Academic Editors: Fernando Fernandez-Aranda, Janet Treasure and Empar Lurbe

Received: 10 October 2021 Accepted: 24 October 2021 Published: 26 October 2021

**Publisher's Note:** MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

**Copyright:** © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).

as well as with increased psychological burden, such as depression, low self-esteem, body image disturbances, perceived stress, and lowered quality of life [7].

The frequent co-morbidity of BED and obesity may suggest that both conditions are part of a broad spectrum of eating-related behaviors, implying that patients could transition from one condition to another [8]. This idea is consistent with recent studies linking obesity with comorbid BED and obesity without BED to shared phenotypical, in part clinical, features. For example, early life adversities such as trauma have been associated with the development of both BED and obesity [9,10], possibly due to lasting impairments in coping mechanisms and metabolic alterations due to stress [11,12]. In a similar vein, insecure attachment styles that develop in early childhood have been associated with emotional eating, eating unhealthy food, and binge eating [13], which studies link to the pathogenesis of BED and obesity [14,15]. Neurobiological studies also show that dopaminergic and glutamatergic pathways play a crucial role in developing and maintaining both conditions [16], further corroborating the idea of a shared continuum between obesity with comorbid BED and obesity without BED.

Patients with BED and comorbid obesity also differ from obese individuals without BED regarding a variety of phenotypical features. Patients with BED and obesity display higher levels of impulsivity than obese individuals without BED, in general, and especially toward food cues [17,18]. Neurobiological studies have shown that BED patients with obesity show lower activity levels in brain areas responsible for control and self-regulatory processes than obese individuals without BED [17]. Patients with BED have lower response inhibition abilities when presented with food cues in a go-no-go task, a finding associated with decreased activation of the prefrontal control network, which is active during successful no-go (withhold) trials in non-BED obese individuals [19]. Evidence also suggests a more compromised hormonal regulation of hunger and satiety in BED compared to obesity, for example, as mirrored in findings of blunted postprandial ghrelin suppression in BED compared with obesity [20]. In addition, Schulz and Laessle [21] found that depression weakens self-regulation in obese BED patients but not in obese individuals without BED, suggesting a possible link between depression and binge eating behavior. Finally, a recent study from our group showned that negative mood was associated with decreased food avoidance in obese BED patients only, but not in obese individuals without BED [22].

The evidence is less consistent on commonalities and disparities between obese patients with comorbid BED and obese individuals without BED concerning eating-related symptomatology other than binge eating. Strong concerns about shape and weight are core features BED shares with other EDs like anorexia nervosa or bulimia nervosa [23,24], and significant concerns of shape and weight also emerge in connection with obesity without BED in large community samples [25]. Similarly, several eating styles have been associated with obesity and comorbid BED in comparison with obesity without BED, such as emotional eating [22,26–30], eating in response to stress [31], and lower success in dieting and restraint [32], although especially research on the role of restraint has generated inhomogeneous results [33,34]. Newer concepts such as food craving and the strong desire to eat certain foods show stronger correlations with binge eating than obesity [35–37]. Food addiction, which among others, describes a loss of control over eating, cravings, and continued excessive food consumption contrary to the knowledge of adverse consequences [38], is also associated with a higher frequency of binge episodes and emotional eating [39,40]. At the same time, food addiction may play a role in obesity, too [41].

Further exploration of the commonalities and disparities between obesity with comorbid BED and obesity without BED is warranted, considering the results may help identify specific targets of prevention and intervention. Existing therapeutic approaches and weight loss strategies for obesity, such as dietary programs or physical exercise, are often unsuccessful or do not lead to enduring weight reductions [7,42]. Obese patients with BED also exhibit smaller weight reductions compared with obese individuals without an ED following weight-loss surgery [43,44]. Cognitive behavioral therapy (CBT), which functions as the foundation of BED treatment, aims to modify eating behaviors and has been

found to lead to a remission of binge episodes among 64.4% of patients, including positive effects in terms of co-occurring psychological impairments [32,45]. However, the evidence for long-term results after cessation of CBT is still disappointing [32,46], suggesting BED treatment needs further improvement.

Thus far, the commonalities and differences in phenotypical features between obese BED patients and obese individuals without BED have been mapped across a range of studies but are seldom explored within a single investigation. One cannot exclude that differences in study design or sample composition account for some inconsistencies across findings, suggesting the need for a more comprehensive investigation. A comprehensive investigation also allows for the assessment the relative contribution of different sets of phenotypical and clinical features in grouping and distinguishing obese patients with BED from obese individuals without BED, aiding in theory development and prognostic application. Here, we conducted an exploratory study in which we assessed eatingrelated symptomatology (shape and weight concerns [23,24], emotional eating [26–30,47], dieting [32], food craving [37], and food addiction [48]), general psychopathology (impulse control impairments [17], depression [34]), and early life experiences (childhood traumatic events [9,10], attachment styles [14,15]) using standardized questionnaires. Specifically, we aimed to comprehensively compare obese patients with BED against obese individuals without BED as well as healthy, normal-weight controls in terms of these features, using univariate analyses and dimensionality reduction techniques.
