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BACKGROUND Bulimia nervosa (BN) and related syndromes characterized by binge eating (BN-S) vary considerably in illness severity and course. Utilizing the National Institute of Mental Health’s (NIMH) Research Domain Criteria (RDoC) framework, we developed a model positing that the same set of physiological consequences of weight suppression (WS, defined as difference between highest and current adult body weight) contribute to binge-eating severity and maintenance by 1) increasing drive/motivation to consume food (Reward Valuation-Effort [RV-E]), and 2) decreasing ability for food consumption to lead to a state of satiation/satisfaction (Reward Satiation). OBJECTIVE Our funded project aimed to test concurrent associations among WS, physiological factors (leptin concentrations, postprandial glucagon-like peptide 1 [GLP-1] response), behavioral indicators of RV-E (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 if WS predicts BN-S maintenance in longitudinal models and if posited mediators also predict BN-S maintenance (aim 2); and determine if associations between WS and BN-S severity and maintenance are mediated by alterations in leptin, GLP-1 response, RV-E, and Reward Satiation (aim 3). METHODS We aimed to recruit a sample of N=320 women with BN-S or non-eating disorder controls, with body mass index from 16 to 35 kg/m2, for a longitudinal study including diagnostic interviews, questionnaires, height, weight and percent body fat measurement, weight history, fasting leptin, postprandial glucagon-like peptide 1 (GLP-1) and insulin responses to a fixed meal, and ad lib meal and progressive ratio tasks to behaviorally measure Reward Satiation and RV-E, respectively, at baseline, with at least n=250 providing data at 6- and 12-month follow-up. Data will be analyzed using structural equation models to test posited pathways. RESULTS Data collection began November 2016 and ended April 2023, with a pause on in person data collection from March 2020 to February 2021 due to the COVID-19 pandemic. Of N=399 eligible women enrolled, 290 (73%) women provided clinical, behavioral, and biological data at baseline, and 249 (86%) participants, representing 62% of those enrolled, 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 longitudinal data, supported solely through federal funding, can inform questions emerging from recent interest and controversy surrounding use of GLP-1 agonists for binge eating. CLINICALTRIAL Not applicable
BACKGROUND Bulimia nervosa (BN) and related syndromes characterized by binge eating (BN-S) vary considerably in illness severity and course. Utilizing the National Institute of Mental Health’s (NIMH) Research Domain Criteria (RDoC) framework, we developed a model positing that the same set of physiological consequences of weight suppression (WS, defined as difference between highest and current adult body weight) contribute to binge-eating severity and maintenance by 1) increasing drive/motivation to consume food (Reward Valuation-Effort [RV-E]), and 2) decreasing ability for food consumption to lead to a state of satiation/satisfaction (Reward Satiation). OBJECTIVE Our funded project aimed to test concurrent associations among WS, physiological factors (leptin concentrations, postprandial glucagon-like peptide 1 [GLP-1] response), behavioral indicators of RV-E (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 if WS predicts BN-S maintenance in longitudinal models and if posited mediators also predict BN-S maintenance (aim 2); and determine if associations between WS and BN-S severity and maintenance are mediated by alterations in leptin, GLP-1 response, RV-E, and Reward Satiation (aim 3). METHODS We aimed to recruit a sample of N=320 women with BN-S or non-eating disorder controls, with body mass index from 16 to 35 kg/m2, for a longitudinal study including diagnostic interviews, questionnaires, height, weight and percent body fat measurement, weight history, fasting leptin, postprandial glucagon-like peptide 1 (GLP-1) and insulin responses to a fixed meal, and ad lib meal and progressive ratio tasks to behaviorally measure Reward Satiation and RV-E, respectively, at baseline, with at least n=250 providing data at 6- and 12-month follow-up. Data will be analyzed using structural equation models to test posited pathways. RESULTS Data collection began November 2016 and ended April 2023, with a pause on in person data collection from March 2020 to February 2021 due to the COVID-19 pandemic. Of N=399 eligible women enrolled, 290 (73%) women provided clinical, behavioral, and biological data at baseline, and 249 (86%) participants, representing 62% of those enrolled, 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 longitudinal data, supported solely through federal funding, can inform questions emerging from recent interest and controversy surrounding use of GLP-1 agonists for binge eating. CLINICALTRIAL Not applicable
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