Guest post: The Cognitive Effects of Anorexia

By: Lauren Goette
Lauren Goette received her B.S. in Psychology from Cal Poly, San Luis Obispo June 2017, and plans to become a licensed professional counselor in the future. Having personally struggled with anorexia, Lauren has become an advocate for mental health, working as a Peer Health Educator at Cal Poly and speaking out against the stigma surrounding mental illness. This was a paper she wrote her senior year (published with permission). ​

    The deadliest mental disorder in existence, Anorexia Nervosa (AN) threatens the lives of millions of US citizens each year. According to Arcelus, Mitchell, Wales, and Nielsen (2011), anorexia has the highest mortality rate of any mental disorder. In fact, it has been estimated that anywhere from five to twenty percent of individuals with AN will die from the disorder (“Anorexia Nervosa,” n.d.). This exceptionally high mortality rate is largely the result of anorexics’ self-induced starvation, which can be achieved through methods such as calorie restriction and excessive exercise (“Feeding and Eating Disorders,” 2013). As a result of these behaviors, anorexia can lead to serious physical problems, such as slow heart rate, low blood pressure, reduced bone density, severe dehydration, fatigue, hair loss, and a plethora of other physiological issues (“Health Consequences of Eating Disorders,” n.d.). And while there are numerous physical complications that result from this disorder, a significant amount of damage is also inflicted on the cognitive level. A variety of studies conducted in the past two decades have shed light on the devastating cognitive impacts of anorexia, as well as the promising positive effects of refeeding. Current evidence shows, as a result of semi starvation, individuals struggling with anorexia can experience drastic structural brain changes, inhibited cognitive abilities, and memory impairments, which may be improved with weight restoration.
Structural Brain Changes
    One of the most severe physical and psychological costs of anorexia is structural brain changes, which can cause significant harm to the cognitive functioning and overall mental health of anorexia sufferers. In the short term, a diet deficient in calories and nutrients, often coupled with excessive exercising, can lead to loss of both white and gray matter (Sidiropoulos, 2007). Prolonged caloric restriction promotes “abnormal reward responses to food and a deviation from a healthy feeling/perception of the body when eating.” These structural changes may, in part, explain why anorexics continually avoid food consumption, as the act itself appears to elicit a negative perception and/or sensation of the body. Additionally, this reduction of gray matter in may also contribute to the disturbance of the brain’s typical reward responses which encourage food consumption.
Cognitive Impairments
    Often the direct result of structural brain changes, AN sufferers can experience a wide range of cognitive difficulties. Higgs (2009) explored the impact of interference from diet-related thoughts on anorexics’ cognitive abilities. On a cognitive task, restrained eaters’ reaction times when imagining eating cake were significantly slower compared to when they imagined drinking water. On the other hand, unrestrained eaters' reaction times did not significantly differ between the cake or the water conditions. Higgs maintained that the cognitive impairments displayed by restrained eaters were the direct result of a “reduction in processing capacity due to interference from diet-related thoughts.” With this reduction in processing capacity, dieters’ ability to perform basic cognitive tasks was drastically diminished, highlighting how impactful caloric restriction can be on AN individual's thoughts and on their execution of simple cognitive tasks.
    In addition to these milder cognitive issues, AN sufferers can also develop chronic cognitive deficits. Specifically, Gillberg et al. (2010) found, eighteen years after AN onset, anorexics had more attention, executive function, and mentalizing problems. Anorexia was found to be associated with “a range of neuropsychological problems that are present long after the eating disorder… is no longer an important feature.” Even after starvation has ceased, weight-restored anorexia survivors can experience lingering cognitive issues. Gillberg et al. suggested that this is the result of severe structural damage which can leave important cognitive facilities critically damaged. Moreover, Fowler et al. (2006) found that even “relatively severe” neurocognitive impairments have the potential to adversely affect AN sufferers’ daily social and occupational functioning in the long term. These impairments can have a substantially negative effect on recovered individuals’ quality of life, making typically simple cognitive tasks exceptionally difficult to accomplish.
Memory Impairments
    Along with cognitive difficulties, AN can also cause notable memory impairment. Kemps, Tiggeman, Wade, Ben-Tovim, and Breyer (2006) found that anorexic individuals’ frequent obsessive eating-disordered thoughts actively prevent their working memory from operating effectively, which can lead to various issues with basic memory functions such as recall. Chan et al. (2013) also found anorexic’s impairment in memory functions to be positively correlated with BMI. In other words, the lower an AN sufferer’s BMI, the worse their memory functions were, and vice versa. Kingston, Szmukler, Andrewes, Tress, and Desmond (1996) also discovered an association between anorexics’ lower weight and poorer performance on memory tasks. Kingston et al. maintained that this poor performance was directly related to anorexics’ degree of weight loss, concluding that anorexics’ memory performance declines with their decrease in weight. Chan et al. proposed that this correlation between BMI and memory impairment indicates that anorexics’ memory deficits may, in part, be associated with malnutrition, however current research remains inconclusive.
Weight Restoration
    Having focused largely on the starvation-induced structural, cognitive, and memory impairments of AN, it is also imperative to recognize the simplest yet most effective treatment for such damage: weight restoration. Though not a “cure-all,” weight restoration, accomplished through the refeeding of the anorexic patient, has the potential to reverse much of the structural and cognitive damage caused by the disorder. In terms of brain matter recovery, Sidiropoulos (2007) demonstrated how weight restoration resulted in the return of white matter to premorbid levels. Simply by increasing caloric intake, anorexic patients were able to recover all of the white matter they had lost throughout the course of their disorder. Similarly, Wagner et al. (2006) found that weight restoration in long-term recovered anorexic individuals resulted in the reversal of structural brain abnormalities. These results imply that weight restoration has the power to reverse structural brain damage, and restore any and all white matter lost to anorexia.
    Focusing on the psychological implications of structural brain recovery, Bernardoni et al. (2016) found a strong association between partial weight restoration and improvements in affect and eating disorder symptoms. With even minor increases in weight, recovering anorexics experienced significant improvements to their psychological wellbeing. On the cognitive side, Hatch et al. (2009) discovered that weight-restored individuals were notably faster on cognitive tasks, and exhibited superior verbal fluency and working memory. Hatch et al. concluded that, with refeeding and weight gain, cognitive impairments in weight-restored AN sufferers appeared to normalize.
    Despite the existing support for weight restoration, it has noteworthy limitations. First and foremost, complete structural brain repair is not entirely possible through weight restoration While Sidiropoulos (2007) did find significant improvements in the quantity of white matter recovered in weight-restored individuals, in truth, some gray matter loss persisted. In spite of the recovery of white matter to premorbid levels, previously anorexic individuals sustained irreversible gray matter loss, which remained unaffected by their increased weight. Secondly, weight restoration fails to improve distorted cognitions about body image. Even after weight restoration, Bernardoni et al. (2016) revealed that patients remained dissatisfied with their bodies. Lastly, weight restoration fails to recover weight-restored individuals’ memory abilities. Nikendei et al. (2010), discovered that deficits in immediate and delayed story recall in currently ill AN patients persisted even after these patients were weight-restored. Nikendei et al. suggested that this was the result of a so-called “scar effect” on the brain caused by chronic starvation. They maintained that this scar effect may play an important role in the etiology and/or persistence of AN, and might also explain why memory impairments sustained during AN are seemingly irreparable.
Conclusion
    The vast body of anorexia research available today highlights both the extensive damage AN can cause to anorexics’ brain structure, cognitive abilities, and memory, in addition to the reparative power of weight restoration. Tragically, for individuals struggling with AN, the damage sustained throughout the course of the disorder can inhibit their brains’ basic cognitive functions. The structural brain changes caused by AN can lead to an irreversible loss of brain matter, as well as serious complications with cognitive and memory functioning. Anorexia nervosa can make simple cognitive and memory tasks, such as attention and recall, exceedingly difficult to accomplish. These cognitive and memory impairments, which can be caused by both structural brain damage and cognitive interference, can make everyday functioning a challenge. Not to mention, the irreversible nature of some of this damage can cause long-term impairment, even in weight-restored individuals. Despite the seemingly endless list of structural, cognitive, and memory complications caused by AN, weight restoration may hold the key to the recovery of both brain matter and cognitive abilities. In spite of its shortcomings, weight restoration has the ability to effectively repair the structural brain damage and cognitive impairment caused by anorexia nervosa.

References

• Anorexia Nervosa. Retrieved December 03, 2016, from https://www.nationaleatingdisorders.org/anorexia-nervosa
• Arcelus, J., Mitchell, A. J., Wales, J., & Nielsen, S. (2011, July). Mortality Rates in Patients With Anorexia Nervosa and Other Eating Disorders. JAMA Psychiatry, 68(7), 724-731. doi:10.1001/archgenpsychiatry.2011.74.
• Bernardoni, F., King, J. A., Geisler, D., Stein, E., Jaite, C., Natsch, D., . . . Ehrlich, S. (2016, April 15). Weight restoration therapy rapidly reverses cortical thinning in anorexia nervosa: A longitudinal study. NeuroImage, 130, 214-222. Web. November 26, 2016.
• Chan, T. W., Ahn, W., Bates, J. E., Busemeyer, J. R., Guillaume, S., Redgrave, G. W., . . . Courtet, P. (2013). Differential impairments underlying decision making in anorexia nervosa and bulimia nervosa: A cognitive modeling analysis. International Journal of Eating Disorders, 47(2), 157-167. doi:10.1002/eat.22223
• Chui, H. T., Christensen, B. K., Zipursky, R. B., Richards, B. A., Hanratty, M. K., Kabani, N. J., . . . Katzman, D. K. (2008). Cognitive Function and Brain Structure in Females With a History of Adolescent-Onset Anorexia Nervosa. Pediatrics, 122(2). doi:10.1542/peds.2008-0170
• Feeding and Eating Disorders - DSM-5. (2013). Retrieved November 12, 2016, from http://www.dsm5.org/Documents/Eating Disorders Fact Sheet.pdf
• Fowler, L., Blackwell, A., Jaffa, A., Palmer, R., Robbins, T. W., Sahakian, B. J., & Dowson, J. H. (2005). Profile of neurocognitive impairments associated with female in-patients with anorexia nervosa. Psychological Medicine, 36(04), 517. doi:10.1017/s0033291705006379
• Gillberg, I. C., Billstedt, E., Wentz, E., Anckarsäter, H., Råstam, M., & Gillberg, C. (2010). Attention, executive functions, and mentalizing in anorexia nervosa eighteen years after onset of eating disorder. Journal of Clinical and Experimental Neuropsychology, 32(4), 358-365. doi:10.1080/13803390903066857
• Hatch, A., Madden, S., Kohn, M. R., Clarke, S., Touyz, S., Gordon, E., & Williams, L. M. (2009). In first presentation adolescent anorexia nervosa, do cognitive markers of underweight status change with weight gain following a refeeding intervention? International Journal of Eating Disorders, 295-306. doi:10.1002/eat.20695
• Health Consequences of Eating Disorders. (n.d.). Retrieved December 04, 2016, from https://www.nationaleatingdisorders.org/health-consequences-eating-disorders
• Higgs, Suzanne. "Impairment of cognitive performance in dietary restrained women when imagining eating is not affected by anticipated consumption." Eating Behaviors 8 (2006): 157-61. Web. 25 Nov. 2016.
• Kemps, E., Tiggeman, M., Wade, T., Ben-Tovim, D., & Breyer, R. (2006). Selective working memory deficits in anorexia nervosa. European Eating Disorders Review, 14, 97-103. doi:10.1002/erv.685
• Kingston, K., Szmukler, G., Andrewes, D., Tress, B., & Desmond, P. (1996). Neuropsychological and structural brain changes in anorexia nervosa before and after refeeding. Psychological Medicine, 26(01), 15. doi:10.1017/s0033291700033687
• Nikendei, C., Funiok, C., Pfüller, U., Zastrow, A., Aschenbrenner, S., Weisbrod, M., . . . Friederich, H. (2010). Memory performance in acute and weight-restored anorexia nervosa patients. Psychological Medicine, 41(04), 829-838. doi:10.1017/s0033291710001121
• Sidiropoulos, M. (2007, January). Anorexia nervosa: The physiological consequences of starvation and the need for primary prevention efforts. McGill Journal of Medicine, 10(1), 20-25. Web. 25 Nov. 2016.
• 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. doi:10.1016/j.biopsych.2005.06.014