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How Does Anorexia Affect the Brain?

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Anorexia nervosa (AN) is a disorder of undereating, and results in profound nutritional depletion. Weight loss and nutrient deficits affect every organ in the body. While most of these changes are largely reversible, the brain can suffer permanent damage if AN persists without treatment. It’s difficult to elucidate the exact amount of time required to cause damage, but numerous studies over the last forty years reveal what and how changes take place when the body is deprived of nutrition.

How Does Anorexia Affect the Brain?

How Does the Brain Develop?

Brain development starts when the fetus grows in the womb. Cortical folding, otherwise known as gyrification, occurs mostly in utero, and the final folding pattern remains relatively unchanged after birth and as the child develops. Neurons grow and migrate and make connections with one another throughout this phase, and this continues long after birth into childhood, and, in parallel, unnecessary connections are eliminated in a process called pruning.

By eighteen years old, the brain has completed the pruning process, and the networks of neurons that orchestrate all kinds of human behavior have been formed. The frontal lobe of the brain continues to develop until the early 20s. As humans age, the brain naturally shrinks slightly. Substances and psychiatric illness can have profound effects on where and how quickly the brain’s structure and function changes. (1,9,11)

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Does Anorexia Brain Damage Occur?

People with anorexia nervosa have altered brain structure on brain scans. In particular, there is a loss of brain tissue, which leads to a widening of the gaps between folds (sulci) and a shrinking of the folks themselves (gyri). The ventricles that contain cerebrospinal fluid (CSF) also widen. (1) 

CSF is the fluid that nourishes, protects, bathes, and supports healthy neural tissue. Those with AN have larger ventricles that contain more CSF. Computed tomography (CT) scans show that the brains of people with alcohol use disorder (colloquially known as alcoholism) are similar to the brains of those with AN, likely due to similar nutritional deficiencies. (1) The degree of brain shrinkage correlates with duration of illness in people with AN, which illustrates that the effects of nutritional and calorie deficits are cumulative. (3) 

Magnetic resonance imaging (MRI) studies also have discovered that reductions in brain volume, reduced gray matter volume, ventricular enlargement and higher CSF volume are associated with AN. (3) In addition, starvation actually changes the folding pattern of the brain which is usually invariant after the gyrification process, or stable after birth, as we mentioned above. However, these abnormal alterations in the folding patterns from nutritional depletion can be restored with partial weight restoration. (9)

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Brain Tissue: White & Gray Matter

The brain contains two types of tissue: white and gray matter. Gray matter makes up the outer layer of the brain and has a high concentration of neuron cell bodies. This plays a significant role in allowing humans to think and function normally. White matter also contains neurons, but they are coated in a layer called myelin. This allows messages between neurons to travel quickly and efficiently. (4) 

MRI studies show significant shrinkage of gray matter volume in two parts of the brain: the frontal lobe and left insula. These regions play important roles in regulating emotions, which researchers suspect contribute to the cognitive deficits associated with chronic AN. (5) 

MRI brain scans show that regional and global gray matter volume were similar for those who had recovered long-term from AN when compared to healthy controls (those without AN) of the same age. (6)

The amount of weight loss, age of onset, and illness duration do not independently predict or correlate with specific brain volume changes. Studies do show, however, that those with chronic AN tend to have more significant cortical white matter and cerebellar volume losses. Researchers coin this as a trait or “scar” of the illness on an MRI scan. (7)

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Are These Changes Reversible?

Many studies have tried to determine how long it takes during and after recovery for the brain to recover, and for things like volume and gyrification to normalize. One study showed that in people who were able to partially restore their weight (>10% body mass index increase), cortical (brain) thickness increased by about 0.06mm/month during brief weight restoration therapy that lasted three months. (8) 

In brain CT scans taken of people who regained a healthy body weight, many did not see a reversal of ventricle widening, but there was a significant lessening in the degree of sulcal widening, meaning that the gaps between folds grew narrower again, and brain tissue volume was increasing again to normal levels. (2) 

The patterns of brain tissue loss in the brain mirrors those seen in suicide attempts, anxiety disorders, and autistic spectrum disorder, in that similar brain regions seem to be infolved.The impacted brain regions are known to play important roles in impulse control, , attention, self-regulation, and social interactions. Damage to these regions likely contributes to the many neuropsychological processes, including mood and behavioral challenges, that make recovering from AN difficult. (10) 

Not all brain changes seen in AN are consequences of the disorder. Some might actually contribute to the initial reduction in food intake. For example,one study found that alterations in the medial orbitofrontal cortex, insula, and striatum were related to taste pleasantness and reward sensitivity in people with AN. Researchers posited that these alterations might explain the food avoidance behaviors commonly seen in those who struggle with eating disorders. These results remained consistent when researchers accounted for confounds such as age, depression, anxiety, and medications. (11)

Within Health provides virtual care and treatment for anyone with an eating disorder. Our clinical care team is practiced in helping patients recover from anorexia nervosa, and any comorbid mental health disorders. Call our team to learn how to get started.

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Frequently asked questions


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  2. ​​Dolan RJ, Mitchell J, Wakeling A. Structural brain changes in patients with anorexia nervosa. Psychol Med. 1988 May;18(2):349-53. doi: 10.1017/s0033291700007893. PMID: 3399587.
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  7. Seitz J, Walter M, Mainz V, Herpertz-Dahlmann B, Konrad K, von Polier G. Brain volume reduction predicts weight development in adolescent patients with anorexia nervosa. J Psychiatr Res. 2015 Sep;68:228-37. doi: 10.1016/j.jpsychires.2015.06.019. Epub 2015 Jul 2. PMID: 26228424.
  8. Bernardoni F, King JA, Geisler D, Stein E, Jaite C, Nätsch D, Tam FI, Boehm I, Seidel M, Roessner V, Ehrlich S. Weight restoration therapy rapidly reverses cortical thinning in anorexia nervosa: A longitudinal study. Neuroimage. 2016 Apr 15;130:214-222. doi: 10.1016/j.neuroimage.2016.02.003. Epub 2016 Feb 11. PMID: 26876474.
  9. Bernardoni F, King JA, Geisler D, Birkenstock J, Tam FI, Weidner K, Roessner V, White T, Ehrlich S. Nutritional Status Affects Cortical Folding: Lessons Learned From Anorexia Nervosa. Biol Psychiatry. 2018 Nov 1;84(9):692-701. doi: 10.1016/j.biopsych.2018.05.008. Epub 2018 May 23. PMID: 29910027.
  10. Brodrick BB, Adler-Neal AL, Palka JM, Mishra V, Aslan S, McAdams CJ. Structural brain differences in recovering and weight-recovered adult outpatient women with anorexia nervosa. J Eat Disord. 2021 Sep 3;9(1):108. doi: 10.1186/s40337-021-00466-w. PMID: 34479625; PMCID: PMC8414694.
  11. Frank GK, Shott ME, Hagman JO, Mittal VA. Alterations in brain structures related to taste reward circuitry in ill and recovered anorexia nervosa and in bulimia nervosa. Am J Psychiatry. 2013 Oct;170(10):1152-60. doi: 10.1176/appi.ajp.2013.12101294. PMID: 23680873; PMCID: PMC3789862.
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