Saturday, October 1, 2022

Understanding Anorexia Nervosa

 Anorexia nervosa is a disorder that stems from anxious thoughts and behaviors. It has the highest mortality rate of all psychiatric illnesses due to its chronicity and high relapse rate. The high mortality rate and relapse rate highlights a need for better treatment options for anorexia nervosa. In individuals struggling with this illness, long periods of caloric fasting lead to a reduced feeling of anxiety and periods of healthy caloric intake increase feelings of anxiety. The increased feelings of anxiety when eating makes recovery even more difficult as anxious thoughts are often what individuals are trying to avoid in the first place. In addition, it is interesting to note that stress signals and food intake signals, like hunger, are both processed in the hindbrain. Recent studies studying rat brains have found that hindbrain neurons, GLP-1 and PrRP, have been found to have reduced activation during periods of caloric deficiency. It is suspected that these neurons are altered or shut off in anorexia nervosa resulting in the reduction of anxiety and stress observed in brains experiencing chronic food deprivation. Often in treatment for psychiatric diseases, treating behavioral symptoms are the main and only therapeutic option. However, understanding the underlying physiological mechanisms is important in psychiatric illnesses. These mechanisms have the potential to lead to behavioral symptoms and it is important to understand for providing better treatment options, especially when it comes to psychiatric diseases with a high mortality rate like anorexia nervosa.


Genn, R. F., Tucci, S. A., Thomas, A., Edwards, J. E., & File, S. E. (2003). Age-associated sex differences in response to food deprivation in two animal tests of anxiety. Neuroscience & Biobehavioral Reviews27(1-2), 155-161.

Resmark G, Herpertz S, Herpertz-Dahlmann B, Zeeck A. Treatment of Anorexia Nervosa-New Evidence-Based Guidelines. J Clin Med. 2019 Jan 29;8(2):153. doi: 10.3390/jcm8020153. PMID: 30700054; PMCID: PMC6406277.

Starzomska M, Rosińska P, Bielecki J. Chronic anorexia nervosa: Patient characteristics and treatment approaches. Psychiatr Pol. 2020 Aug 31;54(4):821-833. English, Polish. doi: 10.12740/PP/OnlineFirst/118601. Epub 2020 Aug 31. PMID: 33386730.

 Maniscalco, J. W., & Rinaman, L. (2017). Interoceptive modulation of neuroendocrine, emotional, and hypophagic responses to stress. Physiology & behavior176, 195-206.


3 comments:

  1. It is undeniable that Anorexia Nervosa has a lot of biological causes underlying the disorder. However, I could not help but wonder if there are also culture aspects involved in the manifestation process and the display of the disorder. Up until 1980s, it was argued that Anorexia was not found in countries outside of the United States, with little cases in South America and Europe, and no incidents found in Asia. After an excessive amount of research, scientists in Asia, specifically China, only found ten possible patients that might have anorexia. However, the interesting things that might give Asian anorexia its name of "atypical anorexia" is the way that the disease manifest itself. Instead of having the conception of the fear of fatness and body dysmorphic disorder that Western patients had; Asian Anorexia symptoms could be associated with a response to an emotional stressor in a person stemming from cultural and historical context rather than a reaction concerning one's body image (Old Chineses believed that being able to eat is to have good luck, so there was little stigma around large body shape at that time). However, this soon changed due to globalization of medical information, resulting in a steep increase in the number of patients with Western version of Anorexia Nervosa, and not the Atypical Asian Anorexia.
    It was suggested that the shift in symptoms exhibition resulting from the generalization and adoption of "Western" medical definitions, such as the "DSM system." The legitimization of the disorder through increased media attention had introduced two new aspects in the relationship between Anorexia and those affected. Firstly, the presence of a standardized "symptom pool" had created the urge within patients to have their internal suffering recognized. The mental disorder was no longer just an outlet for their penned-up frustration; rather, it had become an identity that was shaped by the media's coverage on the matter. The need to have their feelings validated had moved the affected individuals toward producing symptoms that will correspond to the medical diagnostics of the time, even if the changes in symptomatic displays meant a change in the underlying cause, shifting from emotional distress to body dysmorphic obsession. Secondly, the involvement of "Western categories" and heightened media attention had changed the linear, one-way causative relationship that individuals had with Anorexia into an endless "feedback loop" that was continuously reinforced by the patients, the doctor, and the surrounding society. The patients saw media headlines, adopted the symptoms, and came to doctors for help. The doctor diagnosed the patients with their displayed symptoms and collected data, which they would use to make medical publications and suggestions. The media would then pick up on the doctors' recommendations and create articles that feed the information back to the patients. Therefore, once the patients assimilated their symptoms to the flow of the media and Western diagnostic tools, it would be difficult to identify the condition's original cause.

    Lee, S. (2001). Fat phobia in anorexia nervosa: Whose obsession is it? In M. Nasser, M. A. Katzman, & R. A. Gordon (Eds.), Eating disorders and cultures in transition. (pp. 40–54). Brunner-Routledge.
    Watters, E. (2010). Crazy Like Us: The Globalization of the American Psyche. Free Press.

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  2. I found your blog to be really interesting Cassidy! I would 100% agree that understanding the cellular and physiological mechanism is a key component to understand this illness, but also establish therapeutic regimens. I think that it could also expand on preventive measures of Anorexia. I would also agree with Thu on the notion of how culture may play a role in the development of this illness. I believe that there's a lot of intersectionality coming to play when it comes to understanding the basis of this illness and how it translates into the feeling of anxiety. An aspect that I think would be beneficial is to examine how the gut-brain-axis comes into play. Seemingly, studies are currently looking at how the gut microbiome may play an essential role in anorexia. I think that what we know from the literature of the imbalance of bacteria can cause mood changes, anxiety, and depression as a response.

    https://www.sciencedirect.com/science/article/pii/S235293931830054X#:~:text=Dysregulation%20of%20gut%2Dbrain%20axis%20in%20anorexia%20nervosa.,gut%20microbiota%20and%20immune%20system.

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  3. This is a very interesting finding. I wonder if the reduced activation of hindbrain neurons like GLP-1 and PrRP lead to downstream effects like the increase or decrease in certain hormones associated with metabolism. I read one study that indicated that metabolic disruption - even before the onset of disease - can possibly explain some of the reason why certain individuals are more susceptible than others and why recovery is so difficult (Watson 2019). For example, those individuals who are predisposed to having a low BMI are at higher risk for developing anorexia nervosa (Watson 2019). Interestingly, many genes thought to be associated with anorexia nervosa were expressed even more in the cerebellum than in the rest of the brain (Watson 2019), supporting your research's findings that the hindbrain may be a key player in the disease. It it good to see a disease which is so often approached from just the psychological perspective also be examined through another lens.

    Watson, H, et al. (2019) Genome-wide Association Study Identifies Eight Risk Loci and Implicates Metabo-Psychiatric Origins for Anorexia Nervosa. Nature Genetics, 51(8): 1207-1214.

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