Abstract

Background: Women with type 1 diabetes (T1D) are 2.4 times more likely to develop an eating disorder than their nondiabetic peers. In addition, T1D has been reported as a risk factor associated with the development of an eating disorder. Objective: To identify the biological disruptions and psychological pressures unique to a person with T1D that create a higher risk for developing an eating disorder. Design and Methods: Conducted a three-year review of literature, articles and research studies on biological systems impacted by T1D, and on the psychological factors involved in eating disorders. Merged the research with case-study evidence obtained from Diabulimia Helpline clients and online support group members through discussions, posts and responses to questions. Results: A number of physiological consequences of the destruction or removal of beta cells are known precursors to the onset of an eating disorder. Insulin is required for proper regulation of leptin, neuropeptide Y and dopamine, all of which are involved in the consumption and use of energy. While insulin analogs have made great strides, they do not perfectly mimic natural insulin or it’s interactions with other hormones and neurochemicals in the body. In addition, the more “out of range” a person’s blood glucose is, the more disrupted are these physiological mechanisms. The absence of amylin disrupts satiety mechanisms both directly in the brain and indirectly in the intestine through uncontrolled gastric emptying. In addition, certain character traits that are associated with eating disorders, such as avoiding thoughts and emotions or black and white thinking, can be exacerbated with a T1D diagnosis. Conclusion: The development of T1D increases the number of risk factors a person has for developing an eating disorder, some of which are biological in nature and thus cannot be avoided. We can also see how biology becomes psychology when, for example, a reduction of leptin creates a risk of binging which in turn creates a risk for insulin omission. Disclosure D. Lee-Akers: None. J. Simon: None. E. Akers: None.

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