The Neuroscience of Eating Disorders

Written By: Laura Meng

During the 19th century, Sir William Gull formally proposed the clinical term Anorexia nervosa (AN) to encompass a set of homogeneous and aberrant thought processes and behaviours: a salient pursuit of weight loss despite low body weight, fear of weight gain, substantial value attributed to thinness, and specific physiological impacts, including amenorrhea and emaciation.(1) Since then, the Diagnostic Statistical Manual of Mental Disorders-Issue V has additionally included Bulimia nervosa (BN), Binge eating disorder (BED), and not otherwise specified subcategories of eating disorders (EDs).(2) BN comprises alternating episodes of binging—consumption of food beyond satiation—and compensatory behaviours, including purging, abuse of laxatives, and excessive exercise.(1) EDs are often temporally comorbid with affective psychiatric disorders, including anxiety and depression. They are among the highest morbidity of psychiatric disorders, and exhibit a high rate of suicide and relapse.(3)


A unifying neuropsychological dimension of Idée fixe: the “domination of mental life” associated with food consumption and an inability to inhibit these thoughts is present in EDs.(2) It is proposed that maladaptive habit formation, neuromodulator dysfunction, and stress contribute significantly to their course of development.(3)


Both clinical trials and rodent models suggest that an imbalance of goal directed behaviours (GDB) and habitual behaviours can result in compulsivity: a repeated inability to inhibit inappropriate responses despite adverse consequences.(4) GDB or action-outcome learning involves the presence of a cognitive link between the action with its desired reward. GDB are responsive to the magnitude of the reward, and a decline in action performance is expected if the value of the reward decreases; thus, they are sensitive to reward devaluation. Amygdalal, ventral striatal, dorsalmedial striatal (DMS), and orbitalfrontal cortical (OFC) activity are observed during GDB.(3) As a behaviour is repeated, habitual behaviours or stimulus-response learning occurs. Habitual behaviours are relatively insensitive to both devaluation and the action outcome. Instead, they are specific responses elicited by specific environmental cues. The anatomical areas active during habitual learning include the dorsalateral striatum (DLS) and the dorsolateral prefrontal cortex.(4) In patients with EDs, habitual behaviours are resistant to change.(2)


A trans-diagnostic model of EDs propose that compulsivity is present in AN, BN, and BED, and can be treated through targeted psychotherapy.(6) In clinical paradigms, a deficit in DMS and OFC activity was present in patients with AN compared to controls while in rodent models of AN, higher activity of the DLS was observed. These findings suggest a deficit in GDB and/or excessive habit formation contribute to the compulsivity of AN.(4) Dopamine is pivotal to the cortical-striatal systems that underlie GDB-habit formation through modulating intracellular signaling cascades. Among its other functions, serotonin modulates affective states, and selective serotonin reuptake inhibitors are often utilized as an adjunct in current treatments of eating disorders.(5) Both these neuromodulators exhibit deviations from expected functioning in individuals with eating disorders, though their specific mechanism is currently ambiguous. Furthermore, rodent models and self-reports in patients delineate the significance of stress in shaping behaviour: stress often precedes the deleterious compensatory behaviours, including binging and purging, observed across EDs.(6)


Continued psychiatric and neuroscience development iterate the importance of approaching EDs through multiple facets.(5) A randomized trial comparing the efficacy of non-specific psychotherapy VS psychotherapy that targets Regulating Emotions and Changing Habits (REaCH) aimed to improve AN treatment through refining an existing therapeutic technique.(6) Neurobiological models, including the development of a neurocognitive endophenotype of compulsion, rodent models utilizing subneuronal knockouts, and continued efforts in elucidating the genetic biomarkers common to EDs illustrate an integrative approach to understanding EDs. Sincere efforts from students, researchers, patients, and clinicians alike continue to further our understanding and development of future treatments for individuals with eating disorders.



1.) Gruber, R. (2016). Biological Psychiatry: Eating Disorders [Powerpoint Presentation].






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