The Neuroscience of Anorexia Nervosa: What do we Know and Why do we Care?

Written by MEDA undergraduate intern, Louisa Oppenheim

Throughout my undergraduate Psychology education, I’ve become increasingly interested in the biological bases of behavior. Combined with my interest in the eating disorders field, I’ve wondered if the brains of people with eating disorders differ from people without eating disorders.

It turns out that eating disorders have a strong biological basis. Since genetics accounts for 50-80% of the risk of developing an eating disorder [1], an understanding of the biological perspective is more important than ever.  Although psychosocial factors (e.g. temperament, personality, family situation) are undoubtedly important, the neuroscience of eating disorders explains why some people develop eating disorders over others, even if they grew up in similar conditions. Focusing on anorexia nervosa (AN), it also helps explain how people with AN can restrict and maintain a low weight while a larger percentage of the population struggles with dieting.

One of the answers to the neuroscience of AN lies in neurotransmitter (brain chemical) activity, specifically the activity of serotonin and dopamine. People with AN have altered activity at serotonin and dopamine receptors [2]. Since serotonin is involved with satiety and dopamine is associated with the brain’s reward system, altered receptor activity may explain why people with AN have reduced hunger signals and alterations in their food reward system.

Through measuring the brain function of patients with AN, researchers can understand how brain activity circuits are correlated with certain traits and symptoms characteristic of patients with AN, such as impaired cognitive functioning and food/taste processing. In one study, researchers underwent fMRI scanning, which measures brain activity via blood flow changes in the brain, while completing a memory task. Although their performance on the task did not differ from healthy controls, people with AN over engaged the areas of the brain involved with memory, integrating information, and overall cognitive functioning (parts of the temporal and parietal lobes). Interestingly, when AN patients underwent weight restoration and completed the task again, their brain activity did not differ from healthy controls, demonstrating that weight restoration may help improve efficiency of cognitive functioning [3].

Understanding brain function can also help us understand hunger signals in AN. When given sugar, people recovered from AN have decreased activity in the “primary taste cortex” (right anterior insula). Located deep within the brain, the role of the anterior insula is to integrate and evaluate information about hunger and taste [4].

So, altered brain activity in this region, even following recovery, may imply that this brain difference is hard-wired, or present before AN’s onset. Also, these research findings may explain why it is so difficult for people with AN to perceive hunger signals, and consequently, nutritionally recover.

Along with functional differences, researchers are trying to understand how brain structure (brain volume levels) differs in people with AN. Brain structure is measured through MRI scanning, a technique that uses strong magnets and radio waves to create a vivid image of the brain. In one MRI study, researchers found that people with AN have significantly less grey matter volume when compared to age-matched healthy controls. (Grey matter is mostly made up of dendrites and neuronal cell bodies, which receive and integrate signals from other neurons, respectively.) But, when they gain weight, grey matter volume is restored to normal levels [5, 6]. These results demonstrate the negative impact of malnutrition on the brain, but also the positive impact of weight restoration in restoring brain volume, emphasizing the importance of nutritional recovery in AN.

Although overall grey matter volume is restored following weight restoration, some smaller, regional grey matter volumes in structures involved with cognitive flexibility, or the ability to shift thought processes, are still significantly smaller than healthy controls (supplementary motor area and anterior cingulate cortex) [7, 8]. So, these differences may contribute to the inflexible and perfectionist personality sometimes found in people struggling with (and recovered from) AN [9].

Although researchers have made significant progress in understanding the neuroscience of AN, there are some current limitations in the field. One of the main limitations (when comparing AN to healthy controls) is the trait versus state problem. In other words, if we find a brain difference in AN patients, we don’t know if that brain difference predisposed them to AN (trait-dependent) or developed as a result of AN (state-dependent) [1, 10]. By completing longitudinal studies (measuring the brain several times throughout AN’s course) and using recovered people as subjects (like some of the studies above), we can start to understand which brain alterations are trait- versus state-dependent.

People with AN and their loved ones, along with clinicians and researchers, can benefit from knowledge about the neuroscience of AN. We can start to understand why some characteristics of AN are difficult to treat and why AN is hard to recover from. At a larger level, understanding AN as a hard-wired brain disorder (and not the sufferer’s fault) can help reduce the stigma for those suffering and their loved ones.


[1] 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.

[2] Culbert, K. M., Racine, S. E., & Klump, K. L. (2015). Research Review: What we have learned about the causes of eating disorders – a synthesis of sociocultural, psychological, and biological research. Journal of Child Psychology and Psychiatry, 56(11), 1141–1164.

[3] Castro-Fornieles, J., Caldú, X., Andrés-Perpiñá, S., Lázaro, L., Bargalló, N., Falcón, C., … Junqué, C. (2010). A cross-sectional and follow-up functional MRI study with a working memory task in adolescent anorexia nervosa. Neuropsychologia, 48(14), 4111–4116.

[4] Oberndorfer, T. A., Frank, G. K. W., Simmons, A. N., Wagner, A., McCurdy, D., Fudge, J. L., … Kaye, W. H. (2013). Altered Insula Response to Sweet Taste Processing After Recovery From Anorexia and Bulimia Nervosa. American Journal of Psychiatry, 170(10), 1143–1151.

[5] Castro-Fornieles, J., Bargalló, N., Lázaro, L., Andrés, S., Falcon, C., Plana, M. T., & Junqué, C. (2009). A cross-sectional and follow-up voxel-based morphometric MRI study in adolescent anorexia nervosa. Journal of Psychiatric Research, 43(3), 331–340.

[6] Wagner, A., Greer, P., Bailer, U. F., Frank, G. K., Henry, S. E., Putnam, K., … Kaye, W. H. (2006). Normal Brain Tissue Volumes after Long-Term Recovery in Anorexia and Bulimia Nervosa. Biological Psychiatry, 59(3), 291–293.

[7] Mühlau, M., Gaser, C., Ilg, R., Conrad, B., Leibl, C., Cebulla, M. H., … Nunnemann, S. (2007). Gray Matter Decrease of the Anterior Cingulate Cortex in Anorexia Nervosa. American Journal of Psychiatry, 164(12), 1850–1857.

[8] Friederich, H.-C., Walther, S., Bendszus, M., Biller, A., Thomann, P., Zeigermann, S., … Herzog, W. (2012). Grey matter abnormalities within cortico-limbic-striatal circuits in acute and weight-restored anorexia nervosa patients. NeuroImage, 59(2), 1106–1113.

[9] Kaye, W. H., Wierenga, C. E., Bailer, U. F., Simmons, A. N., & Bischoff-Grethe, A. (2013). Nothing tastes as good as skinny feels: the neurobiology of anorexia nervosa. Trends in Neurosciences, 36(2), 110–120.

[10] Frank, G. K. W. (2015). Recent Advances in Neuroimaging to Model Eating Disorder Neurobiology. Current Psychiatry Reports, 17(4).