Investigational drugs for the treatment of binge eating disorder (BED): an update.

Introduction: Binge eating disorder (BED) is the most common eating disorder and is frequently associated with psychiatric and medical comorbidities and functional impairment. Although psychological treatments have been the cornerstones of BED treatment, pharmacologic interventions also play an important part of the multimodal management of this condition.Areas covered: This review examines investigational, approved and other pharmacological agents for the treatment of BED. We searched PubMed and clinicaltrials.gov to identify pharmacological interventions for the management of this condition.Expert opinion: BED pharmacological studies have incorporated new drug targets based on our enhanced understanding of the pathophysiology of BED. Neurobiological dysregulation in the reward center and impulse control circuitry and related disturbances in dopamine neurotransmission are among the neurobiological explanations that have been suggested for BED. These mechanisms serve as a pharmacodynamic foundation for the development of new compounds such as lisdexamfetamine (LDX) and dasotraline. Despite these advances, pharmacological trials in BED have numerous challenges that must be overcome. For most compounds studied, larger and more definitive trials is a high priority.

Clinical phenotype and genetic risk factors for bipolar disorder with binge eating: an update.

Introduction: Clinical and genetic study of psychiatric conditions has underscored the co-occurrence of complex phenotypes and the need to refine them. Bipolar Disorder (BD) and Binge Eating (BE) behavior are common psychiatric conditions that have high heritability and high co-occurrence, such that at least one quarter of BD patients have BE (BD + BE). Genetic studies of BD alone and of BE alone suggest complex polygenic risk models, with many genetic risk loci yet to be identified. Areas covered: We review studies of the epidemiology of BD+BE, its clinical features (cognitive traits, psychiatric comorbidity, and role of obesity), genomic studies (of BD, eating disorders (ED) defined by BE, and BD + BE), and therapeutic implications of BD + BE. Expert opinion: Subphenotyping of complex psychiatric disorders reduces heterogeneity and increases statistical power and effect size; thus, it enhances our capacity to find missing genetic (and other) risk factors. BD + BE has a severe clinical picture and genetic studies suggests a distinct genetic architecture. Differential therapeutic interventions may be needed for patients with BD + BE compared with BD patients without BE. Recognizing the BD + BE subphenotype is an example of moving towards more precise clinical and genetic entities.

Comparing cognitive behavioural therapy for eating disorders integrated with behavioural weight loss therapy to cognitive behavioural therapy-enhanced alone in overweight or obese people with bulimia nervosa or binge eating disorder: study protocol for a randomised controlled trial.

BACKGROUND: Around 40 % of individuals with eating disorders of recurrent binge eating, namely bulimia nervosa and binge eating disorder, are obese. In contrast to binge eating disorder, currently there is no evidence base for weight management or weight loss psychological therapies in the treatment of bulimia nervosa despite their efficacy in binge eating disorder. Thus, a manualised therapy called HAPIFED (Healthy APproach to weIght management and Food in Eating Disorders) has been developed. HAPIFED integrates the leading evidence-based psychological therapies, cognitive behavioural therapy-enhanced (CBT-E) and behavioural weight loss treatment (BWLT) for binge eating disorder and obesity respectively. The aim of the present study is to detail the protocol for a randomised controlled trial (RCT) of HAPIFED versus CBT-E for people with bulimia nervosa and binge eating disorder who are overweight/obese. METHOD/DESIGN: A single-blind superiority RCT is proposed. One hundred Brazilian participants aged ≥ 18 years, with a diagnosis of bulimia nervosa or binge eating disorder, BMI > 27 to < 40 kg/m(2), will be recruited from both community and clinics and individually randomised to a therapy arm. Five groups of ten participants will receive the experimental intervention (HAPIFED) and the other five groups of ten the control intervention (CBT-E). Both therapies are manualised, and in this RCT will comprise 1 individual session and 29 office-based group sessions over 6 months. Assessment points will be at baseline, end of therapy, and 6 and 12 months after end of therapy. The primary outcome of this intervention will be reduced weight. Secondary outcomes will be improved metabolic indicators of weight management, reduction in eating disorder symptoms including improved control over eating, improved adaptive function, physical and mental health-related quality of life, and reduced levels of depression and anxiety. DISCUSSION: This study will be the first to investigate a psychological therapy that aims to assist weight management in people with co-morbid overweight or obesity bulimia nervosa as well as with binge eating disorder. It will have the potential to improve health outcomes for the rapidly increasing number of adults with co-morbid obesity and binge eating disorder or bulimia nervosa. TRIAL REGISTRATION: US National Institutes of Health clinical trial registration number NCT02464345 , date of registration 1 June 2015.

Impact of binge eating disorder in the psychopathological profile of obese women.

OBJECTIVE: Our objective was to evaluate the psychopathological profile of obese women with binge eating disorder (BED) using the Symptom Checklist-90 (SCL-90). METHODS: Two hundred twelve obese women who seek for weight loss treatment were sequentially selected to participate in the study. Binge eating disorder was diagnosed using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Binge eating disorder severity was assessed using Binge Eating Scale. Depressive symptoms were assessed using Beck Depression Inventory. The psychopathological profile was assessed using the SCL-90. RESULTS: Binge eating disorder was diagnosed in 54 patients (26.6%). Obese patients with BED presented significant higher scores in all domains of SCL-90 (P < .05 for all) in comparison with obese patients without BED. A significant relationship was found among Binge Eating Scale, Beck Depression Inventory, and all domains of the SCL-90 (P < .05 for all). After linear regression, obsessivity-compulsivity (P = .03), interpersonal sensitivity (P = .0064), paranoid ideas (P = .03), and psychoticism (P = .01) were independently related to the severity of BED. CONCLUSION: Obese women with BED presented a more severe psychopathological profile than obese controls. Among all, obsessivity-compulsivity, interpersonal sensitivity, paranoid ideas, and psychoticism seem to be strongly linked to BED severity.