review.

The salience network (SN) plays a central role in cognitive control by integrating sensory input to guide attention, attend to motivationally salient stimuli, and recruit appropriate functional brain-behavior networks to modulate behavior. Mounting evidence suggests that disturbances in SN function underlie abnormalities in cognitive control and may be a common etiology underlying many psychiatric disorders. Such functional and anatomical abnormalities have been recently apparent in studies and meta-analyses of psychiatric illness using functional magnetic resonance imaging (fMRI) and voxel-based morphometry (VBM). Of particular importance, abnormal structure and function in major cortical nodes of the SN, the dorsal anterior cingulate cortex (dACC) and anterior insula (AI), have been observed as a common neurobiological substrate across a broad spectrum of psychiatric disorders. In addition to cortical nodes of the SN, the network’s associated subcortical structures, including the dorsal striatum, mediodorsal thalamus, and dopaminergic brainstem nuclei, comprise a discrete regulatory loop circuit. The SN’s cortico-striato-thalamo-cortical loop increasingly appears to be central to mechanisms of cognitive control, as well as to a broad spectrum of psychiatric illnesses and their available treatments. Functional imbalances within the SN loop appear to impair cognitive control, and specifically may impair self-regulation of cognition, behavior, and emotion, thereby leading to symptoms of psychiatric illness. Furthermore, treating such psychiatric illnesses using invasive or non-invasive brain stimulation techniques appears to modulate SN cortical-subcortical loop integrity, and these effects may be central to the therapeutic mechanisms of brain stimulation treatments in many psychiatric illnesses. Here, we review clinical and experimental evidence for abnormalities in SN cortico-striatal-thalamic loop circuits in major depression, substance use disorders, anxiety disorders, schizophrenia, and eating disorders. We also review emergent therapeutic evidence that novel invasive and non-invasive brain stimulation treatments may exert therapeutic effects by normalizing abnormalities in the salience network loop, thereby restoring capacity for cognitive control. Finally, we consider a series of promising directions for future investigations on the role of SN cortico-striatal-thalamic loop circuits in the pathophysiology and treatment of psychiatric disorders.

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Cortico-Striatal-Thalamic Loop Circuits of the Salience Network: A Central Pathway in Psychiatric Disease and Treatment.

Background
Eating disorders are severe psychiatric disorders with a complex etiology involving transactions among sociocultural, psychological, and biological influences. Most research and reviews, however, focus on only one level of analysis. To address this gap, we provide a qualitative review and summary using an integrative biopsychosocial approach.

Methods
We selected variables for which there were available data using integrative methodologies (e.g., twin studies, gene-environment interactions) and/or data at the biological and behavioral level (e.g., neuroimaging). Factors that met these inclusion criteria were idealization of thinness, negative emotionality, perfectionism, negative urgency, inhibitory control, cognitive inflexibility, serotonin, dopamine, ovarian hormones. Literature searches were conducted using PubMed. Variables were classified as risk factors or correlates of eating disorder diagnoses and disordered eating symptoms using Kraemer et al.'s (1997) criteria.

Findings
Sociocultural idealization of thinness variables (media exposure, pressures for thinness, thin-ideal internalization, thinness expectancies) and personality traits (negative emotionality, perfectionism, negative urgency) attained ‘risk status’ for eating disorders and/or disordered eating symptoms. Other factors were identified as correlates of eating pathology or were not classified given limited data. Effect sizes for risk factors and correlates were generally small-to-moderate in magnitude.

Conclusions
Multiple biopsychosocial influences are implicated in eating disorders and/or disordered eating symptoms and several can now be considered established risk factors. Data suggest that psychological and environmental factors interact with and influence the expression of genetic risk to cause eating pathology. Additional studies that examine risk variables across multiple levels of analysis and that consider specific transactional processes amongst variables are needed to further elucidate the intersection of sociocultural, psychological, and biological influences on eating disorders.

Research Review: What we have learned about the causes of eating disorders – a synthesis of sociocultural, psychological, and biological research

Recent findings suggest the existence of a frontoparietal control system consisting of flexible hubs that regulate distributed systems (e.g., visual, limbic, motor) according to current task goals. A growing number of studies are reporting alterations of this control system across a striking range of mental diseases. We suggest this may reflect a critical role for the control system in promoting and maintaining mental health. Specifically, we propose that this system implements feedback control to regulate symptoms as they arise (e.g., excessive anxiety reduced via regulation of amygdala), such that an intact control system is protective against a variety of mental illnesses. Consistent with this possibility, recent results indicate that several major mental illnesses involve altered brain-wide connectivity of the control system, likely altering its ability to regulate symptoms. These results suggest that this "immune system of the mind" may be an especially important target for future basic and clinical research.

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The Frontoparietal Control System A Central Role in Mental Health

https://isiarticles.com/bundles/Article/pre/pdf/34957.pdf

Difficulties in emotion regulation across the spectrum of eating disorders

The aim of this meta-analysis was to summarise data from neuropsychological studies on inhibitory control to general and disease-salient (i.e., food/eating, body/shape) stimuli in bulimic-type eating disorders (EDs). A systematic literature search was conducted to identify eligible experimental studies. The outcome measures studied included the performance on established inhibitory control tasks in bulimic-type EDs. Effect sizes (Hedges' g) were pooled using random-effects models. For inhibitory control to general stimuli, 24 studies were included with a total of 563 bulimic-type ED patients: 439 had bulimia nervosa (BN), 42 had anorexia nervosa of the binge/purge subtype (AN-b), and 82 had binge eating disorder (BED). With respect to inhibitory control to disease-salient stimuli, 12 studies were included, representing a total of 218 BN patients. A meta-analysis of these studies showed decreased inhibitory control to general stimuli in bulimic-type EDs (g = −0.32). Subgroup analysis revealed impairments with a large effect in the AN-b group (g = −0.91), impairments with a small effect in the BN group (g = −0.26), and a non-significant effect in the BED group (g = −0.16). Greater impairments in inhibitory control were observed in BN patients when confronted with disease-salient stimuli (food/eating: g = −0.67; body/shape: g = −0.61). In conclusion, bulimic-type EDs showed impairments in inhibitory control to general stimuli with a small effect size. There was a significantly larger impairment in inhibitory control to disease salient stimuli observed in BN patients, constituting a medium effect size.

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Inhibitory control in bulimic-type eating disorders: a systematic review and meta-analysis.

Background. In this meta-analysis we review the findings from neuropsychological studies on set-shifting in people with eating disorders (EDs) or overweight/obesity. Method. Four databases (PubMed, PsycINFO, PSYNDEX and Web of Science) were searched for eligible studies. Effect sizes (ESs) were pooled using random-effects models. Moderator analyses were conducted for ED and overweight/obese subgroups, adult/adolescent samples and measures of set-shifting. Results. Sixty-four studies with a total of 1825 ED patients [1394 anorexia nervosa (AN), 376 bulimia nervosa (BN) and 55 binge eating disorder (BED)] and 10 studies with a total of 449 overweight/obese individuals were included. The meta-analysis revealed a small to medium ES for inefficient set-shifting across all three ED diagnoses (Hedges’ g = –0.45). Subgroup analyses yielded small to medium ESs for each ED subtype (g = –0.44 for AN, –0.53 for BED, –0.50 for BN), which did not differ significantly. There was a medium ES for restricting type AN (ANR; g = –0.51) but no significant ES for binge/purge type AN (AN/BP; g = –0.18). A medium ES was found across obesity studies (g = –0.61). The ES across overweight studies was not significant (g = –0.07). Adult samples did not differ from adolescent samples in either ED or overweight/obesity studies. The different set-shifting measures were associated with largely varying ESs. Conclusions. The meta-analysis provides strong support that inefficient set-shifting is a salient neuropsychological phenomenon across ED subtypes and obesity, but is less prominent in AN/BP and overweight. Compulsivity seems to be a common underlying factor supporting a dimensional and transdiagnostic conceptualization of EDs and obesity.

Set-shifting ability across the spectrum of eating disorders and in overweight and obesity: a systematic review and meta-analysis.

Objective

To investigate neuropsychological mechanisms of impulsivity in patients with bulimia nervosa (BN) and binge-eating disorder (BED).



Method

Nineteen BN patients and 31 age- and body-mass-index (BMI)-matched healthy controls (c-BN) as well as 54 overweight and obese BED patients and 43 age- and BMI-matched healthy controls (c-BED) were investigated using an inhibitory control task (stop signal task, SST) and a decision-making under risk task (game of dice task, GDT).



Results

Compared to c-BN, BN patients demonstrated significant greater stop signal reaction times in the SST, but no differences for the frequency of risky decisions in the GDT. BED patients did not differ from c-BED in the SST or the GDT.



Discussion

BN but not BED patients differed from their respective control groups concerning the “stopping” component of impulsivity. These differences in motor inhibition may contribute to the behavioral distinctions in binge-eating behavior between BN and BED. © 2013 Wiley Periodicals, Inc. (Int J Eat Disord 2013; 46:721–728)

Inhibitory control and decision making under risk in bulimia nervosa and binge‐eating disorder

Objective:
Eating disorders are serious psychosomatic disorders with high morbidity and lifetime mortality. Inadequate response to current therapeutic interventions constitutes a challenging clinical problem. A better understanding of the underlying neurobiological mechanisms could improve psychotherapeutic and drug treatment strategies.

Method:
A review highlighting the current state of brain imaging in eating disorders related to the anxiety and pathological fear learning model of anorexia nervosa (AN) and the impulsivity model of binge eating in bulimia nervosa (BN).

Results:
Available neuroimaging studies in patients with acute AN primarily suggest a hyper-responsive emotional and fear network to food, but not necessarily to eating disorder-unrelated, salient stimuli. Furthermore, patients with AN show decreased activation in the ventral fronto-striatal circuits during the performance of a cognitive flexibility task. Results in patients with BN primarily suggest a hypo-responsive reward system to food stimuli, especially to taste reward. Additionally, patients with BN exhibit impaired brain activation in the inhibitory control network during the performance of general response–inhibition tasks.

Discussion:
Anxiety and pathological fear learning may lead to conditioned neural stimulus-response patterns to food stimuli and increased cognitive rigidity, which could account for the phobic avoidance of food intake in patients with acute AN. However, further neurobiological studies are required to investigate pathological fear learning in patients with AN. Patients with BN may binge eat to compensate for a hypo-responsive reward system. The impaired brain activation in the inhibitory control network may facilitate the loss of control over food intake in patients with BN. © 2013 by Wiley Periodicals, Inc. (Int J Eat Disord 2013; 46:425–432)

Mudan Wu

Papers

Difficulties in emotion regulation across the spectrum of eating disorders

Inhibitory control in bulimic-type eating disorders: a systematic review and meta-analysis.

Set-shifting ability across the spectrum of eating disorders and in overweight and obesity: a systematic review and meta-analysis.

Inhibitory control and decision making under risk in bulimia nervosa and binge‐eating disorder

Neurocircuit function in eating disorders