Naomi G. Hill

Introduction: Although individuals with bulimia nervosa (BN) demonstrate elevated reward sensitivity and reward valuation‐effort (RV‐e) compared to controls, whether BN differs from its other specified feeding or eating disorder variant (OSFED‐BN), remains unclear. Further, whether differences best reflect categorical distinctions or correlations with symptom severity is unknown. This study examined whether trait and behavioural reward indicators differentiate BN, OSFED‐BN, and controls, predict diagnostic status, and correlate with bulimic symptom severity. Methods: Participants were 349 women (153 BN, 118 OSFED‐BN, 78 controls). Group comparisons, multinomial logistic regression, and correlational analyses were conducted on the Sensitivity to Punishment/Sensitivity to Reward‐Reward subscale (SPSRQ‐Reward), Behavioural Activation System‐Drive (BAS‐Drive) scale, and progressive ratio tasks assessing RV‐e for food and game rewards. Results: BN and OSFED‐BN demonstrated higher SPSRQ‐Reward scores than controls but did not differ from each other. OSFED‐BN, but not BN, showed higher food and game RV‐e compared to controls. SPSRQ‐Reward predicted higher odds of BN or OSFED‐BN versus controls, whereas BAS‐Drive predicted lower odds. SPSRQ‐Reward was positively associated with bulimic symptom frequencies. Food RV‐e was inversely associated with purging frequency. Discussion: Findings supported the role of reward‐related processes in contributing to both dimensional and categorical differences between BN, OSFED‐BN, and controls.

Objective: Gastrointestinal (GI) disturbances and eating disorder symptoms commonly co‐occur. Hypervigilance and anxiety about GI symptoms may motivate eating disorder behaviors to manage and/or avoid GI symptoms. We hypothesized that GI‐specific anxiety would be more strongly associated with dietary restriction and purging than GI‐specific hypervigilance. Further, we hypothesized that distinguishing between GI‐specific anxiety and hypervigilance would have incremental validity over using an existing measure of GI‐anxiety and related constructs initially developed for patients with irritable bowel syndrome, the Visceral Sensitivity Index. Methods: Three hundred and eighty‐two undergraduate students with elevated eating pathology (83.5% female, 87.4% White) completed questionnaires assessing GI‐specific hypervigilance and anxiety, the Visceral Sensitivity Index, and eating disorder symptoms. Participants were recruited with elevated shape/weight‐oriented eating pathology ( N = 309) and elevated avoidant/restrictive food intake disorder‐related eating pathology ( N = 73). Analyses were pre‐registered. Results: Regarding dietary restriction, the relative weight of GI‐specific anxiety did not differ from that of GI‐specific hypervigilance. Further, neither variable provided incremental validity over the Visceral Sensitivity Index in understanding restriction. Regarding purging, GI‐specific anxiety was not more strongly associated with purging than GI‐specific hypervigilance. However, GI‐specific anxiety, but not GI‐specific hypervigilance, demonstrated incremental validity over the Visceral Sensitivity Index in explaining purging. Conclusion: Distinguishing between GI‐specific hypervigilance and anxiety adds incremental validity in understanding purging but not restriction. Future research should examine whether addressing anxious cognitions about GI symptoms improves purging outcomes.

Objective: Individuals with binge‐spectrum eating disorders (EDs) engage in varying degrees of maladaptive and adaptive exercise. Elevated shape/weight concern is associated with engagement in maladaptive and adaptive exercise. No research has examined whether specific facets of shape/weight concern (e.g., fear of weight gain) are associated with degree of maladaptive versus adaptive exercise engagement. Method: Participants were 124 adults with binge‐spectrum EDs enroled in outpatient trials of Enhanced Cognitive Behaviour Therapy. Linear regression models examined associations between each facet of shape and weight concern concurrently at pre‐treatment and degree of maladaptive versus adaptive exercise at pre‐treatment (i.e., percentage maladaptive exercise episodes of total exercise episodes). We explored these relationships across treatment and diagnostic groups. Results: Greater pre‐treatment fear of weight gain was associated with a greater degree of pre‐treatment maladaptive exercise ( p = 0.027). This pattern was marginally significant in the longitudinal model ( p = 0.057) and was upheld within the BN‐spectrum ( p 's < 0.041) but not the BED‐spectrum group. Discussion: Accounting for all other facets, fear of weight gain may function as a risk factor for engagement in a greater degree of maladaptive exercise pre‐ and post‐treatment. Future research should examine the mechanisms underlying associations between fear of weight gain and maladaptive exercise engagement.

Background: Bulimia nervosa and related syndromes (BN-S) characterized by binge eating vary considerably in illness severity and course. Using the Research Domain Criteria framework of the National Institute of Mental Health, we developed a model positing that the same set of physiological consequences of weight suppression (WS; defined as the difference between the highest and current adult body weight) contribute to binge-eating severity and maintenance by (1) increasing the drive or motivation to consume food (reward valuation effort [RVE]) and (2) decreasing the ability for food consumption to lead to a state of satiation or satisfaction (reward satiation). Objective: Our funded project aimed to test concurrent associations among WS, physiological factors (leptin concentrations and postprandial glucagon-like peptide 1 [GLP-1] response), behavioral indicators of RVE (breakpoint on progressive ratio tasks) and reward satiation (ad-lib test meal intake), self-report of these core constructs, and binge-eating severity in BN-S (aim 1); test prospective associations to determine whether WS predicts BN-S maintenance in longitudinal models and whether posited mediators also predict BN-S maintenance (aim 2); and determine whether associations between WS and BN-S severity and maintenance are mediated by alterations in leptin levels, GLP-1 response, RVE, and reward satiation (aim 3). Methods: We aimed to recruit a sample of 320 women with BN-S or noneating disorder controls, with BMI from 16 kg/m2 to 35 kg/m2, for our study. The study included diagnostic interviews; questionnaires; height, weight, and percentage of body fat measurements; weight history; fasting leptin level; postprandial GLP-1 and insulin responses to a fixed meal; and ad-lib meal and progressive ratio tasks to behaviorally measure reward satiation and RVE, respectively, at baseline, with at least 78.1% (250/320) of the participants providing data at 6- and 12-month follow-up visits. Data will be analyzed using structural equation models to test posited pathways. Results: Data collection began in November 2016 and ended in April 2023, pausing in-person data collection from March 2020 to February 2021 due to the COVID-19 pandemic. Of 399 eligible women enrolled, 290 (72.7%) provided clinical, behavioral, and biological data at baseline, and 249 (62.4%) provided follow-up data. Measures demonstrated strong psychometric properties. Conclusions: We seek to identify biobehavioral predictors to inform treatments that target key factors influencing the severity and course of binge eating. These data, supported solely through federal funding, can inform questions emerging from recent interest and controversy surrounding the use of GLP-1 agonists for binge eating. International Registered Report Identifier (IRRID): RR1-10.2196/66554

BACKGROUND Bulimia nervosa and related syndromes (BN-S) characterized by binge eating vary considerably in illness severity and course. Using the Research Domain Criteria framework of the National Institute of Mental Health, we developed a model positing that the same set of physiological consequences of weight suppression (WS; defined as the difference between the highest and current adult body weight) contribute to binge-eating severity and maintenance by (1) increasing the drive or motivation to consume food (reward valuation effort [RVE]) and (2) decreasing the ability for food consumption to lead to a state of satiation or satisfaction (reward satiation). OBJECTIVE Our funded project aimed to test concurrent associations among WS, physiological factors (leptin concentrations and postprandial glucagon-like peptide 1 [GLP-1] response), behavioral indicators of RVE (breakpoint on progressive ratio tasks) and reward satiation (ad-lib test meal intake), self-report of these core constructs, and binge-eating severity in BN-S (aim 1); test prospective associations to determine whether WS predicts BN-S maintenance in longitudinal models and whether posited mediators also predict BN-S maintenance (aim 2); and determine whether associations between WS and BN-S severity and maintenance are mediated by alterations in leptin levels, GLP-1 response, RVE, and reward satiation (aim 3). METHODS We aimed to recruit a sample of 320 women with BN-S or noneating disorder controls, with BMI from 16 kg/m2 to 35 kg/m2, for our study. The study included diagnostic interviews; questionnaires; height, weight, and percentage of body fat measurements; weight history; fasting leptin level; postprandial GLP-1 and insulin responses to a fixed meal; and ad-lib meal and progressive ratio tasks to behaviorally measure reward satiation and RVE, respectively, at baseline, with at least 78.1% (250/320) of the participants providing data at 6- and 12-month follow-up visits. Data will be analyzed using structural equation models to test posited pathways. RESULTS Data collection began in November 2016 and ended in April 2023, pausing in-person data collection from March 2020 to February 2021 due to the COVID-19 pandemic. Of 399 eligible women enrolled, 290 (72.7%) provided clinical, behavioral, and biological data at baseline, and 249 (62.4%) provided follow-up data. Measures demonstrated strong psychometric properties. CONCLUSIONS We seek to identify biobehavioral predictors to inform treatments that target key factors influencing the severity and course of binge eating. These data, supported solely through federal funding, can inform questions emerging from recent interest and controversy surrounding the use of GLP-1 agonists for binge eating. INTERNATIONAL REGISTERED REPORT RR1-10.2196/66554

Objective: Negative affect is central to eating disorder maintenance models; identifying mechanisms underlying this link may inform specific treatment targets. The current study evaluated which emotions (i.e., distress, fear, and moral emotions) were most strongly linked to feeling fat and tested feeling fat as a longitudinal mediator of the relationship between these emotions and restricting or binge eating (https://osf.io/3d5cq/).Method: Community adults (N = 714, M[SD] age = 41.5[13.7], 84.6% female, 85.9% white) provided data at baseline, 3‐month, and 6‐month follow‐up. Relative weights analysis examined which emotion categories exhibited the strongest longitudinal relationships with feeling fat. Cross‐lagged panel models tested feeling fat as a mediator of the relationship between emotions and eating disorder behaviors.Results: Distress and moral emotions were the strongest emotional predictors of feeling fat. Feeling fat predicted binge eating (p's < 0.001), but not restricting (p's ≥ 0.832), in random effects cross‐lagged panel models. Feeling fat partially mediated the longitudinal relationship between distress and binge eating (p = 0.044); however, this effect became nonsignificant after adjusting for BMI (p = 0.354). Feeling fat did not mediate relationships between moral emotions and binge eating or between either distress or moral emotions and restricting (p's ≥ 0.638).Discussion: Feeling fat was associated with binge eating, not restricting, highlighting the importance of specificity in maintenance models. Because the mediating effect of feeling fat was accounted for by body size, factors associated with body size, such as internalized weight stigma, may be more relevant mediators of the relationship between negative emotions and eating disorder behaviors. Future research on feeling fat should adjust for body size.

ObjectiveSome individuals meet the criteria for atypical anorexia nervosa and another eating disorder simultaneously. The current study evaluated whether allowing a diagnosis of atypical anorexia nervosa to supersede a diagnosis of bulimia nervosa (BN) or binge-eating disorder (BED) provided additional information on psychological functioning.MethodsArchival data from 650 university students (87.7% female, 69.4% white) who met Eating Disorder Diagnostic Survey for DSM-5 eating disorder criteria and completed questionnaires assessing quality of life, eating disorder-related impairment, and/or eating pathology at a single time point. Separate regression models used diagnostic category to predict quality of life and impairment. Two diagnostic schemes were used: the DSM-5 diagnostic scheme and an alternative scheme where atypical anorexia nervosa superseded all diagnoses except anorexia nervosa. Model fit was compared using the Davidson-Mackinnon J test. Analyses were pre-registered ().ResultsAllowing an atypical anorexia nervosa diagnosis to supersede a BN or BED diagnosis provided better fit to the data for eating disorder-related impairment (p = .02; n = 271), but not physical, psychological, or social quality of life (p's >= .33; n = 306). Allowing an atypical anorexia nervosa diagnosis to supersede a BN or BED diagnosis provided a better fit in cross-sectional models predicting purging (p = .02; n = 638), but not body dissatisfaction, binge eating, restricting, or excessive exercise (p's >= .08; n's = 633-647).DiscussionThe current data support retaining the DSM-5 diagnostic scheme. More longitudinal work is needed to understand the predictive validity of the atypical anorexia nervosa diagnosis.Public SignificanceThe current study examined how changes to the diagnostic categories for eating disorders may change how diagnoses are associated with quality of life and impairment. Overall, findings suggest that the diagnostic hierarchy should be maintained.

Sexual abuse or assault (SA) history is associated with eating disorder severity and psychiatric comorbidity, including post-traumatic stress disorder (PTSD). Beyond persistent alterations in mood and cognitions characterizing PTSD, PTSD due to SA may contribute to greater increases in negative affect and body image concerns following food intake in bulimic syndromes (BN-S). To test this, participants (n = 172) with BN-S who reported PTSD due to SA, PTSD due to other forms of trauma, or neither completed clinical interviews and momentary reports of negative affect and shape/weight preoccupation before and after food intake. Participants with PTSD, regardless of trauma source, reported higher purging frequency whereas PTSD due to SA was associated with more frequent loss of control eating. For one task, changes in negative affect following food intake differed across the three groups. Negative affect decreased significantly in participants with PTSD without SA whereas nonsignificant increases were observed in those with PTSD with SA. Results of the present study suggest that source of trauma in PTSD may impact likelihood that eating regulates affect and provide insight into ways current treatments may be adapted to better target purging in BN-S comorbid with PTSD.

Objective: Individuals with bulimia nervosa (BN) engage in both maladaptive (i.e., compulsive and/or compensatory) and adaptive exercise (e.g., for enjoyment). No research has examined whether those who engage in adaptive, compulsive, and/or compensatory exercise exhibit differences in BN pathology or treatment outcome compared to those not engaging in exercise, limiting intervention efficacy.Method: We examined associations of baseline exercise engagement with baseline and posttreatment BN pathology among 106 treatment‐seeking adults (M_age = 37.4, SD_age = 12.95, 87.74% female, 68.87% White) enrolled across four clinical trials of outpatient enhanced cognitive behavioral therapy for BN (range: 12–16 sessions). Analysis of covariances examined associations between baseline exercise type and baseline/posttreatment global eating pathology, dietary restraint, loss‐of‐control (LOC) eating, and purging frequency.Results: Those engaging in only adaptive exercise reported lower global eating pathology compared to those engaging in compulsive‐only exercise (Est = −1.493, p = .014, M_diff = −.97) while those engaging in baseline compulsive exercise reported less LOC eating compared to those not engaging in exercise (Est = −22.42, p = .012, M_diff = −12.50). Baseline engagement in compulsive‐only exercise was associated with lower posttreatment global eating pathology compared to baseline engagement in no exercise (Est = −.856, p = .023, M_diff = −.64) and both compulsive and compensatory exercise (Est = .895, p = .026, M_diff = −1.08).Discussion: Those engaging in compulsive, compensatory, adaptive, and no exercise exhibit different patterns and severity of BN pathology. Future research is needed to position treatments to intervene on maladaptive, while still promoting adaptive, exercise.Public significance statement: No research to date has examined whether those who engage in adaptive, compulsive, and/or compensatory exercise exhibit differences in BN pathology or treatment outcome compared to those not engaging in exercise, limiting targeted intervention efforts. We found that those engaging in compulsive, compensatory, and adaptive exercise exhibit different patterns of BN pathology and that adaptive exercise engagement was related to lower cognitive eating disorder symptoms at baseline.