Obesity, defined as an excessive accumulation of body fat (body mass index (BMI) ≥ 30.0 kg/m2
], presents one of the most prevalent health conditions in the Western world [2
]. During the last decade, research on the causal and maintaining factors of obesity has focused on executive functioning and neural characteristics [3
]. Executive functions represent a range of higher cognitive capacities enabling goal-directed behavior including inhibition, cognitive flexibility, planning, or decision-making [6
]. Importantly, impairments in general executive functions in individuals with obesity, for example, reduced inhibition and planning, were linked to unsuccessful weight-loss related behavior, such as poor dietary quality and less success in weight loss therapies [8
]. In order to provide targeted treatment options for executive dysfunctions, the specification of neuropsychological profiles in the obesity spectrum is warranted [10
In this context, a recent review showed substantial similarities between executive functions in obesity and substance use disorder, including increased impulsive decision-making and an attentional bias towards disorder-related stimuli in both conditions [11
]. In addition to these neuropsychological abnormalities, several neuroimaging studies documented a considerable overlap between obesity and substance use disorder regarding functional alterations in frontal brain regions and meso-corticolimbic circuits, which are involved in reward processing and decision-making [11
Recent research hypothesized that certain foods, especially high-fat and high-sugar foods, elicit addictive-like behavioral responses in vulnerable individuals characterized by high impulsivity and reward sensitivity through the activation of reward-related brain circuits [12
]. This so-called food addiction (FA) hypothesis has been controversially discussed [15
], since certain aspects of substance use symptomatology, including symptoms of withdrawal or tolerance, have not been demonstrated regarding food [21
]. FA is mainly operationalized as a trait based on a self-report questionnaire to assess food-related addictive behavior, the Yale Food Addiction Scale 2.0
(YFAS 2.0) [22
]. Although FA was found in individuals across the weight range, it was often described in the context of obesity, with highly varying prevalence of 6.7–56.8% in samples of treatment-seeking individuals who were overweight or obese [14
]. Two recent studies specifically investigated alterations in executive functioning in individuals with obesity and trait FA, showing that higher versus lower FA severity in obesity was related to poorer decision-making, greater attentional impairments [23
], significantly poorer inhibition and cognitive flexibility assessed via self-report questionnaires and a computerized neuropsychological test battery [24
]. Individuals with obesity and trait FA, may therefore present with a specific neuropsychological profile in the obesity spectrum.
Likewise, the clinical eating disorder diagnosis of binge-eating disorder (BED) [25
] has been associated with addictive-like eating behavior [26
]. According to the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) [25
], the core feature of BED is represented by recurrent episodes of objective binge eating, which are characterized by a feeling of loss of control over eating while consuming an unambiguously large amount of food in a discrete period of time. BED is not associated with regular inappropriate compensatory behaviors, such as vomiting or excessive exercising [25
]. Among treatment-seeking individuals with overweight and obesity, 23.9% presented with comorbid BED [28
]. Individuals with BED were repeatedly found to show impairments in executive functioning exceeding those observed in obesity only, including increased impulsivity, reward sensitivity, rash spontaneous behavior, risky decision-making, and reduced inhibition [29
]. These alterations were found in general executive functioning tasks [30
] as well as in food-related tasks [30
], strengthening the assumption of a specific neuropsychological profile of individuals with obesity and comorbid BED.
Even though trait FA and the diagnosis of BED have a significant number of behavioral symptoms in common (e.g., consumption of large amounts of food, loss of control, continued use despite negative consequences, cravings) and show a comorbidity of 57.0–72.2% in treatment-seeking and population-based samples with obesity [39
], no study has yet compared the neuropsychological profiles of individuals with obesity presenting with or without FA and BED.
In the context of executive functions in obesity as described above, we therefore aimed to investigate general executive functions, specifically decision-making, reward sensitivity, cognitive flexibility, inhibition, and cognitive control in four distinct groups of individuals with obesity: those with FA, BED, FA plus BED (FA/BED), and a control group of otherwise healthy individuals with obesity (OB) stratified to the other groups based on age, sex, and BMI. Among the four groups, we assumed that individuals with OB would show the highest levels of executive functioning. For those with FA, we particularly expected poorer decision-making, cognitive control, inhibition, and flexibility than for OB. Furthermore, we assumed that individuals with BED would perform significantly worse than individuals with OB in tasks investigating impulsivity, reward sensitivity, and inhibition. Due to a lack of evidence, no evidence-based hypothesis was derived regarding possible differences on executive functioning between individuals with trait FA and those with BED. However, based on a recent finding that individuals with FA plus BED displayed greater eating disorder and general psychopathology than individuals with BED only [40
], we suggested cumulative adverse effects on executive functioning. Thus, individuals with FA/BED were expected to show lower levels of executive functioning than individuals with OB, FA, and BED only.
The present study aimed at investigating the associations of trait FA and the DSM-5 diagnosis of BED regarding executive functions in adults with obesity. It was found that individuals with BED showed lower executive functioning, characterized by a higher variability in reaction times and less feedback integration, compared to otherwise healthy individuals with obesity. Contrary to expectations, there were no differences in executive functioning among individuals with FA, FA/BED, and obesity only. The results thus suggest a BED-specific, but not a FA-specific, neuropsychological profile in individuals with obesity. The combined presentation of trait FA and BED was not associated with greater impairments in executive functioning compared to their single presentations.
The fact that individuals with obesity and BED displayed a significantly higher variability in their reaction times compared to the OB group is similar to findings showing a high variability in reaction times in ADHD [62
]. ADHD is highly comorbid to obesity and BED and is associated with comparable neuronal processes [62
]. In ADHD, it is usually believed that the variability of response times reflects occasional gaps in attention [62
], which could be related to high distractibility, making an attentional shift and the detection of task-irrelevant stimuli, for example, food cues, more likely. Another result was the significant and medium-sized difference between the BED and the OB group in the learning to learn score in the WCST, in accordance with recent research [37
]. The negative learning to learn score indicated that individuals with BED became less rather than more efficient on consecutive trials of the WCST [57
]. Hypothetically, this could be caused by an inability to appropriately integrate the feedback in order to improve performance, as previously evidenced in BED [29
]. Transferred into everyday life, the deficient processing of feedback to improve performance could be related to a lack of feedback integration in daily learning, such as feedback given by one’s own body after an objective binge-eating episode in order to prevent such an episode from occurring again, leaving an individual without control [65
]. In this context, it is worth noting that the BED group did not display heightened depressive symptoms compared to the OB and FA group. Observed differences between the BED and OB group can therefore not be attributed to increased general psychopathology, but were related to BED diagnosis.
Contrary to the two previous studies investigating executive functions in individuals with trait FA [23
], demonstrating that higher versus lower FA severity in obesity was related to poorer decision-making, inhibition, and cognitive flexibility, no other performance score reached significance in the present study. The hypothesis that individuals with obesity and FA may present with a specific neuropsychological profile in the obesity spectrum was therefore not supported in this clinical treatment-seeking sample. It is of note, however, that the FA group mostly presented with mild and moderate FA symptomatology only, allowing to speculate that FA severity was not high enough to be accompanied by cognitive impairments in this sample. On the other hand, this result could also reflect the assumption that BED, as a clinical eating disorder diagnosis, is associated with more cognitive impairments than subjective trait FA.
The hypothesis of cumulative effects on executive dysfunctions in individuals with FA plus BED was not confirmed in the present study, since the FA/BED group did not display lower performance compared to the OB, FA, or BED group in any of the tasks under investigation. Notably, the FA/BED group reported considerably more depressive symptoms compared to the OB group, with an average in the range of a major depression [48
], and thus contradicts neuropsychological evidence of impaired executive functioning in individuals with depression [66
]. However, the underlying mechanisms of this finding cannot currently be identified. Therefore, this result needs replication in larger, independent samples of individuals with FA/BED.
4.1. Methodological Considerations
When interpreting the results several strength and limitations have to be mentioned. First, using well-established measures, the diagnosis of BED was derived from an expert interview, the EDE 17.0D [44
], and trait FA was assessed via the established self-questionnaire YFAS 2.0 [22
]. Second, the OB group was stratified to the other groups and groups were mutually exclusive regarding trait FA and objective binge-eating episodes. Third, executive functioning was measured with established, standardized, and computerized tasks. Critically, the relatively small group sizes have to be mentioned, as only medium-to-large-sized effects could be detected with adequate power. Additionally, there might be an assessment bias across diagnostic groups, as FA was assessed with a self-administered questionnaire, while BED diagnosis was made by clinical expert interview, suggesting that trait FA and BED mirror different levels of clinical severity. Furthermore, no food-specific tasks were used. Various studies have shown a stronger association between executive functions in food-related tasks in relation to binge-eating behavior [30
]. Lastly it is important to note that the design of this study was cross-sectional; therefore, causal conclusions about the direction of observed effects are not indicated.
4.2. Implications and Future Directions
The current study identified greater executive dysfunctions in individuals with obesity and comorbid BED compared to those with obesity only. Clinically, the assessment of eating disorder symptomatology, specifically a diagnosis of BED, seems therefore indicated in individuals with obesity. In these individuals, an increase in neuropsychological impairments is likely to interfere with standard treatment options [8
] and may thus constitute a specific target for intervention, for example, via cognitive remediation therapy [41
]. Based on this study’s results, an in-depth investigation in the variability of reaction times (alertness tasks) is indicated, especially considering the effects of food stimuli, as current research points to an increased attentional bias towards food cues in individuals with BED e.g., [66
Regarding trait FA, this study revealed no impairments in executive functioning other than a tendency towards higher choice-impulsivity, which could be related to the high proportion of individuals characterized by low FA severity in the FA group. Studies investigating executive functions in individuals with obesity and more severe FA are therefore needed. Alternatively, it could be argued that similarities in executive functioning between individuals with obesity plus trait FA and individuals with substance use disorder as recently shown [12
] only manifest on a neurobiological [12
] and not on a neuropsychological level. To further differentiate these aspects of addictive-like eating behavior, future research is warranted to specifically investigate neuronal and neuropsychological overlaps and distinctive features between trait FA and substance use disorder, especially in the context of disorder-related stimuli (e.g., food stimuli).
It was surprising that the observed large differences in attentional variability and conceptual learning between the BED and OB group did not manifest in the FA/BED group, particularly as this group presented as the most impaired group concerning mental health, with more depressive symptoms than the OB group. The assessment of trait FA in individuals with versus without BED may therefore be helpful to determine identify individuals at risk for greater mental health impairment and in need of more intensive treatment. Further research into the neuropsychological characteristics of individuals with FA plus BED is however warranted, preferably using larger samples and a longitudinal study design in order to evaluate the effects of trait FA plus BED on weight trajectories and treatment outcome in individuals with obesity.