The Multidisciplinary Approach in the Treatment of Eating (PDF)

Georgia State University Georgia State University ScholarWorks @ Georgia State University ScholarWorks @ Georgia State University Nutrition Masters Projects Department of Nutrition Summer 8-13-2020 The Multidisciplinary Approach in the Treatment of Eating The Multidisciplinary Approach in the Treatment of Eating Disorders Disorders Laura Brown Follow this and additional works at: https://scholarworks.gsu.edu/nutrition_mastersprojects Recommended Citation Recommended Citation Brown, Laura, "The Multidisciplinary Approach in the Treatment of Eating Disorders." , Georgia State University, 2020. doi: https://doi.org/10.57709/18985221 This Project is brought to you for free and open access by the Department of Nutrition at ScholarWorks @ Georgia State University. It has been accepted for inclusion in Nutrition Masters Projects by an authorized administrator of ScholarWorks @ Georgia State University. For more information, please contact [email protected]  The Multidisciplinary Approach in the Treatment of Eating Disorders By Laura Lane Brown B.S., Middle Tennessee State University, 2004 M.B.A., Middle Tennessee State University, 2006 Committee Members: Jessica Todd, MS, RD, LD, Marci Soran, Linda Buchanan, PhD, Carrie Poline, DO, Christine Engstrom, MS, RD, LD, CEDRD-S 2020 Master’s capstone project submitted in partial fulfillment of the requirements for the Master of Science degree in Coordinated Program, Nutrition Byrdine F. Lewis College of Nursing and Health Professions Georgia State University Atlanta, GA  P a g e 2 | 53 Table of Contents Acronyms ................................................................................................................................... 4 Introduction ................................................................................................................................ 6 Eating Disorder Prevalence........................................................................................................ 6 Feeding & Eating Disorder Types .............................................................................................. 7 Risk Factors ............................................................................................................................... 8 Screening & Diagnosis ............................................................................................................... 9 Warning Signs & Symptomology ...............................................................................................10 Suicidality & Eating Disorders ...................................................................................................15 Neurochemistry .........................................................................................................................15 Metabolism ...............................................................................................................................17 Determining Levels of Care (LOC) ............................................................................................18 Inpatient Hospitalization ..................................................................................................................... 18 Residential Treatment ......................................................................................................................... 19 Partial Hospitalization Program .......................................................................................................... 19 Intensive Outpatient Program ............................................................................................................ 20 Outpatient Treatment ......................................................................................................................... 20 The Multidisciplinary Team........................................................................................................21 Physician ............................................................................................................................................. 21 Psychotherapist ................................................................................................................................... 22 Registered Dietitian ............................................................................................................................ 22 Other Coordinated Staff & Specialists ................................................................................................ 23 Family Members ................................................................................................................................. 24 Treatment Approaches ..............................................................................................................24 Cognitive Behavioral Therapy ............................................................................................................. 24 Interpersonal Therapy......................................................................................................................... 25 Dialectical Behavioral Therapy ............................................................................................................ 25 Acceptance & Commitment Therapy .................................................................................................. 26 Family-Based Therapy ......................................................................................................................... 26 Exposure Therapy ............................................................................................................................... 27 Narrative Therapy ............................................................................................................................... 28 Group Therapy .................................................................................................................................... 28 Intuitive Eating .................................................................................................................................... 28 Health at Every Size ............................................................................................................................. 29  P a g e 3 | 53 Pharmacology & Supplementation ............................................................................................30 Pharmacology ..................................................................................................................................... 30 Supplementation................................................................................................................................. 31 Other Medical & Nutritional Protocols .............................................................................................. 33 Coordination & Communication .................................................................................................35 Barriers to Treatment ................................................................................................................35 Medical Perspective ............................................................................................................................ 35 Dietitian Perspective ........................................................................................................................... 36 Patient Barriers ................................................................................................................................... 37 Financial Cost & Insurance .................................................................................................................. 38 Conclusion ................................................................................................................................38 Methods ....................................................................................................................................38 Appendix 1: LOC Guidelines .....................................................................................................40 Appendix 2: Video Screenshots ................................................................................................41 References ...............................................................................................................................48  P a g e 4 | 53 Acronyms ACT – acceptant and commitment therapy ALT – alanine aminotransferase AN-ERP – exposure response prevention for anorexia APA – American Psychiatric Association ARFID – avoidant/restrictive food intake disorder AST – aspartate aminotransferase AN – anorexia nervosa BED – binge eating disorder BMI – body mass index BN – bulimia nervosa BUN – Blood urea nitrogen CBT – cognitive behavior therapy CCK - cholecystokinin DA – dopamine DBT – dialectical behavior therapy ED – eating disorders ERP-B – exposure response prevention for binging ERP-P – exposure response prevention for purging FSH – follicle stimulating hormone GAPS – Guidelines for Adolescent Preventative Services HAES – health at every size HVA – homovanillic acid IBW – ideal body weight IE – intuitive eating IGF-1 – insulin-like growth factor 1 IOP – intensive outpatient program IPT – interpersonal therapy LH – luteinizing hormone LOC – levels of care MAOIs – monoamine oxidase inhibitors MED- DBT – multi-diagnostic complex eating disorder dialectical behavior therapy MRI – magnetic resonance imaging NICE – National Institute for Health and Clinical Excellence NPY – neuropeptide Y OCD – obsessive compulsive disorder OSFED – other specified feeding or eating disorder PHP – partial hospitalization program PYY – peptide tyrosine tyrosine PTSD – post traumatic stress disorder RANZCP – Royal Australian and New Zealand College of Psychiatrists  P a g e 5 | 53 RD – registered dietitian RMR – resting metabolic rate RO-DBT – radically-open DBT SUD – substance use disorder SSRI – serotonin re-uptake inhibitor TCAs - Tricyclic antidepressants UFED – unspecified feeding or eating disorder  P a g e 6 | 53 Introduction Eating disorders (ED) are characterized by severe disturbances in eating behavior and body weight.1 They encapsulate a broad range of compulsive food and eating related disturbances that are considered one of the more malicious psychiatric disorders.2 Disturbances may include persistent dietary restraint, starvation, low weight, overvaluation of body shape, body dysmorphia, periodic overeating, purging, overweight, and aversion to food based on sensory and texture aversions.2 The etiology of eating disorders is multi-factorial including genetic, biological, individual, family, psychological, and socio-cultural and as such require a multi- disciplinary treatment approach.3 EDIN: Education and Insight on Eating Disorders, is a local non-profit working to create awareness and provide education on eating disorders to those struggling with EDs, caregivers, and medical and therapeutic professionals in the metro Atlanta area. Currently, they offer a wide variety of educational resources including in-person and web-based presentations and educational curriculum. The purpose of this literature review is to explore the current research on eating disorders including, but not limited to, prevalence, etiology, metabolism, neurochemistry, and the multi-disciplinary roles of the treatment team. The ultimate goal of this capstone project is to provide a comprehensive and educational video aimed at improving ED knowledge in the professional community. Eating Disorder Prevalence National and global studies indicate an increase in the overall prevalence of ED over recent years.1 It is estimated that up to 70 million individuals worldwide and 30 million individuals in the United States will have an eating disorder during their lifetime.4-6 In Georgia, there are around 339,500 people who suffer from ED.7 In both Canada and the United Kingdom, it is estimated that ED are third highest chronic condition among girls ages 15-19 years old.2,8 Although ED are traditionally thought to be confined to Western countries, studies have highlighted a higher prevalence in Asia and developing Middle-Eastern countries.1 ED affect all ages, genders, ethnicities, and sexualities. Approximately 95% of initial cases in both males and females occurred by the age of 25, with the highest mean annual prevalence around the age of 21 years.9 Although the estimated annual prevalence of ED is lower comparative to other disease states, the cumulative lifetime burden is high at 14.3% for male and 19.7% for female individuals.9 The stereotypical ED patient is an affluent, white female adolescent, but males can also suffer from greater body dissatisfaction as well as problematic eating behaviors.3 Additionally, the LGBTQIA+ community have shown a higher prevalence than their straight counterparts.3 Caucasians are the largest ethnic group affected by ED, but Mexican-American, African Americans, and Asians have been shown to be at risk as well.3 African American women have been shown to be at equal risk as their Caucasian counterparts, specifically for bulimia nervosa.3 As the second deadliest mental illness behind opiate addiction, one person dies every 62 minutes from an ED.10 When the initial onset occurs during adolescence, it can result in up to a 25-year reduction in lifespan as well as impaired quality of life.11 The most prevalent ED is other specified feeding or eating disorder (OSFED), followed by binge eating disorder (BED),  P a g e 7 | 53 bulimia nervosa (BN), and anorexia nervosa (AN).9 As the majority of research has focused on AN, BN, and BED, we will further detail prevalence by category. Feeding & Eating Disorder Types The American Psychiatric Association has outlined and defined diagnostic criteria for eight main ED in the Diagnostic and Statistical Manual of Mental disorders (DSM-V). As we review the diagnostic criteria for each category, it is important to note that individuals should be carefully evaluated for an eating disorder regardless of other criteria if they are unable to maintain or attain a healthy weight, height, body composition or sexual maturation for gender or age.3 AN is characterized by the restriction of energy intake resulting in significantly low body weight, intense fear of weight gain or the persistent behavior that interferes with weight gain despite low body weight, and a disturbance in body image, or persistent lack of recognition of the seriousness of their current low body weight.12 There are two other subtypes of AN, atypical and binge-purge AN. Atypical AN is similar to the standard AN, but patients are not significantly underweight.13 Roughly between 42.1%-56.2% of those with AN will meet at least one criteria for another DSM-5 disorder.14 The most common being anxiety and major depressive disorders.14 Substance abuse is also present at a rate between 13%-27%.14 It is estimated that males represent between 10-25% of those patients diagnosed with anorexia nervosa and are at a higher risk of dying than their female counterparts partly due to a lack of education around diagnosing eating disorders and a lack of awareness of eating disorders in the male population.15 Anorexia has one of the highest mortality rates of all ED with an approximate mortality rate of 20%.12 More recent evidence supports that those suffering from AN will still meet full diagnostic criteria more than two decades after onset of AN.2 Less than half of those with AN will completely recover.16 Around 30% will show improvement while 25% maintain a chronic course.16 BN is detailed as recurrent episodes of binge eating and inappropriate compensatory behaviors to prevent weight gain with a frequency of at least once per week for three months.12 Those that suffer from BN often express self-evaluation that is unduly influenced by body shape and weight. In this context, binge eating is described as eating an excessive amount of food in a discrete period of time along with a sense of lack of control.12 Compensatory behaviors may include use of laxatives, diuretics, vomiting, fasting, or excessive exercise. Of particular note, BN occurs in the absence of AN.12 The lifetime prevalence of BN is estimated between 1.7-2.9% with peak incidence between 16-20 years of age in females.14 Although studies vary, the male lifetime prevalence is estimated to be between 0.13% and 1.34%.17 Although BN is more prevalent than AN, it is generally diagnosed at a later stage.3 This can partly be attributed to the tendency for those with BN to be at weight or overweight as well as poor health screening practices across disciplines.3 The prognosis for BN is slightly better than those with AN.16 Around 50% will recover, while 30% will maintain disordered behaviors.16 Newly added to the DSM-V is binge eating disorder (BED). Similar to BN, BED consists of recurrent episodes of binge eating that occur at least once per week for three months, however  P a g e 8 | 53 without the additional compensatory behaviors as is the case in BN.12 It is associated with symptoms such as eating more rapidly, feeling uncomfortably full, eating while not feeling hungry, and eating alone due to embarrassment and/or feelings of self-disgust.12 Patients often note marked distress around binge eating. It occurs in the absence of AN and BN.12 The lifetime prevalence of BED in males and females is around 2.0% and 3.5%, respectively.5,17 As this has been newly added to the DSM-V, there is limited research available. Other recently added ED to the DSM-V include, pica, rumination, avoidant/restrictive food intake disorder (ARFID), other specified feeding or eating disorder (OSFED), and unspecified feeding or eating disorder (UFED). A diagnosis of pica is classified as eating of one or more nonnutritive, nonfood substances on a persistent basis over a period of at least 1 month that is inappropriate to the developmental level of the individual.18 It occurs in the absence to any cultural or socially normative practices.18 Furthermore, if the eating behavior coincides with another mental disorder such as autism, a separate diagnosis of pica should only occur if severe enough to warrant additional clinical attention.18 Rumination features repeated regurgitation of food over a period of at least one month and the regurgitated food may be re-chewed, re- swallowed or spit out.18 Similar to pica, if the behavior coincides with another mental disorder, diagnosis of rumination should only be considered if it is severe enough to warrant the additional diagnosis.18 It can only occur in the absence of BN, AN, BED, and ARFID.18 The current prevalence data on both rumination and pica is inconclusive, however an increased prevalence in those with intellectual disabilities is noted.18 ARFID is noted when there is an eating or feeding disturbance with the persistent failure to meet nutritional needs associated with significant weight loss or growth failure, significant nutritional deficiency, dependency on enteral/supplemental feeding or marked with interference with psychosocial functioning.12 These symptoms are not explained by lack of food availability, other medical illnesses, or cultural practices and occurs in the absence of AN, BN, or body image disturbances.12 The OSFED category is for those eating disorders causing significant distress, but not meeting the criteria for the other diagnostic categories.12 OSFED has a lifetime prevalence estimated around 7.6%.1 Night eating syndrome, purging disorder, subthreshold binge eating disorder, low frequency/limited duration BN, and atypical AN would be classified under this category.12 The last category, UFED covers eating disorders where there is presentation of clinically significant symptoms, but they do not meet the full criteria for other ED.12 Additionally, subclinical eating disorder behaviors such as binge eating, purging, laxative abuse, and fasting for weight loss is nearly as common among males as to females.15 Risk Factors There are several risk factors associated with the development of ED that cover a variety of genetic, physiological, environmental, psychological or temperamental factors. From a genetic or physiological standpoint, those that have a history of gastrointestinal problems, brain abnormalities, childhood obesity, and early pubertal maturation may be more susceptible.3,18 From a familial side, those with a first-line relative with a history of an eating disorder, bipolar and depressive disorders, as well as a history of alcohol or substance abuse have an increased  P a g e 9 | 53 risk. Additionally, those that have experienced family anxiety, are part of cultures or occupations that value thinness, or have had a history of neglect, physical, emotional, or sexual abuse are more predisposed.18 From a temperamental view, there are some key personality characteristics. Those with BN are often characterized with increased impulsivity and risk- taking behavior, while patients diagnosed with AN often have a difficult time expressing negative feelings, exhibit low self-esteem, and show some degree of constraint.3 Comorbid anxiety disorders, autism, obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, or those that display obsessional or perfectionistic traits are associated with the development of ED.18 Lastly, those with a history of dieting, obesity, and/or an increased focus on weight or body image either from themselves or from family members may be more vulnerable.3 Screening & Diagnosis Being able to correctly diagnose ED is paramount in the treatment and prognosis of a patient with an eating disorder. Early intervention is associated with a better prognosis, so it is essential that health care professionals be familiar with the early signs and symptoms of ED.16 Unfortunately, many cases of ED are missed by health practitioners. In fact only half of all cases of AN and one-third of BN cases are ever detected by the healthcare system.14 According to Murray only 26% of those with ED will receive any consultation for symptoms let alone engage in supported treatments.2 Approximately 20% of females and 13% of males will go into treatment.2 Since the initial onset of ED is skewed towards adolescence and young adulthood, it suggests that this is a prime time for prevention efforts, while the higher prevalence later in life highlights the importance of identification and treatment for long term prognosis.9 ED are multi-factorial and as such require a multi-disciplinary team approach. At a minimum treatment teams include a physician, dietitian, and psychologist or therapist. Patients may initially present for treatment at any one of these team members and may not even realize they have an eating disorder.16 Thus understanding how to screen and what to watch out for with regards to signs and symptoms is imperative among all practitioners. On a basic behavioral level, there are some symptoms that are associated with ED and should highlight to look further into identifying and diagnosing. If a patient exhibits a strong tendency for extreme physical activity, frequent meal skipping, restrictive eating patterns, thinness as a valued goal, unrealistic goals, poor coping skills related to life events, and/or withdrawal from friends then a deeper investigation should be warranted.3 Children that have obsessive-compulsive traits such as perfectionism, having to follow rules, and concern about mistakes are much more likely to develop an ED than those that do not, so practitioners should be watchful.19 There are a number of screening tools that can be utilized to assist in the detection and diagnosis of ED. The most widely known is the SCOFF questionnaire which only consists of 5 questions.12 1) Do you make yourself sick because you feel uncomfortably full?12 2) Do you worry that you have lost control over how much you have eat?12 3) Have you recently lost more than one stone (6.35 kg) in a 3-month period? 4) Do you believe yourself to be fat when others say you are thin?12 5) Would you say that food dominates your life?12 If the client answers 2 or more questions with a yes, then a diagnosis of AN or BN may be likely.12 Bright Futures and the  P a g e 10 | 53 Guidelines for Adolescent Preventative Services (GAPS) are also useful evidenced-based screening forms.3 The Bright Futures screening tool utilizes a variety of questions including how do you feel about the way you look, how do you feel about your weight, are you trying to change your weight, and do you ever fast, vomit, or take laxatives or diet pills to control your weight.3 The GAPS guidelines recommends screening adolescents annually for ED and to inquire about body image and dieting patterns.3 However, according to the National Institute for Health and Clinical Excellence (NICE) guidelines, the most effective screening tool probably remains the practitioner thinking about the possibility of an eating disorder.12,20 Warning Signs & Symptomology In addition to screening tools, there are a number of warning signs or symptoms that can aid in the detection and identification of ED. A detailed client history is critical in the assessment process and in determining the level of care. Significant symptoms can be divided into five main categories: cardiovascular, gynecological, gastrointestinal, psychological, and other.14 Common symptoms of someone with AN include hypotension with a systolic blood pressure below 99 mm HG and/or a diastolic blood pressure below 50 and bradycardia with a heart rate below 60 beats per minute.3,14 It is important to note that patients, parents, and even physicians may link a slow heart rate as a sign of fitness, when it could be a sign of decompensation as is the case in malnutrition.3 Additionally, around 30-50% of patients with AN have mitral valve prolapse. With severe malnutrition, cardiac muscle diminishes, but the size of the valve does not, leading to prolapse.3,14 Another possible complication in those with AN who also purge via self-induced vomiting is the development of pneumomediastinum, a condition where air leaks into the mediastinum.14 It is hypothesized that malnutrition causes thinning of the alveolar walls and connective tissue, which can predispose patients to pneumomediastinum when intrathoracic pressure increases such as is the case during vomiting.14 Patients have also shown congestive heart failure, dysrhythmias, orthostatic hypotension, pericardial effusion, syncope, and electrocardiographic abnormalities.3 In addition, patients with BN who abuse ipecac, which contains alkaloid emetine, are at risk for cardiomyopathy, which can result in heart failure and ventricular arrhythmias when taken in excess.14 From a gastrointestinal perspective, delayed gastric and colonic emptying, abdominal pain and distention are all common complaints in those with AN and BN.3,14 Those with AN are higher at risk for this and are often diagnosed with gastroparesis, gastric distention, gastroesophageal reflux, constipation, and superior mesenteric artery syndrome.3,14 BN patients who self-induce vomiting often complain of painful swallowing, hoarseness, dysphagia, and heartburn secondary to gastroesophageal reflux.14 Patients who abuse laxatives may complain of diarrhea and abdominal cramping.14 With regards to constipation, it is important to not treat with stimulant laxatives such as Senna-Gen and bisacodyl due to the potential for long-term abuse, which puts the patient at risk for developing colonic nerve cell damage causing cathartic colon syndrome.14 Patients who have a history of abusing stimulant based laxatives may develop rebound constipation.14 Other common gastrointestinal issues include acute pancreatitis, Barrett’s esophagus, bloody diarrhea, esophagitis, esophageal rupture, gallstones, and  P a g e 11 | 53 perforation or rupture of the stomach. Barret’s esophagus occurs from chronic gastroesophageal reflux that affects the lining of the esophagus causing it to thicken and become red.14 Mallory-Weiss tears and parotid hypertrophy are primarily seen in those with BN. Mallory-Weiss tears or lower esophageal tears that typically occur due to violent vomiting.14 Parotid hypertrophy is the chronic enlargement of the parotid glands in those who purge via vomiting as seen in BN and atypical AN binge-purge type.14,21 The tale-tale signs of enlarged parotid glands is swelling of the cheeks.14 Additionally acid reflux from self-induced vomiting and damage to the esophageal sphincters can affect the pharynx and larynx and can lead to the development of laryngopharyngeal reflux.22 The regurgitated acidic contents can come into contact with the vocal cords and surrounding areas resulting in hoarseness, dysphagia, chronic cough, and repeated sore throats.22 The most prominent gynecological symptoms among females is irregular menstrual cycles, amenorrhea, or delayed pubertal development in adolescents. In female patients with AN development of hypothalamic amenorrhea syndrome can occur resulting from variable reduction in pulsatile hypothalamic GnRH gonadostat signaling to the pituitary gland resulting in failure of ovulation.23 As a result of this gonadotropin failure, individuals with AN have decreased levels of the sex hormones, estradiol, estrone, progesterone, and testosterone.23 Menstrual irregularities are also common in BN although usually less severe and prevalent than in cases of AN.23 Typically, this functional hypogonadotropic, hypogonadism-induced amenorrhea reflects a temporary and reversible disturbance in function.23 According to Golden et al., menses can be expected to resume at a weight that exceeds 90-93% of ideal body weight.24 However, other studies have demonstrated more variable weights than predicted weights.23 Additionally, there is some evidence that weight loss may not be the only factor causing amenorrhea. Amenorrhea can precede significant weight loss in about one-quarter of women and can persist even after weight restoration, while other women may resume menstruation despite a low body weight.23 It is thought that adaptive hormonal responses to sociocultural-psychic stress, excessive exercise and chronic nutritional energy deficiency along with reduced thyroid and leptin levels may also contribute.23 From a medical standpoint, treatment efforts should focus on the overall treatment of the ED as there is little inherent value in administering female sex hormones (i.e. birth control) as withdrawal bleeding can promote a false sense of well-being and minimize the need for therapy.23 Men with AN display a few abnormalities of reproductive hormones including low testosterone, LH, and FSH which may lead to poor semen quality, reproductive suppression, decreased sperm motility, and an increase in immature sperm number.23,25 It is important to note that pregnancy in women with an ED is still possible. At least 1 in 20 women experience some form of an eating disorder in pregnancy with the highest risk for those with a history of an eating disorder.26 A 2013 study found that 7.5% of women receiving their first routine ultrasound scan during pregnancy met the criteria for an eating disorder.27,28 Another study showed that 28% of subjects displayed disordered eating symptoms and psychological and behavioral traits associated with ED during pregnancy.29 Unfortunately, 93.3% of the women in this study were not identified by their medical practitioners.29 This is especially important as it is associated with a greater incidence of complications for mother and  P a g e 12 | 53 child. Those with BN have 2x the risk for hyperemesis gravidarum, increased weight gain, and miscarriage.26,30-32 Mothers with BED are at risk for increased weight gain and pre-term delivery. AN has been associated with low weight gain during pregnancy33.26,30,31 All mothers are at higher risk for gestational diabetes, hypertension, and pre-eclampsia.26,30,31 The child on the other hand is at risk for being large or small for gestational age, smaller head circumference, stillbirth, low birth weight, low APGAR scores, breach, and cleft lip and/or palate.26,31 Even 2-6 months post-partum, mother and child are at continued risk. The mother is more likely to stop breastfeeding, increase eating disorder behaviors including quick weight loss, and are 5X more likely to develop mood disorders such as depression.31 The baby is more at risk for decreased child feeding, low mother-child attachment, and roughly 17% will have failure to thrive within the 1st year.31 Psychological co-morbidities and dual diagnosis are prominent in ED. The presence of comorbidity is a strong indicator of poorer long-term outcomes and is associated with more severe symptoms.34 In a study of more than 2400 hospital patients with an eating disorder, researchers found that more than 97% had one or more co-occurring conditions. The study further found that 94% had co-occurring mood disorders such as major depression, 56% with anxiety disorders, 20% had obsessive-compulsive disorder, 22% with post-traumatic stress disorder (PTSD), and 22% with alcohol or substance abuse disorder.19 In fact, two-thirds of people with AN had signs of an anxiety disorder before the onset of their eating disorder.19 Further supporting the high prevalence of comorbid psychiatric disorders, a national representative survey found that 95% of respondents with BN, 79% with BED, and 56% with AN met the criteria for at least one other psychiatric disorder.5 Among those BN respondents, they also noted that 64% met the criteria for three or more co-occurring psychiatric disorders.5 As one of the top 3 comorbid psychiatric disorders, PTSD can occur when a person is exposed to a traumatic event such as death, threatened death, actual or threatened serious injury or sexual violence.18 This exposure can result from the direct experience with the traumatic event, witnessing the event in-person, learning of a traumatic event that occurred to a close family member or friend, or first-hand, repeated experiences or extreme exposure to adverse details of the traumatic event.18 Symptoms of PTSD can be grouped into four main categories including intrusion symptoms, avoidance, negative alterations in mood, and alterations in arousal and reactivity.18 Some of these symptoms may include flashbacks, nightmares, irritability, angry outbursts, exaggerated startle, problems concentrating, insomnia, being overly watchful, numbing, forgetting, partial amnesia, negative beliefs around oneself, others, or the world, and self-blame.18 Evidence suggests that ED patients may be sensitive or vulnerable to stress and its consequences. Two national representative studies have shown that individuals with BN, BED, or binge eating have higher rates of PTSD symptoms than those without ED.5,35 The lifetime prevalence of PTSD among BN groups range between 38-44%.5,35 Additionally, women who were victims of assault were 1.86X more likely to develop BN than if they hadn’t been victimized.35,36 In another study looking at PTSD and AN, the researchers found that 13.7% of participants met the criteria for PTSD.37 When they delved further into the results, they found that AN purging subtype had higher odds of PTSD than standard AN.37 Another study found that 48% of females and 68% of males with AN, up to 41% of females and  P a g e 13 | 53 24% of males with BN, and up to 35% of females and 16% of males with BED have experienced some form of sexual violence.36 Unresolved trauma and/or PTSD may be an important factor in the maintenance of eating disorder symptoms. Similar to the way substance abuse may be used to self-medicate, binge eating and/or purging may also help reduce the hyperarousal or anxiety symptoms associated with trauma as well as help numb or avoid traumatic experiences.38 These behaviors are reinforcing, making it difficult to break the cycle.38 As a result, individuals with ED complicated by trauma and PTSD need treatment for both conditions utilizing a trauma-informed, integrated approach.38 Of note, the best approach to address both PTSD and ED remains debated, but work so far primarily focusses on cognitive behavioral therapy with integrated treatment for the eating disorder.38 Additionally, personality disorders occur commonly in individuals with ED. In a meta-analysis examining the prevalence of personality disorders and ED, they found that avoidant personality disorder, dependent personality disorder, and obsessive-compulsive personality disorder (OCD) were commonly associated in both AN and BN, while borderline personality disorder, which is marked by impulsivity and instability is common among BED.39 Additionally comorbid substance use disorders (SUD) are common with roughly 1 in 5 individuals developing a SUD at some point in their lifetime and roughly 1 in 10 meet current criteria for a SUD.40 The lifetime prevalence of comorbid SUD among adults with AN, BN, BED, and subthreshold BED is estimated between 23-37%.40 In a meta-analysis, researchers found that among the highest prevalence of comorbid SUD was tobacco (36.1 ± 23.1%), caffeine (23.8 ± 12.5%), alcohol (20.6 ± 16.0%), or any other illicit drug (19.8 ± 19.6%), cannabis (14.5 ± 16.0%), and cocaine (13.7 ± 23.4%).40 Lifetime SUD comorbidity is higher among females, Caucasians, and individuals with BN and binge-purge behaviors.40 It is estimated that roughly 20% of individuals being treated for a SUD report binge eating.41 Of men with BED, 40.4% report having struggled with a SUD.42 ED and SUD share many common risk factors including brain chemistry, family history, low-self-esteem, anxiety, and depression.43 They also share similar characteristics such as compulsive behavior, social isolation, and risk for suicide.43 Successful treatment of comorbid psychiatric diagnoses and SUD in patients with ED can be challenging when the patient is malnourished as starvation can have a significant impact on mood and cognition and some psychiatric symptoms may improve with weight restoration.3 Beyond the gastrointestinal, cardiovascular, reproductive, and psychological issues associated with ED, there is a vast array of other signs or symptoms. Other affected areas include dermatologic, endocrine, skeletal, hematologic, neurologic and fluid and electrolyte balances. Hematologic effects of ED include bone marrow suppression, mild anemia, leukopenia, thrombocytopenia, impaired cell-mediated immunity, and low sedimentation rate.3 Neurologically speaking patients might have cortical atrophy, myopathy, peripheral neuropathy, and even seizures.3 From a dermatological standpoint, patients often present with brittle nails, alopecia, lanugo on the arms and sides of their face, and dry skin and hair.3,14 Acrocyanosis, alopecia, hypercarotenemia, and knuckle calluses also known as Russel’s sign have been noted.3 Russel’s sign is indicative of self-induced vomiting in BN patients.3 Hypercortisolism, growth retardation or short stature, low T3 syndrome and partial diabetes insipidus or an inability to concentrate urine has been noted in adolescents with ED.3  P a g e 14 | 53 The skeletal ramifications are detrimental and include osteoporosis, osteopenia, and fractures.3 As a disease characterized by low bone mass and deterioration of the microarchitectural structure of the bone, osteoporosis results in bone fragility and nontraumatic fractures due to low bone mass.23 Osteoporosis is present in almost 40% of patients with AN, while osteopenia is present in 92%. This is particularly of concern as peak bone mass generally occurs between the ages of 17 and 22, which often coincides with the onset of AN.23 Once amenorrhea is present, the estrogen-progesterone deficiency plays a role in hindering bone development and promoting bone resorption.23 In addition to the hypothalamic hypogonadal state addressed above, excess hydrocortisone secretion, low insulin-like growth factor 1 (IGF-1), and low androgen levels are often present.14 Low levels of IGF-1 reduce the levels of osteocalcin and can cause abnormalities in osteoblasts.23 The elevated cortisol levels are also inversely related to levels of osteocalcin.23 All of these factors together, are likely to promote the rapid and aggressive bone loss in individuals.23 Other signs of ED include poor dentition in BN and complaints of fatigue, peripheral edema, and bloating.3,14 Fluid and electrolyte imbalances are a major concern for those with ED. Laboratory results such as blood count and electrolytes should be reviewed. In more severe cases of AN, anemia, leukopenia, hypoglycemia, and hypophosphatemia have been noted.14 The more concerning electrolyte abnormalities occur in the early stages of refeeding in patients with AN.14 Refeeding syndrome is the clinical complications that can occur as the result of fluid and electrolyte shifts during aggressive nutritional rehabilitation of malnourished patients and can potentially be fatal when not detected or treated early in nutritional rehabilitation.44 When reintroducing glucose into the diet it stimulates insulin secretion to help promote uptake of glucose as well as potassium, magnesium, and phosphorus into the cells.14 Phosphorus is then used for protein and glycogen synthesis and is quickly depleted.14 This process leads to a state of hypophosphatemia that causes adenosine triphosphate depletion which impairs muscle contraction in the heart and diaphragm resulting in cardiopulmonary failure.14 Additionally, the increased uptake of magnesium and potassium into cells further contribute to cardiac arrhythmias and muscle weakness.14 In BN patients, lab results can point to metabolic alkalosis, hypochloremia, and hypokalemia.14 The frequency of hypokalemia and hypochloremia in patients who purge through vomiting has been shown to be related to the frequency of daily purging.14 In one study, more than 40% of patients who purged twice a day or more became hypokalemic.14,45 Hypokalemia puts them at risk for atrial and ventricular arrhythmias. Both vomiting and diuretics produce a contraction alkalosis secondary to dehydration and subsequent activation of the renin-angiotensin system.14 Pseudo-Bartter syndrome may develop due to purging and creating a chronic state of dehydration and hypokalemia.14 When the renin-angiotensin system is stimulated, it causes an increased amount of aldosterone to be secreted, which then attempts to restore intravascular volume via increasing sodium absorption in the distal convoluted tubule, but at the expense of potassium and hydrogen excretion. This is important to note as aggressive fluid administration can lead to rapid and severe edema.14 Other known fluid and electrolyte imbalance complications in ED patients include decreased glomerular filtration rate, elevated blood urea nitrogen (BUN), hyponatremia, and ketonuria.3,14