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Reports of eating disorders (EDs) have risen since the start of the COVID-19 pandemic.13 Several justifiable explanations for these increases have been offered, including social isolation, reduced access to therapy and treatment, disrupted routines, and stress.13
While these consequences of the COVID-19 pandemic have likely contributed to the rise in EDs, other explanations have been overlooked.
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Few, if any, people have suggested that becoming ill with COVID-19 and its impact on the body might be contributing to the recent increase in EDs.
While we still don’t know a lot about COVID-19, evidence suggests that the disease causes a significant inflammatory response,1; 14 leading to the development of autoimmune and inflammatory diseases for some individuals (e.g., multisystem inflammatory syndrome).2; 14
The nature of COVID-19’s inflammatory consequences, why they manifest, and who gets them, however, remains unclear. This uncertainty about the lasting effects of COVID-19 on the immune system makes it challenging to determine exactly how it could contribute to ED development.
Another problem is that, despite emerging evidence that problems with the immune system can cause EDs, we still aren’t certain why this is.8; 9
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The Immune System
The complexity of the immune system makes it challenging to determine how COVID-19 impacts it.
In simple terms, an immune system is a group of many different organs, tissues, and cells in the body and brain that protect us from threats (e.g., viruses and infections) to our well-being.
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White blood cells recognize and kill health threats throughout the body by making antibodies against them. White blood cells also alert the rest of the body to the health threat via special messengers called cytokines. Meanwhile, in the brain, special immune cells called microglia and astrocytes work together to detect health threats and protect the brain from foreign intruders. The gut also plays a special role in immunity by developing immune cells and regulating the immune response.4
The immune system doesn’t always work properly, though. Certain lifestyle choices (e.g., smoking), stress and anxiety, autoimmunity, genetics, or illness can alter how the immune system operates.
For example, an autoimmune disorder is a disease where the immune system attacks its own healthy cells rather than attacking foreign threats. It does this via autoantibodies, which are proteins that tell the immune system to attack its own cells. Autoimmune disorders result in persistent inflammation, a weakened defense against threats, and dysregulation of bodily functions. For example, Type 1 Diabetes (T1D) is an autoimmune disorder where the body attacks pancreatic β cells, which produce insulin. Consequently, people with T1D lack insulin-producing cells.
So far, researchers have found that COVID-19 can dysregulate the immune system in ways that contribute to chronic inflammation, gut problems (e.g., altered gut microbiota),3 and the development of autoimmunity after recovery.14; 15
These health consequences of COVID-19 could potentially contribute to ED development.
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Inflammation and Autoimmunity as Causes for Eating Disorders?
How the immune system contributes to ED development is unclear, though emerging evidence suggests that there are overlaps in genetics and biological pathways involved in immune response and eating disorders.5; 6; 7
It’s important to remember that people don’t always begin food restricting to lose weight. In some cases, individuals with certain illnesses, such as cancer, develop anorexia in response to inflammation, which alters appetite.8 In a similar way, inflammation from COVID-19 could contribute to the development of EDs.
One way inflammation has been shown to contribute to EDs is by disrupting hunger and fullness cues.
For example, rodent research has shown that rodents with high levels of pro-inflammatory cytokines are more susceptible to developing anorexic-like behavior (e.g., food restriction and excessive physical activity) than rodents with lower levels of pro-inflammatory cytokines.7 Similarly, rodents with abnormal levels of immune cells (e.g., microglia) in the hippocampus (i.e., the brain’s eating center) voluntarily restrict their food intake, leading to weight loss.6
These findings suggest that changes in the number of immune cells or how long these cells are activated can disrupt hunger and fullness cues and increase physical activity in ways that increase ED susceptibility. Chronic inflammation from COVID-19 could, therefore, increase susceptibility to developing an ED.
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Problems with the gut during COVID-19 (e.g., changes in microbiota composition) could also contribute to ED onset, as gut issues can initiate an immune response and alter eating behavior. For example, imbalances in certain gut bacteria can disrupt how we experience hunger and fullness cues,11 as well as change our moods in ways that might contribute to disordered eating (e.g., increased depression or anxiety).12 Gut inflammation might also cause stomach discomfort or pain, resulting in disinterest in eating or body dissatisfaction.10
Certain autoimmune disorders might also cause EDs. While the link between autoimmunity and ED development has only recently been explored, we know that some people with EDs have autoantibodies that attack appetite-regulating hormones.8; 9 These bodily dysfunctions might disrupt how these individuals experience hunger and fullness, resulting in ED development.
What’s Next?
While we don’t know if COVID-19’s lasting impact on the immune system increases ED susceptibility, these questions need further consideration.
As researchers continue determining how COVID-19 impacts the body, they will need to focus on how possible inflammatory consequences of COVID-19 impact appetite, mood, anxiety, the gut, and body satisfaction, all of which contribute to ED development.
In the same sense, those researching EDs need to continue exploring how problems with the immune system can contribute to ED development. Only when these relationships are understood can we fully determine how COVID-19 might be contributing to the recent increase in EDs.13
References
1)Jose, R.J., & Manuel, A. (2020). COVID-19 cytokine storm: The interplay between inflammation and coagulation. The Lancet Respiratory Medicine. doi: 10.1016/S2213-2600(20)30216-2.
2)Galeotti, C., & Bayry, J. (2020). Autoimmune and inflammatory diseases following COVID-19. Nature Reviews Rheumatology, 16, 413-414.
3)Zuo, T., Zhang, F., Lui, G.C., Yeoh, Y.K., Li, A.Y., Zhan, H.,…& Ng, S.C. (2020). Alterations in gut microbiota of patients with COVID-19 during time of hospitalization. Gastroenterology, 159, 944-955.
4)Wu, H.J., & Wu, E. (2012). The role of gut microbiota in immune homeostasis and autoimmunity. Gut Microbes. doi: 10.4161/gmic.19320.
5)Howard, D., Negraes, P., Voineskos, A.N., Kaplan, A.S., Muotri, A.R., Duvvuri, V., & French, L. (2020). Molecular neuroanatomy of anorexia nervosa. Scientific Reports, 10. doi: 10.1038/s41598-020-67692-1.
6)De Luca, S.N., Sominsky, L., Soch, A., Wang, H., Ziko, I., Rank, M.M., & Spencer, S.J. (2019). Conditional microglia depletion in rats leads to reversible anorexia and weight loss by disrupting gustatory circuitry. Brain, Behavior, and Immunity, 77, 77-91. https://doi.org/10.1016/j.bbi.2018.12.008.
7)Milton, L.K., Patton, T., O’Keeffe, M., Oldfield, B.J., & Foldi, C.J. (2022). In pursuit of biomarkers for predicting susceptibility to activity-based anorexia in adolescent female rats. International Journal of Eating Disorders, 55, 664-677. doi: 10.1002/eat.23705.
8)Sirufo, M.M., Magnanimi, L.M., Ginaldi, L., & De Martinis, M. (2022). Anorexia nervosa and autoimmune comorbidities: A bidirectional route? CNS Neuroscience & Therapeutics, 28, 1921-1929.
9)Hommer, R.E., & Swedo, S.E. (2017). Anorexia and autoimmunity: Challenging the etiologic constructs of disordered eating. Pediatrics, 140. doi: 10.1542/peds.2017-3060.
10)Beese, S.E., Harris, I.M., Dretzke, J., & Moore, D. (2019). Body image dissatisfaction in patients with inflammatory bowel disease: A systematic Review. BMJ Open Gastro.
11)Han, H., Yi, B., Zhong, R., Wang, M., Zhang, S., Ma, J.,…& Zhang, H. (2021). From gut microbiota to host appetite: Gut microbiota-derived metabolites as key regulators. Microbiome, 9.
12)Forsythe, P., Sudo, N., Dinan, T., Taylor, V.H., & Bienenstock, J. (2010). Mood and gut feelings. Brain, Behavior, and Immunity, 24, 9-16. https://doi.org/10.1016/j.bbi.2009.05.058.
13)Lin, J.A., Hartman-Munick, S.M., Kells, M.R., Milliren, C.E., Slater, W.A., Woods, E.R.,…& Richmond, T.K. (2021). The impact of the COVID-19 pandemic on the number of adolescents/young adults seeking eating disorder-related care. Journal of Adolescent Health, 69, 660-663.
14)Yong, S.J. (2021). Long COVID or post-COVID-19 syndrome: Putative pathophysiology, risk factors, and treatments. Infectious Diseases, 53, 737-754.
15)Gracia-Ramos, A.E., Martin-Nares, E., & Hernández-Molina, G. (2021). New onset of autoimmune diseases following COVID-19 diagnosis. Cells, 10.
