Kathrin Schag

Bio: Kathrin Schag is an academic researcher from University of Tübingen. The author has contributed to research in topics: Binge eating & Impulsivity. The author has an hindex of 14, co-authored 31 publications receiving 1377 citations.

Food‐related impulsivity in obesity and Binge Eating Disorder – a systematic review

Abstract: Impulsivity towards food has been recognized as a potential factor leading to increased food intake in obesity. Patients suffering from binge eating disorder (BED) form a specific subgroup of obese people that might be characterized by increased impulsivity. These assumptions, although, have yet to be verified. Therefore, this review evaluates evidence for food-related impulsivity in obese people with and without BED and examines possible differences between both populations. More precisely, evidence for the two components of impulsivity is analyzed separately: evidence for reward sensitivity, specifically, the urge for appetitive stimuli and evidence for rash-spontaneous behaviour such as acting disinhibited with no regard for the consequences. Our search resulted in 51 articles demonstrating generally increased food-related impulsivity. We found particular emphasis on increased reward sensitivity in obese people, which appeared to be more pronounced in people with BED. There was little and conflicting evidence, however, concerning increased rash-spontaneous behaviour in obese people without BED, but consistent evidence of an increase in obese people with BED. All in all, the evidence supports the view that BED represents a specific phenotype of obesity with increased food-related impulsivity. Taking these specific deficits into account can enhance the effectiveness of weight reduction programmes and psychotherapy.

Food-Related Impulsivity in Obesity and Binge Eating Disorder—A Systematic Update of the Evidence

Abstract: The specific eating pattern of Binge Eating Disorder (BED) patients has provoked the assumption that BED might represent a phenotype within the obesity spectrum that is characterized by increased impulsivity. Following the guidelines of the PRISMA statement (preferred reporting items for systematic reviews and meta-analyses), we here provide a systematic update on the evidence on food-related impulsivity in obese individuals, with and without BED, as well as normal-weight individuals. We separately analyzed potential group differences in the impulsivity components of reward sensitivity and rash-spontaneous behavior. Our search resulted in twenty experimental studies with high methodological quality. The synthesis of the latest evidence consolidates conclusions drawn in our initial systematic review that BED represents a distinct phenotype within the obesity spectrum that is characterized by increased impulsivity. Rash-spontaneous behavior in general, and specifically towards food, is increased in BED, while food-specific reward sensitivity is also increased in obese individuals without BED, but potentially to a lesser degree. A major next step for research entails the investigation of sub-domains and temporal components of inhibitory control in BED and obesity. Based on the evidence of impaired inhibitory control in BED, affected patients might profit from interventions that address impulsive behavior.

Impulsivity in Binge Eating Disorder: Food Cues Elicit Increased Reward Responses and Disinhibition

Abstract: Background Binge eating disorder (BED) represents a distinct eating disorder diagnosis. Current approaches assume increased impulsivity to be one factor leading to binge eating and weight gain. We used eye tracking to investigate both components of impulsivity, namely reward sensitivity and rash-spontaneous behaviour towards food in BED for the first time. Methods Overweight and obese people with BED (BED+; n = 25), without BED (BED−; n = 26) and healthy normal-weight controls (NWC; n = 25) performed a free exploration paradigm measuring reward sensitivity (experiment 1) and a modified antisaccade paradigm measuring disinhibited, rash-spontaneous behaviour (experiment 2) using food and nonfood stimuli. Additionally, trait impulsivity was assessed. Results In experiment 1, all participants located their initial fixations more often on food stimuli and BED+ participants gazed longer on food stimuli in comparison with BED− and NWC participants. In experiment 2, BED+ participants had more difficulties inhibiting saccades towards food and nonfood stimuli compared with both other groups in first saccades, and especially towards food stimuli in second saccades and concerning sequences of first and second saccades. BED− participants did not differ significantly from NWC participants in both experiments. Additionally, eye tracking performance was associated with self-reported reward responsiveness and self-control. Conclusions According to these results, food-related reward sensitivity and rash-spontaneous behaviour, as the two components of impulsivity, are increased in BED in comparison with weight-matched and normal-weight controls. This indicates that BED represents a neurobehavioural phenotype of obesity that is characterised by increased impulsivity. Interventions for BED should target these special needs of affected patients.

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

Abstract: 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)

Psychosomatic Medicine in Germany: More Timely than Ever

Abstract: 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

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

Abstract: 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.