Purpose of review

Eating disorders are severe psychiatric disorders with a suspected complex biopsychosocial cause. The purpose of this review is to synthesize the recent literature on brain imaging in eating disorders.

Recent findings

Food restriction as well as binge eating and purging behaviors are associated with lower regional brain volumes or cortical thickness, but those changes largely return to normal with normalization of weight and eating behavior. Computational modeling has started to identify patterns of structural and functional imaging data that classify eating disorder subtypes, which could be used in the future, diagnostically and to better understand disorder-specific psychopathology. The prediction error model, a computational approach to assess dopamine-related brain reward function, helped support a brain-based model for anorexia nervosa. In that model, the conscious motivation to restrict conflicts with body signals that stimulate eating. This conflict causes anxiety and drives a vicious cycle of food restriction.

Summary

Novel brain research supports the notion that eating disorders have distinct neurobiological underpinnings. This new knowledge can be used to describe disease models to patients and develop novel treatments.

Introduction

Anorexia nervosa is a severe psychiatric illness and no medication has been approved for its treatment. This lack of biological treatments requires the development of new directions for pharmacological research.

Areas covered

There is modest but emerging evidence that dopamine D2 and serotonin 1A and 2A receptor agonistic and antagonist medication might be beneficial for weight gain, although the underlying mechanisms are uncertain. Improving quality of life including treating comorbid conditions is an additional important outcome measure, but this has not been well researched. Biological and psychological risk factors together with neurobiological alterations during the illness maintain the disorder 's pathophysiology. Neuroscience research can be used to understand those interactions and advance the research agenda. The authors discuss the above as well as give perspectives on future research.

Expert opinion

If a multidisciplinary approach that includes evidence-based psychotherapy shows unsatisfactory success in weight normalization and cognitive-emotional recovery, then more experimental treatments that are safe and have indicated treatment effectiveness should be tried to augment treatment. Identification and treatment of comorbid conditions to improve quality of life of the patient should also be part of the treatment regimen, even if the effect on weight gain is uncertain.

Anorexia nervosa is a severe psychiatric disorder most commonly starting during the teenage-years and associated with food refusal and low body weight. Typically there is a loss of menses, intense fear of gaining weight, and an often delusional quality of altered body perception. Anorexia nervosa is also associated with a pattern of high cognitive rigidity, which may contribute to treatment resistance and relapse. The complex interplay of state and trait biological, psychological, and social factors has complicated identifying neurobiological mechanisms that contribute to the illness. The dopamine D1 and D2 neurotransmitter receptors are involved in motivational aspects of food approach, fear extinction, and cognitive flexibility. They could therefore be important targets to improve core and associated behaviors in anorexia nervosa. Treatment with dopamine antagonists has shown little benefit, and it is possible that antagonists over time increase an already hypersensitive dopamine pathway activity in anorexia nervosa. On the contrary, application of dopamine receptor agonists could reduce circuit responsiveness, facilitate fear extinction, and improve cognitive flexibility in anorexia nervosa, as they may be particularly effective during underweight and low gonadal hormone states. This article provides evidence that the dopamine receptor system could be a key factor in the pathophysiology of anorexia nervosa and dopamine agonists could be helpful in reducing core symptoms of the disorder. This review is a theoretical approach that primarily focuses on dopamine receptor function as this system has been mechanistically better described than other neurotransmitters that are altered in anorexia nervosa. However, those proposed dopamine mechanisms in anorexia nervosa also warrant further study with respect to their interaction with other neurotransmitter systems, such as serotonin pathways.

Anorexia nervosa is a severe psychiatric illness associated with food avoidance. Animal models from Berridge et al. over the past decade showed that environmental ambience, pleasant or fear inducing, can trigger either appetitive (desire) or avoidance (dread) behaviors in animals via frontal cortex, nucleus accumbens dopamine D1 and D2 receptors, and hypothalamus. Those mechanisms could be relevant for understanding anorexia nervosa. However, models that translate animal research to explain the psychopathology of anorexia nervosa are sparse. This article reviews animal and human research to find evidence for whether this model can explain food avoidance behaviors in anorexia nervosa. Research on anorexia nervosa suggests fear conditioning to food, activation of the corticostriatal brain circuitry, sensitization of ventral striatal dopamine response, and alterations in hypothalamic function. The results support the applicability of the animal neurocircuitry derived model and provide directions to further study the pathophysiology that underlies anorexia nervosa.

Anorexia nervosa is a complex psychiatric illness associated with food restriction and high mortality. Recent brain research in adolescents and adults with anorexia nervosa has used larger sample sizes compared with earlier studies and tasks that test specific brain circuits. Those studies have produced more robust results and advanced our knowledge of underlying biological mechanisms that may contribute to the development and maintenance of anorexia nervosa. It is now recognized that malnutrition and dehydration lead to dynamic changes in brain structure across the brain, which normalize with weight restoration. Some structural alterations could be trait factors but require replication. Functional brain imaging and behavioral studies have implicated learning-related brain circuits that may contribute to food restriction in anorexia nervosa. Most notably, those circuits involve striatal, insular, and frontal cortical regions that drive learning from reward and punishment, as well as habit learning. Disturbances in those circuits may lead to a vicious cycle that hampers recovery. Other studies have started to explore the neurobiology of interoception or social interaction and whether the connectivity between brain regions is altered in anorexia nervosa. All together, these studies build upon earlier research that indicated neurotransmitter abnormalities in anorexia nervosa and help us develop models of a distinct neurobiology that underlies anorexia nervosa.

Anorexia nervosa (AN) is a serious eating disorder characterized by self-starvation and extreme weight loss. Pseudoatrophic brain changes are often readily visible in individual brain scans, and AN may be a valuable model disorder to study structural neuroplasticity. Structural magnetic resonance imaging studies have found reduced gray matter volume and cortical thinning in acutely underweight patients to normalize following successful treatment. However, some well-controlled studies have found regionally greater gray matter and persistence of structural alterations following long-term recovery. Findings from diffusion tensor imaging studies of white matter integrity and connectivity are also inconsistent. Furthermore, despite the severity of AN, the number of existing structural neuroimaging studies is still relatively low, and our knowledge of the underlying cellular and molecular mechanisms for macrostructural brain changes is rudimentary. We critically review the current state of structural neuroimaging in AN and discuss the potential neurobiological basis of structural brain alterations in the disorder, highlighting impediments to progress, recent developments, and promising future directions. In particular, we argue for the utility of more standardized data collection, adopting a connectomics approach to understanding brain network architecture, employing advanced magnetic resonance imaging methods that quantify biomarkers of brain tissue microstructure, integrating data from multiple imaging modalities, strategic longitudinal observation during weight restoration, and large-scale data pooling. Our overarching objective is to motivate carefully controlled research of brain structure in eating disorders, which will ultimately help predict therapeutic response and improve treatment.

Eating disorders are severe psychiatric illnesses with a typical age of onset in adolescence. Brain research in youth and young adults may help us identify specific neurobiology that contributes to onset and maintenance of those disorders. This article provides a state-of-the-art review of our current understanding of the neurobiology of anorexia nervosa and bulimia nervosa. This includes brain structure and function studies to understand food restriction, binge-eating or purging behaviors, cognitive and emotional factors, as well as interoception. Binge-eating disorder and avoidant restrictive food intake disorder are also discussed, but the literature is still very small.

Endurance or aerobic exercise has many physical and mental health benefits, but less is known about the specific impact that cardiovascular activity may have on dopamine-associated brain circuits involved in reward processing and mood regulation in humans. Understanding such effects will help to explain individual differences in both exercise uptake and maintenance. This study evaluated neural response to a classical taste-conditioning reward prediction error task with the use of functional magnetic resonance imaging, along with data on self-reported aerobic exercise among healthy young adult females (N = 111). Results indicated positive associations between reported aerobic exercise and regional brain response that remained significant after multiple comparison correction for the right medial orbital frontal cortex response to unexpected sucrose receipt (r = 0.315, p = .0008). The medial orbitofrontal cortex is implicated in reward and outcome value computation and the results suggest that aerobic exercise may strengthen this circuitry, or reciprocally, higher orbitofrontal cortical activity may reinforce exercise behavior. The findings aid in developing a model of how exercise engagement can modify reward-circuit function and could be used therapeutically in conditions associated with altered brain salience response.