Diseases and Disorders

The Neurology Behind Eating Disorders

Emily Yuan


Abstract

Eating disorders are biopsychosocial disorders that affect eating habits. They can come in many forms, such as anorexia, bulimia, and binge eating disorder, with anorexia having the highest death rate among mental illnesses [1]. Despite the undeniable impact that societal pressure and social media have on the development of eating disorders, genetic factors that dictate brain development play a significant role in the onset of these life changing diseases as well [3]. Studies have shown that individuals with eating disorders have altered activity in multiple brain areas and have abnormal neurotransmitter activity [1].

 

Eating Disorders

    Eating disorders are serious mental illnesses that affect over 30 million Americans. These disorders stem from biological, psychological, and social factors and are described by having abnormal eating habits, ranging from anorexia nervosa to pica to orthorexia. Although there definitely are environmental factors that play a large role in the onset of these diseases, such as societal pressure, there is also a neurological basis for eating disorders. Before delving into the details about the cellular mechanisms altered in victims, we need to first understand how these disorders affect individuals.

 

The Anorexic Thought Process

    So what is going on inside the mind of someone with an eating disorder? Research has found that those with eating disorders think differently from most people. It was initially thought that individuals with anorexia nervosa were able to override primary drives through self control. This self control is exercised by anorexics when constantly choosing low fat and low calorie food. However,  even when they attempted to recover from the eating disorder, they were unable to overcome their desire to opt for the low calorie and low fat food options, demonstrating that the persistent selection of these foods is not simply a matter of self control [1]. Although this study focused on individuals with anorexia nervosa, these differences in thought processes can also be seen in people with other eating disorders, such as bulimia or Prader-Willi syndrome [1].

    Dr. Joanna Steinglass conducted a study to understand how eating disorders impact decision making when it comes to food. She used fMRI imaging to monitor the brain activity of women with anorexia nervosa (AN) and healthy controls (HC) as they made food related decisions. The women were asked to choose between two items – chocolate cake and carrots. Unsurprisingly, the women with anorexia prefered the carrots  to the chocolate cake. However, they used a different brain structure than healthy individuals to make their decision. As opposed to the prefrontal cortex, patients suffering from anorexia nervosa utilized the dorsal striatum [1]. Since the dorsal striatum plays a key role in decision making, rewards, and habitual behaviors, an increase in this area’s activity suggests that the anorexic subjects’ decisions to eat the carrots were habitual [1]. No matter how hard they tried, their brains would automatically direct them towards the lower calorie option [1].


 

    In AN (Fig. 1), a correlation with choice values was observed in the dorsal striatum, whereas no above threshold correlation was observed in HC (Fig. 2). Additionally, no above-threshold correlations were observed in the ventral striatum in either group, and no differences were found between HC and AN groups. (b) Parametric analysis of choice strength showed significantly greater activity in the dorsal striatum in the AN than in the HC group. (c) To illustrate the pattern across the dorsal and ventral striata, in an independent analysis, data was extracted from the right caudate, right nucleus accumbens, and right putamen. Differences between the HC and AN groups were seen in the caudate, but not in the nucleus accumbens or putamen [1].

 

Neurotransmitters

    Studies have shown that abnormalities regarding several neurotransmitters are associated with the onset of eating disorders. The two that have been the most extensively studied are the mood regulating hormone serotonin and histamine [2].

    Anorexics often have reduced levels of serotonin in their blood, since they do not have enough nutrients to synthesize this neurotransmitter [2]. As they continuously starve themselves, the body responds by increasing the number of serotonin receptors to utilize the remaining serotonin more efficiently [2]. These receptors are still present after individuals recover, often making them anxious and emotional when they eat [2]. People who have been previously diagnosed with anorexia physically feel better when they abstain from eating for this reason, making recovery extremely difficult without professional help [4]. In addition, anorexic patients are more likely to have a mutated 5-HT2A receptor for serotonin [4]. This mutated receptor increases the amount of serotonin in the brain during a non-starved state, leading to anxiety and obsessive behavior [10]. Since food further increases serotonin levels, the discomfort associated with increased serotonin deters anorexics from eating, a major obstacle in the road to recovery [10].

    Individuals with bulimia are also affected by abnormalities in serotonin levels. In contrast to anorexics, whose psychological symptoms are caused by increased serotonin levels, bulimics have lower than average levels of serotonin after long periods without eating, such as during sleep. The decreased serotonin levels leads to binge eating and irritability when these individuals wake up [12]. Serotonin affects binge eating disorder in a similar fashion, where the depressed mood caused by low serotonin levels leads to binge eating

    Histamine also plays a central role in the development of anorexia nervosa. Histamine is often associated with the immune system, but it is also linked  to appetite and taste perception [10]. Increases in histamine concentration in the blood decreases food intake, while blocking these histamine receptors increases hunger [10]. Additionally, histaminergic activity is increased by sudden food intake after starvation, discouraging the individual from eating [10]. Histamine’s effect on the body is mediated by the H1 receptor, which is found in higher concentrations in certain areas of the brain affected by eating disorders [5]. The increased number of histamine receptors increases the body’s sensitivity to histamine fluctuations, thus decreasing hunger within that individual.

 

Genetics

    Relatives of individuals with anorexia nervosa are over 10 times more likely to have an eating disorder, yet not everyone with an eating disorder has a relative with that same disorder [7]. The trend of familial eating disorders can have two explanations. The traits can be heritable and passed down to children genetically, or these traits can be learned, as exposure to behaviors can evoke those same behaviors in children [7]. What does this mean? Eating disorders most likely stem from a variety of factors. There have been no conclusive results about the reason behind eating disorder development. Some studies have found that there is a strong genetic influence in developing eating disorders, while others have found that environmental factors play a more significant role [7].

    Twin studies using identical and fraternal twins helped to differentiate between the effects of environmental and genetic factors. These studies found that identical twins had a higher similarity in developing anorexia and bulimia than fraternal twins, and they estimated that binge eating, self-induced vomiting, and dietary restraints were between 46-72 percent heritable [3]. Attitudes about body image and weight preoccupation were estimated to be  32 to 72 percent genetic [3]. These attitudes were also found to develop later in life. Studies of 11 year olds have found no significant genetic variation in body perception, while the variance in these attitudes can be accounted for by genetics in 53 to 57 percent of 17 year olds [3]. This correlates with the average age of onset for anorexia nervosa, which is 16-17 and bulimia nervosa, which is 18-19 [6]. Personality traits related to the development of eating disorders, such as increased level of emotionality, stress reactivity, and perfectionism, have also been found to be influenced by genetics [3].

    Molecular genetics studies have been used to try to identify genes linked to eating disorders, with certain groups reporting an increase in the -1438/A allele of the 5-HT2A gene as well as other serotonin-related genes in individuals with anorexia nervosa [3]. The 5-HT2A gene codes for the serotonin 2A receptor, which increases the amount of serotonin receptors in a non-starved state [10]. This receptor is involved in many complex mental illnesses with research still underway about its specific function [8]. Women with anorexia are more likely to have a mutated 5-HT2A serotonin receptor [3]. Another study found a possibility for linkage of anorexia and bulimia on chromosomes 4, 11, 13, and 15 with the peak NPL score on chromosome 4 [3].

    More research must be done to come to more conclusive results about the specific genes related to eating disorders; however, there is an indisputable correlation between genetics and eating disorders [3]. While some studies have been done to support these genetic findings [3], others have found that eating disorders are really a combination of genetic and environmental factors. There are currently three types of genetic environments (G-E) identified: Passive, Evocative, and Active [9]. A genetic environment is the interaction between the predisposed genetics and the environment a person is exposed to. Passive G-E occurs simply though the sharing of genetic information. Evocative G-E occurs when family members reinforce certain perceptions that are predisposed by genetics. Active G-E is when an individual who is genetically predisposed to have an eating disorder actively seeks out an environment that reinforces their perspective as a result of their genetically determined qualities [9].

 

Treatment and Further Research

    Of course, an important goal of eating disorder research is to develop a better understanding of these disorders and develop better treatment plans for victims. Correlation studies that analyze the predictors of treatment success for anorexia nervosa found that self-reported emotional avoidance (behavioural/cognitive avoidance, low acceptance) and submissive behaviour predicted clinical outcomes [13]. Social cognitive (emotion recognition, emotional theory of mind) and neurocognitive performance (set-shifting, detail focus) had limited predictive ability [13]. While eating disorder treatment is sometimes successful, many victims suffer from relapse [13].

    Although there have been many studies done on various aspects of eating disorders and eating disorder treatment, there is a huge amount of uncertainty regarding each of the eating disorders. In comparison to many of the other significant mental illnesses, eating disorders receive only a fraction of the funding per patient [14]. For example, the NIH budget for eating disorders is only ⅓ that of PTSD, despite the fact that anorexia nervosa is the deadliest mental disorder [14].

    As shown in the studies above, there have been many links drawn between different factors and the onset of eating disorders; however, these correlations have not allowed scientists to pinpoint an exact cause for this deadly disease [14]. Since many different factors lead to the development of eating disorders, research cannot be restricted to the cellular level. Especially in a society where media plays a huge role in our lives,  psychological and sociological studies must be conducted to evaluate the impact the environment has on affected individuals [14].


References


  1. Statistics & Research on Eating Disorders. (2018, April 05). Retrieved from https://www.nationaleatingdisorders.org/statistics-research-eating-disorders

  2. Oldershaw, A., Lavender, T., & Schmidt, U. (n.d.). Are socio-emotional and neurocognitive functioning predictors of therapeutic outcomes for adults with anorexia nervosa? Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/29744972

  3. 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.

  4. 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

  5. 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

  6. Lyons, L. (2017, January 04). Eating Disorders, Environmental or Biological? Retrieved March 04, 2018, from https://www.eatingdisorderhope.com/blog/eating-disorders-environmental-biological

  7. Raote I, Bhattacharya A, Panicker MM. Serotonin 2A (5-HT2A) Receptor Function: Ligand-Dependent Mechanisms and Pathways. In: Chattopadhyay A, editor. Serotonin Receptors in Neurobiology. Boca Raton (FL): CRC Press/Taylor & Francis; 2007. Chapter 6. https://www.ncbi.nlm.nih.gov/books/NBK1853/

  8. Bulik, C. M., PhD. (2013, November 07). The Role of Genetics in Eating Disorders. Retrieved March 04, 2018, from https://uncexchanges.org/2011/04/11/the-role-of-genetics-in-eating-disorders/

  9. About Eating Disorders. (n.d.). Retrieved March 04, 2018, from http://www.anorexiabulimiacare.org.uk/about/about-eating-disorders

  10. Ishizuka, T., & Yamatodani, A. (2012). Integrative role of the histaminergic system in feeding and taste perception. Frontiers in Systems Neuroscience, 6, 44. http://doi.org/10.3389/fnsys.2012.00044 Retrieved: 10/02/2018

  11. Morisita, J., Sato, Y., Adachi, M., Itoh, M., & Hongo, M. (2009). Increased brain histamine H1 receptor binding in patients with anorexia nervosa. Biological Psychiatry, 65 (4), 329-335 Retrieved: 10/02/2018

  12. Berrettini, W. (2004). The Genetics of Eating Disorders. Psychiatry (Edgmont), 1(3), 18–25. Retrieved: 10/02/2018

  13. Báez-Mendoza, R., & Schultz, W. (2013). The role of the striatum in social behavior. Frontiers in Neuroscience, 7, 233. http://doi.org/10.3389/fnins.2013.00233 Retrieved: 10/02/2018

  14. Foerde, Karin et al. “Neural Mechanisms Supporting Maladaptive Food Choices in Anorexia Nervosa.” Nature neuroscience 18.11 (2015): 1571–1573. PMC. Web. 6 Jan. 2018. Retrieved: 10/02/2018

Emily Yuan

Emily Yuan


I’m a science enthusiast in the Richard Montgomery High School IB Class of 2019. I think brains are absolutely awesome and fascinating, and became involved in IYNA in 2017 right before competing in the DC Brain Bee. Outside of IYNA, I’m involved in several community initiatives, including SEDAA and Paper Bridges. I also love art and baking!