Eating disorder behaviors can range from dangerous caloric restriction to eating that feels out of control—often combined with unhealthy weight control behaviors, such as self-induced vomiting or laxative abuse. Anorexia nervosa, bulimia nervosa, and binge eating disorder are the most prevalent eating disorders. Diagnostically, anorexia nervosa requires low body weight, intense fear of or behavior that interferes with weight gain, and disturbance in the perception of one’s weight or shape.
Criteria for bulimia nervosa include recurrent binge eating (eating a large amount of food in a discrete period of time accompanied by a sense of loss of control) and actions meant to counteract weight gain (eg, self-induced vomiting), as well as overvaluation of body weight or shape. Binge eating disorder involves recurrent binge eating without inappropriate compensatory behavior. Individuals with eating disorders frequently report extreme body dissatisfaction, anhedonia, anxiety, and difficulty tolerating negative emotions, although these are not required for diagnosis.
The cause of eating disorders remains unknown. Given that eating disorders reflect a discrepancy between the physiological need to eat and the drive to eat, it has been hypothesized that these individuals have a fundamental disturbance of appetite regulation. In recent years, advances in brain imaging have provided new insights into neural pathways that play a role in emotions, reward, salience, and inhibition of eating.
CASE VIGNETTE
Mabel is a 16-year-old girl who is hospitalized with unstable vital signs and a BMI of 17.5. Her family describes her as an anxious, shy, and perfectionistic child who tended to ruminate about academics, social relationships and, more recently, food. Mabel says that she has always been a picky eater. She started to lose weight after she got braces and switched to softer foods 2 years ago. She reports that her food rules became progressively more restrictive and she began exercising regularly. She became increasingly anhedonic, cognitively rigid, and sensitive to perceived criticism. She interprets her family’s efforts to support her weight restoration efforts as “nagging” and judgmental.
Current treatments—psychotherapy or pharmacotherapy—often have limited efficacy in ameliorating eating disorder symptoms and may not fully normalize eating behavior. Furthermore, many psychological interventions used to treat eating disorders are adaptations of treatments for other psychiatric disorders (eg, depression, anxiety) and were not developed for the specific, unique needs of patients with eating disorders.
The lack of a mechanistic understanding of eating disorders has thwarted efforts to develop more powerful, evidence-based interventions. Alterations in brain circuitry linked to reward and inhibition in particular appear to be involved in the maladaptive eating behavior characteristic of anorexia nervosa, bulimia nervosa, and binge eating disorder.
Neurocircuitry overview
What is it about the brains of those with eating disorders that might drive dysfunctional eating behavior? It is well known that gut and hypothalamic mechanisms contribute to the regulation of energy metabolism and eating behaviors. However, in recent years, studies in humans have revealed that higher-order, corticolimbic systems likely play a role in the pathophysiology of eating disorders.1 These systems integrate behavior with eating and can override homeostatic signals (Figure 1).
The first of these networks codes for perceived importance of a food stimulus and comprises the insula and anterior cingulate. The insula, along with the frontal operculum, also processes basic sensory information about food. The second pathway includes the nucleus accumbens, putamen, and caudate, as well as the orbitofrontal cortex and amygdala. These regions code for the rewarding and motivating value of eating and contribute to approach or avoidance behavior.
The third network helps control consumption based on consideration of both short- and long-term outcomes (eg, weight gain). It includes the dorsal caudate and dorsal anterior cingulate, lateral prefrontal cortex, and parietal cortex. These systems interactively weigh the reward value of food and the consequences of consuming it, and they integrate this information with homeostatic and motivational drives to guide eating behavior.
Mounting evidence suggests that an altered balance of reward and inhibition may contribute to disordered eating.1 In anorexia nervosa, severely restricted food intake appears to be related to overactive inhibitory control in combination with underactive reward circuitry. In contrast, dysregulation of both inhibitory and reward drives may manifest in the alternating over- and under-consumption characteristic of bulimia nervosa. Binge eating disorder may be related to altered sensitivity of ventral reward regions. Findings also suggest that these brain-based differences are linked to temperament traits, such as anxiety and harm avoidance, which persist after remission and may underlie the development of eating pathology.
Dr Ely and Dr Berner are Postdoctoral Fellows, and Dr Wierenga is Associate Professor of Psychiatry at the University of California, San Diego. Dr Kaye is Professor and Program Director of the Eating Disorders Treatment and Research Program in the department of psychiatry at the University of California, San Diego. The authors report no conflicts of interest concerning the subject matter of this article.
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