Binge eating disorder

Abstract

Binge eating disorder (BED) is characterized by regular binge eating episodes during which individuals ingest comparably large amounts of food and experience loss of control over their eating behaviour. The worldwide prevalence of BED for the years 2018-2020 is estimated to be 0.6-1.8% in adult women and 0.3-0.7% in adult men. BED is commonly associated with obesity and with somatic and mental health comorbidities. People with BED experience considerable burden and impairments in quality of life, and, at the same time, BED often goes undetected and untreated. The aetiology of BED is complex, including genetic and environmental factors as well as neuroendocrinological and neurobiological contributions. Neurobiological findings highlight impairments in reward processing, inhibitory control and emotion regulation in people with BED, and these neurobiological domains are targets for emerging treatment approaches. Psychotherapy is the first-line treatment for BED. Recognition and research on BED has increased since its inclusion into DSM-5; however, continuing efforts are needed to understand underlying mechanisms of BED and to improve prevention and treatment outcomes for this disorder. These efforts should also include screening, identification and implementation of evidence-based interventions in routine clinical practice settings such as primary care and mental health outpatient clinics.

Figure 1:. Timeline of the evolution of classification criteria for BED.

The first description of binge eating is attributed to the American psychiatrist Albert J Stunkard in the late 1950s, while another American psychiatrist, Walter W Hamburger, a few years earlier laid the foundation for the understanding that obesity entails also emotional aspects. These early notions focus on binge eating as a behaviour, and it took two decades until binge eating was introduced as a core symptom of an eating disorder, bulimia nervosa (BN), in the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM). Fourteen years later, BED was included as a research diagnosis into the fourth edition of the DSM, including a more specified definition of binge eating as a core psychopathology and a time criterion. BED was finally recognized as an official diagnosis in DSM-5 a decade later. Compared with the research criteria, the DSM-5 criteria include a loosening of the time criterion with binge eating episodes occurring at least once a week over three months necessary to fulfil the diagnosis. BED is also included in the International Classification of Diseases 11^th Revision (ICD-11). The ICD has loosened criteria around the ‘large amount’ of food ingested, allowing subjective binge eating, which will put challenges towards consistent application of diagnostic criteria. EDNOS, eating disorder not otherwise specified.

Figure 2:. Lifetime prevalence of binge eating disorder

World map displaying lifetime prevalence for binge eating disorder (BED) for different regions ^,–. For most regions, only the pooled lifetime prevalence (an average of male and female prevalence) is available.

Figure 3:. Schematic display of pathways of Gut-brain communication.

Eating behaviour is regulated by a complex interaction of the gastrointestinal, endocrine and central nervous system. Hormonal signalling from the gastrointestinal system to brain structures involved in homeostatic regulation (the hypothalamus), reward system functioning (the striatum) and cognitive control (the prefrontal cortex) influencing behavioural outcomes involved in the regulation of eating behaviour, such as processes of decision-making and emotion regulation, which are altered in individuals suffering from BED.

Figure 4:. Food intake regulation.

Different peptide hormones, including ghrelin, leptin and insulin, promoting hunger and satiety signals are directly secreted from the gastrointestinal tract and predominantly communicate with brain regions involved in homeostatic regulation and reward system functioning. Research on alterations in gut-brain communication in binge eating disorder (BED) is in its infancy; however, putative dysregulated peptide hormone functioning has been hypothesized to be associated with altered hunger-satiety signalling in individuals with BED.

Figure 5:. Brain circuits involved in the pathopsychology of BED.

Neuropsychological impairments of binge eating disorder (BED) have been explored in several brain imaging studies. The neurological basis of binge eating is composed of the hypothalamus (H) that regulates energy balance, such as food intake stimulated by gut hormones, the reward system that is representing motivational-affective functions (comprising the amygdala (Am), nucleus accumbens (Nac), ventral tegmental area (VTA), ventral striatum (VS) and orbitofrontal / ventromedial prefrontal cortex (OFC)), and cortical regions that are responsible for inhibitory control processes (comprising the prefrontal cortex (PFC), dorsolateral PFC (DLPFC), anterior cingulate cortex (ACC); insula and inferior frontal gyrus not shown). These three systems interact while binge eating episodes and mirror main components of impulsivity, that is, reward sensitivity and inhibitory control.