Recent advances in developing and screening candidate pharmacotherapies for psychiatric disorders have depended on rodent models. Eating disorders are a set of psychiatric disorders that have traditionally relied on behavioral therapies for effective long-term treatment. However, the clinical use of Lisdexamfatamine for binge eating disorder (BED) has furthered the notion of using pharmacotherapies for treating binge eating pathologies. While there are several binge eating rodent models, there is not a consensus on how to define pharmacological effectiveness within these models. Our purpose is to provide an overview of the potential pharmacotherapies or compounds tested in established rodent models of binge eating behavior. These findings will help provide guidance for determining pharmacological effectiveness for potential novel or repurposed pharmacotherapies.

BACKGROUND: Having reliable information to make decisions about the allocation of healthcare resources is needed to improve well-being and quality-of-life of individuals with eating disorders (EDs). EDs are a main concern for healthcare administrators globally, particularly due to the severity of health effects, urgent and complex healthcare needs, and relatively high and long-term healthcare costs. A rigorous assessment of up-to-date health economic evidence on interventions for EDs is essential for informing decision-making in this area. To date, health economic reviews on this topic lack a comprehensive assessment of the underlying clinical utility, type and amount of resources used, and methodological quality of included economic evaluations. The current review aims to (1) detail the type of costs (direct and indirect), costing approaches, health effects, and cost-effectiveness of interventions for EDs; (2) assess the nature and quality of available evidence to provide meaningful insights into the health economics associated with EDs.
METHODS: All interventions for screening, prevention, treatment, and policy-based approaches for all Diagnostic and Statistics Manual (DSM-IV and DSM-5) listed EDs among children, adolescents, and adults will be included. A range of study designs will be considered, including randomised controlled trials, panel studies, cohort studies, and quasi-experimental trials. Economic evaluations will consider key outcomes, including type of resources used (time and valued in a currency), costs (direct and indirect), costing approach, health effects (clinical and quality-of-life), cost-effectiveness, economic summaries used, and reporting and quality assessments. Fifteen general academic and field-specific (psychology and economics) databases will be searched using subject headings and keywords that consolidate costs, health effects, cost-effectiveness and EDs. Quality of included clinical studies will be assessed using risk-of-bias tools. Reporting and quality of the economic studies will be assessed using the widely accepted Consolidated Health Economic Evaluation Reporting Standards and Quality of Health Economic Studies frameworks, with findings of the review presented in tables and narratively.
CONCLUSIONS: Results emanating from this systematic review are expected to highlight gaps in healthcare interventions/policy-focused approaches, under-estimates of the economic costs and disease-burden, potential under-utilisation of ED-related resources, and a pressing need for more complete health economic evaluations.

The dynorphin (DYN)/kappa opioid receptor (KOR) system has increasingly been investigated as a possible pharmacotherapeutic target for alcohol use disorder, but findings on the direction of its effects have been mixed. Activation of KORs by DYN has been shown to elicit dysphoric effects, and the DYN/KOR system has canonically been considered particularly important in driving alcohol intake through negative reinforcement in dependent states. However, this review also highlights its activity in opposing the positive reinforcement that drives alcohol intake at earlier stages. Both DYN and KORs are concentrated in the extended amygdala, a set of interconnected regions that includes the bed nucleus of the stria terminalis, central nucleus of the amygdala, and nucleus accumbens shell. This review focuses on the role of the DYN/KOR system in the extended amygdala in ethanol use. It begins by examining the effects of ethanol on the expression of DYN/KOR in the extended amygdala, expression of DYN/KOR in alcohol-preferring and alcohol-avoiding animals, and the effects of knocking out DYN/KOR genes on ethanol intake. Then, it examines the effects on ethanol use in both dependent and nondependent states from systemic pharmacological manipulations of DYN/KOR and from specific manipulation of this system in regions of the extended amygdala. We propose that greater expression and binding of DYN/KOR, by reducing the positive reinforcement that drives early stages of intake, initially acts to prevent the escalation of ethanol drinking. However, prolonged, binge-like, or intermittent ethanol intake enhances levels of DYN/KOR in the extended amygdala such that the system ultimately facilitates the negative reinforcement that drives later stages of ethanol drinking. This review highlights the potential of the DYN/KOR system as a target that can affect different outcomes across different stages of ethanol drinking and the development of alcohol use disorder.