Should Binge Eating Disorder Be Included in the DSM-V? A Critical Review of the State of the Evidence
Department of Psychology, Wesleyan University, Middletown, Connecticut 06459, USA. Annual Review of Clinical Psychology
(Impact Factor: 12.67).
02/2008; 4(1):305-24. DOI: 10.1146/annurev.clinpsy.4.022007.141149
Binge eating disorder (BED) was introduced in 1994 as a provisional eating disorder diagnosis. The core symptom is recurrent binge eating in the absence of inappropriate compensatory behaviors and/or extreme dietary restraint. This review examines the status of the literature on BED according to five criteria that have been proposed to determine whether BED warrants inclusion in the psychiatric nosology as a distinct eating disorder. We conclude that each of these criteria was met. There is a commonly accepted definition of and assessment approach to BED. The clinical utility and validity of BED have been established, and BED is distinguishable from both bulimia nervosa and obesity. BED should be included in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders.
Available from: Rebecca R Klatzkin
- "BED is associated with considerable psychological and physiological dysfunction that distinguishes it from obesity       ; it aggregates in families independently of obesity and is caused in part by familial factors distinct from those for obesity . Yet, additional studies are needed to further differentiate the BED phenotype from the obesity phenotype in order to inform treatment development  . "
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ABSTRACT: This study investigated cardiovascular functioning, mood, and eating-related psychological factors at rest and in response to mental stress in three groups of women: 1) Obese women with Binge Eating Disorder (BED; n=9); 2) Obese non-BED women (n=15); and 3) Normal weight (NW) non-BED women (n=15). Compared to both obese and NW non-BED women, obese women with BED showed heightened overall blood pressure and reported greater depression symptoms, perceived stress, and eating-related psychopathology. Additionally, obese women with BED reported greater overall negative affect and state anxiety compared to obese non-BED women. The heart rate response to stress was blunted in the obese BED group compared to the other groups, but this effect was no longer significant after controlling for baseline differences in depression. Correlational analyses revealed a positive association between stress-induced changes in hunger and cardiovascular measures only in obese women with BED. Longitudinal studies are needed to determine if stress dysregulation and stress-induced increases in hunger contribute to the onset and/or maintenance of BED. In particular, studies utilizing an additional NW BED control group are warranted in order to further examine the impact of BED above and beyond the impact of obesity on psychophysiological functioning and to inform the growing literature regarding stress-related factors that distinguish the BED and obesity phenotypes.
Copyright © 2015. Published by Elsevier Inc.
- "For the cunent mental conditions, we argued for a dysfunctional right FL network that supports or fails, respectively, to adapt ongoing thoughts and impulses to behavioral requirements. This conjecture suggests that some diagnostic clusters, or at least some of their symptoms, could be merged into this wider phenotype representing a diagnostic altemative to the traditional one in which the current number ofdiagnostic categories are kept, modified, or increased in numbers (e.g., Starcevic, 2006; Striegel-Moore & Franko, 2008). The basic suggestion here is neither new nor unconventional as shown by the ongoing and controversial debate on the form and content of the DSM-V (Frances & Widiger, 2012; Kendler & First, 2010; Nesse & Stein, 2012).Itis neither new when considering recent approaches linking ED to relative dysfunctional allocentric processing, a function also associated with the right hemisphere (Riva, 2012; Riva &. "
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ABSTRACT: The major features in eating disorders are a preoccupation with food and its consumption and body dissatisfaction. Diagnostic manuals provide clusters of criteria according to which affected individuals can be categorized into one or other group of eating disorder. Yet, when considering the high proportion of comorbidities and ignoring the content of the symptoms (food, body), the major features seem to yield obsessional-compulsive, addictive, and impulsive qualities. In the present article, we review studies from the neuroscientific literature (mainly lesion studies) on eating disorder, obsessive-compulsive disorder, impulse control disorder, and addiction to investigate the possibility of a wider phenotype that can be related to a common brain network. The literature localizes this network to the right frontal lobe and its connectivities. This network, when dysfunctional, might result in a behavior that favors the preoccupation with particular thoughts, behaviors, anxieties, and uncontrollable urges that are accompanied by little scope for ongoing behavioral adjustments (e.g., impulse control). We reason that this network may turn out to be equally involved in understudied mental conditions of dysfunctional body processing such as muscle dysmorphia, body dysmorphic disorder (including esthetic surgery), and xelomelia. We finally consider previous notions of a wider phenotype approach to current diagnostic practice (using DSM), such as the possibility of a model with a reduced number of diagnostic categories and primary and secondary factors, and to etiological models of mental health conditions.
Available from: David Castle
- "A related concern is that although the sample appeared to cover the spectrum of severity of dietary restraint, formal diagnoses of eating disorders were not conducted, and given that a convenience sample of university students was recruited, it is likely that many of the participants would not meet criteria for an eating disorder diagnosis. Similarly, although we exclusively recruited women in order to be consistent with previous literature , binge eating is also common among men . As such, it is possible that the frequency of binge eating episodes and the strength of association between negative mood and binge eating onset is weaker in the present study than would be anticipated for a clinical population that sampled both men and women. "
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Although a wealth of studies have tested the link between negative mood states and likelihood of a subsequent binge eating episode, the assumption that this relationship follows a typical linear dose–response pattern (i.e., that risk of a binge episode increases in proportion to level of negative mood) has not been challenged. The present study demonstrates the applicability of an alternative, non-linear conceptualization of this relationship, in which the strength of association between negative mood and probability of a binge episode increases above a threshold value for the mood variable relative to the slope below this threshold value (threshold dose response model).
A sample of 93 women aged 18 to 40 completed an online survey at random intervals seven times per day for a period of one week. Participants self-reported their current mood state and whether they had recently engaged in an eating episode symptomatic of a binge.
As hypothesized, the threshold approach was a better predictor than the linear dose–response modeling of likelihood of a binge episode. The superiority of the threshold approach was found even at low levels of negative mood (3 out of 10, with higher scores reflecting more negative mood). Additionally, severity of negative mood beyond this threshold value appears to be useful for predicting time to onset of a binge episode.
Present findings suggest that simple dose–response formulations for the association between negative mood and onset of binge episodes miss vital aspects of this relationship. Most notably, the impact of mood on binge eating appears to depend on whether a threshold value of negative mood has been breached, and elevation in mood beyond this point may be useful for clinicians and researchers to identify time to onset.
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