National Eating Disorders Association

Although eating disorders result from the interplay of a variety of cultural and biological factors, the brain is central to understanding why some people develop eating disorders, why people stay ill, and how they can recover. In recent years, scientists have made tremendous strides in understanding the brain science of eating disorders.

Based on evidence from hundreds of studies, it appears that one of the factors that make a person more likely to develop an eating disorder is how their brain functions. Researchers have identified specific neurobiological differences in the brains of people with anorexia, bulimia, or binge eating disorder. These differences affect how we eat, as well as things like mood, anxiety, personality, and decision-making.

This section will introduce you to the basics of eating disorder neurobiology, and how various neural systems work together in individuals with eating disorders.


Neurons send signals to each other using chemicals known as neurotransmitters. The type and amount of neurotransmitters released will tell neighboring neurons whether to become active or to stay silent.

The body produces an array of neurotransmitters and their receptors, which are proteins on the surface of the cell that recognize a specific neurotransmitter and relay the signal from the outside to the inside of the cell. Small variations in the shape and number of receptors, as well as the amount of neurotransmitter produced—known as polymorphisms—exist in the population, which increase or decrease the amount of neurotransmitter in the synapse (the small space between a neuron and its neighbors) and our sensitivity to it. These variations have been linked to a variety of mental illnesses, including eating disorders.

For eating disorders, there are two primary neurotransmitters you need to know about: serotonin and dopamine. Each of these neurotransmitters has an influence in how we think and behave, our personalities, and even perhaps our risk for developing an eating disorder.


Given that serotonin (sometimes referred to as 5-hydroxytryptophan) helps control everything from memory and learning to sleep, mood, and appetite, researchers quickly began to look for potential relationships between polymorphisms in serotonin receptor genes and eating disorders.

A variety of studies have found alterations in the serotonin system in individuals currently ill with anorexia nervosa and those recovered from the disorder. Researchers found that people who are currently suffering from anorexia have significantly lower levels of serotonin metabolites in their cerebrospinal fluid than individuals without an eating disorder. This is likely a sign of starvation, since the body synthesizes serotonin from the food we eat. After long-term recovery from anorexia, however, individuals have significantly elevated serotonin levels (Kaye et al., 1991). In this study, the researchers found that higher levels of serotonin correspond with levels of anxiety and obsessive behavior. Geneticists have also found that individuals with anorexia are slightly more likely to carry a particular variant of the 5HT2A serotonin receptor, which is thought to increase the amount of serotonin in the brain during the non-starved state (Gorwood et al., 2002).

In an article published in 2009 in Nature Neuroscience, leading eating disorder researcher Walter Kaye hypothesizes that starvation actually makes people with anorexia feel better by decreasing the serotonin in their brains (Kaye, Fudge, & Paulus, 2009). As they continue to starve themselves, however, the brain responds by increasing the number of serotonin receptors to more efficiently utilize the remaining serotonin. So in order to keep feeling better, the person needs to starve themselves further, creating the illness’s vicious cycle. When someone with anorexia starts eating again, however, serotonin levels spike, causing extreme anxiety and emotional chaos, which makes recovery difficult without adequate support.

Individuals with bulimia also have dysfunctions in their serotonin circuitry. Those with bulimia, however, appear to have somewhat different alterations than those with anorexia. When going without food for longer periods of time (such as during sleep), those with bulimia had a larger drop in serotonin levels than women without eating disorders, which led to binge eating and increased irritability (Steiger et al., 2001). Researchers also found that women with bulimia who carried a particular variant of a serotonin receptor were also significantly more impulsive (Bruce et al., 2005). Abnormalities in the serotonin system were also found to persist after recovery, hinting that these  differences may have been present before the onset of the disorder (Kaye et al., 2001).

Serotonin alterations in binge eating disorder appear fairly similar to those found in bulimia, although the research is more limited in this area. Researchers generally believe that individuals with BED also suffer from chronically low serotonin levels, which is thought to contribute to binge eating in an attempt to relieve the depressed mood caused (in part) by this low serotonin (Haedt-Matt & Keel, 2011). Genetics studies have supported this idea, as variants in a serotonin transporter gene were associated with increased binge eating severity in the general population (Akkermann et al., 2010). Further studies found an association between impulsivity and strict dieting with serotonin receptor genes and binge eating in young women (Racine et al., 2009).


Dopamine is commonly thought of as the “pleasure” chemical, due to its links with rewarding behaviors and drugs of abuse. Although dopamine is involved in reward-motivated behavior (such as studying to get good grades, or going to work early to get a raise), it also helps regulate movement, memory, hormones and pregnancy, and sensory processing (Beaulieu & Gainetdinov, 2011). Like serotonin, the overlap of processes controlled by dopamine and eating disorderrelated symptoms caused researchers to investigate potential associations.

In anorexia, the leading hypothesis is that the disorder is associated with an over-production of dopamine, leading to anxiety (Bailer et al., 2012a), harm avoidance (Bailer et al., 2012b), hyperactivity and the ability to go without pleasurable things like food (Kontis & Theochari, 2012). Research has shown that bulimia is associated with lower levels of both dopamine and certain of its receptors, and that binge eating is significantly associated with dopamine release in certain parts of the brain (Broft et al., 2012). Binge eating disorder has been linked to a hyper-responsiveness to rewards such as food, which makes eating more rewarding and pleasurable than in people without this disorder (Davis et al., 2012) and leads to a continuation of compulsive overeating (Bello & Hajnal, 2010).

You can read more about the effects of dopamine in the section on Reward.


Akkermann, K., Nordquist, N., Oreland, L., & Harro, J. (2010). Serotonin transporter gene promoter polymorphism affects the severity of binge eating in general population. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 34(1), 111-114. doi: 10.1016/j.pnpbp.2009.10.008

Bailer, U. F., Narendran, R., Frankle, W. G., Himes, M. L., Duvvuri, V., Mathis, C. A., & Kaye, W. H. (2012). Amphetamine induced dopamine release increases anxiety in individuals recovered from anorexia nervosa. International Journal of Eating Disorders, 45(2), 263-271. DOI: 10.1002/eat.20937

Bailer, U. F., Frank, G. K., Price, J. C., Meltzer, C. C., Becker, C., Mathis, C. A., ... & Kaye, W. H. (2012b). Interaction between serotonin transporter and dopamine D2/D3 receptor radioligand measures is associated with harm avoidant symptoms in anorexia and bulimia nervosa. Psychiatry Research: Neuroimaging. doi:10.1016/j.pscychresns.2012.06.010

Bello, N. T., & Hajnal, A. (2010). Dopamine and binge eating behaviors. Pharmacology Biochemistry and behavior, 97(1), 25-33. doi: 10.1016/j.pbb.2010.04.016

Beaulieu, J. M., & Gainetdinov, R. R. (2011). The physiology, signaling, and pharmacology of dopamine receptors. Pharmacological reviews, 63(1), 182-217. doi: 10.1124/ pr.110.002642

Broft, A., Shingleton, R., Kaufman, J., Liu, F., Kumar, D., Slifstein, M., ... & Walsh, B. T. (2012). Striatal dopamine in bulimia nervosa: A pet imaging study. International Journal of Eating Disorders, 45(5), 648-656. DOI: 10.1002/eat.20984

Bruce, K. R., Steiger, H., Joober, R., Kin, N. M. K., Israel, M., & Young, S. N. (2005). Association of the promoter polymorphism− 1438G/A of the 5‐HT2A receptor gene with behavioral impulsiveness and serotonin function in women with bulimia nervosa. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 137(1), 40-44.

Davis, C., Levitan, R. D., Yilmaz, Z., Kaplan, A. S., Carter, J. C., & Kennedy, J. L. (2012). Binge eating disorder and the dopamine D2 receptor: Genotypes and sub-phenotypes. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 38(2), 328-335. doi: 10.1016/j.pnpbp.2012.05.002

Kontis, D., & Theochari, E. (2012). Dopamine in anorexia nervosa: a systematic review. Behavioural Pharmacology, 23(5 and 6), 496-515. doi: 10.1097/FBP.0b013e328357e115

Haedt-Matt, A. A., & Keel, P. K. (2011). Revisiting the affect regulation model of binge eating: A meta-analysis of studies using ecological momentary assessment. Psychological bulletin, 137(4), 660. doi: 10.1037/a0023660

Kaye, W. H., Gwirtsman, H. E., George, D. T., & Ebert, M. H. (1991). Altered serotonin activity in anorexia nervosa after long-term weight restoration: does elevated cerebrospinal fluid 5-hydroxyindoleacetic acid level correlate with rigid and obsessive behavior? Archives of General Psychiatry, 48(6), 556. doi: 10.1001/archpsyc.1991.01810300068010

Kaye, W. H., Frank, G. K., Meltzer, C. C., Price, J. C., McConaha, C. W., Crossan, P. J., ... & Rhodes, L. (2001). Altered serotonin 2A receptor activity in women who have recovered from bulimia nervosa. American Journal of Psychiatry, 158(7), 1152-1155. doi:10.1176/appi.ajp.158.7.1152

Kaye, W. H., Fudge, J. L., & Paulus, M. (2009). New insights into symptoms and neurocircuit function of anorexia nervosa. Nature Reviews Neuroscience, 10(8), 573-584. doi:10.1038/nrn2682

Gorwood, P., Ades, J., Bellodi, L., Cellini, E., Collier, D. A., Di Bella, D., ... & Treasure, J. (2002). The 5-HT2A-1438G/A polymorphism in anorexia nervosa: A combined analysis of 316 trios from six European centres. Molecular psychiatry, 7(1), 90-94. doi: 10.1038/sj/mp/4000938

Racine, S. E., Culbert, K. M., Larson, C. L., & Klump, K. L. (2009). The possible influence of impulsivity and dietary restraint on associations between serotonin genes and binge eating. Journal of psychiatric research, 43(16), 1278-1286. doi: 10.1016/j.jpsychires.2009.05.002

Steiger, H., Young, S. N., Ng Ying Kin, N. M. K., Koerner, N., Israel, M., Lageix, P., & Paris, J. (2001). Implications of impulsive and affective symptoms for serotonin function in bulimia nervosa. Psychological Medicine, 31(01), 85-95.