Published: 2021
Neuroscience is an area of research that explores brain communication (i.e. how cells “talk” with each other) with the goal of understanding our thoughts, behaviours, and bodily functions.
Like a text message, brain cells send chemical messages to other brain cells that tell our body what it needs (e.g. sleep), how we feel (e.g. sad), and what we worry about (e.g. weight gain). This information influences our thoughts, actions, and health.
Understanding how the brain influences our thoughts and behaviours is important because, if we know how the brain functions during illnesses (e.g. eating disorders), we can develop better preventative measures and treatments for people who have them. Neuroscience research can also help to justify the need for care, as it can demonstrate that eating disorders benefit from medical treatment.
Studying eating disorders from a neuroscience perspective, however, is challenging. The brain is constantly changing, and there’s still a lot we don’t know about it. Also, every brain is different. This makes it difficult to determine neurobiological causes for eating disorders.
One way that researchers determine neurobiological causes for eating disorders is by seeing if eating disorder symptoms (e.g. high anxiety) are still present in recovered individuals. The rationale is that, if the symptom is present even when the eating disorder is not, that symptom is likely to have been around before the eating disorder (i.e. may have caused the eating disorder).
One cause for eating disorders is negative thinking [1]. It has been shown that people with eating disorders have negative thoughts more frequently than people without eating disorders [2; 3; 4], and that eating disorder behaviour (e.g. binge eating or food restriction) follows negative thinking (e.g. negative social comparisons and self-evaluations [4; 1]. This is true across most types of eating disorders (e.g. bulimia, orthorexia,[5; 6] anorexia,[7] atypical anorexia,[7; 8] and binge eating disorder).
People with eating disorders have frequent negative thoughts because, as brain studies show, they focus on threatening information (e.g. weight or food) more often than people without eating disorders [9; 10; 11; 12]. Frequent negative thinking contributes to eating disorder onset by increasing stress on the body, which changes how the brain functions. For people with eating disorders, frequent negative thinking might lead to biological changes that make coping with negative thoughts especially difficult [13].
Eating disorder behaviour (e.g. binge eating) can present as a coping mechanism for negative thinking [14]. For example, for people with bulimia or binge eating disorder, binge eating might be a way for them to briefly escape negative thoughts [15; 16]. This is because, as brain imaging studies show, people who develop bulimia or binge eating disorder are motivated to eat for different reasons than people who don’t binge eat [17].
In contrast, food restriction might be a coping strategy for people with anorexia. This is because the body’s chemical hunger messenger, ghrelin, can also reduce anxiety [18; 19]. When people without anorexia restrict their food intake, ghrelin is sent to the brain to tell them that they need to eat. When people with anorexia restrict their food intake their brains receive a lot more ghrelin than people without anorexia [20; 21]. Therefore, restricting food intake can reduce anxiety for people with anorexia.
Brain scans also show that people with anorexia symptoms find high-calorie foods less rewarding than people without anorexia symptoms; this could be due to how their brains communicate information about food reward [22; 23]. It’s unclear, though, if increased ghrelin signalling causes anorexia or if it’s a consequence of malnutrition [24; 25].
Changes in brain chemicals, such as serotonin, also contribute to eating disorder onset by shaping our personalities [26]. Differences in personalities contribute to the development of different eating disorders [27].
Neuroscience research shows that high levels of serotonin cause personality traits common in anorexia (e.g. perfectionism, anxiousness, rigidity, and compulsivity) [27; 28; 29]. Consequently, having high levels of serotonin increase the likelihood that someone will develop personality traits that cause anorexia [27].
People with bulimia nervosa or binge eating disorder, in contrast, have lower serotonin levels than people without these disorders [30]. Low levels of serotonin have been associated with personality traits common in eating disorders that include binge eating (e.g. high impulsivity and low mood) [27; 31]. This suggests that low levels of serotonin increase an individual’s risk of developing personality traits that cause one of these disorders.
Because these serotonin differences are present in recovered individuals and might have a genetic component [30; 32], differences in serotonin levels are likely to be a cause, rather than a consequence, of eating disorders [27].
Neuroscience can also explain body image concerns in eating disorders. People with anorexia symptoms overestimate their body size more often than people without these symptoms [33]. Neuroscientists think that this is because their brains “talk” about their bodies in ways that favour negatively biased self-references [34; 35]. These body overestimations persist in recovery and, therefore, might contribute to eating disorder onset [36].
People with eating disorders also struggle with bodily cues in ways that contribute to eating disorder development. Bodily cues are internal messages that inform people about the state of their bodies (e.g. when they are hungry). Listening and responding appropriately to these cues (e.g. feeling hungry and eating) is called “interoceptive awareness” [37].
People of all weights with most eating disorder types have low interoceptive awareness [22; 38] This means they can’t accurately recognise when they are hungry, full, or experiencing certain emotions. For example, people with avoidant/restrictive food intake disorder (ARFID) receive fullness cues sooner during a meal than people without ARFID [39]. This prevents them from relying on their bodies to know when to stop eating. Low interoceptive awareness can be both a cause and consequence of an eating disorder [40; 41].
Poor gut health also contributes to eating disorder onset by influencing our thoughts and behaviours [42; 43]. Scientists are only just beginning to understand how the gut causes mental illness and, consequently, few studies have explored its role in eating disorders. One study found that people with anorexia have a gut low in bacterial diversity, which might reduce interoceptive awareness [44]. Less is known about how the gut might cause other eating disorders, though gut discomfort is a known cause for ARFID [42].
Childhood gut discomfort is a known cause for ARFID, as the unpleasantness of eating can lead to food restriction and aversions to hunger and fullness cues (i.e. poor interoceptive awareness)[45]. Additionally, bad (e.g. choking) and unpleasant sensory experiences (e.g. dislike of certain textures) with food can cause ARFID [46]. These sensory experiences in ARFID overlap with autism [47]. The brains of people with ARFID, like those of people with autism, might be biased to communicate unpleasant information about food texture, smell, colour, and taste [48]. Because so much brain development happens during childhood, these early life experiences with food (e.g. food avoidance) shape future eating behaviour, which can include the development of ARFID.
[1] Sala, M., Brosof, L., & Levinson, C. (2019). Repetitive negative thinking predicts eating disorder behaviours: A pilot ecological momentary assessment study in a treatment seeking eating disorder sample. Behaviour Research and Therapy, 112, 12-17.
[2] Kukk, K., & Akkermann, K. (2017). Fluctuations in negative emotions predict binge eating both in women and men: An experience sampling study. Eating Disorders, 25, 65-79.
[3] Palmieri, S., Mansueto, G., Scaini, S., Caselli, G., Sapuppo, W., Spada, M., Sassaroli, S., & Ruggiero, G. (2021). Repetitive negative thinking and eating disorders: A mate-analysis of the role of worry and rumination. Journal of Clinical Medicine, 10, 1-16.
[4] Cardi, V., Matteo, R., Gilbert, P., & Treasure, J. (2014). Rank perception and self-evaluation in eating disorders. International Journal of Eating Disorders, 47, 543-552.
[5] Strahler, J. (2021). Trait mindfulness differentiates the interest in healthy diet from orthorexia nervosa. Eating and Weight Disorders, 26, 993-998.
[6] Koven, S., & Abry, A. (2015). The clinical basis of orthorexia nervosa: Emerging Perspectives. Neuropsychiatric Disease and Treatment, 11, 385-394.
[7] Pauls, A., Dimitropoulos, G., Marcoux-Louie, G., Singh, M., & Patten, S. (2020). Psychological characteristics and childhood adversity of adolescents with atypical anorexia nervosa versus anorexia nervosa. Eating Disorders, 24, 1-13.
[8] Weinbach, N., Sher, H., Bohon, C. (2018). Differences in emotion regulation difficulties across types of eating disorders during adolescence. Journal of Abnormal Child Psychology, 46, 1351-1358.
[9] Seidel, M., King, J., Ritschel, F., Boehm, I., Geisler, D., Bernardoni, F.,…& Ehrlich, S. (2018). Processing and regulation of negative emotions in anorexia nervosa: An fMRI study. NeuroImage: Clinical, 18, 1-8.
[10] Renwick, B., Campbell, I., & Schmidt, U. (2013). Review of attentional bias modification: A brain-directed treatment for eating disorders. European Eating Disorders Review, 21, 464-474.
[11] Luo, Y., Mendoza, C., Pelfrey, S., Lohrenz, T., Gu, X., Montague, P., & McAdams, C. (2021). Elevated neurobehavioural responses to negative social interactions in women with bulimia nervosa. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging.
[12] Bauer, A., Schneider, S., Waldorf, M., Brakes, K., Huber, T., Adolph, D., & Vocks, S. (2017). Selective visual attention towards oneself and associated state body satisfaction: An eye-tracking study in adolescents with different types of eating disorders. Journal of Abnormal Child Psychology, 45, 1647-1661.
[13] Rojo, L., Conesa, L., Bermudez, O., & Livianos, L. (2006). Influence of stress in the onset of eating disorders: Data from a two-stage epidemiologic controlled study. Psychosomatic Medicine, 68, 628-635.
[14] MacNeil, L., Esposito-Smythers, C., Mehlenbeck, R., & Weismoore, J. (2012). The effects of avoidance coping and coping self-efficacy on eating disorder attitudes and behaviours: A stress-diathesis model. Eating Behaviours, 13, 293-296.
[15] McCuen-Wurst, C., Ruggieri, M., & Allison, K. (2017). Disordered eating and obesity: Associations between binge eating disorder, night-eating syndrome, and weight-related comorbidities. Annals of the New York Academy of Sciences, 1411, 96-105.
[16] Turton, R., Chami, R., & Treasure, J. (2017). Emotional eating, binge eating, and animal models of binge-type eating disorders. Current Obesity Reports, 6, 217-228.
[17] Steinglass, J., Berner, L., Attia, E. (2019). Cognitive neuroscience of eating disorders. Psychiatric Clinics of North America, 42, 75-91.
[18] Chuang, J., & Zigman, J. (2010). Ghrelin’s role in stress, mood, and anxiety regulation. International Journal of Peptides, 2010, 1-5.
[19] Maniscalco, J. & Rinaman, L. (2018). Vagal interoceptive modulation of motivated behaviour. Physiology (Bethesda), 33, 151-167.
[20] Nedvídkova, J., Krykorková, I., Barták, V., Papezová, H., Gold, P., Alesci, S., & Pacak, K. (2003). Loss of meal-induced decrease in plasma ghrelin levels in patients with anorexia nervosa. The Journal of Clinical Endocrinology & Metabolism, 88, 1678-1682.
[21] Breithaupt, L., Chunga-Iturry, N., Lyall, A., Cetin-Karayumak, S., Becker, K., Thomas, J.,…& Eddy, K. (2020). Developmental stage-dependent relationships between ghrelin levels and hippocampal white matter connections in low-weight anorexia nervosa and atypical anorexia nervosa. Psychoneuroendocrinology, 119.
[22] Holsen, L., Lawson, E., Christensen, K., Klibanski, A., & Goldstein, J. (2014). Abnormal relationships between the neural response to high- and low- calorie foods and endogenous acylated ghrelin in women with active and weight-recovered anorexia nervosa. Psychiatry Research, 223, 94-103.
[23] Olivo, G., Zhukovsky, C., Salonen-Ros, H., Larsson, E., Books, S., & Schiöth, B. (2019). Functional connectivity underlying hedonic response to food in female adolescents with atypical AN: The role of somatosensory and salience networks. Translational Psychiatry, 9.
[24] Monteleone, A., Monteleone, P., Grave, R., Nigro, M., Ghoch, M., Calugi, S.,...Maj, M. (2016). Ghrelin response to hedonic eating in underweight and short-term weight restored patients with anorexia nervosa. Psychiatry Research, 235, 55-60.
[25] Schalla, M., & Stengel, A. (2018). The role of ghrelin in anorexia nervosa. International Journal of Molecular Science, 19.
[26] Bailer, U., & Kaye, W. (2011). Serotonin: Imaging findings in eating disorders. Current Topics in Behavior Neuroscience, 6, 59-79.
[27] Steiger, H. (2004). Eating disorders and the serotonin connection: State, trait, and developmental effects. Journal of Psychiatry & Neuroscience, 29, 20-29.
[28] Isaksson, M., Ghaderi, A., Wolf-Arehult, M., & Ramklint, M. (2021). Overcontrolled, undercontrolled, and resilient personality styles among patients with eating disorders. Journal of Eating Disorders, 9.
[29] Zastrow, A., Kaiser, S., Stippich, C., Walther, S., Herzog, W., Tchanturia, K.,…& Friederich, H.C. (2009). Neural correlates of impaired cognitive-behavioural flexibility in anorexia nervosa. American Journal of Psychiatry, 166, 608-616.
[30] Monteleone, P., Tortorella, A., Castaldo, E., & Maj, M. (2005). Association of a functional serotonin transporter gene polymorphism with binge eating disorder. American Journal of Medical Genetics Part B, 141B, 7-9.
[31] Kessler, R., Hutson, P., Herman, B., & Potenza, M. (2016). The neurobiological basis of binge-eating disorder. Neuroscience & Behavioural Reviews, 63, 223-238.
[32] Moskowitz, L., & Weiselberg, E. (2017). Anorexia nervosa/atypical anorexia nervosa. Current Problems in Pediatric and Adolescent Health Care, 47, 70-84.
[33] Cornelissen, K., McCarty, K., Cornelissen, P., & Tovée, M. (2017). Body size estimation in women with anorexia nervosa and healthy controls using 3D avatars. Scientific Reports, 7.
[34] Zhang, A., Leow, A., Zhan, L., GadElkarim, T., Moody, S., Khalsa, S., Strober, M., & Feusner, J. (2016). Brain connectome modularity in weight-restored anorexia nervosa and body dysmorphic disorder. Psychological Medicine, 46.
[35] Serino, S., Dakanalis, A., Gaudio, S., Carrà, G., Cipresso, P., Clerici, M., & Riva, G. (2015). Out of body, out of space: Impaired reference frame processing in eating disorders. Psychiatry Research, 230, 732-734.
[36] Eshkevari, E., Rieger, E., Longo, M., Haggard, P., & Treasure, J. (2014). Persistent body image disturbance following recovery from eating disorders. International Journal of Eating Disorders, 47, 400-409.
[37] Quigley, K., Kanoski, S., Grill, W., Barrett, L., & Tsakiris, M. (2021). Functions of interoception: From energy regulation to experience of the self. Trends in Neuroscience, 44, 29-38.
[38] Martin, E., Dourish, C., Rotshtein, P., Spetter, M., & Higgs, S. (2019). Interoception and disordered eating: A systematic review. Neuroscience & Behavioral Reviews, 107, 166-191.
[39] Becker, K., Mancuso, C., Dreier, M., Asanza, E., Breithaupt, L., Slattery, M., Plessow, F., Micali, N., Thomas, J.,…& Lawson, E. (2021). Ghrelin and PYYY in low-weight females with avoidant/restrictive food intake disorder compared to anorexia nervosa and healthy controls. Psychoneuroendocrinology, 129.
[40] Murphy, J., Brewer, R., Catmur, C., & Bird, G. (2017). Interoception and psychopathology: A developmental neuroscience perspective. Developmental Cognitive Neuroscience, 23, 45-56.
[41] Price, C., & Hooven, C. (2018). Interoceptive awareness skills for emotion regulation: Theory and approach of mindful awareness in body-oriented therapy (MABT). Frontiers in Psychology, 9.
[42] Murray, H., Kuo, B., Eddy, K., Breithaupt, L., Becker, K., Dreier, M., Thomas, J., & Staller, K. (2020). Disorders of gut-brain interaction common among outpatients with eating disorders including avoidant/restrictive food intake disorder. International Journal of Eating Disorders, 54, 952-953.
[43] Hozer, P. (2017). Interoception and gut feelings: Unconscious body signals’ impact on brain function, behavior, and belief processes. Processes of Believing: The Acquisition, Maintenance, and Change in Creditions, pp. 435-442.
[44] Butler, M., Perrini, A., & Eckel, L. (2021). The role of the gut microbiome, immunity, and neuroinflammation in the pathophysiology of eating disorders. Nutrients, 13.
[45] Zucker, N., Via, M., Craske, M., Foukal, M., Harris, A., Datta, N., Savereide, E., & Masow, G. (2020). Feeling and body investigators (FBI) – ARFID division: An acceptance-based interoceptive exposure treatment for children with ARFID. International Journal of Eating Disorders, 52, 466-472.
[46] Thomas, J., Lawson, E., Micali, N., Misra, M., Deckersbach, T., & Eddy, K. (2017). Avoidant/restrictive food intake disorder: A three-dimensional model of neurobiology with implications for etiology and treatment. Current Psychiatry Reports, 19, 54.
[47] Mayes, S., & Zickgraf, H. (2019). Atypical eating behaviors in children and adolescents with autism, ADHD, other disorders, and typical development. Research in Autism Spectrum Disorders, 64, 76-83.
[48] Galiana-Simal, A., Muñoz-Martinez, V., & Beato-Fernandez, L. (2017). Connecting eating disorders and sensory processing disorder: A sensory eating disorder hypothesis. Global Journal of Intellectual & Developmental Disabilities, 3, 1-3.