Glen Forester

Objective: Food craving is a central feature of binge‐eating disorder (BED) and may be a proximal mechanism linking environmental food cues to binge eating. Although laboratory studies show that food cues elicit craving and ecological momentary assessment (EMA) studies show that craving predicts binge eating, no study has tested whether craving is the momentary mechanism linking naturalistic food‐cue exposure to binge eating. We tested this prospective within‐person mediational model in daily life among individuals with BED. Method: Adults with BED ( N = 43) completed a 10‐day EMA protocol. Multilevel structural equation modelling tested the within‐person pathway from momentary food‐cue exposure to craving to subsequent binge eating, controlling for prior craving and prior binge eating. Results: At the within‐person level, food‐cue exposure predicted increased craving, which in turn predicted a greater likelihood of subsequent binge eating, supporting a significant mediation effect. Conclusions: These findings provide the first EMA‐based evidence that food‐cue exposure increases binge‐eating risk in BED through momentary increases in craving. Results highlight cue‐induced craving as a potential key mechanism underlying binge eating and suggest that interventions targeting craving regulation and cue reactivity may improve treatment outcomes.

Objective: Emerging evidence suggests that eating disorder (ED) pathophysiology involves metabolic alterations, and preliminary data indicate that ketogenic interventions may reduce symptom severity. We tested whether exogenous ketone supplementation modulates neural responses in individuals with anorexia nervosa (AN) and bulimia nervosa (BN) during a task previously shown to elicit altered prediction‐error signaling in ED populations. Method: Twenty‐two participants across the AN and BN spectrum (AN: n = 8; OSFED‐AN: n = 9; BN: n = 4; OSFED‐BN: n = 1) spanning a wide range of ages (19.0–52.1 years) and body mass index (BMI: 17.2–46.2) were studied in a randomized, double‐blind, placebo‐controlled crossover design. On separate days, participants consumed 10 g beta‐hydroxybutyrate (BHB) or placebo prior to completing a taste‐based conditioning task during electroencephalography (EEG). Trial‐level neural sensitivity to prediction error during unexpected taste receipt and omission was indexed using the reward positivity (RewP/FRN) and late positive potential (LPP) event‐related potentials (ERPs), cortical markers of outcome salience linked to dopaminergic and noradrenergic systems. Results: Active BHB increased blood ketone levels. Compared to placebo, BHB was associated with a significant reduction in LPP sensitivity to unsigned prediction error ( p = 0.028), controlling for diagnosis, comorbidity, and medication use. Poorer self‐esteem was associated with a smaller ketone‐related reduction in LPP sensitivity ( p = 0.002). Discussion: These findings suggest that EEG‐based measures can capture prediction‐error processing during cue‐taste learning and that exogenous ketones may attenuate neural sensitivity to salient taste outcomes in EDs. Further research is needed to determine whether such modulation translates into clinically meaningful changes in illness behavior.

Accruing evidence suggests that personality-based approaches to eating disorder classification may offer several advantages over current diagnostic models, with prior research consistently identifying three personality-based groups characterized by either (1) high levels of impulsivity and dysregulation (termed the “undercontrolled” group), (2) high levels of rigidity and avoidance (termed the “overcontrolled” group), or (3) relatively normative levels of personality functioning (termed the “low psychopathology” group). Cognitive inflexibility (i.e., difficulty adjusting thoughts or behaviors) has theorized relevance to eating disorders. However, prior research has frequently failed to observe differences in cognitive inflexibility across eating disorder diagnostic groups. The present study aimed to identify personality-based groups in an eating disorder sample, and then to examine the relations between these groups and behavioral measures of cognitive inflexibility. 83 men and women who met DSM-5 criteria for anorexia nervosa or bulimia nervosa completed self-report questionnaires to assess trait-level approach/avoidance behaviors and impulsivity, as well as behavioral tasks assessing attentional set-shifting and reversal learning, two facets of cognitive inflexibility. Latent profile analysis of measures assessing approach/avoidance behaviors and impulsivity supported a three-class model replicating the undercontrolled, overcontrolled, and low psychopathology groups. Notably, the low psychopathology group was characterized by elevated reward responding. One-way ANOVAs indicated that the low psychopathology group demonstrated heightened perseverative errors (an indicator of impaired reversal learning) relative to the other groups. No group differences were observed for attentional set-shifting errors or probabilistic switch errors. Findings from the present study provide additional support for personality-based classification approaches identifying undercontrolled, overcontrolled, and low psychopathology eating disorder groups. Results also suggest that reward-related processes may contribute to disorder maintenance in the low psychopathology group, indicating potentially meaningful targets for intervention. This study supports previous research indicating that individuals with eating disorders can be subdivided into three groups with either (1) high levels of impulsivity and dysregulation (termed the “undercontrolled” group), (2) high levels of rigidity and avoidance (termed the “overcontrolled” group), or (3) relatively normative levels of personality functioning (termed the “low psychopathology” group). This study also indicates that individuals in the “low psychopathology group” may experience abberations in reward functioning (e.g., elevated drive for rewards and difficulty adjusting to changing reward contingencies) that may contribute to eating disorder persistence.

Objective: Binge eating appears to be associated with impulsivity, especially in response to negative affect (i.e., negative urgency). However, negative urgency is typically assessed via self‐report, which captures only some aspects of urgency and may be subject to bias. Few studies have examined impulsivity following experimental manipulations of affect in binge‐eating samples.Method: In the present study, individuals who engage in regular binge eating completed a behavioural impulsivity (go/no‐go) task with high‐ and low‐calorie food stimuli, once following negative affect induction and once following neutral affect induction.Results: Greater behavioural impulsivity to high‐calorie food cues while in a negative (and not a neutral) affective state was associated with more frequent binge‐eating behaviour. Further, this behavioural measure of negative urgency uniquely accounted for variance in binge‐eating frequency when controlling for self‐reported negative urgency, suggesting that behavioural measures may be a useful complement to self‐report measures.Discussion: These findings provide novel and compelling evidence for the relationship between negative urgency and binge eating, highlighting negative urgency as a potentially important target for intervention.

Background: Loss of control eating is more likely to occur in the evening and is uniquely associated with distress. No studies have examined the effect of treatment on within-day timing of loss of control eating severity. We examined whether time of day differentially predicted loss of control eating severity at baseline (i.e. pretreatment), end-of-treatment, and 6-month follow-up for individuals with binge-eating disorder (BED), hypothesizing that loss of control eating severity would increase throughout the day pretreatment and that this pattern would be less pronounced following treatment. We explored differential treatment effects of cognitive-behavioral guided self-help (CBTgsh) and Integrative Cognitive-Affective Therapy (ICAT).Methods: Individuals with BED (N = 112) were randomized to receive CBTgsh or ICAT and completed a 1-week ecological momentary assessment protocol at baseline, end-of-treatment, and 6-month follow-up to assess loss of control eating severity. We used multilevel models to assess within-day slope trajectories of loss of control eating severity across assessment periods and treatment type.Results: Within-day increases in loss of control eating severity were reduced at end-of-treatment and 6-month follow-up relative to baseline. Evening acceleration of loss of control eating severity was greater at 6-month follow-up relative to end-of-treatment. Within-day increases in loss of control severity did not differ between treatments at end-of-treatment; however, evening loss of control severity intensified for individuals who received CBTgsh relative to those who received ICAT at 6-month follow-up.Conclusions: Findings suggest that treatment reduces evening-shifted loss of control eating severity, and that this effect may be more durable following ICAT relative to CBTgsh.