Orthorexia Nervosa Prevalence in US Adults with Type 1 and Type 2 Diabetes
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Orthorexia Nervosa Prevalence in US Adults with Type 1 and Type 2 Diabetes A Thesis SUBMITTED TO THE FACULTY OF THE UNIVERSITY OF MINNESOTA BY Caitlyn Jahn Shoemaker IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE Dr. Scott Crow, MD, Advisor January 2020 © Caitlyn Jahn Shoemaker 2020 Acknowledgements The process of this thesis was not without some obstacles and pitfalls along the way. For helping me navigate the process from the beginning, I extend my sincerest gratitude to my adviser, Scott Crow. Thank you as well to Scott and my other committee members Jillian Lampert, PhD, MPH, RD, LD, FAED and Jennifer Linde, PhD, for taking time to review this work and to hear my defense. I would also like to send hugs back to my mom Cyndy Jahn, my dogs Violet and Jackson, and my friends and family in New Jersey and beyond for all the hugs you gave me when I doubted my abilities and myself throughout this time, in spirit and real-time. I am extremely grateful to my forever friend, Savannah Bennett, for proofreading this work, and for providing moral support throughout my entire graduate school experience—even as she works long hours herself on yet another graduate degree. Thank you to my Simmons University undergraduate adviser, Dr. Lisa Brown PhD, RDN, LDN, for encouraging me to pursue a graduate degree and for bolstering my passion for dietetics. Finally, I extend greatest thanks to Liz Fayram CEDRD, RD, LDN for bringing the concept of Orthorexia Nervosa to my attention in the first place—I may never have known what it was or what a major health issue it was if not for your breadth of knowledge and diagnostic skills. i Dedication To my mama, Violet, and Jackson You have been the calm waves in my life storm and my guides over and through the mountains and valleys on my life journey. You’ve never let me drown or fall. To Casey You are the Pusheen to my pizza, the Archie to my Edith, and the Superman to my Wonder Woman. You are my forever love and my forever rock, and the best partner-in-crime there ever was or ever will be. ii Abstract Background The disordered eating pattern Orthorexia Nervosa has been examined in groups from health professionals to those with defined eating disorders (EDs). The prevalence has not fully been established. Orthorexia shares the isolation/malaise aspects of defined EDs. Because people with diabetes (DM) often struggle with food/EDs and treatment relies on limiting processed foods, people with diabetes may display Orthorexia symptomatology. However, Orthorexia has rarely been examined in people with diabetes—and never in a US adult population. Objective Determine prevalence of Orthorexia in people with diabetes, specifically US adults. Other aims: determine association between Orthorexia Nervosa and (1) quality-of- life (QOL); (2) overall disordered eating habits; (3) disordered eating habits in people with insulin- dependent diabetes; (4) body image perception in people with diabetes. Hypothesis Due to its suggested symptomology and similarities to established EDs, Orthorexia Nervosa is prevalent in people with diabetes. Methods The survey was comprised of five previously validated surveys: SF-36, EAT-26, DEPS- R, Hopwood Body Image Scale, and ORTO-15. Results The rates of Orthorexia Nervosa did not differ significantly between DM1 and DM2 diabetes types (67.4 and 62.3, respectively). Our hypotheses regarding quality of life and eating habits of insulin-dependent diabetes were not supported. Eating disorder behaviors decreased significantly in our sample, which did not support the hypothesis that some behaviors would be positively correlated. Body image satisfaction increased significantly with Orthorexia symptomology, which was contrary to our hypothesis but at the same time, intriguing. Conclusion Orthorexia is prevalent in people with diabetes. Diabetes health professionals should recognize/screen for Orthorexia. iii Table of Contents List of Tables ………………………………………………………………………………….v List of Figures ………………………………………………………………………………..vi List of Abbreviations ………………………………………………………………….….vii Background and Review of the Literature ………………………………….....1 Methods ………………………………………………………………………………………...15 Research Design ………………………………………………………………………………….….15 Participants and Data Collection Procedures …………………………………………..16 Measures ………………………………………………………………………………………………...17 Analysis …………………………………………………………………………………………….…….21 Results …………………………………………………………………………………………...23 Demographics ……………………………………………………………………………….……23 What is the Orthorexia Nervosa prevalence in US Adults with diabetes?.…..24 Orthorexia Nervosa and quality of life in people with diabetes . ……………….…………………………………………..……25 Orthorexia Nervosa and typical eating disorder behaviors in people with diabetes ……………………………………25 Orthorexia Nervosa and disordered eating behaviors in people with insulin-dependent diabetes …………..……..... 25 Orthorexia Nervosa and body image perception in people with diabetes ………………………………….……………….…...25 Orthorexia Nervosa and demographic factors.………………………………………….………………………………………………….……...25 Discussion …………………………………………………………………………………..…..27 Conclusion …………………………………………………………………………………...….31 Bibliography …………………………………………………………………………………...33 Appendix A: Original Sources of Measures…………………………………….…41 iv List of Tables Table 1: Reliability, Measures of Central Tendency, and Variability of Scales ……………………………………………………………………………..22 Table 2: Demographics of Survey Participants ………………………………………………….23 Table 3: Frequency distributions/Correlations of ORTO-15 Total Scales, ORTO-15 Subscales and Other Scales ………………………………………………………...……26 Table 4: Frequency distributions/Correlations of ORTO-15 Total Scale, ORTO-15 Subscales, and Demographics …………………………………………………………..27 v List of Figures Figure 1: Combined Total Prevalence of Orthorexia Nervosa in Study Sample ……………………...24 vi List of Abbreviations 1. AN- Anorexia Nervosa 2. BN- Bulimia Nervosa 3. BED- Binge Eating Disorder 4. ED- Eating Disorder 5. DM 1/ DM 2- Type 1/ Type 2 diabetes mellitus 6. SAD-Standard American Diet 7. DSM-5- Diagnostic Statistical Manual-5 8. OSFED- Other Specified Feeding and Eating Disorders 9. UFED- Unspecified Feeding and Eating Disorders 10. HDL- High Density Lipoprotein 11. GI- Glycemic Index 12. GL- Glycemic Load 13. DKD- Diabetic Kidney Disease 14. SF-36- Short Form-36 items 15. QOL- Quality of Life 16. EAT-26- Eating Attitudes Test- 26 items 17. DEPS-R- Diabetes Eating Problems Survey-Revised 18. ORTO-15- Bratman Orthorexia Questionnaire- 15 items vii Background and Review of the Literature Diabetes and Sugar Intake It is well understood that the compound glucose is needed as the main source of metabolic fuel for basic daily nutrition and energy needs. The brain alone utilizes about 60% of total glucose in the body. Carbohydrates—whether from fruits and starchy vegetables or from grains—are the origin of glucose (and glycogen its storage form in muscles and the liver). Under normal metabolic (non-diabetic) conditions, glucose can come from two main sources: either directly from food (fed) or from non-carbohydrate sources via glycogenolysis or gluconeogenesis (fasting)1. Glucagon dominates during fasting, while insulin secretion is inhibited. In the post-prandial fed state, insulin is upregulated via the pancreatic islet cells, glucagon is suppressed and anabolic processes such as lipogenesis occur1. In people with diabetes, however, the mechanism of glucose regulation is drastically altered. Diabetes, according to the American Diabetes Association, is a grouping of metabolic diseases whose pathogeneses are characterized by impaired glucose regulation (chronic hyperglycemia interspersed with bouts of hypoglycemia) via compromised insulin action or secretion2. In diabetes, similar to healthy individuals, glucose comes from glycogenolysis or gluconeogenesis. However, even with exogenous insulin to regulate glucose diffusion rate into the cells, there is still not enough natural plasma insulin to regulate the above processes. In the post-prandial state, the exogenous insulin cannot fully suppress glucagon secretion so glucose spills freely into the blood, resulting in hyperglycemia2,3 While there are several manifestations of diabetes, this study focuses on two types: Type 1 and Type 2. 1 Overview of Diabetes Mellitus Types and Mechanisms Type 1 Diabetes- There are two forms of type 1 diabetes: immune-mediated and idiopathic2,3. Immune- mediated Type 1 diabetes- The predominant form is autoimmune in nature, known as “in-sulin-dependent” or “juvenile-onset”, diabetes2,3. It is present in roughly 5-10% of diabetes cases and is due to the near-complete or complete destruction of β cells in the pancreas. Fasting hyperglycemia presents along with various antibodies as part of the heightened immune response. Sudden ketoacidosis is often another initial symptom of the disease, particularly in children who experience faster cell destruction than adults2,3. Unlike type 2 who may or may not use exogenous insulin, type 1 patients must use exogenous insulin permanently. The patients are usually not overweight, and may even experience rapid weight loss4. Idiopathic Type 1 diabetes- This form not only involves a complete lack of pancreatic production of insulin and ketoacidosis, but also shows no evidence of autoimmune destruction of the pancreatic β cells3. It is suggested in the literature that this form comprises a very small number of cases, and is inherited3 and insulin may be required as needed, depending on the case3. Type 2 Diabetes- Roughly 90-95%