THE PRESENCE OF EATING DISORDER TENDENCIES IN FEMALE ADOLESCENT PATIENTS WITH DEPRESSION, ANXIETY OR SUBSTANCE ABUSE: EATING ATTITUDES

AND BODY IMAGE DISTURBANCES

A Dissertation Presented to the Faculty of the College of Health Sciences of TUI University In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy in Health Sciences

by Nadine King September 2009

UMI Number: 3405319

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 2009 Nadine King

TUI UNIVERSITY COLLEGE OF HEALTH SCIENCES CYPRESS, CALIFORNIA 90630

THE PRESENCE OF EATING DISORDER TENDENCIES IN FEMALE ADOLESCENT PATIENTS WITH DEPRESSION, ANXIETY OR SUBSTANCE ABUSE: EATING ATTITUDES AND BODY IMAGE DISTURBANCES This dissertation, written by Nadine King Submitted to the Faculty of TUI University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY IN HEALTH SCIENCES Approved by: __________________________________ Dr. Edith Neumann, VP for Academic Affairs ___________________________________ Dr. Mihaela Tanasescu, Doctoral Program Director Date:_________________________________ We, the undersigned, certify that we have read this dissertation and approve it as adequate in scope and quality for the Doctor of Philosophy. Dissertation Committee: _________________________________ Chair, Dr. Sana Ghaddar _________________________________ Member, Dr. Frank Gomez ______________________________________ Member, Dr. Marian Levy

BIOGRAPHICAL SKETCH Nadine Kings career of over 30 years in the field of Nutrition began after graduation from Hunter College of the City University of New York with a BS, then an MS, in Nutrition. She has worked in nursing homes as a consultant and Food Service Director for 27 years. In addition, she has worked in home health, hospital dietetics, and teaching and has been a member of a university research team in the area of lipid research. Presently she treats private patients as well as serves as a consultant to several assisted living facilities. As a Registered Dietitian, she has grown to appreciate the importance of proper nutrition in the overall health of our population. She has worked with ethnically and culturally diverse populations in order to adapt the principles of her profession to the lifestyles of those who have different religious and/or cultural issues as relate to food choices and methods of preparation. King was introduced to the area of eating disorders through her work at a university clinic in Tennessee, where she was asked to utilize her knowledge as a part of the treatment team consisting of an MD and a therapist. Multidisciplinary treatment for eating disorders is now the standard of care. She then became involved in the Eating Disorder Coalition

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of Tennessee. Upon receiving her PhD, she plans to continue her clinical work as well as teach the principles of nutrition and attitudes towards food to the medical and lay communities. We are now facing challenges presented by the rise in lifestyle-related diseases in America and Western Europe. King hopes to enhance her ability to make significant contributions to our society. On a personal level, she is married to a physician and has two adult children. She was born and raised in New York. She relocated to Memphis, Tennessee in 1977.

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I dedicate this paper to the four special men in my life: To my father, Myron, who was always there for me with encouragement and advice. To my husband, Paul, who has been critiquing my work since high school and who is so special and patient and has been looking forward to the completion of this PhD. To my son, Marc, who came to the house for every online class to assist me with the computer in order to hear/see the lecture, send my work, and teach me the ins and outs of the computer age. To my son, Scott, who called to see how the classes were progressing and always asked, Did the computer give you difficulty tonight?

ACKNOWLEDGEMENTS I give special thanks to the following people who have given me support throughout this odyssey process of writing a dissertation so that I may place three more letters (PhD) after my name: James Lock, MD, PhD, from Stanford, who reviewed the outline and gave me early direction; David M. Garner, PhD, for giving me permission to use the EAT-26; Dr. Jan H. Rosenvinge for a discussion of his questionnaire; and the dissertation chair, Sana Ghaddar, RD, PhD, and committee members, Frank Gomez, PhD, and Marian Levy, Dr.PH, RD, for their input, revisions, and vision. Grateful acknowledgement is given to my former professors during my bachelors program, Dr. Mary Ludden and Dr. Lenora Moragne, who have remained my sounding boards during these many years. Thanks to my husband, Dr. Paul King, for his insights into the teenaged mind and to my many colleagues and friends for their support. Finally, thanks to the clients and facilities that participated in the study. This dissertation is about young people needing to change a complex set of patterns of behavior. I hope that in a small way I have been able to be of service.

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TABLE OF CONTENTS LIST OF TABLES<<<<<<<<<<<<<<.<.<<<.. ix LIST OF FIGURES<<<<<<<<<<<<<<.<<<<. xi LIST OF ABBREVIATIONS<<<<<<<<<<..<<..<.. xii CHAPTER 1: Introduction<<<<<<<<<<<...<<< 1 CHAPTER 2: Problem Statement<<<<<<<<<<<< 5 Research Questions<<<<<<<<<<<<.<< 6 CHAPTER 3: Literature Review<<<<<<<<<<<<.. 8 Diagnostic Criteria and Medical Complications<<<<<<<<..<< 9 Epidemiology of Eating Disorders<<<<.<<<.. 16 Risk Factors for Eating Disorders<<<<<<.<< 19 EDNOS<<<<<<<<<<<<<<<<<.<< 44 Treatment of Eating Disorders<<<<<<<<<. 45 The Concept of Disordered Eating<<<<.<<<.. 58 The Concept of Loss of Control (LOC)<<<<<<. 59 CHAPTER 4: Conceptual Framework<<<<<<<<<< 61 CHAPTER 5: Hypothesis/Research Questions<<<<.<<. 65 CHAPTER 6: Methodology<<<<<<<<<<<<<<.. 71

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Characteristics of the Study Population<<<<<<<<<<<<<<<. 87 Summaries of Research Questions<<<<<<<.. 97 CHAPTER 7: Limitations/Delimitations<<<<<<<<< 102 Discussion<<<<<<<<<<<<<<<<<< 106 CHAPTER 8: References<<<<<<<<<<<<.<<<.. 114 APPENDIX<<<<<<<<<<<<<<<<<.<<<<. 140

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LIST OF TABLES Table 1: Research Questions, Study Variables, and Statistical Tests<<<<<<<<<<<<<<<<<<.

83

Table 2: Sample Size in Adult Co-morbidity Studies<<<<. 85

Table 3: Demographics of the Study Population<<<<<<

89

Table 4: Hospital vs. Community Group Analysis<<<<<

92

Table 5: Study Variable Differences and Risks in Psychiatric and Community Groups (N=144)<<<<<<<. 94

Table 6: Analysis of Participant Characteristics and Diagnostic Tests<<<<<<<<<<<<<<<<<...

96

Table 7: Comparisons Between Hospital and Community Populations<<<<<<<<<<<<<<<<

96

Table 8: Observation of Risks (EAT-26/BSQ-34) Between Groups (Hospital vs. Community)<<<<<<<<<<<...

97

Table 9: Age Distribution Between Groups (Hospital vs. Community)<<<<<<<<<<<<<<<<<<<<<. 99

Table 10: BMI Distribution Between Groups (Hospital vs. 100 Community)<<<<<<<<<<<<<<<<<<<<<.

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Table 11: Predictors of Risk of Developing an Eating Disorder<<<<<<<<<<<<<<<<<<<<<<<

101

Table 12: Study Limitations and Recommendations<<<<.

103

LIST OF FIGURES

Figure 1: Conceptual Framework<<<<<<<<<<<<

63

Figure 2: Distribution of Clients Throughout Study & Attrition Rate<<<<<<<<<<<<<<.<<<<<.

88

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LIST OF ABBREVIATIONS AN = Anorexia Nervosa BDD = Body Dysmorphic Disorder BDI = Beck Depression Inventory BMI = Body Mass Index BSQ-34 = Body Shape Questionnaire-34 BN = Bulimia Nervosa CBT = Cognitive Behavioral Therapy CIDI = Composite International Diagnostic Interview DSM-IV-TR = Diagnostic & Statistical Manual of Mental Disorders, Fourth Edition, Text Revision EAT-26 = Eating Attitude Test-26 EDI = Eating Disorder Inventory EDNOS = Eating Disorder Not Otherwise Specified FDA = Food and Drug Administration GAD = Generalized Anxiety Disorder GI = Gastrointestinal MINI = Mini International Neuropsychiatric Interview NPL = Nonparametric Linkage OCD = Obsessive Compulsive Disorder

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PANSS = Positive and Negative Syndrome Scale RD = Registered Dietitian SSRI = Selective Serotonin Reuptake Inhibitor YRBS = Youth Risk Behavior Surveillance

xiii

THE PRESENCE OF EATING DISORDER TENDENCIES IN FEMALE ADOLESCENT PATIENTS WITH DEPRESSION, ANXIETY OR SUBSTANCE ABUSE: EATING ATTITUDES AND BODY IMAGE DISTURBANCES

Nadine King, PhD TUI University 2009

ABSTRACT The objective of this study was to examine the prevalence of eating disorder symptoms and body image disturbance in a group of adolescent females. The study included two groups: inpatient group recruited from a psychiatric hospital diagnosed with mood disorder and/or substance use disorder, and a community group recruited from the schools. The study measured attitude toward eating and body image using the EAT-26 and the BSQ-34. No significant differences were observed in the risk of developing an eating disorder between the psychiatric group and the community group (x2 (1) = 2.29, p > .05). A significant difference was observed in age (t (144) = -.614, p < .01) and Body Mass Index (t (122.72) = 3.57, p < .01). Body Mass Index and anxiety were shown to be significant predictors of disordered eating in both

study groups. Predictors of increasing the risk of developing an eating disorder were BMI (OR = 1.17, 95% CI 0.800, 0.946), Group (OR = 1.43, 95% CI 0.729, 3.255 and Anxiety (OR = 1.11, 95% CI 0.839, 0.924). We can conclude that eating disorder risk factors are more prevalent among females suffering from problems related to being overweight and anxious. Therefore, public health efforts should focus on helping young girls cope with anxiety to prevent development of co-morbidities related to unhealthy eating.

CHAPTER ONE Introduction

Eating disorders are a serious and growing problem with both psychiatric and medical consequences, including death. Of the three categories of eating disorder, anorexia nervosa (AN) may be the least common but has the highest mortality rate of 10% after 10 to 20 years of illness. The three categories of eating disorders are AN, bulimia nervosa (BN), and eating disorder not otherwise specified (EDNOS). Eating disordered individuals show disturbed eating behavior as well as a perceptual disturbance about body shape and/or weight. From a developmental perspective, acceptance of ones body shape and image is an important task in the adolescent years. Anorexia Nervosa is defined as a disorder characterized by a prolonged refusal to eat, resulting in emaciation, amenorrhea, emotional disturbance concerning body image, and fear of becoming obese (APA, 2000). BN is defined as a disorder characterized by an insatiable craving for food, often resulting in episodes of continuous eating, often followed by purging (APA, 2000). In a study that examined 36,320 public school students (French, Stacy, Downes, Resnick, & Blum, 1995), the

researchers found that dieting or perception of the need to diet were strongly related to fear of being unable to control eating and to poor body image. Those with the most severe symptoms developed an eating disorder, primarily BN (Fairburn, Cooper, Doll, & Welch, 1999). Many patients, especially adolescents, who present for treatment of an eating disorder do not meet full diagnostic criteria for AN or BN and are therefore classified as having EDNOS. Eating disorder not otherwise specified represents the largest population of eating disordered patients who present for treatment. Additionally, the prevalence of co-morbid psychiatric illness in the patient with an eating disorder has an impact on the treatment of the patient. There are no studies at present that examine co-morbid eating disorder symptoms of psychiatrically disturbed adolescents. This is a serious gap in our scientific knowledge, especially since co-morbidity is more the norm than the exception in child and adolescent psychiatry. Adolescent anxiety disorders and disruptive behavioral disorders have frequently been found to be co-morbid with depression. Adolescents with substance use disorder may also have co-morbid disorders that must be addressed and treated. Current research has focused on the following co-morbid disorders associated with

substance use disorders: attention-deficit hyperactivity disorder (ADHD), bipolar disorder, and major depression. Anorexia Nervosa, BN, and EDNOS have not as yet been identified as co-morbid disorders. The research supports integrative treatment models for substance abuse and co-morbid psychiatric disorders. If in the substance-abusing adolescent female population there is a significant degree of eating disorder pathology, then this co-morbidity would also have to be addressed. To date, there have been no published studies taking a look at this possible co-morbidity. The study described here examined the prevalence of missed cases of adolescents at risk of developing an eating disorder, as measured by participants scores on the Eating Attitudes Test-26 (EAT-26), pertaining to perception of food, and the Body Shape Questionnaire-34 (BSQ-34), pertaining to perception of body image. This study also attempted to identify predictors that might increase adolescents risk of developing symptoms of an eating disorder, so that more emphasis could be placed on prevention among this identified patient population. Results gained from this study may increase awareness of predictive factors and lead to appropriate family and/or treatment interventions. Eating disorder co-morbidity must be assessed and treated when adolescents present

for psychiatric and/or substance abuse treatment. This will improve the prognosis and outcome as these young individuals enter adulthood.

CHAPTER TWO Problem Statement

The recognition and effective management of eating disorders is a significant and meaningful problem that lends itself to a research effort. Achieving and maintaining normal body weight and a normal pattern of eating are essential components of adolescent development. Many adolescent girls who are diagnosed with mood disorders, anxiety disorders, and substance use disorders also have dysfunctional cycles of chaotic eating patterns. These often are not recognized and/or not treated. The behavior, though, is so dysfunctional that it affects social relationships. Twerski (1977) stated that the absence of self-esteem is found in every eating problem. I hope to show that eating disorders are far more common as a component of the psychopathology of disturbed adolescent girls than has been previously thought. Thus far there have been only five randomized, controlled studies that focused on adolescents with AN. In BN, there have been no adolescent studies; the only published studies, to the best of my knowledge, focused on adults. EDNOS, which represents the largest of the eating disorder treatment populations, has not been studied at all. The numbers of patients studied is

very small due to the rigorous criteria used to make a diagnosis of an eating disorder according to the American Psychiatric Associations Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR). This paper hopes to broaden the conceptualization of eating disorders by showing their prevalence in a psychiatric population in treatment for other disorders.

Research Questions

Research Question I Do psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder have a higher risk of developing an eating disorder, based on EAT-26 score > 20 and/or a BSQ score > 110, when compared with healthy student female participants drawn from the community?

Research Question II Do psychiatrically disturbed and substance-abusing, adolescent, hospitalized females not previously diagnosed with an eating disorder have a difference in age when compared with healthy female student participants drawn from the community?

Research Question III Do psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder have a difference in body mass index (BMI) distribution for developing an eating disorder, when compared to healthy female student participants drawn from the community?

Research Question IV What are the predictors of increased risk of developing an eating disorder among psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder, as well as healthy student female participants drawn from the community?

CHAPTER THREE Literature Review

Eating disorders in the child and adolescent population can lead to serious medical and psychiatric problems. The prevalence rates of eating disorders are estimated to be 0.5% to 5% of adolescent females. Severe consequences can include premature death or lifelong morbidity (Fisher, Golden, & Katzmon, 1995; Steiner & Lock, 1998). AN is characterized by a refusal to maintain body weight at or above a minimal normal weight (<85% of expected weight for age and height or body mass index <17.5 kg/m2) or a failure to show the expected weight gain during growth. People diagnosed with AN often have an intense fear of gaining weight, are preoccupied with weight, and have denial of their current low weight. There are two subtypes of AN: binge-purge and restrictive. Patients who meet all clinical criteria for AN but continue menses are diagnosed with EDNOS. These patients often regularly use inappropriate measures for weight control, such as chewing and spitting out food or purging. On the other hand, patients with BN have recurrent episodes of binge eating and compensatory behavior to prevent weight gain (e.g., vomiting, laxative abuse, diuretics, and enemas). Both

anorexia and bulimia may feature excessive exercise. However, individuals with bulimia are often in the normal range of body weight (APA, 2000).

Diagnostic Criteria and Medical Complications Diagnostic Criteria for Anorexia Nervosa The diagnostic criteria for AN are found in the DSM-IV-TR and are as follows (APA, 2000): A. Refusal to maintain body weight at or above a minimally normal weight for age and height (i.e., weight loss leading to maintenance of body weight <85% of that expected; or failure to make expected weight gain during period of growth, leading to body weight <85% of that expected). B. Intense fear of gaining weight or becoming fat, even though classified as being underweight for age and height. C. Disturbances in the way in which ones body weight or shape is experienced, undue influence of body weight or shape on selfexamination, or denial of the seriousness of the current low body weight. D. Existence of amenorrhea in postmenarchal females, with the absence of a least three consecutive menstrual cycles. A woman is considered to have amenorrhea if her periods occur only following hormone therapy estrogen administration.

10 Specific Type of Anorexia Nervosa. a) Restricting Type: During the current episode of AN, the person has not regularly engaged in binge-eating or purging behavior (e.g., selfinduced vomiting or the misuse of laxatives, diuretics, or enemas). b) Binge-Eating/Purging Type: During the current episode of AN, the person has regularly engaged in binge-eating or purging behavior (e.g., self-induced vomiting or the misuse of laxatives, diuretics, or enemas).

Medical Complications of Anorexia Nervosa Patients diagnosed with AN have weight markedly decreased due to malnutrition. They often display sunken cheeks, prominent bony protuberances, and muscle wasting. They choose to wear thick layers of clothing due to low body temperature, have acrocyanosis (coldness and blueness) of the hands and feet, have fine downy hair (lanugo) that is present over the arms, back, and abdomen, and have dry and brittle scalp hair. They also have low resting pulse and low blood pressure on standing (Shamire, Golden, Arden, Filiberto, & Shenker, 2003). Electrocardiogram abnormalities including prolonged QTc intervals may result in ventricular arrhythmias and sudden death (Isner, Roberts, Heymsfield, & Yager, 1985). Hematologically, patients diagnosed with AN tend to have low white blood cell, red blood cell,

11

and platelet counts. Leukopenia (low white blood cell count) is seen as secondary to bone marrow suppression (Sharp & Freeman, 1993). Gastrointestinal (GI) problems associated with AN include constipation and bloating from delayed gastric emptying and decreased GI motility. Metabolic rate slows down due to starvation, decreased lean body mass, and decreased caloric requirements. In contrast to other forms of malnutrition, serum albumin levels are usually normal. Endocrine changes associated with AN includes pubertal delay and amenorrhea, with low levels of the pituitary and ovarian hormones that control menstruation. In most instances, the amenorrhea is associated with weight loss, but in 20% of cases the loss of menses preceded significant weight loss (Golden, 1997). Amenorrhea is usually caused by a combination of malnutrition, increased exercise, emotional stress, and low body weight. Activation of the hypothalamic-adrenal axis causes high levels of serum cortisol to be produced. The most serious complication of prolonged amenorrhea and low estrogen state is a substantial decrease in bone mass, or osteopenia (Bachrach, Guido, Katzman, Litt, & Marcus, 1990; Mahasmita, 2003; Soyka, 2002; Soyka, Grinspoon, Levitsky, Herzog, & Klibanski, 1999). Osteopenia is related to a combination of poor nutrition, low body weight, excessive exercise, high cortisol, and estrogen deficiency. Osteopenia in girls

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with anorexia is more severe than that seen in women with other conditions. Adolescence is a critical time for formation of bone mass, which will not occur with anorexia. Young girls diagnosed with AN are at increased risk of bone fractures, and osteopenia that occurs in adolescence may not be completely reversible (Soyka, 2002). A study of women who had been in recovery from AN for an average of 21 years reported a positive correlation between the presence of pathological bone fractures and a lower bone mineral density of the hip when compared to controls (Hartman et al., 2000).

Diagnostic Criteria for Bulimia Nervosa The DSM-IV-TR diagnostic criteria for BN are as follows (APA, 2000): A. Recurrent episodes of binge eating, defined as an episode of binge eating characterized by both of the following: a. Eating in a discrete period of time (e.g., within any two-hour period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances. b. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much is eaten).

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B. Recurrent inappropriate compensatory behavior in order to prevent weight gain (e.g., self-induced vomiting, misuse of laxatives, diuretics, enemas, or other medications, fasting, or excessive exercise). C. Both binge eating and inappropriate compensatory behaviors both occur, on average, at least twice a week for at least three consecutive months. D. Self-evaluation is unduly influenced by body shape and weight. E. The disturbance does not occur exclusively during episodes of Anorexia Nervosa. Criterion A for BN, as mentioned above, addresses amount and duration of binge eating, as well as the accompanying psychological state. Some individuals with bulimia, however, do not eat large amounts but are nonetheless focused on the loss of control. Criterion B for BN covers misuse of laxatives and excessive exercise. Excessive exercise is defined as continuous excessive exercise for a minimum of twice a week for three consecutive months. This helps to differentiate BN from EDNOS. Criterion D reflects perception of ones body. Specific Type of Bulimia Nervosa. a. Purging Type: During the current episode of BN, the person has regularly engaged in self-induced vomiting or the misuse of laxatives, diuretics, or enemas.

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b. Nonpurging Type: During the current episode of BN, the person has used other inappropriate compensatory behaviors, such as fasting or excessive exercise, but has not regularly engaged in self-induced vomiting or the misuse of laxatives, diuretics, or enemas.

Medical Complications of Bulimia Nervosa In patients with bulimia, hypokalemia (reduced potassium) is the most frequently found electrolyte disturbance. Hypokalemia is associated with vomiting or diuretic use and can result in cardiac arrhythmia. Patients may suffer from muscle weakness, congestive heart failure, cardiac arrest, and even sudden death due to excessive use of ipecac, which induces vomiting (Schiff et al., 1986). As a result of binge eating and vomiting, 10% to 30% of patients with BN may have enlargement of the parotid and salivary glands (Ogren, Hueiler, Pearson, Antonson, & Moore, 1987). Recurrent vomiting may also increase erosion of the dental enamel, owing to stomach acid, and as evidenced on the anterior teeth. Additionally, patients with BN may suffer from gastroesophageal reflux disease, esophagitis leading to chest pain, and even esophageal rupture. Small tears in the esophagus may sometimes be inferred from blood present in the vomit.

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Diagnostic Criteria for Eating Disorder Not Otherwise Specified The diagnostic criteria for EDNOS according to DSM-IV-TR are as follows (APA, 2000): A. All of the criteria for AN are met, except that the individual has regular menses. B. All of the criteria for AN are met, except that, despite substantial weight loss, the individuals current weight is in the normal range. C. All of the criteria for BN are met, except that binges occur at a frequency of less than twice a week or for the duration of less than three months. D. The individual is of normal body weight and regularly engages in inappropriate compensatory behavior after eating small amounts of food (e.g., self-induced vomiting after the consumption of two cookies). E. The individual repeatedly chews and spits out, but does not swallow, large amounts of food. F. Binge-eating disorder (i.e., recurrent episodes of binge eating in the absence of the regular use of inappropriate compensatory behaviors characteristic of BN).

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Epidemiology of Eating Disorders Prevalence rates of AN and BN appear to vary from 1% to 3%, respectively, and among men the incidence is approximately one-tenth of that in women (Hoek & VanHoeken, 2003). Anorexia Nervosa has become the third most common chronic illness among adolescent girls after obesity and asthma (Lucas, Beard, OFallon, & Kurland, 1991). Chronic AN with longterm morbidity has a mortality rate of 3% to 10%, with suicide occurring in up to 5% of patients diagnosed (Steiner & Lock, 1998). In a study of ethnic differences and body image concerns at Yale University, it was found that Caucasian girls had a significantly higher level of dietary restraint and body image dissatisfaction than Hispanic girls or African American girls (White & Grilo, 2005). While no prevalence figures are available for EDNOS, it is important to keep in mind that EDNOS can apply to those individuals who engage in inappropriate compensatory behaviors. Data indicate that a number of women will purge, spit out food, and abuse diet pill and/or diuretics in an effort to reduce their weight (Roerig et al., 2003). A study by Guarda, Coughlin, and Cummings (2004) looked at adolescents who chew and spit out food. Garry and colleagues (2003) described the abuse of diet pills by teenage

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girls. Bell and colleagues (2004) examined abuse of over-the-counter herbal weight loss supplements. The U.S. Food and Drug Administration (FDA) recently banned the sale of over-the-counter diet supplements containing ephedra following reports of medical complications and death (FDA, 2004). Clearly, further studies are needed that incorporate the severely disturbed population that represents the majority of eating disorders presenting for treatment. Studies indicate that AN has a younger age of onset compared with BN. The incidence of all eating disorders is less than 2.8% by the age of 18 and 1.3% by ages 19 to 23 (Lewinsohn, Striegel-Moore, & Seely, 2000). The onset of AN typically occurs during the peripubertal or postpubertal period (Lucas, Beard, OFallon, & Kurland, 1988 & 1991). Prepubertal AN does exist, but it is uncommon. However, disturbances in eating and weight-related behaviors are clearly present among preadolescent girls (Sands, Tricker, Sherman, Asmatas, & Maschette, 1997). There is no definitive answer as to why puberty increases the risk of AN, but one theory suggests that puberty increases a girls vulnerability to pressure to be thin in the context of a changing body (Gowers & Shore, 2001).

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Although most studies show the majority of patients diagnosed with AN to be White women, there is growing evidence of eating disorders among women of color (Chamorro & Flores-Ortiz, 2000; Davis & Katzman, 1999; French et al., 1997). In a study of Black and Hispanic women at Yale University, it was found that eating concerns plus depressive affect was a significant predictor of body image concern (Hrabosky & Grilo, 2007). Further, while dieting and emphasis on weight and body image are common in highly developed countries (Striegel-Moore, Silberstein, & Rodin, 1986), evidence of AN on Curacao shows that it occurs in other countries as well (Hoek, vanHartere, vanHoekin, & Susser, 1998). Exposure to cultural ideals of thinness seems almost universal, especially in Western countries, but only a small percentage of the population will develop an eating disorder. There may be a genetic predisposition to the susceptibility to cultural pressure (Bulik et al., 2003). A link has been found between parental education and AN in a large population study of female twins (Walters & Kendler, 1995). In an epidemiological study of 1,713 youths hospitalized with an eating disorder, 92% were female, and 78% were non-Hispanic White with a mean age of 15.3 years (Calderon, Vanderstoep, Collett, Garrison, & Toth, 2007).

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A study of 902 high school students found that 13.7% of the girls tested had a positive score on the EAT-26, indicating abnormal eating attitudes. Positive scores were correlated with low self-esteem and problematic relationships with one or both parents (Saporetti, Sancini, Bassoli, Castelli, & Pellai, 2004).

Risk Factors for Eating Disorders

Female Sex as a Risk Factor Being female is probably the single most reliable risk factor for AN. One study utilized the Survey for Eating Disorders questionnaire to examine female versus male prevalence of eating disorders in a sample of 1,960 adolescents (1,026 girls and 934 boys), all 14 to 15 years of age. Among the girls, lifetime prevalence was 0.7% for AN and 1.2% for BN. Among the boys, the prevalence 0.2% for AN and 0.4% for BN. Prevalence of EDNOS was quite high among both sexes, at 14.6% for females and 5% for males (Kjelsas, Bjormstrom, & Gotestam, 2004). A literature review by Hoek and van Hoeken (2003) found that the prevalence rate for BN was 1% among women and 0.1% among men; for AN, the prevalence was 0.3% among women and statistically insignificant among men. These findings were similar to those of a large study that included 8,116

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Ontario residents, in which the female to male ratio of BN was 10 to 1 (Garfinkel et al., 1996). AN typically occurs during the peripubertal or postpubertal period (Lucas, Beard, OFallon, & Kurland, 1991). Disturbances in eating behavior are clearly present in preadolescent girls (Graber, Brooks-Gunn, Parkoff, & Warren, 1994), but the period of highest risk coincides with puberty (Lucas et al., 1991). During puberty, girls may be more vulnerable to pressure to be thin as their bodies are changing (Gowers & Shore, 2001). Weight concerns and dieting are normative in developed countries, but the precise role of sociocultural factors in increasing risk for AN is unclear. A large percentage of movie stars in magazines are quite thin, but only a small number develop an eating disorder. Perfectionism is thought to play a role in increased risk for developing an eating disorder (Bulik et al., 2003). Female sex appears to be a risk factor across ethnicities. French and colleagues (1997) collected data from 17,159 ethnically diverse adolescent females in a school survey in which body dissatisfaction and a perception of being overweight were correlated with dieting and binge eating. Ethnic subcultures do not appear to protect against broader cultural influences in the United States.

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Chamorro & Florez-Ortiz (2000) studied 139 Mexican American women using the Eating Attitudes Test-26 (EAT-26). The study showed that second generation women had a positive correlation with the part of the EAT that deals with control of eating and perceived pressure from others to gain weight. The differing of the values in different generations of Mexican American women appears to create special pressures that may lead to disordered eating.

Perinatal Risk Factors Shoebridge & Gowers (2000) noted a higher rate of maternal anxiety during pregnancy among the mothers of girls who developed eating disorders. Forty consecutive referrals of adolescent girls diagnosed with AN were compared with controls in a case control method. Significant indices of high maternal anxiety (p < .008) and later age for first sleeping away from home (p < .009) were reported. Other indices include near exclusive childcare (p < .02) and infant sleep difficulties (p < .048). Therefore, maternal anxiety may be a contributor to later development of AN in daughters. Favaro, Tenconi, & Santonastaso (2006) looked at the obstetric records of subjects with AN, BN, and no eating disorder. All subjects at Padua Hospital in Padua, Italy were studied via medical records from January 17,

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1971 to December 30, 1979. The sample comprised over 114 patients with AN, 73 patients with BN, and 554 controls. Maternal complications such as anemia, diabetes mellitus, pre-eclampsia, placenta infarction, neonatal cardiac problems, and hyperactivity were shown to be significant predictors of AN. Each maternal factor independently had a p value < .05. The risk of developing AN increases with the total number of obstetrical complications. Significant obstetrical complications for BN included neonatal hyporeactivity, early eating problems, and low birth weight for gestational age.

Personality Traits as Risk Factors Andeluh, Tchanturia, Rabe-Hesketh, and Treasure (2003), in a case control study, retrospectively looked at a sample of adult women with eating disorders to assess the predictive value of childhood obsessive-compulsive personality (OCD). Forty-four women with AN, 28 women with BN, and 28 healthy controls with no psychiatric disorder and no medical problems were interviewed and completed a self-report inventory. Childhood obsessive personality traits had a high predictive value for the development of eating disorders. The estimated odds ratio increased by a factor of 6.9 for each obsessive trait (95% CI = 2.9 16.4, p < .001). Women with childhood

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perfectionism and rigidity had significant higher rates of co-morbid OCD in addition to the eating disorder. A prospective study from Spain sampled 2,562 girls aged 12 to 21 years for a baseline assessment in a longitudinal study (Gual et al., 2002). The goal was to study the relationships of self-esteem and personality with eating disorders. Since this was a baseline assessment, the study was cross-sectional using multivariable logistic regression of a 36-item self-esteem scale and the Eysenck inventory scale. Eating disorders were strongly associated with low self-esteem (7.98, 95% CI = 3.48.8) and high levels of neuroticism (9.49, 95% CI = 3.724.5). Other researchers have also looked at perfectionism as a risk factor for an eating disorder. Bulik and colleagues (2003) interviewed female twin pairs born from 1934 to 1974 a total of four times between 1988 and 1997. Three perfectionism subscales were used: concerns over mistakes, personal standards, and doubts about actions. Univariate logistic regression analysis showed the odds ratios for concerns over mistakes to be 1.88 (p < .01) for AN and 1.96 (p < .0001) for BN, compared with 1.11 for major depression and 0.75 for alcohol abuse/dependence (p < .05). Doubts about actions had odds ratios of 2.27 (p < .001) for AN and 2.02 (p < .001) for BN. Therefore, concerns over

24

mistakes and doubts about actions were significantly associated with both AN and BN but not with other psychiatric disorders. Even after remission of symptoms for the disorder of AN or BN, traits like perfectionism continue to be persistent. Srinivesagam and colleagues (1995) tested 20 subjects who seemingly had recovered from AN. They were at normal weight with regular menses for one year. These subjects were compared with 16 controls. The instruments used were the Eating Disorder Inventory (EDI) and two different scales for perfectionism. Compared with controls, the women with a history of AN had a greater need for order and precision, even after recovery. Disordered eating, too, tends to be persistent. Kother and colleagues (2001) studied 800 children and their mothers. Subjects received DSM-based assessment in 1975, 1983, 1985, and 1992. Early onset BN was associated with a 9-fold increase in risk for late adolescent BN and a 20-fold increase in risk for adult BN. If BN developed in late adolescence, there was a 35-fold increase in risk for adult BN.

Parental Obesity as a Risk Factor Parental obesity is more of a risk factor for BN than for AN (Fairburn, Welch, Doll, Davies, & OConnor, 1997). A study looking at parental weight

25

of women with AN showed no correlation, in that parents weight was not different than that of controls (Halmi, Stuess, & Goldberg, 1978).

Dieting as a Risk Factor The prevalence of dieting, defined as a restricted intake of calories with the goal of losing weight, has been estimated to be between 14% and 77% (French, Perry, Leon, & Fulkerson, 1994). French and colleagues (1995) studied 33,393 adolescents in grades 712, using a health behavior survey. Differences in psychosocial and health behavior risk factors by frequently dieting and purging were assessed with multivariate logistic regression. Dieting frequency was associated with binge eating (female OR = 1.46, male OR = 1.53) and poor body image (female OR = 0.56, male OR = 0.63). These adolescents also had a greater frequency of alcohol and tobacco use. The above correlation suggests that frequent dieting may be a general adolescent risk taking behavior. Fairburn and colleagues (2005) studied the development of eating disorders in a population of 2,992 young women who were dieting. A questionnaire was given to 17,144 women, and 10,077 (58.8%) questionnaires were returned. Dieting was defined as eating restraint using a subscale from the Eating Disorder Examination Questionnaire. The subjects had a mean age

26

of 19.83 years (SD = 2.36) and a mean BMI of 23.22 (SD = 3.74). The severity of dietary restraint and eating disorder features was assessed using the selfreport Eating Disorder Examination Questionnaire as well as an Eating Disorder Examination, an interview technique developed by Dr. Fairburn. Assessment occurred on four occasions over two years. Participants who did and did not develop an eating disorder were compared in terms of their scores on the global subscale of the Eating Disorder Examination. Follow-up with the questionnaire suggested that 457 respondents might have developed an eating disorder. Ten of the women developed AN (9.6%), 19 developed BN (18.3%), and 75 developed EDNOS (72.1%). Cox regression analysis showed that low BMI, defined as < 19 kg/m2, and high scores on five items of the Eating Disorder Examination Questionnaire were identified as predictive of developing an eating disorder. The items were preoccupation with food and eating, desire to have an empty stomach, frequency of purging, fear of losing control over eating, and preoccupation with shape or weight. The study correctly identified 70% of future diagnoses (95% CI = 60.2 78.8) with a 25% rate of false positives (95% CI = 73.4 76.8). The dieters who developed eating disorders had more disturbed eating habits than those who did not, as well as features such as eating in secret, fear of losing control, and desire to have a completely empty stomach.

27

The National Task Force on the Prevention and Treatment of Obesity (2000) concluded that dieting and weight loss was not associated with the development of eating disorders.

Co-morbid Psychiatric Disorders as Risk Factors It is known that co-morbid disorders of anxiety, depression, and substance use are found in adults with eating disorders. Godart and colleagues (2000) studied the co-morbidity of eating disorders and anxiety disorders, looking at the presence of anxiety in an eating disorder population. Sixty-three subjects with a diagnosed eating disorder were assessed using the Composite International Diagnostic Interview (CIDI). Eighty-three percent of the subjects with AN and 71% of those with BN had at least one lifetime diagnosis of an anxiety disorder. The most frequent type of anxiety disorder was social phobia. The anxiety disorder predated the onset of the eating disorder in 75% of subjects with AN and 88% of subjects with BN. The same group of investigators (Godart et al., 2003) used the Mine International Neuropsychiatric Interview (MINI) to assess 271 women with AN or BN and 271 community volunteer controls. The rate of anxiety disorders in the group with an eating disorder (71%) was significantly higher than that found in the control group. Similarly, the

28

anxiety disorder preceded the eating disorder. Bulik and colleagues (1997) compared the prevalence and age of onset of the anxiety disorder relative to the primary diagnosis in 68 women with AN, 116 women with BN, 56 women with major depression and no eating disorder, and 98 random controls. In 90% of the women with AN, 94% of those with BN, and 71% of those with major depression, the anxiety disorder preceded the primary diagnosis (p < .01). A multivariate logistic regression showed an odds ratio for overanxious disorder (OR = 11.8) that was elevated for AN. BN had significant elevations in the odds ratios for both overanxious disorder and social phobia. A study of links between eating disorders and psychiatric co-morbidity showed that Axis I anxiety disorders were more closely linked to the severity of eating disorder symptoms than were affective or substance use disorders. Multivariate analysis in a sample of 277 women revealed the correlation of eating disorder symptoms with specific co-morbidities (Spindler & Milos, 2007). A large sample of individuals from the Price Foundation collaborative genetics study was used to investigate the prevalence of anxiety disorders and their relationship to eating disorders and age of onset (Kaye, Bulik, Thornton, Barbarick, & Masters, 2004). First, the demographic and clinical characteristics

29

of 672 patients were noted, and patients were assessed using DSM-IV criteria for anxiety disorders. Second, the mean age of onset of anxiety disorder and eating disorder were determined. Then, the demographic and clinical measures for healthy women were compared to those of women with remitted or active ED. Approximately two-thirds of the eating disordered women reported one or more lifetime co-morbid anxiety disorder, especially OCD (41%) and social phobia, (20%). Again, in the majority of subjects, the anxiety disorder preceded the eating disorder (Kaye et al., 2004). Forty-two percent of the women with eating disorders had one or more anxiety disorders in childhood. Interestingly, even those women who had never had an anxiety disorder and who had been recovered from an eating disorder for at least 12 months nonetheless had higher levels of anxiety and perfectionism than healthy controls. This conclusion, however, has not been reached by everyone. Sodersten and Bergh (2006) argued that when dropout rates were taken into account, the expression of OCD before AN was rare. Their evidence did not support OCD as a risk factor for the development of AN. Further research has examined whether the presence of anxiety disorders is related to depression in subjects with eating disorders. In a recent

30

study, Godart, Curt, Perdereau, and colleagues (2005) administered the MINI to 271 subjects with AN or BN and determined by univariate analysis that nearly all instances of an anxiety disorder were related to a major depressive episode. There were differences in terms of degree of risk. Generalized anxiety disorder (GAD) was the most frequent disorder in AN and BN subjects in this study. A major depressive episode was 2.4 to 4.2 times more frequent when GAD was present. OCD increased the risk of depression by 3.5 and was present in almost 25% of subjects (Godart et al., 2005). In another study of eating disorders with co-morbid OCD, the MINI and the Yale-Brown Obsessive-Compulsive Scale were administered to 89 subjects (aged 1530 years) meeting a DSM-IV diagnosis of eating disorder and to 89 matched controls (Speranza et al., 2001). Current and lifetime prevalence of OCD in subjects with an eating disorder was higher than in the general population (15.7% and 19% versus 0% and 1.1%, p < .05). The authors concluded that eating disorders and OCD share a genetic vulnerability that predisposes individuals to develop obsessional and compulsive symptoms focused on food and body image. In another articulation of data from this population, researchers (Speranza et al., 2001) pointed out that AN patients had a slightly higher current and lifetime co-morbidity than BN patients (19%

31

and 22.4% versus 9.7% and 12.9%). The OCD diagnosis preceded the eating disorder diagnosis. Finally, though, the OCD scores of the underweight patients were not significantly higher than those of the normal weight patients, suggesting that obsessive thinking is not an important characteristic for the development of the eating disorder. Patients with BN have a high rate of co-morbidity with other psychiatric disorders. In particular, high rates of affective disorders, chemical dependency problems, and anxiety disorders have been described among patients and, in some studies, among their relatives. One study examined 31 female patients with BN, 29 women who had been recovered from BN for one year or more, and 19 healthy women. The Yale-Brown Obsessive-Compulsive Scale was administered. The scores of the women with BN (mean = 13.1, SD = 10.6) were significantly higher than those of the recovered women (mean=7.9, SD=7.0), and both these groups scored significantly higher than the controls (mean = 1.9, SD = 2.6). The conclusion reached was that OCD symptoms persisted after recovery (vonRanson, Kaye, Weltzin, Rao, & Matsunaga, 2001). Silberg and Bulik (2005) did a longitudinal study of 408 monozygotic and 198 dizigotic female twin pairs, 8 to 13 years old and 14 to 17 years old, from the Virginia Twin Study of Adolescent Behavioral Development. This

32

study pointed to an association between eating disorders and depression, overanxious disorder, and separation anxiety disorder. These authors also suggested that a genetic factor plays a role in the development of anxiety, depression, and eating disorders throughout development of eating disorder symptoms. Other studies have looked at patients with eating disorders and the occurrence of alcohol abuse. A prospective study at the Harvard Eating Disorders center (Keel et al., 2003) assessed 136 females with AN and 110 females with BN every six to twelve months for 8.6 years. Twenty-seven percent of the sample reported a lifetime history of alcohol use disorder, and 10% developed alcohol use disorder over the course of the study. A substantial number of patients with an eating disorder develop alcohol problems, especially women with depression and those over-concerned with body image. The Washington University St. Louis group studied the relationship between BN and alcohol dependence among women (Duncan et al., 2006). This study sought to determine whether women with BN and alcohol dependence were similar to women who had BN but not alcohol dependence or to women who had alcohol dependence but not BN. The study enlisted 407

33

female relatives from a study of alcoholism. There were 30 women with BN and alcohol dependence, 55 women with BN and no alcohol dependence, and 322 women with alcohol dependence and no BN. Bivariate analysis showed that, compared to the women with only one of these disorders, women with both BN and alcohol dependence were more likely to have drug dependence, conduct disorder, and major depression, and to engage in unsafe sex. The data may suggest that co-morbidity of BN and alcohol dependence was associated with more severe psychopathology. A recent study of co-morbidity of body dysmorphic disorder (BDD) and eating disorders is unique in that it examined a psychiatric population for symptoms of an eating disorder (Ruffolo, Phillips, Menard, Fay, & Weisberg, 2006). Two hundred individuals with a DSM-IV diagnosis of BDD completed questionnaires as well as interviews measuring body image, symptom severity, psychosocial functioning, and quality of life. Results showed that 32.5% of subjects with BDD had had a co-morbid ED: 9% for AN, 6.5% for BN, and 17.5% for EDNOS. Comparisons between the BDD patients with an eating disorder and those without am eating disorder revealed a higher proportion of the group with co-morbidity being hospitalized for psychiatric

34

issues. These findings have implications for the assessment and treatment of co-morbid body image disorders. In a study examining psychiatric co-morbidity in a population with eating disorders at New York Hospital, 86 of 105 inpatients with an eating disorder (81.9%) had depression, anxiety, or substance dependence as a comorbid diagnosis. The patients with restrictive-type AN were more likely than those with BN to have developed an eating disorder before the other Axis I disorders. Ninety-three percent of the population had a co-morbid Axis I disorder, and 69% had an Axis II disorder. Personality disorders were common (Brown, Sunday, & Halmi, 1994). A similar study of 229 women showed 73% of subjects with AN, 60% of subjects with BN, and 82% of subjects with mixed AN and BN symptoms had a current co-morbid Axis I diagnosis, most commonly major depression. (Herzog, Keller, Sacks, Yeh, & Lavari, 1992). The Childrens Hospital in Seattle, using the Pediatric Health Information System database, found a co-morbidity rate of 68% among adolescent inpatients with an eating disorder (Calderon et al., 2007).

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Issues of Attachment in Relationships as a Risk Factor Women with eating disorders tend to be insecure in their attachment with parents and to have fears of abandonment and lack of autonomy in relationships (Kenny & Hart, 1992). The more insecure the mother-daughter relationship is, the greater the disordered eating pathology that is noted (Heesacker & Neimeyer, 1990). A study by Shoebridge and Gowers (2000) showed that girls with AN had high levels of distress at first separation, a later age of sleeping away from home, and a high rate of near-exclusive maternal childcare. Studies of family environment have shown a greater degree of family pathology in BN than in AN. Physical abuse, violence among family members, and excessive parental control were more common for patients with BN (Schmidt, Tiller, & Treasure, 1993), while excessive maternal protectiveness seemed more common for patients with AN (Walters & Kendler, 1995). Individuals with eating disorders report more adverse life events and more problems with interpersonal relationships than healthy controls (Striegel-Moore, Silberstein, & Rodin, 1993). Horesch et al. (1995) found that the adolescents with AN reported more adverse life events compared with

36

healthy controls, and in a study of discordant sisters by Karwantz and colleagues (2001), the sister with AN reported more teasing about breast development.

Genetics as a Risk Factor Family studies have given us clear information that there may be genetic transmission of eating disorders or at least an increased susceptibility to eating disorders within some families. In a study by Strober and colleagues (2000) the rates of eating disorders were obtained for 1,831 relatives of 504 probands using family history and interviews. The relative risk of syndromal AN was 11.3 and 12.3 in the female relatives of anorexic and bulimic probands respectively. The relative risk of BN was 4.2 and 4.4 for the female relatives of anorexic and bulimic probands respectively. The conclusion reached was that eating disorders have a cross transmission in families. The stereotyped clinical signs, sex distribution, and age of onset support a biological vulnerability (Kaye & Strober, 1999). In an epidemiological study examining patterns of co-morbidity and familial aggregation, comparisons were made of risks of eating disorders and psychiatric disorders in firstdegree biological relatives (Lilenfeld et al., 1998). The research team used direct interviews to select subjects with eating disorders and matched

37

controls. The population consisted of 26 females with restrictive AN, 47 females with BN, and 44 female controls, as well as 460 biological relatives. The relatives of both anorexic and bulimic probands showed increased risk of eating disorders, major depressive disorder, and OCD. Risk of substance dependence was elevated among the relatives of bulimic probands compared with the relatives of anorexic probands. Results point to a significantly greater lifetime prevalence of eating disorders among the relatives of individuals with eating disorders as compared with the relatives of non-eating disordered controls. There are also the suggestion that obsessive-compulsive personality traits may be a specific familial risk factor for AN. In a sample of 969 girls with EAT scores > 20, high EAT scores were correlated with high maternal EAT scores (OR = 2.8, 95% CI = 1.55.2; Yanez, Peix, Atseria, Aman, & Brug, 2007). A study involving 6, 916 adolescent girls and 5,618 adolescent boys looked for predictors of eating disorder behavior. The results illustrated that girls under 14 years of age whose mothers had a history of eating disorders were three times more likely than their peers to start purging (OR = 2.8, 95% CI = 1.35.9; Field et al., 2008).

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More recent studies have focused on heritability in terms of specific chromosomes and genes. One multicenter study examined 192 families with at least two affected relatives who met diagnostic criteria for an eating disorder (Grice et al., 2002). A nonparametric linkage (NPL) analysis test was not significant but returned a score of 1.80 at marker D4S2367 on chromosome 4. An NPL score of three or more is specific. The test was again performed on a subgroup of families (N = 37) in which at least two affected relatives had a diagnosis of restrictive AN. The NPL score was then 3.03 at marker DIS3721 on chromosome 1p. Genotyping additional markers in this region gave an NPL of 3.45, showing an anorexia susceptibility locus on chromosome 1p. These results were similar to a linkage analysis study measuring psychiatric, personality, and temperament phenotypes of individuals from 196 families (Devlin et al., 2002). These family members were accessed through an AN proband as well as the genotyping of 387 markers across the genome. A linkage analysis of the affected sibling was performed. The investigators found three suggestive rates with the greatest link at chromosome 1 (p < .00003). Another candidate gene that has been recently investigated for a possible link to eating disorders is the gene for insulin-like growth factor z,

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IGF2 (Bacher-Melman et al., 2005). This gene located on chromosome 11p15.5 has a metabolic action on the stimulation of insulin. One area of interest is a possible association of a single nucleotide polymorphism in the 31 untranslated region of the IGF2 gene (ApaI) and body mass index. This gene predisposes to weight gain. Using the EAT-26 test, the authors concluded that these individuals may become pathological dieters, with excessive dieting possibly evolving into abnormal behaviors and then into eating disordered syndromes.

Athletics as a Risk Factor Athletic activities, especially ballet and gymnastics, have been investigated as risk factors for the development of AN (Abraham, 1996; Bettle, Bettle, Neumarker, & Neumarker, 1998). These activities in particular have received much attention because of the high levels of exercise and the pressure for thinness (Klump, Ringham, Marcus, & Kaye, 2001). The prevalence of AN is 4 to 25 times higher in ballet dancers when compared with the general population (Garner & Garfinkel, 1980). Ballet dancers not only have scores on measures of eating behavior similar to those with AN, but the disturbance persists even after retirement from ballet (Khan et al., 1996). In a study of former female college gymnasts (N = 22) and matched

40

controls, symptoms were assessed using the Eating Disorder Inventory-2 (OConnor, Lewis, Kirchner, & Cook, 1996). Preoccupation with weight was stable over time for the controls. The gymnasts had experienced more preoccupation with weight than controls during the time they were participating in college gymnastics (p < .03), but this abated after retirement from the sport. In a study of 900 female athletes, it was found that the eatingdisordered group had feelings associated with both disordered eating and disordered exercise, such as feeling bad if unable to exercise a certain amount of time (OR = 1.53; 95% CI = 1.341.74). The feelings were considered more significant than the exercise amount or frequency (Boyd, Abraham, & Luscombe, 2007).

The Role of Societal Pressure to be Thin Not only is it widely presumed that the female ideal of thinness celebrated by the media has a deleterious effect on vulnerable girls and women, but this assumption has received scientific attention as well. A study of 238 female undergraduates indeed showed media influence on eating disorder symptoms, gender-role endorsement, ideal body stereotype, and body satisfaction (Stice, Schupak-Neuberg, Shaw, & Stein, 1994).

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In a prospective longitudinal investigation of 231 adolescent girls, initial pressure to be thin predicted a subsequent growth in body dissatisfaction (Stice, 2001). Body dissatisfaction then resulted in dieting and negative affect, which in turn resulted in bulimic symptoms. Therefore, pressure to be thin and the thin-ideal internalization lead to the development of behaviors (dieting, negative affect) that seemed to encourage bulimic symptoms. An interesting study involving 120 young women randomly assigned subjects to an experimental condition in which a very thin female complained that she felt fat and voiced the intention to diet, or to a control situation in which body image was not discussed (Stice, Maxfield, & Wells, 2003). The results showed that the experimental condition produced an increase in body dissatisfaction, but not the negative affect needed to result in bulimic symptoms. The precise role of societal pressure in eating disorders remains to be identified. Societal emphasis on thinness is nearly universal in Western countries, but only a small number of women will develop AN. For BN, on the other hand, perceived pressure to be thin may create a scenario of body dissatisfaction leading to dieting and negative affect that may contribute to

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the development of the disorder in at-risk individuals. The effects of media pressure to be thin may be stronger for those girls with pre-existing body image disturbances (Cattarin, Thompson, Thomas, & Williams, 2000). Similarly, individuals who are at a higher weight may experience external pressure from family or friends to be thin, resulting in bulimic symptoms (Stice & Whitenton, 2002); however, some studies do not support this association (Cattarin & Thompson, 1994). The internalization of thinness as an ideal has been shown to cause body dissatisfaction, which predicts increases in diet attempts and bulimic symptoms (Stice, 2001; Stice, Presnell, & Spangler, 2002). Indeed, interventions that focus on decreasing body dissatisfaction improve negative affect and bulimic symptoms (Bearman, Stice, & Chase, 2003). The effect of internalizing a thin idea may be more pronounced in girls that tend to be heavier (Stice & Whitenton, 2002).

The Role of Risk-Taking Behaviors In 1990 the Centers for Disease Control and Prevention developed the Youth Risk Behavior Study (YRBS), an in-school survey using self-completed paper and pencil questionnaires given to students in a group setting. The YRBS samples 13,000 to 14,000 students in grades nine through twelve

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enrolled in about 150 public and private high schools. Measurement is spread among different types of risk taking, with eating disorders, drugs, and suicide being a few of the categories. This is a cross sectional design repeated every two years (Grunbaum et al., 2002). The YRBS administered in 2001 found that White (19.7%) and Hispanic (23.1%) girls were significantly more likely than African American (15%) girls to report having gone 24 or more hours without eating in order to control weight. Vomiting or laxative use to control weight was reported by 10.8% of Hispanic girls, 8.2% of White girls, and 4.2% of African American girls (Grunbaum et al., 2002). Another study examined the health-damaging behavior of girls versus boys (Lowry, Galuska, Fulton, Wechsler, & Kann, 2002). In this study, fasting, the use of diet pills, vomiting, or laxative abuse were reported by 18.8%, 10.9%, and 7.5% of White, Hispanic, and African American girls respectively, compared with 6.4%, 4.4%, and 2.2% of boys. It is unclear if the girls would meet DSM-IV criteria for an eating disorder, since the questions do not cover all the diagnostic criteria. On the other hand, the YRBS is valuable in that it does identify those female adolescents practicing risky and health-damaging behaviors.

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Eating Disorder Not Otherwise Specified (EDNOS) Large gaps exist in our current knowledge of eating disorders, especially in regard to EDNOS. The few randomized, controlled trials in the literature deal with full-syndrome AN or BN but do not address EDNOS. However, incidence of EDNOS appears to be on the rise. In fact, one study of treatment approaches for AN took six years to recruit 37 subjects who met all strict diagnostic criteria for AN (Robin et al., 1999). Many, if not most, patients treated in clinical settings do not meet full criteria for AN or BN and thus are characterized as having EDNOS. In a 2005 study by Fairburn and Brohn, the percentage of adolescents diagnosed with EDNOS was 72.1%, compared with 9.6% diagnosed with BN. A study of differences between adolescents and young adults who presented to an eating disorders program found a high incidence of EDNOS in both populations, but it was higher among adolescents (Fisher, Schneider, Burns, Symons, & Mandel, 2001). One study of adolescents 14 to 15 years of age found the prevalence of EDNOS to be 14.6% in girls and 5% in boys (Kjelsas, Bjornstrom, & Gotestam, 2004). Another study by Fisher & colleagues (2001) compared adolescents and adults and found that both groups who sought treatment had a high prevalence of EDNOS. The literature to date strongly

45

suggests that most eating disordered adolescents fail to meet full criteria for AN or BN. EDNOS, as a category, is largely subsyndromal AN or BN (Fairburn & Brohn, 2005). EDNOS is the most common category of eating disorder (Brewerton, 2002), yet there is a dearth of research on it. We hope to show that the symptoms necessary for a diagnosis of EDNOS occur both in psychiatrically disturbed and substance-abusing adolescent girls. EDNOS has only recently been recognized as a distinct disorder, and although it is the most prevalent disorder in adolescents, it is underdiagnosed. Treatment of Eating Disorders

Psychosocial Treatments for Adolescents with AN Russell and colleagues from the Maudsley Hospital in London published the first randomized, controlled trials on the treatment of adolescents with AN (Russell, Szmukler, Dare, & Eisler, 1987). After 10 weeks in the hospital, patients were referred for outpatient treatment. Twenty-one adolescents received either a year of individual therapy or a year of family therapy. The individual sessions worked on the model of supportive therapy. The family therapy followed the Maudsley method in which the parents were helped to take control over the way the patients ate. Once weight loss was

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brought under control, responsibility for continued management moved to the patient. At the conclusion of one year, six out of 10 patients in family therapy had a favorable outcome, compared to only one out of 11 patients in individual therapy. The percentage of regained weight was greater in the family therapy group, and five out of 10 patients kept their weight above 85% average body weight compared to one out of 11 in individual therapy. Le Grange, Eisler, Dare, & Russell (1992) then went on to compare two types of Maudsley method family therapy: co-joint sessions versus separate sessions for patient and parents. Their study included 18 patients, aged 15 to 18 years, with duration of illness of 13.7 + 8.4 months and at a mean percentage of ideal body weight of 77.9% + 7.6%. Results indicated a favorable outcome for both groups over a six-month period. The small number of patients, however, made for a lack of statistical significance. A larger study by Eisler and colleagues (2000) randomly assigned 40 patients to one of two treatments. Patient age was 15.5 + 1.6 year; duration of disorder was 12.9 + 9.4 months. Treatment took place over one year in an average of 16 sessions. Each group improved in terms of percentage of average body weight and BMI (p < .001).

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In a randomized, controlled trial by Robin, Siegel, Koepke, Moye, & Tice (1994), 37 patients in two treatment groups were randomly assigned to receive either individual or family therapy. Treatment took place over 12 to 18 months and included consultation with a dietitian. At the end of treatment, 66% of all patients had achieved their target weight, while 80% of patients in the family therapy group had reached their target weight. Of interest are two possibly confounding factors in this study: hospitalization and extensive dietary intervention. The favorable outcome may have been owing to the dietary counseling, due to the fact that the decline in scores on conflict over eating occurred even though the family interaction did not change. Also, without a no-treatment control group it is impossible to rule out that the positive result in both experimental groups was due to the dietary counseling. A randomized clinical trial by Robin and colleagues (1999) compared behavioral family systems therapy with ego-oriented individual therapy in a cohort of 37 adolescent girls meeting criteria for diagnosis of AN. The therapeutic goals were to restore weight and to address eating attitudes, comorbid depression, and family relationships. Results showed that both approaches, followed 12 to 18 months, were significantly effective.

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Another randomized, controlled trial compared two 16-week family therapy interventions (Geist, Heinman, Stephens, Davis, & Katzman, 2000). In this study, the subjects had a six-week inpatient stay during which they were placed on a re-feeding program. Although the two groups did not differ in outcome, 59% refused to enter the study. The above randomized, controlled trials are limited due to small population size and insufficient statistical power to detect significant differences between treatments. Further, more research is needed that uses standardized assessment tools and ones that investigate the long-term effects of treatment. One long-term study had a discouraging relapse rate of nearly onethird (Keel, Dorer, Frankno, Jackson, & Herzog, 2005). Women with a diagnosed eating disorder (N = 246) were followed-up every six months for nine years. Patients with a diagnosis of BN or AN, binge-purge type, were likely to return to bulimic patterns. It has been suggested that a migration of the disorder may occur over time, so that an eating disorder may start as AN but later become BN or EDNOS (Fairburn & Harrison, 2003).

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Psychosocial Treatment for Adolescents with Bulimia Nervosa (BN) There is to date no randomized, controlled trial in the literature looking specifically at adolescents with BN. Although studies on effective treatment of adults with BN may not apply well to adolescents, they thus far present the only evidence-based treatment. There have been a large number of randomized, controlled trials of cognitive behavior therapy (CBT) in adults with BN (National Institute for Clinical Excellence, London, 2004). CBT eliminated binge eating and purging in approximately one-third to one-half of trials. Further, pathological dieting behavior decreased, and patients attitudes about body shape and weight improved.

Psychosocial Treatment for Adolescents with Eating Disorder Not Otherwise Specified (EDNOS) Most adolescent patients who present in need of treatment for disordered eating are most appropriately diagnosed with EDNOS. Thus, effective treatment of adolescents ideally addresses both anorexic and bulimic behaviors. Further, treatment needs to be adjusted to accommodate for developmental variability of adolescents (Weisz & Hawley, 2002). It is the variability of the adolescent symptoms that causes the study of EDNOS to be the most challenging. Treatment programs for adolescents with an eating

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disorder must accommodate a range of different pathological symptoms, in which the intervention should match the particular clinical needs of the patient. This is outlined in the practice guidelines for the treatment of patients with eating disorders of the American Journal of Psychiatry (2006), which stated that the biopsychosocial impact of eating disorders creates the need for a multidisciplinary team. This model, developed at the University of Utah, includes a physician, a registered dietitian (RD), and a mental health professional. The RD performs an initial nutrition interview, works with the patient on a food diary, educates the patient about the consequences of the eating disorder, assists in establishing weight goals, and helps the patient gain control through a dietary plan. In motivating the patient for behavior change, the RD must address the pathological food issues as well as the behaviors associated with those issues. Wilson (1999) stated that, in order to be effective, nutrition therapy requires knowledge of cognitive behavior principles. The flexibility of a CBT approach is well suited to address the wide spectrum of eating-disordered behavior in adolescents. Maladaptive beliefs and thoughts are challenged and were replaced with more accurate perceptions and attitudes involving nutrition. Using the stages of change

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model, the nutritionist was able to move the patient from pre-contemplation to contemplation, from preparation to action, and finally to maintenance (Prochaska, 1998). Therefore, the RD can assist the eating-disordered adolescent with purposeful/individualized changes in food choices, meal planning, and development of a regular pattern of eating. Furthermore, the nutritionist approach can encompass dealing with eating and body image issues in the adolescent patient as well as in the patients family. Developmentally, both the setting of limits and the granting of autonomy in regard to food become crucial issues. For that reason and others, parental involvement in treatment is beneficial. Inclusion of parents has been shown to be effective in randomized, controlled data looking at adolescent AN and at childhood obesity (Golan & Weizman, 2001).

Family Therapy Family therapy appears to emerge as an essential treatment for eating disorders in young people (Honig, 2000). Family interventions mobilize the strength of the family to help the adolescent. Any combination of either combined therapy of parents and child separate sessions or parent counseling seems to be acceptable. A study by Robin and colleagues (1999) showed improvement of symptoms with behavioral family systems therapy. In this

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study of 37 adolescents with AN, behavioral family systems therapy was compared to ego-oriented individual therapy. Both treatments improved eating attitudes, but the family approach produced greater weight gain and higher rates of resumption of menstruation. Early studies of the Maudsley family systems model indicate success in adolescent AN (Lock, 2002) and BN (Dodge, 1995). This model often will put the parents in charge of re-feeding the adolescent.

Pharmacological Treatment for Anorexia Nervosa (AN) There are few controlled studies on pharmacological management of eating disorders in adolescents since few medications have FDA approval for use in children. There have, however, been four placebo-controlled trials of antidepressants for AN. Results showed the effect was not significant (Attia, Haiman, Walsh, & Flater, 1998; Biederman, 1985; Halmi, Eckert, LaDu, & Cohen, 1986; Lacey & Crisp, 1980). If we take into account the rate of comorbid depression in eating disorders, we might expect a greater effect. It has been hypothesized that the effect of malnutrition may interfere with the action of the drug. Specifically, depletion of serotonin resulting from starvation might interfere with the effectiveness of selective serotonin reuptake inhibitor (SSRI) antidepressants (Delgado et al., 1990).

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Nearly 50 years ago there was enthusiasm about the proposed role of chlorpromazine (Thorazine), the first antipsychotic medication, in the treatment of AN. Two small, placebo-controlled trials found little efficacy (Vandereycken, 1984). The newer antipsychotics were later introduced and were found to produce weight gain as a prominent side effect. There was again consideration of the potential usefulness of antipsychotics, especially olanzapine (Zyprexa), in the treatment of eating disorders (Boachie, Goldfield, & Spetique, 2003; Powers, Santana, & Bannon, 2002). There were open-label studies launched, and in one conducted by Powers and colleagues in 2002, 10 of 14 patients gained a mean of 8.75 pounds. Powers, Simpson, and McCormick (2005) later proposed that future diagnostic descriptors might include AN with psychotic features, referring to the delusion of being fat and the presence of auditory hallucinations. Powers and colleagues selected 39 patients who met the DSM-IV criteria for AN: 45% had restrictive type, and 55% had binge-purge type. Thirty-six were female, three were male, mean age was 26 years, and mean BMI was 16. These patients were assessed using the Positive and Negative Syndrome Scale (PANSS), which was developed by Kay (1990) to assess the positive and negative symptoms of schizophrenia. The PANSS scores of these 39 patients

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with AN were then compared to validated reference scores from 240 patients with schizophrenia (Powers, Simpson, & McCormick, 2005). The mean PANSS score for the AN patients was 33 (SD = 6.1) and for the schizophrenia patients was 39.6 (SD = 9.3). There was a significant overlap in the scores with nearly 70% of patients having some psychotic symptoms. Interviews indicated that some heard an anorectic voice telling them not to eat, and some were convinced that they were fat despite evidence to the contrary. Several patients voiced the delusion that if food touched their plate they would gain weight even if they did not eat it. Twenty-seven patients were suspicious that their families were secretly adding calories to the food. Patients were frequently emotionally withdrawn or had blunted affect. These are tantalizing results, but a multi-site, randomized, double-blind, placebo-controlled study is needed. Other medications that have been studied include lithium, which has weight gain as a side effect; there was one controlled trial that showed little benefit (Gross et al., 1981).

Pharmacological Treatment for Bulimia Nervosa (BN) There have been two double-blind trials on the safety and efficacy of the antidepressant fluoxetine (Prozac) in the treatment of BN. The Fluoxetine

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Bulimia Nervosa Collaborative Study Group (1992) conducted an eight-week, multi-center, placebo-controlled, randomized trial comparing luoxetine at 20 mg/day, fluoxetine at 60mg/day, or placebo in 387 women who reported at least three binge and purge episodes per week for at least six months. There was a one-week placebo-only period after which those women who showed a 75% improvement were excluded. Patients recorded the number of bingepurge episodes in a diary and participated in several measurements including the EAT assessment. Overall, fluoxetine at 60mg/day was superior to placebo in reducing binge eating (p < .001) and vomiting (p < .001). Patients receiving fluoxetine at 20 mg/day showed a significant reduction in vomiting (p < .021) but not in binge eating (p < .453). There were also significant improvements on the EAT and other scales. Goldstein and colleagues compared fluoxetine at 60 mg/day with placebo in a 16-week, randomized, controlled, double-blind, multi-center trial (Goldstein, Wilson, Thompson, Potvin, & Rampey, 1995). The study had 398 subjects meeting the diagnostic criteria for BN. Efficacy was measured by change in the number of vomiting and binge eating episodes per week. Response rate was defined as a 50% decrease in the number of episodes. Fluoxetine at 60 mg/day was superior to placebo in reducing the number of

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episodes of vomiting (p < .002) and binge eating (p < .005). Improvement was also seen on the EDI (p < .006) and both scales of the Clinical Global Impression (p < .0001). The improvement was seen in both depressed and non-depressed patients with bulimia (Goldstein, Wilson, Ascroft, & al-Banna, 1999). A review of treatment trials showed that the combination of CBT and antidepressants has become the standard of therapy (Mitchell, Raymond, & Specker, 1993). Walsh, Wilson, & Loeb (1997) conducted a randomized, double-blind, placebo-controlled trial in 120 women meeting the criteria for BN. Patients were randomized and assigned to one of the five treatment groups: CBT + placebo, CBT + active medication, supportive therapy + placebo, supportive therapy + active medication, or active medication alone. Patients randomized to an active medication group received desipramine at 200-300mg/day for eight weeks. If binge frequency had not decreased by 75% or if side effects were intolerable, then the desipramine was tapered to discontinuation, and fluoxetine at 60mg/day was started. Results showed that CBT was superior to supportive psychotherapy in reducing binge eating and vomiting. CBT + active medication was superior to active medication alone in

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reducing vomiting frequency. Two-thirds of patients were switched from desipramine to fluoxetine due to side effects or a lack of improvement.

Multidisciplinary Approach to the Treatment of Eating Disorders The first clinical pathway for AN was developed at Packard Childrens Hospital of Stanford (Lock, 1999). A treatment team consisted of adolescent medicine physicians, child psychiatrists, nurses, and RDs. The RD, experienced in working with young people, assisted the patient in setting up meal plans and exchanges. The RD needed to be able to confront dysfunctional behavior such as excessive exercise, purging, or inadequate caloric intake if suspected (Rome et al., 2003). Knowledge about body shape distortion and eating-disordered behavior would enable the RD to evaluate adolescent psychiatric patients in general. Most treatment programs today include an exercise program, a spiritual component, and an RD-administered nutritional intervention (Eiger, Christie, & Sucher, 1996). The American Academy of Child and Adolescent Psychiatry (AACAP) has published treatment guidelines for a variety of psychiatric disorders that affect children and adolescents. The multidisciplinary approach with the integral involvement of an RD has been emphasized (AACAP Practice Guidelines, 1998). The APA has also published practice guidelines with

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emphasis given to the importance of collaboration among health care professionals including RDs (APA, 2000).

The Concept of Disordered Eating In a study ending in 2004, 17.1% of children and adolescents in the United States were found to be overweight, defined as a BMI at or above the 95th percentile for age and sex. There was no significant difference by age or racial/ethnic group (Ogden et al., 2006). Being overweight is associated with an increased risk of excessive preoccupation with weight and shape, dieting, and binge eating (Tanofsky-Kraff et al., 2005). There is also an association between being overweight and unhealthy methods of weight control including binging, purging, and the use of diet pills to control weight (Austin, Field, Wiecha, Peterson, & Gortmaker, 2005). Elevated weight, shape concerns, and a negative evaluation of oneself have been implicated in risk for developing an eating disorder (Jacobi, Hayward, deZwaan, Kraemer, & Agras, 2004). Such features can lead to a vicious cycle of being overweight, using weight control measures that lead to disordered eating, and then further weight gain due to the inability to control affect (Stice, Presnell, Shaw, & Rohde, 2005). Disordered eating can lead to full-blown eating disorders in which the cycle consists of binge eating followed by purging or

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binge eating without any restrictive measures (Kotler et al., 2001). A pattern of disordered eating results in significant threats to ones physical and psychological health. There is a significant risk of further weight gain and the development of an eating disorder (Goldschmidt, Aspen, Sinton, Tanofsky-Kraff, & Wilfley, 2008). Body dissatisfaction may change with normal fluctuations in shape or weight but a consistent pattern of concern with shape and weight or thin body preoccupation has been associated with the development of an eating disorder (McKnight Investigation, 2003).

The Concept of Loss of Control (LOC) Overweight children and adolescents are less likely to utilize healthy weight control measures and are less likely to be engaged in regular family meals (Neumark-Sztainer, Eisenberg, Fulkerson, Story, & Larson, 2008). In a study of 126 children and adolescents seeking residential care for obesity, episodes of binge eating were reported in 36.5% (Decaluwe, Braet, & Fairburn, 2003). The evidence suggests that binge eating involves the over-consumption of large amounts of food, and that LOC is linked to weight gain (Stice et al., 2005). Loss of control behavior then leads to adverse consequences such as

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negative mood (Tanosky-Kraff et al., 2005), anxiety, depression, and body dissatisfaction (Morgan et al., 2002). Although few adolescents meet the criteria for full syndrome binge eating disorder (Stice, Presnell, & Bearman, 2001) there is prevalent sub-threshold binge eating, particularly in overweight adolescents, with prevalence estimates ranging from 20% (Isnard, Michel, & Frelut, 2003) to 30% (Decaluwe et al., 2003). Adolescents who did report subthreshold binge eating behavior have greater distress, depressive symptoms, and anxiety (Isnard et al., 2003). The children reporting LOC episodes, regardless of the amount of food consumed, were heavier and had more psychological distress than those with no LOC episodes (Morgan et al., 2002; Tanofsky-Kraff et al., 2005). Therefore, it appears that LOC is a stronger indicator of additional psychopathology than the amount of food consumed, as well as being a crucial component in the use of the term binge eating as it applies to adolescents. The overweight youth are significantly more likely to report binge eating than youth of normal weight (Tanofsky-Kraff et al., 2005). Clinically, LOC appears to be a significant issue in adolescent overeating.

CHAPTER FOUR Conceptual Framework

There have been numerous published studies that have examined the correlation between eating disorders and co-morbid psychiatric disorders. Many patients diagnosed with eating disorders have symptoms of major depression and/or substance use disorder. Although there is some variation among patients with AN and among those with BN as to their particular pattern of psychiatric co-morbidity, there is a high correlation for comorbidity across the literature. Furthermore, the majority of eatingdisordered patients presenting for treatment carry the diagnosis of EDNOS, which at the present time has not been adequately studied. In addition, we are seeing a rise in the number of adolescents and adults being diagnosed with an eating disorder (especially EDNOS), and treatment centers for eating disorders have grown over the past decade. Evidence-based research is largely centered on discreet treatments for discreet disorders (Weisz, Donnenberg, Han, & Kauneckis, 1995). Unfortunately, todays adolescent psychiatric patient displays multiple problems. The Great Smoky Mountain Study of Youth found that the

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prevalence of psychiatric disorders among youth was 20%. Thirty three percent had more than one diagnosis (Costello et al., 1996). Studies by Weisz and colleagues in public mental health clinics in Los Angeles found the modal number of diagnoses among youth was five (Weisz, Donnenburg, Han, & Weiss, 1995). There is a lack of developed research on the effectiveness of treatment for youth with more than one problem, which presents serious obstacles to the delivery of services. It was our hypothesis that perceptions about eating and body image disturbances cut across diagnostic categories and would likely be found in young women being treated for psychiatric disorders and substance use disorders. (The relative rarity of eating disorders in the male population precludes excluding young men from this study.) The absence of self-esteem may well be the fundamental issue leading to compensatory action by the adolescent in an unconscious manner. Adolescents being treated for psychiatric disorders will often have unwarranted feelings of inadequacy, which are stressful and distressing, and may give rise to maladaptive behavior. These behaviors may include self-mutilation, sexual promiscuity, drug abuse, and even physical aggression.

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The research questions that we attempted to answer involve the degree of existing eating disorder symptoms in two groups of female adolescents: inpatients and a community group (Figure 1). Figure 1. Conceptual Framework Female Adolescent Inpatients Ethnicity Parents Weight History of Eating Disorder Dieting Depression High Risk Athletics Substance Abuse Female Adolescents in the Community

Patient Demographics Age BMI

Scores Denoting Risk of Developing an Eating Disorder Measured by EAT-26 > 20 or BSQ-34 > 110

The inpatient treatment group had a diagnosed psychiatric disorder made by a child and adolescent psychiatrist. The diagnostic categories we considered were depression/anxiety and substance use disorder. The adolescent community group had no history of psychiatric disorder, substance use disorder, or medical problems and no psychiatric treatment. The purpose of this study was to see if psychiatrically disturbed and substance-abusing

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females who had never been previously diagnosed with an eating disorder had a higher likelihood of developing a co-morbid eating disorder based on EAT-26 and BSQ-34 scores. Furthermore, we examined age as a continuous variable and BMI as a discrete variable in the psychiatric population as well as in the community population. We hoped to determine predictors of increased risk of developing an eating disorder in both populations. If our hypothesis proved to be true, it would have important treatment ramifications in their treatment. It would add another dimension to the successful psychiatric treatment of these youngsters.

CHAPTER FIVE Hypothesis/Research Questions

Primary Research Question: Research Question I Do psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder have a higher risk of developing an eating disorder, based on EAT-26 score > 20 and/or a BSQ score > 110, when compared to healthy student female participants drawn from the community? Hypothesis I-A. Ho: Psychiatrically disturbed and substance-abusing, hospitalized, adolescent females do not have a higher risk of developing an eating disorder when compared to their comparative group drawn from the community. Ha: Psychiatrically disturbed and substance-abusing, hospitalized, adolescent females do have a higher risk of developing an eating disorder when compared to their comparative group drawn from the community.

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Secondary Research Questions: Research Question II Do psychiatrically disturbed and substance-abusing, adolescent, hospitalized females not previously diagnosed with an eating disorder have a difference in age when compared with healthy female student participants drawn from the community? Hypothesis II-A. Ho: Psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder do have an age difference for developing an eating disorder compared with the comparative group drawn from the community. Ha: Psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder do not have an age difference for developing an eating disorder compared with the comparative group drawn from the community.

Research Question III Do psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder have a difference in BMI distribution for developing an eating disorder, based on an EAT-26 score

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> 20 and/or a BSQ score > 110, when compared to healthy female student participants drawn from the community? Hypothesis III-A. Ho: The BMI values that increase the risk for eating disorders among psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder is the same as in the healthy female student participants drawn from the community. Those with BMI values < 19 will have a higher EAT and/or BSQ scores in both groups. Ha: The BMI values that increase the risk for eating disorders among psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder will be different from those of the healthy female student participants drawn from the community.

Research Question IV What are the predictors of increased risk of developing an eating disorder among psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder, as well as healthy student female participants drawn from the community?

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Hypothesis IV-A. Ho: Depression/anxiety, substance abuse, age, gender, parental obesity, genetics, and athletic level (ballet and gymnastics) are not predictors of increasing the risk of developing an eating disorder among psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder. Ha: Some of the above mentioned factors are associated with increased risk of developing an eating disorder among psychiatrically disturbed and substance-abusing, hospitalized, adolescent females not previously diagnosed with an eating disorder.

Discussion The work of Weisz and colleagues (1995a) as well as the Great Smokey Mountain Study (Costello et al., 1996) indicated that co-morbid disorders occurring in youth are underdiagnosed. The lack of research on effective treatments for youth with more than one psychiatric problem presents serious problems for the proper delivery of services. The recognition that co-morbid disorders are more common than previously thought, leads to a more fundamental question of how we may define mental health in youth (Jensen & Hoagwood, 1997). Our research attempted to show the prevalence of eating

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disorders as an additional co-morbidity in need of consideration in the adolescent population. The presence of an active substance use disorder as a risk-taking behavior indicated a possible strong association with eating disorders. It is our research that may uncover untreated eating disorder symptoms in patients being treated for substance abuse. This finding will have implications in the treatment planning for the adolescent. Clinicians will then begin to look for symptoms of an eating disorder in the population that they serve. Increasing the awareness of occult eating disorder pathology will result in a more comprehensive treatment for these patients. According to Gardner (1996), body image includes two components. One component is a perception, an estimation of size and appearance. The other component is an attitude that relates to feelings and attitudes towards ones own body. Garner and Garfinkel (1981) do point out that alterations in body image involve a perceptual distortion and a cognitive-affective alteration that shows dissatisfaction with ones figure. Eating-disordered patients have a multi-dimensional problem involving perceptual alterations, a negative attitude towards ones body, and resulting behavioral alterations (Garfinkel & Garner, 1982).

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We set out to illustrate that psychiatrically disturbed adolescent females have eating perceptions and body image concerns similar to those with a primary diagnosis of an eating disorder. If this proved to be true then psychosocial interventions will need to be formulated to address those issues.

CHAPTER SIX Methodology Research Design This was a cross sectional study with two non-equivalent adolescent groups designed to examine the prevalence of distortions in eating attitudes and body image disturbances in adolescent girls 12 to 17 years of age. The inpatient study population had been diagnosed with depression/anxiety and/or substance use disorder. The total score of the EAT-26 (perception of eating) and the total score of the BSQ-34 (perception of body image), the dependent variable, identified participants as having a risk of developing an eating disorder based on the cut-off scores of EAT > 20 or BSQ > 110. We compared a study group of inpatient adolescent females with a comparative adolescent student group drawn from the community. The groups were matched for gender and age. Each participant and parent was required to read and sign a consent form (Appendix). The study obtained a university review board approval from Touro University International for human protection.

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Sampling and Recruitment This sample may best be described as a non-probability purposive sample. The researcher controlled as much as possible for the independent variables of the study groups. There was a study group and a community student group. The study group was composed of adolescent females hospitalized at a psychiatric facility with DSM-IV-TR diagnoses of depression/anxiety and/or substance use disorder. Other psychiatric disorders were excluded. The community student group was composed of adolescent girls recruited from local middle schools and high schools. This group had no previous medical diagnosis of a psychiatric disorder. The recruitment area spanned from Memphis, Tennessee to Olive Branch, Mississippi and to Tupelo, Mississippi. The inpatient population was recruited from one free-standing psychiatric facility in Olive Branch, Mississippi. The community clients were recruited from local public and/or private schools.

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Study Conduct Inpatient Group. 1. The administrator and medical director of the potential participating hospital were contacted to obtain permission for participating in this research study. 2. When the hospital granted permission for participation in the study, the researcher then set a meeting with the attending child psychiatrist(s), nurse(s), and social worker(s) to gain their approval for participation and discuss study details. 3. After the attending child psychiatrist performed the psychiatric evaluation, and after the social worker completed the psychosocial assessment, the potential patient participants were selected. 4. During parents first visit to the hospital, the study was explained to both parent and child. If the parents permitted their children to participate in the study, they were asked to sign the consent form. 5. The patient participants were asked to complete the study packet prepared by the researcher after the parents left the hospital. The participants were instructed to return the packet to the nurse when completed. The participants were also encouraged to ask the nurse or researcher any question and to complete the questionnaire as much as they were able. The

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packet included: the EAT-26, the BSQ-34, the Depression Anxiety Stress Scales-21 (DASS-21), and demographic forms. The questionnaires were selfadministered to avoid any confounding effect associated with answering or administration bias. 6. The researcher took the questionnaires from the nurse and examined them for incompleteness and/or discrepancies; the participants would have been contacted if either were present. If not at least 95% complete, the questionnaire was excluded from analysis. 7. The researcher calculated BMI values and entered them and the scores of the EAT-26, BSQ-34, and DASS-21 questionnaires into the Statistical Package for the Social Sciences (SPSS) program for statistical analysis.

Community Group. 1. The researcher visited the schools during the time set by school administration. 2. A short presentation about the study and its benefits to the community was presented to the participating class members (teachers, students, and parents of the students). Students who agreed to participate in the study were asked along with their parents to sign consent and assent forms.

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3. After granting approval for participation, the researcher distributed to the students the study packets (outlined above in addition to a demographic questionnaire). The students were oriented on how to answer the questions to ensure accuracy and completeness. They were asked to take the study packet to their desks to complete the questions and return them to the teacher/researcher when done. The students were encouraged to ask questions if the need arose. 4. When all packets were returned to the teachers/ researcher, the researcher obtained height and weight data. 5. All questionnaires were reviewed for incompleteness and checked for discrepancies; the participants were contacted if either were present. As in the case of inpatient participation, any questionnaire that had less than 95% completeness was excluded from analysis.

Study Population Inclusion Criteria 1. All patients, along with their parents/guardian, who agreed to sign the consent form.

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2. All participants, including the adolescent study group of healthy females, were female, between the ages of 1217 years, and residing in the Memphis, Tennessee area or counties in Northern Mississippi. 3. All participants were on grade level in regular classes to assure that they understood the questionnaires. 4. All participants were currently attending school, since school dropout would be a serious adverse psychosocial factor that may interfere with the results. 5. The inpatient group had a DSM-IV-TR psychiatric diagnosis of depression/anxiety and/or substance use disorder. They were recruited from Parkwood Hospital in Olive Branch, Mississippi. Exclusion Criteria 1. Had a diagnosis of schizophrenia or bipolar disorder. 2. Were not on grade level or were in special education. 3. Had a diagnosis of any medical condition that may interfere with their behavior toward food intake and body image. These conditions included: diabetes, renal disease, thyroid disease, Cushings syndrome, cancer, or lupus. 4. Had been diagnosed with, or had ever received treatment for, a specific eating disorder.

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Data Collection The same data (anthropometry and four questionnaires) were collected from both studied groups (adolescent student group and adolescent inpatient group).

Anthropometry Body weight and height were used to calculate participants BMI. BMI in kg/m2 is calculated as weight in kg divided by height in meters-squared. For both groups (the inpatient group and the community student group), weight was measured using the Health-O-Meter digital lithium scale, model HDL938 (Sunbeam Products Inc). Weight measurements were taken to the nearest 0.5 kg, with light clothing and no shoes. Two measurements were obtained, and if discrepancy in weight measurement was detected, a third measurement was obtained to ensure accuracy. Measurements of height were taken to the nearest 0.1 cm in doubles. Height was measured with a measuring tape attached to a vertical wooden pole. Two measurements were obtained, and if discrepancy in height measurement was detected, a third measurement was obtained to ensure accuracy. Measurements were performed by a Registered Nurse or Licensed Practical Nurse in the hospital and by the researcher in the community setting.

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Questionnaires A total of four questionnaires were used in this study: a demographic questionnaire, two questionnaires to assess attitudes towards food (EAT-26) and body image (BSQ-34), and one questionnaire to assess for depression/anxiety (DASS-21). All study questionnaires were selfadministered. The demographic questionnaire was constructed by the investigator. It included questions pertaining to age, birthplace, and whether there was a medical condition that might exclude the respondent from the study. The EAT-26, adapted from Garner & Garfinkel (1979), was utilized in the 1998 National Eating Disorders Screening Program and has been the most widely used standardized instrument in assessing symptoms and attitudes in patients with eating disorders or prone to developing eating disorders. This questionnaire is a test that evaluates attitudes and preoccupations in relation to food, weight, and exercise. An individual with an EAT-26 score of 20 or greater is considered at risk of developing an eating disorder (Cooper, Taylor, Cooper, & Fairburn, 1987). This instrument has exhibited adequate validity and reliability (Garner, 1993, 1997) in the English language for identifying eating disorders. Cronbach alpha demonstrated adequate reliability of .98. It consists of 26 questions divided into two sections. Section I includes questions

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1 25, with a scoring of responses of always, usually, often, sometimes, rarely, and never to items such as Am terrified about being overweight. Responses are scored as always = 3, usually = 2, and often = 1. Question 26 inquires whether the respondent enjoy(s) trying new rich foods and is scored as never = 2, rarely = 2 and sometimes = 1 (Appendix). Individuals with EAT-26 scores > 20 are described as partial syndrome anorectics, suspected anorectics, suspected bulimics, and weight-preoccupied, and are referred for diagnostic interview. Most interesting is the conclusion that most of those identified could be diagnosed with EDNOS (Mumford, Whitehouse, & Chaundry, 1992). The BSQ-34, adapted from Cooper et al. (1987), is utilized to evaluate the fear of putting on weight, feelings of low self-esteem, and body image concerns. The BSQ-34 is a widely used standardized instrument in assessing body image and has been validated for the identification of eating disorders. The importance of the addition of the BSQ-34 to an assessment tool such as the EAT-26 lies in the inclusion of questions that tap into distressing preoccupations with weight and shape, embarrassment in public, and avoidance of activity or exposure of ones body due to self-consciousness, as well as the issue of feeling fat after eating (Rosen, Jones, Ramirez, & Waxman, 1996). The BSQ thus measures feelings of shame and embarrassment about appearance plus body checking and avoiding behaviors. Cronbach alpha

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demonstrated adequate reliability of .882. The test consists of 34 questions with responses of never, rarely, sometimes, often, very often and always. Each answer has a point value ranging from 1 to 6. Total scores are classified into four categories: < 81 = not worried about body shape; 81110 = slightly worried; 111140 = moderately worried; and > 140 = extremely worried. This instrument has adequate validity and reliability (Cooper et al., 1987). The DASS-21, adapted by S. H. Lovibond and P. F. Lovibond, is a shortened version of the DASS-42 containing 21 questions with seven items per scale. The scale is used to measure the emotional states of depression, anxiety, and stress (Lovibond & Lovibond, 1995). The reliability of the DASS21, measured using Cronbachs alpha, was .88 (95% CI = .87.89) for the Depression scale, .82 (95% CI = .80.83) for the Anxiety scale, .9 (95% CI = .89 .91) for the Stress scale, and .93 (95% CI = .93.94) for the total score (Henry & Crawford, 2005). The reliability of the DASS-21 measured, from our study, using Cronbachs alpha was .94 for the depression scale, .81 for the anxiety scale, .88 for the stress scale. The DASS-21 is based on a dimensional rather than a categorical perception of emotional disorder. The assumption (confirmed by research data) is that the differences between depression, anxiety, and stress experienced by normal respondents and clinically

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diagnosed patients are differences of degree of symptom severity (Clara, Cox & Enns, 2001; Crawford & Henry, 2003). The EAT-26 and BSQ-34 questionnaires have both been validated by a number of researchers in English and other languages. Doninger (2005) used the EAT-26 to evaluate 207 female college athletes. In a review article by Garfinkel and Newman (2001) the authors show strong support for the validity, reliability, sensitivity, and specificity of the EAT. It is used as a screening device and has the ability to compare across groups and measure change over time. Boschi & colleagues (2005) evaluated 162 women seeking diet therapy using the EAT-26 and the Three-Factor Eating Questionnaire, showing a high degree of reliability. Castro & colleagues (2004) used the EAT26, the Child and Adolescent Perfectionism Scale, and Beck Depression Inventory (BDI) to assess 71 individuals with anorexia whose mean age was 15.3 years. There were significant correlations among the perfectionism scales, the EAT-26, and the BDI. Dotti and Lazarri (1998) administered the EAT-26 to 1,277 high school students, mostly female, as a screening device. Analysis showed satisfactory reliability with results similar to those of the test author, Garner (1996). Espina, Asuncion-Ortega, Ochoa de Alcia, & Juaniz (2002) administered both the EAT-26 and the BSQ-34 to 969 students 11 to 18 years

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old and found a positive relationship between body shape concern and body weight, irrespective of gender.

Explanation of Dependent and Independent Variables A new categorical variable will be developed that will identify participants as having a risk, versus not having a risk, of developing an eating disorder. This variable will be based on a cut-off score of > 20 on the EAT-26 and/or > 110 on the BSQ-34. This will serve as a dependent variable in Research Question IV and an independent variable for Research Questions II and III. Age is a continuous variable that will serve as a dependent variable for Research Question II. Age will serve as an independent variable for Research Question IV. BMI is a categorical variable that will be divided into 2 categories: > 19 and 19. BMI will serve as a dependent variable for Research Question III and an independent variable for Research Question IV. Other independent variables are predictors: depression/anxiety, substance use disorder, BMI, age, ethnicity, and parental weight (Table 1).

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Table 1. Research Questions, Study Variables, and Statistical Tests

Research Question (RQ) RQ I. Do psychiatrically disturbed and substanceabusing, hospitalized, adolescent females not previously diagnosed with an ED have a higher risk of developing an ED? RQ II. Do psychiatrically disturbed and substanceabusing, hospitalized, adolescent females not previously diagnosed with an ED differ from the community study group by age of developing an ED? RQ III. Do psychiatrically disturbed and substanceabusing, hospitalized, adolescent females not previously diagnosed with an ED have a greater or lesser difference from the community study group in BMI (25) distribution for developing an ED? Independent Variables Study group (hospital patients + community) (nominal) Dependent Variables At risk of developing an ED (dichotomous) Statistical Test Pearson chisquare

Study group at risk for ED (nominal)

Age (continuous)

Independent sample t-test

Study group at risk for ED (nominal)

BMI Independent (dichotomous) Sample t-test (BMI<<BMI><)

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RQ IV. What are the predictors of increasing the Age risk of developing an ED (continuous) among psychiatrically disturbed and substanceAnxiety, BMI, abusing, hospitalized, ethnicity, parental adolescent females not weight, previously diagnosed with dieting, an ED as well as healthy depression, female students drawn substance abuse from the community? (categorical)
Note. BMI = body mass index, ED = eating disorder.

At risk for ED (dichotomous)

Univariate binary logistic regression

Pilot Study after Approval from TUI University After approval from the dissertation committee at TUI University International (TUI) and its Institutional Review Board, Parkwood Hospital was contacted in order to begin a pilot study with five participants. Steps listed in the methodology section were followed and evaluated for availability of information, parental consent, patient compliance, and staff following the protocol. Adjustments were made to the methodology if needed and then be presented to the dissertation advisor and members and to the TUI Ethical Committee.

Identification of Patients at Risk Patients will not receive nutrition counseling as a part of this research. Should a subject be identified through the EAT-26 and BSQ-34 as having a

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susceptibility to an eating disorder, the parent or therapist will be notified in order for the family to seek treatment.

Power Analysis Sample size has varied among published investigations of co-morbidity in eating disorder (Table 2). In this study, the number (N) was calculated for a moderate effect size at N =144 (Steven, 2002). After calculation of the set power at 0.8, with seven variables, each group sample size = 72. This determination was based on a table designed for this and considered the level of significance (alpha = .05), power (.8), standardized (moderate) effect size, number of groups (two), and number of variables (seven). The time frame for the study was dependent on the amount of time required to recruit two groups, N = 72, assuming a moderate effect size. In order to achieve a moderate effect size, the study needed a sample size of 72 girls in each group. N = 144 will give a 94% chance of finding a moderate effect size with an alpha level of p < .05 (Steven, 2002). Table 2. Sample Size in Adult Co-morbidity Studies
Published study Godart et al., 2003 Sample size N = 271 Statistical test p .002 Summary Co-morbidity of anxiety disorder in eating disorder patients

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Keel et al., 2003 Speranza et al., 2001 Bulik et al., 1997

N = 136 N = 89 N = 184

p .001 p .05 OR performed

Alcohol was a significant factor in mortality of women with AN Eating disorder with co-morbid OCD in women 15 30 years old OR overanxious = 13.4 in AN, 6.1 in controls OR OCD = 11.8 in AN OR overanxious = 4.9 in BN OR social phobia = 15.5 in BN, 6.4 in controls

Note. These are articles looking for psychiatric co-morbidity in eating disorders while our study was looking for co-morbid eating disorders in a psychiatric population. The mean n = 170 subjects.

Statistical Analysis of Data SPSS software (SPSS, Inc., Chicago, IL) was used to conduct the following statistical analysis: 1. Descriptive analysis. Continuous variables will be presented as mean standard deviation (SD) while categorical variables will be presented as frequency and percentage. 2. Reliability of the instruments. Cronbachs alpha will be calculated to assess the reliability of the EAT-26, BSQ-34 and DASS-21 in our sample group. 3. Factors associated with high scores on EAT-26 and BSQ-34. Pearson chisquare will be conducted to test for association between EAT-26 and/or BSQ-34 score categories on the one hand and subject groups (new identified variable for patient group vs. community sample), age, and BMI on the

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other hand. Multivariable analysis will then be conducted to examine for predictors of increasing risks of developing an eating disorder among those groups that have been identified as at-risk. We will compare whether the same predictors would be identified in the student control group. Identified predictors will be based on clinical judgment of variables that may increase risk of developing an eating disorder, rather than on statistical significance of variables that will be identified by research questions I III.

Characteristics of the Study Population Catchment Area The population studied consisted of 144 adolescent female participants of whom 50% (72) were recruited from a psychiatric hospital where they had been admitted for treatment of depression/anxiety or substance abuse. The remaining half (50%) were recruited from participating schools in the Shelby County, Tennessee area (Figure 2).

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Figure 2. Distribution of Clients throughout the Study and Attrition Rate

242 Clients

92 recruited; 20 hospital-based participants did not meet criteria

150 recruited; 78 communitybased participants did not meet criteria

144 included Total = 72 Completed study n = 144 Total = 72

n = 72 Hospital patients

n = 72 Community participants

The hospitalized participants attended various schools in Shelby County and the Northern Mississippi area. This is the catchment area for Parkwood Behavioral Health System, a psychiatric and substance abuse facility.

Ethnicity of the Study Population Fifty-one (70%) of the participants in the hospitalized group and 54 (75%) of the participants in the community group were White. African

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Americans numbered 20 (27.7%) in the hospitalized group and 14 (19.4%) in the community group. There were no Asian participants in the hospital group and four (5.5%) in the community group. In the Hispanic group, there was one (1.4%) in the hospitalized group and none in the community sample. For statistical purposes, African Americans, Asians, and Hispanics were grouped together (Table 3).

Cigarette Smoking in the Study Population Current smokers represented 23.6% (17) of the hospitalized participants as compared to 11.1% (8) of the community group. Those who had never smoked composed 55% (40) of the hospitalized group and 79.2% (57) of the community group. There was no significant difference observed in the smoking habits in the two study populations (Table 3).

Body Piercing/Tattoo Habits of the Study Population The hospitalized participants were not significantly different than the community participants in this area. In the hospitalized group, 53.4% had 1 to 3 piercings, and in the community group, 59.4% had 1 to 3 piercings. In the hospitalized group, 4.1% had 4 to 6 piercings as compared to 5.6% in the community group. This was not found to be significant (Table 3). Table 3. Demographics of the Study Population (N=144)

90 Psychiatric n 51 21 Group % 70.8 29.1 Community n 54 18 Group % 75 24.9 Total %

Ethnicity Ethnicity n (%) Caucasian African American, Asian, Hispanic Cigarette Smoking Smoking n (%) Never Currently Stopped <6 mo ago <612 mo ago >1 year ago Body piercing/tattoo habits # of piercings or tattoos 0 1-2 3+

105 (73%) 39 (27.5%)

40 17 5 8 2

55.5 23.6 6.9 11.1 2.7

57 8 2 5 0

79.2 11.1 2.7 6.9 0

67.4 (45%) 17.4 (12%) 4.9 (34%) 9.0 (6.2%) 1.4%

30 26 16

41.6 36.0 22.2

25 32 15

34.7 44.4 20.9

38.2 (26.5%) 40.3 (22%) 21.6 (15%)

Age of Students and Grade in School The community participants mean age was significantly higher (M = 15.57 years, SD = 1.24) than that of the hospitalized participants (M = 14.47

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years, SD = 1.42). Overall, data on age obtained from the medical records at the hospital showed female adolescent admissions tended toward younger ages. The community participant ages started at 13. The hospitalized and the community were both selected based on meeting the criteria for inclusion (p < .001). The community participants mean school grade was also significantly higher (M = 10.22, SD = 1.10) than that of the hospitalized participants (M = 9.19, SD = 1.24; p < .001). The students represented grades 812 (Table 4).

Participants Perception of Parental Weight Seventy-four percent (52) of the hospitalized participants and 66.6% (48) of the community participants considered their mothers weight to be normal. In the hospitalized group, 2.8% (2) of the participants did not have mothers. This difference was found not to be significant (p = .177). Among the hospitalized participants, 76.6% (49) considered their fathers weight to be normal, with the same being true of 66.2% (45) of the community participants. This difference was found not to be significant. Of the hospitalized participants, 11.1% (8) did not have fathers; of the community participants, 5.5% (4) did not have fathers (p = .138; Table 4).

Hours Exercised

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In the hospitalized group, 34.7% did no exercise, compared to 25% in the community group (p = .812). It is worth noting that in both groups, 49.1% exercised more than one hour per week (Table 4). Table 4. Hospital vs. Community Group Analysis (N=144) Hospital group Community group Age of participant Mean (SD) 14.47 (1.42) 15.57 (1.24) 12 yrs 7 0 13 yrs 13 3 14 yrs 15 15 15 yrs 18 14 16 yrs 14 18 17 yrs 5 22 Grade in school Mean (SD) 7th 8th 9th 10th 11th 12th Perception of maternal weight Very thin Thin Normal Overweight Perception of paternal weight Very thin Thin Normal Overweight Hours/week spent exercising, mean (%) 0 hours 9.19 (1.24) 6 18 17 19 12 0 N = 70 3 3 52 (74%) 12 N = 64 2 2 49 (76.6%) 11 10.22 (1.10) 0 4 15 24 19 10 N = 72 3 10 48 (66.6%) 11 N = 68 1 7 45 (66.2%) 15 2.1 6.3 65.3 18.1 4.2 9.0 69.4 16.0

Total 4.9 11.1 20.8 22.2 22.2 18.8

4.2 15.3 22.9 28.5 22.2 6.9

25 (34.7%)

18 (25%)

30%

93 <1 hour 1 hour >1 hour 8 (11.1%) 9 (12.5%) 30 (41.6) 7 (9.7%) 6 (8.3%) 41 (56.9%) 10.4% 10.4% 49.2%

Note: Number of students in group (percentage of group=72).

BMI Differences between the Hospitalized and Community Groups The BMI of the hospitalized participants (M = 24.6kg/m2, SD = 5.51) was significantly higher than the BMI of the community participants ( M = 21.8, SD = 3.62; p = .000; Table 5).

Test Scores in the Hospitalized and Community Groups DASS-21. Significant differences were observed in DASS scores of all three subtests for both the hospital and the community participants: stress (p = .000), anxiety (p = .000), and depression (p = .000; Table 5). Scores on the DASS-stress section for the hospitalized participants (M = 24.11, SD = 9.84) were significantly higher than those for the community participants (M = 10.28, SD = 9.35; p = .000). Likewise, scores on the DASSanxiety section for the hospitalized participants (M = 15.14, SD = 9.32) were significantly higher than those for the community participants (M = 6.11, SD = 7.21; p = .000). Finally, scores on the DASS-depression section for the

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hospitalized participants (M = 23.78, SD = 13.31) were significantly higher than those for the community participants (M = 6.53, SD = 8.25; p = .000).

Table 5. Study Variable Differences and Risks in Psychiatric and Community Groups (N = 144) Hospital SD Community SD Total SD group (M) group (M) (M) BMI DASS/Stress DASS/Anxiety 24.58 24.11 15.14 5.51 9.84 9.32 13.31 10.67 21.80 10.28 6.11 6.53 8.28 3.62 9.35 7.21 8.25 7.80 23.19 17.19 10.63 15.15 9.16 4.85** 11.82** 9.46** 14.0** 9.35**

DASS/Depression 23.78 EAT score >21 indicates ED 10.06

BSQ score 85.86 >110 indicates ED

47.39

84.14

37.08 84.92

41.89

Note.**indicates significance. ED = eating disorder.

EAT-26. Significant difference was observed in the mean EAT-26 scores (p = .001) between the hospital and the community participants (Table 5). The EAT-26 score for the hospital participants (M = 10.06, SD = 10.67) was significantly higher than the EAT-26 score for the community participants (M = 8.28, SD = 7.80; p = .001). Two participants in the hospital group and one

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participant in the community group did not complete the EAT-26. The scores were not clinically significant due to the score being less than 20, as the validity of the EAT-26 depends on a score being greater than 20.

BSQ-34. No significant difference was observed in the mean BSQ-34 scores (p = .824) between the hospital and the community participants (Table 5). The BSQ-34 score for the hospital participants (M = 85.86, SD = 47.39) was not significantly higher than the BSQ-34 score for the community participants (M = 84.14, SD = 37.08; p = .824). Fifteen participants in the hospital group and three participants in the community group did not complete the BSQ-34. The scores were not clinically significant due to the score being less than 110. The validity of the BSQ-34 depends on a score being greater than 110.

Test score correlations. Significant age correlation on the scores of the DASS subtest for stress (x 2 = -.173, p = .038) and depression (x2 = -.244, p = .038) were observed. BMI was significantly correlated with the scores of EAT-26 (x2 = .338, p < .001); BSQ-34 (x2 = .391, p < .001); DASS-stress subscale (x2 = .344, p < .001); DASSanxiety subscale (x2 = .325, p < .001); and DASS-depression subscale (x2=.313, p < .001; Table 6).

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Table 6. Analysis of Participant Characteristics and Diagnostic Tests

EATp 26 value -.014 .873 .338 .304 .041 .001** .001** .130 BSQp 34 value .049 .598 .391 .361 .125 .001** .001** .163 DASS p DASS p -S value -A value -.173 .038* -.047 .575 .314 .274 .024 .001** .001* .779 .325 .303 .106 .001** .001** .206 DAS p S-D value -.244 .003* .313 .242 -.055 .001** .003* .514

Age BMI Wt Ht

Note. **p<.01 and *p<.05. **indicates significance. Ht = height, Wt = weight, S = Stress, A = Anxiety, D = Depression.

There were significant differences in the hospital participants compared to the community participants in the BMIs: F = 11.127, df = 123, p < .001; DASSanxiety subtest F = 6.793, df = 133.60, p < .001; DASS-depression subtest F = 37.48, df = 118.82, p < .001; and DASS-stress subtest F = .291, df = 142, p < .001 (Table 7). Table 7. Comparisons Between Hospital and Community Populations Category Age BMI EAT-26 BSQ-34 DASS-Stress DASS-Anxiety DASSDepression Hospital (M) 14.47 24.58 10.06 85.86 24.11 15.14 23.78 SD 1.42 5.51 10.67 47.39 9.84 9.32 13.31 Community (M) 15.57 21.89 8.28 84.14 10.28 6.11 6.53 SD 1.24 3.62 7.80 37.08 9.35 7.21 8.28 p value < .001** .001* .001* .824 < .001** < .001** < .001**

Note. **indicates significance. ** p<.01 and *p<.05.

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Summaries of Research Questions

Research Question I: Do psychiatrically disturbed and substance-abusing adolescent females (hospital participants) not previously diagnosed with an eating disorder have a higher risk of developing an eating disorder, based on EAT-26 score > 20 and/or a BSQ-34 score > 110, when compared to healthy female students drawn from the community? No significant association was found between study groups Psychiatric (hospital) versus Community and being at risk of developing an eating disorder, 2(1) = 2.29, p = 0.13, indicating that psychiatrically disturbed and substance-abusing (hospital) adolescent females not previously diagnosed with an eating disorder do not have a higher risk of developing an eating disorder, when compared to female students drawn from the community (Table 8).

Table 8. Observation of Risks (EAT-26/BSQ-34) Between Groups (Hospital vs. Community) Study Group Psychiatric, N (%) Community, N (%) Observed at risk 12 (16.7%) 6 (8.3%) Observed not at risk 60 (83.3%) 66 (91.7%)

Note. 2 (1) = 2.29, p = .13. Each study group comprised 72 participants.

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Research Question II: Do psychiatrically disturbed and substance-abusing adolescent females (hospital) not previously diagnosed with no eating disorder have a difference in age for developing an eating disorder when compared to healthy female students drawn from the community? The results of the independent samples t-test were significant, t (144) = 614, p < .01, indicating that a mean difference does exist. There was significant difference in mean age between Hospital and Community groups. The Community group (M = 15.57, SD = 1.24) was significantly older than the Hospital group (M = 14.47, SD = 1.42) (Table 9).

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Table 9. Age Distribution between Groups (Hospital vs. Community) Hospital Variable Age df 144 T -.614** M 14.47 SD 1.42 Community M 15.57 SD 1.24

Note. ** p < 0.01 and * p < 0.05. **indicates significance.

Research Question III: Do psychiatrically disturbed and substance- abusing adolescent females (hospital) not previously diagnosed with an eating disorder have a difference in BMI distribution for developing an eating disorder when compared to healthy female students drawn from the community? The results of the independent samples between two groups were significant, t (122.72) = 3.57, p < 0.01, indicating that a mean difference does exist on the dependent variable BMI between the independent grouping variable with Hospital and Community groups. The Hospital group (M = 24.58, SD = 5.51) was significantly higher than the Community group (M = 21.80, SD = 3.62). Comparison between groups was significant .000** (Table 10).

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Table 10. BMI Distribution between Groups (Hospital vs. Community) as Related to EAT-26 and BSQ-34 Scores
Community Variable BMI .01** .05* Hospital Hospital +/-(M) 24.58 SD 5.51 Community +/-(M) 21.80 SD 3.62

Note. ** p < .01 and * p < .05. ** indicates significance.

Research Question IV: What are the predictors of increasing the risk of developing an eating disorder among psychiatrically disturbed and substance-abusing adolescent females (hospital group) not previously diagnosed with an eating disorder as well as healthy female students drawn from the community? The results of the binary logistic regression predicting risk was significant. Anxiety was a significant predictor of risk for developing an eating disorder, OR = 1.11, 95% CI 0.839-0.924. BMI was also a significant predictor of risk for developing an eating disorder, OR = 1.17, 95% CI 0.800-0.946 (Table 11).

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Table 11. Summary of Risk of Developing an Eating Disorder B SE B df p OR 95% CI for OR DASSAnxiety BMI -.140 .043 1 .001 1.17 .800-.946 -.128 .025 1 .000 1.11 .839-.924

AGE

.598

.138

.98

.99

1.3872.384

ETHNICITY -.045

.299

.53

.64

.533-1.717

DASSDepression GROUP .000

-.122

.167

.852-.920

.020

1.43

.729-3.255

Model 2 (6) = 24.71, p < .01

CHAPTER SEVEN

The purpose of this observational study was to examine predictors for increased risk of developing a pattern of disordered eating. This study included high school students from two different settings: a community group and a group of girls hospitalized for depression/anxiety and/or substance abuse. We posed four hypothetical issues. The first was to show whether a significant difference existed in the presence of an eating disorder in a psychiatric population versus a community population using two standardized tests: EAT-26 and BSQ-34. This current study did not show a significant difference in those test scores between the two groups. We also examined whether age and BMI differences existed between the groups and found significance. That significance was mainly related to the sampling procedure rather than to the eating disorders. The hospitalized girls who met the criteria and volunteered to participate were younger than the community group. This study found that BMI and anxiety were significant predictors for the development of a disordered eating in both study groups: the psychiatric and the community population.

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The study is a significant contribution to the available literature on disordered eating. A review of current available data on co-morbidity showed the prevalence of anxiety disorders to be significantly higher in subjects with eating disorders than in the general community (Swinbourne & Touyz, 2007). However, our study found high levels of anxiety in the psychiatric group but no significant elevations in the scores on the EAT-26 and the BSQ-34. Published studies focused on patients already diagnosed with an eating disorder; however, our study examined a population of psychiatric patients who had not been diagnosed as having an eating disorder. In our study, the nature of the psychiatric disturbances did not seem to impact body image or eating attitude. BMI and anxiety levels were significant predictors for developing an eating disorder in both populations. This may put all teenage girls at risk if they have an elevation in either BMI or anxiety. Those predictors were consistent with the existing research on co-morbidity factors and anxiety in the development of an eating disorder (Gual et al., 2002; Godart, Flament, Pereraeu & Jeammet, 2002; Kaye et al., 2004; Godart et al., 2005).

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It was our aim to identify predictors that increase the risk of developing an eating disorder among females not diagnosed with having an eating disorder.

Characteristics of the Hospital Sample vs. Overweight Youth Seeking Treatment Compared to the community group, the psychiatric hospital group in our study had a significantly higher BMI (Mean difference was 2.78 kg/m2) and scored higher in all areas of DASS-21. These sub-tests measured subjective levels of stress, anxiety, and depression. The young women in the psychiatric group were in the hospital with diagnoses of mood disorder and / or substance abuse. However, results suggest that a positive correlation existed between BMI score and levels of stress, anxiety and depression in this patient population. The observed results of this current study were consistent with the findings of psychopathology found in overweight youngsters who have not been previously diagnosed and / or treated (Morgan et al., 2002; Isnard et al., 2003). Our findings in our population of hospitalized adolescent females are similar to the findings of current available studies on obese youngsters seeking treatment. High levels of depression were correlated with loss of

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control of eating (Goossens, Braet & Decaluwe, 2007). High levels of anxiety in another study x2(1) = 4.38, p = .04 correlated with loss of control (Goossens, Braet, Vlierberghe & Meiss, 2009). Our hospital population had high levels of depression and anxiety. Another study of overweight youth, sponsored by the National Institute of Child Health and Human Development, examined 160 overweight adolescents seeking weight loss treatment. Those overweight girls with binge eating patterns scored higher in negative mood and anxiety symptoms (p < .01) (Glasofer et al., 2007). Other studies involving overweight and treatmentseeking adolescents showed depression to be correlated with loss of control and binge eating (Colles, Dixon, & OBrien, 2008; Glasofer et al., 2007).

The Affect Regulation Model In our study, a population was taken from the adolescent unit of a freestanding psychiatric hospital. Thirty of the 72 female participants (41.7%) were overweight, as measured by BMI > 25 kg/m2. The high levels of stress, anxiety, and depression reported on the DASS subtests demonstrated a significant positive correlation of those negative emotions and higher BMI and the risk of developing an eating disorder. The term emotional eating is seen as a coping mechanism used to reduce negative emotions. Though the

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term initially originated in work with adults, researchers found that young people with loss of control over eating demonstrated a style of emotional eating (Tanofsky-Kraff et al., 2007). Our study supports the evidence of others that a correlation exists between emotional eating and depression/anxiety in treatment-seeking, overweight youngsters (Eddy et al., 2007). (The hospitalized group completed their DASS-21, EAT-26 and BSQ-34 prior to being placed on medication.)

Partial Syndrome Eating Disorders Our study was unable to identify full syndrome eating disorders. The scores on the EAT-26 and BSQ-34 were below threshold. This supports the findings that many adolescents presenting for treatment are diagnosed as partial syndrome or EDNOS (Bunnell et al., 1990; Fairburn & Harrison, 2003). Available studies on adolescents find little meaningful difference between those who meet full criteria and those who are diagnosed with a partial syndrome (Lewinsohn et al., 2000). Sub-threshold levels of eating disorder have predicted the onset of binge eating and purging behavior in late adolescence (Stice & Lock, 1998). Furthermore, longitudinal studies have found that symptoms of eating-related concerns prospectively predict partial syndrome eating disorders (Killen et al., 1996) and the onset of depression

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among initially non-depressed adolescents (Stice, Haywood, Cameron, Killen, & Taylor, 2000).

Negative Affect and Eating Behavior Our group of inpatient young women with significantly higher BMIs and high levels of anxiety can be classified as a negative affect subtype of an eating disorder similar to that of the psychiatric group of adolescent girls studied at Yale (Grilo, 2004). In that group of 137 female adolescents, affect related psychopathologies were found. Our study provided support for Grilos work that included a negative affect subtype when examining risk for the development of both an eating disorder and social maladjustment. Other research with bulimic adults has provided further support for subtyping by negative affect and binge eating disorders (Grilo, Masheb, & Wilson, 2001). Clearly youngsters who lose control over eating suffer with symptoms of psychopathology (Tanofsky-Kraff et al., 2004; Glasofer et al., 2007). Our study adds additional evidence to the available studies that focus on emotional eating. A study of 666 students of both genders, recruited from seven middle schools in Los Angeles County, showed perceived stress, worry, and anxiety to be significantly and positively correlated with emotional eating only in the female group. The authors recommended the use

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of stress reduction techniques to promote positive mood among female students (Nguyen-Rodriquez, Chou, Unger, & Spruijt-Metz, 2008). The above research was also supported by another study done in a New York suburban area high school that included 268 students. It showed that abnormal eating attitudes and behaviors in females were correlated with low self esteem and high levels of anxiety (Fisher, Schneider, Pegler, & Napolitano, 1991). Clearly youngsters who lose control over eating suffer with symptoms of psychopathology (Tanofsky-Kraff et al., 2004; Glasofer et al., 2007). Our study adds additional evidence to the available studies that focus on emotional eating. A study of 666 students of both genders, recruited from seven middle schools in Los Angeles County, showed perceived stress, worry, and anxiety to be significantly and positively correlated with emotional eating only in the female group. The authors recommended the use of stress reduction techniques to promote positive mood among female students (Nguyen-Rodriquez, Chou, Unger, & Spruijt-Metz, 2008). The above research was also supported by another study done in a New York suburban area high school that included 268 students. It showed that abnormal eating attitudes and behaviors in females were correlated with low self-esteem and high levels of anxiety (Fisher, Schneider, Pegler, & Napolitano, 1991). In our study, the dual problem of anxiety and elevated BMI increased the risk for

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disordered eating. Lowering anxiety, therefore, may help prevent the development of an eating disorder (ODea et al., 2000; Nguyen-Rodriquez et al., 2008). In addition, we have only found moderate subjective body shape concerns, even with high BMIs and high anxiety. (Moderate subjective body shape is defined as a score of 111140 on the BSQ-34). Our observed results are similar to a study done on urban teenagers that showed that the selfesteem and anxiety of the obese students did not differ from those students who had a normal body weight (Pastore, Fisher, & Friedman, 1996). Summary

The temporal relationships lead one to suspect that there may be a relationship between diagnosis and eating/body shape attitude, but one cannot state that there is a causal relationship. Furthermore, the questionnaires employed here (the EAT-26 and the BSQ-34) are widely-used screening devices that are not diagnostic in nature but only show, via elevated scores, when there is a potential problem associated with disordered eating. The significance of an elevated score in a particular patient would be open to interpretation, although elevated scores on the questionnaire in a diagnostic group would be significant. Larger sample size and the use of diagnostic instruments for each of the diagnostic categories would give a

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clearer diagnostic picture. In adolescents, co-morbidity is the rule rather than the exception. Future research in this area will need larger study populations tested with several research instruments, so that diagnoses will be clear-cut rather than relying upon the judgment of the clinician. This study required the cooperation of several child psychiatrists in order to include their patients in the study sample; researchers therefore could not be too intrusive in this study.

Study Strength The strength of this study was the ability to use simple screening instruments to point out potential problems in the areas of food attitudes and body image in adolescent girls. We were not attempting to diagnosis an eating disorder; however, we reviewed attitudes and behaviors which, if left untreated, might become an eating disorder in the future. This would certainly aid clinicians in their care of patients.

Treatment Implications for Overweight Females Our study showed that adolescent females with both elevated BMIs and the psychological issue of anxiety are at significant higher risk for developing an eating disorder. Disordered eating combined with increased body weight increases the risk of health complications including diabetes,

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metabolic syndrome, hyperlipidemia, electrolyte imbalance, and hypertension. The combination of eating problem behavior intensifies these risks and can lead to morbidity and mortality at a relatively young age (Goldschmidt, 2008). Our study points to the need to simultaneously treat overweight children as well as those presenting with co-morbid psychiatric symptoms. Treatment and prevention of obesity share the goal of developing and maintaining healthy eating patterns in those youngsters, increasing their quality of life, and prolonging longevity. Study Limitations The study was a cross sectional study that examined attitudes toward food, eating, and body image. This was not a convenience sample due to the necessity of going through the Chief Executive Officer and the Medical Executive Committee in order to apply the questionnaires to hospitalized patients. The researchers also had to overcome bureaucratic obstacles in order to obtain permission to sample community school children. While researchers were able to give the questionnaires to students in school, parents had to give permission. Therefore, information may have been

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passed on by the parent to the student, creating a potential for bias and a potential problem of internal validity for the control sample. Participant identification on the test questionnaires was a potential problem. Respondents may have felt that answers were not confidential, although the researcher reassured participants that they were. The researcher did not have access to the hospital records of hospitalized participants, and therefore socioeconomic information could not be obtained. Likewise, the parents of the community sample were not available to volunteer socioeconomic status. The researcher was told by the schools not to inquire about socioeconomic standing. The researchers did not expect to have a sufficient number of Asian or Hispanic participants compared to White and African-American participants in either group, due to the demographics of the population in the Mid-South region. Further research should perhaps recruit participants from states and/or cities with more ethnic diversity (Table 12).

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Table 12. Study Limitations and Recommendations Limitations Recommendations Administrative obstacles, e.g., gaining permission of Persons conducting research should hospital CEO, medical be employed by facility director and staff, school officials Parental involvement Have a meeting with the community parents prior to the study; ask them not to discuss their opinions with children Once parents return permission slips, assign a number to the questionnaire; respondents may be more forthcoming with truthful answers when certain of anonymity Persons conducting the research should be employed by the facility and therefore able to obtain information from participants charts Conduct research in a more diverse community

Participant identification on test questionnaires

Obtaining socioeconomic data

Representation of study population, e.g., current study sample is representative of area demographics, thus limiting the external generalization of findings

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CHAPTER EIGHT

References Abraham, S. (1996). Characteristics of eating disorder among young ballet dancers. Psychopathology, 29(4), 223229. Psychiatry, 37(suppl), 155. American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (text revision). Washington, DC: Author. American Psychiatric Association Work Group on Eating Disorders. (2000). Practice guidelines for the treatment of patients with eating disorders. American Journal of Psychiatry, 157(suppl 1), 139. Anderluh, M., Tchanturia, K., Rabe-Hesketh, S., & Treasure, J. (2003). Childhood obsessive-compulsive personality traits in adult women with eating disorders: Defining a broader eating disorder phenotype. American Journal of Psychiatry, 160, 242247. Argold, A., Costello, E. J., & Erkanil, A. (1999). Comorbidity. Journal of Child Psychology and Psychiatry, 40, 5787. Attia, E., Haiman, C., Walsh, B. T., & Flater, S. (1998). Does fluoxetine augment the inpatient treatment of anorexia nervosa? American Journal of Psychiatry, 155, 548551. Austin, S. B., Field, A. E., Wiecha, J., Peterson, K. E., & Gortmaker, S. L. (2005). The impact of a school-based obesity prevention trial on disordered weight-control behaviors in early adolescent girls. Archives of Pediatrics and Adolescent Medicine, 159(3), 225230. Bacher-Melman, R., Zobar, A. H., Nemanov, L., Heresco-Levy, U., Gritsenko, I., & Ebstein, R. (2005). Association between insulin-like growth factor 2 gene (IGF2) and scores on the Eating Attitudes Test in nonclinical subjects: a family based study. American Journal of Psychiatry, 162:12, 22562261.

114

115

Bachrach, L. K., Guido, D., Katzman, D., Litt, I. F., & Marcus, R. (1990). Decreased bone density in adolescent girls with anorexia nervosa. Pediatrics, 86, 440447. Bearman, S. K., Stice, E., & Chase, A. (2003). Evaluation of an intervention targeting both depression and bulimic pathology: A randomized prevention trial. Behavior Therapy, 34, 277293. Beidel, D. C. (1991). Social phobia and overanxious disorder in school age children. Journal of the American Academy of Child and Adolescent Psychiatry, 30, 545552. Bell, A., Dorsch, K. D., McCreary, D. R., & Hovey, R. A. (2004). A look at nutritional supplement use in adolescents. Journal of Adolescent Health, 34(6), 508516. Bernstein, G. A., & Borchardt, C. M. (1991). Anxiety disorders in children and adolescence: A critical review. Journal of the American Academy of Child and Adolescent Psychiatry, 30, 519532. Bettle, N., Bettle, O., Neumarker, L. I., & Neumarker, K. (1998). Adolescent ballet school students; their quest for body weight change. Psychopathology, 31(3), 153159. Biederman, J., Herzog, D. B., Rivinus, T. M., Harper, G. P., Ferber, R. A., & Rosenbaurm, J. F. (1985). Amitriptyline in the treatment of anorexia nervosa: A double-blind placebo-controlled study. Journal of Clinical Psychopharmacology, 5, 1016. Birmaker, B., Ryan, N. D., Williamson, D., Brent, D., Kaufman, J., Dahl, R., et al. (1996). Child and adolescent depression: A review of the past ten yearspart 1. Journal of the American Academy of Child and Adolescent Psychiatry, 35, 14271439. Black, B., & Uhde, T. W. (1995). Psychiatric characteristics of children with selective mutism: A pilot study. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 847856.

116

Boachie, A., Goldfield, G. S., & Spettigue, W. (2003). Olanzapine use as an adjunctive treatment for hospitalized children with anorexia nervosa: Case reports. International Journal of Eating Disorders, 33, 98103. Boschi, V., Siervo, M., Papa, A., Bellini, O., & Falconi, C. (2005). Application of the SCOFF, Eating Attitudes Test 26 (EAT 26) and Eating Inventory (TFEQ) Questionnaires in young women seeking diet-therapy. Eat Weight Disorders, 10(2), 7682. Boyd, C., Abraham, S., & Luscombe, G. (2007). Exercise behaviours and feelings in eating disorder and non-eating disorder groups. European Eating Disorder Review, 15(2), 112118. Braet, C., & VanWinckel, M. (2000). Long term follow up of a cognitive behavioral treatment program for obese children. Behavior Therapy, 31, 5574. Braun, D. L., Sunday, S. R., & Halmi, K. A. (1994). Psychiatric co-morbidity in patients with eating disorders. Psychological Medicine, 24, 859867. Brennell, D. W., Shenker, I. R., Nussbaum, M. P., Jacobson, M. S., & Cooper, P. (1990). Subclinical versus formal eating disorders: differentiating psychological features. International Journal of Eating Disorders, 9, 357 362. Brent, D. A., Holder, D., Kolko, K. J., Birmaher, B., Baugher, M., Roth, C., et al. (1997). A clinical psychotherapy trial for adolescent depression comparing cognitive, family and supportive treatments. Archives of General Psychiatry, 54, 877885. Brewerton, T. D. (2002). Bulimia in children and adolescents. Child and Adolescent Psychiatric Clinics of North America, 11, 237256. Bukstein, O. G., & Tarter, R. E. Substance use disorder in children and adolescences. In E. Coffey (Ed.), Textbook of pediatric neuropsychiatry (2nd ed., pp. 595616). New York: American Psychiatric Press.

117

Bulik, C. M., Sullivan, P., Fear, J., & Joyce, P. (1997). Eating disorders and antecedent anxiety disorders: A controlled study. Acta Psychiatrica Scandinavica, 96, 101107. Bulik, C. M., Tozzi, F., Anderson, C., Mazzeo, S., Aggen, S., & Sullivan, P. (2003). The relation between eating disorders and components of perfectionism. American Journal of Psychology, 160, 366368. Burton, E., Stice, E., Bearman, S. K., & Rohde, P. (2007). Experimental test of the affect regulation theory of bulimic symptoms and substance abuse: A randomized trial. International Journal of Eating Disorder, 40, 2736. Cachelin, F. M., & Maher, B. A. (1998). Is amenorrhea a critical criterion for anorexia nervosa? Journal of Psychosomatic Research, 44, 435440. Calderon, R., Vanderstoep, A., Collett, B., Garrison, M. M., & Toth, K. (2007). Inpatients with eating disorders: demographic, diagnostic, and service characteristics from a nationwide pediatric sample. International Journal of Eating Disorders, 40, 622628. Castro, J., Gila, A., Gual, P., Lahortiga, F., Saura, B., & Toro, J. (2004). Perfectionism dimensions in children and adolescents with anorexia nervosa. Journal of Adolescent Health, 35(5), 392398. Cattarin, J. A., Thompson, J. K., Thomas, C., & Williams, R. (2000). Body image, mood, and televised images of attractiveness: The role of social comparison. Journal of Social and Clinical Psychology, 19, 220239. Chambers, W. J., Puig-Antich, J., Tabrizi, M. A., & Davies, M. (1982). Psychotic symptoms in prepubertal major depressive disorder. Archives of General Psychiatry, 39, 921927. Chamorro, R., & Flores-Ortiz, Y. (2000). Acculturation and disordered eating patterns among Mexican American women. International Journal of Eating Disorders, 28(1), 125129. Clara, I. P., Cox, B. J., & Enns, M. W. (2001). Confirmatory factor analysis of the Depression Anxiety Stress Scales in depressed and anxious patients. Journal of Psychopathology and Behavioral Assessment, 23, 6167.

118

Colles, S. L., Dixon, J. B., & OBrien, P. E. (2008). Loss of control is central to psychological disturbance associated with binge eating disorder. Obesity, 16(3), 608614. Cooper, P. J., & Taylor, M. J. (1988). Body image disturbance in bulimia nervosa. British Journal of Psychiatry, 153/2, 3236. Costello, E. J., Angold, A., Burns, B. J., Stangl, D. K., Tweed, D. L., Erkanli, A., et al. (1996). The Great Smoky Mountains Study of youth goals, design, methods, and the prevalence of DSM-III-R disorders. Arch Gen Psychiatry, 53(12), 11291136. Crawford, J. R., & Henry, J. D. (2003). The Depression Anxiety Stress Scales (DASS): Normative data and latent structure in a large non-clinical sample. British Journal of Clinical Psychology, 42, 111131. Das, D., & Thomas, S. E. (2001). An overview of controlled studies of adolescent substance abuse treatment. American Journal of Addiction, 10, 178189. Davis, C., & Katzman, M. (1999). Perfection as acculturation: Psychological correlates of eating problems in Chinese male and female students living in the United States. International Journal of Eating Disorders, 25(1), 6570. Decaluwe, V., Braet, C., & Fairburn, C. G. (2003). Binge eating in obese children and adolescents. International Journal of Eating Disorders. 33(1), 7884. Delgado, P. A., Charnedy, D. S., Price, L. H., Aghajanian, G. K., Landis, H., & Neninger, G. R. (1990). Serotonin function and the mechanism of antidepressant action: Reversal of antidepressant-induced remission by rapid depletion of plasma tryptophan. Archives of General Psychiatry, 47, 411418. Devlin, B., Bacanu, S., Klump, K., Bulik, C., Fichter, M., Halmi, K., et al. (2002). Linkage analysis of anorexia nervosa incorporating behavioral covariates. Human Molecular Genetics, 11, 689696.

119

Dodge, E., Hudes, M., Eisler, I., & Dare, C. (1995). Family therapy for bulimia nervosa in adolescents: An exploratory study. Journal of Family Therapy, 17, 5977. Dotti, A., & Lazzari, R. (1998). Validation and reliability of the Italian EAT-26. Eat, Weight Disorder, 3, 188194. Duncan, A. E., Neuman, R. J., Kramer, J. R., Kuperman, S., Hesselbrock, V. M., & Bucholz, K. K. (2006). Lifetime psychiatric co morbidity of alcohol dependence and bulimia nervosa in women. Drug and Alcohol Dependency, Jan 30 (Epub ahead of print). Eddy, K. T., Tanofsky-Kraff, M., Thompson-Brenner, H., Herzog, D. B., Brown, T. A., & Ludwig, D. S. (2007). Eating disorder pathology among overweight treatment seeking youth: clinical correlates and cross sectional risk modeling. Behavioral Research and Therapy, 45, 23602371. Edman, J. L., Yates, A., Aruquete, M. S., & DeBord, K. A. (2005). Negative emotion and disordered eating among obese college students. Eating Behavior, 6(4), 308317. Eiger, M. R., Christie, B. W., & Sucher, K. P. (1996). Change in eating attitudes: An outcome measure of patients with eating disorders. Journal of the American Dietetic Association, 96(1), 6263. Eisler, I., Dare, C., Hodes, M., Russell, G., Dodge, E., & LeGrange, D. (2000). Family therapy for adolescent anorexia nervosa: The results of a controlled comparison of two family interventions. Journal of Child Psychology and Psychiatry, 41, 727736. Espina, A., Asuncion-Ortega, M., Ochoa de Alcia, T., & Juaniz, M. (2002). Body shape and eating disorders in a sample of students in the Basque Country: A Pilot Study. Psychology in Spain, 6, 311. Fairburn, C. G., & Brohn, K. (2005). Eating Disorder NOS (EDNOS): An examination of the troublesome not otherwise specified (NOS) category in DSM IV. Behavior Therapy, 43, 691701.

120

Fairburn, C. G., Cooper, Z., Doll, H. A., & Davies, B. A. (2005). Identifying dieters who will develop an eating disorder: A prospective, populationbased study. American Journal of Psychiatry, 162, 22492255. Fairburn, C. G., Cooper, Z., Doll, H. A., & Welch, S. L. (1999). Risk factors for anorexia nervosa: Three integrated case-control comparisons. Archives of General Psychiatry, 56, 468476. Fairburn, C. G., & Harrison, P. J. (2003). Eating disorders. Lancet, 361, 407416. Fairburn, C. G., Stice, E., Cooper, Z., Doll, H., Norman, P. A., & OConnor, M. E. (2003). Understanding persistence of bulima nervosa: a five year naturalistic study. Journal of Consulting and Clinical Psychology, 71, 103 109. Fairburn, C. G., Welch, S. L., Doll, H. A., Davies, B. A., & OConnor, M. E. (1997). Risk factors for bulimia nervosa: A community-based casecontrol study. Archives of General Psychiatry, 54, 509517. Favaro, A., Tenconi, E., & Santonastaso, P. (2006). Perinatal factors and the risk of developing anorexia nervosa and bulimia nervosa. Archives of General Psychiatry, 63(1), 8288. Favaro, A., Tenconi, E., Degortes, D., Soave, M., Zanetti, T., Nardi, M. T., et al. (2007). Association between low height and eating disorders: cause or effect? International Journal of Eating Disorder, 40(6), 549553. Field, A. E., Javaras, K. M., Aneja, P., Kitos, N., Camargo, C. A., Taylor, C. B., et al. (2008). Family, peer, and media predictors of becoming eating disordered. Archives of Pediatric Adolescent Medicine, 162(6), 574 579. Fisher, M., Golden, N. H., Katzman, D. K., Kreipe, R. E., Rees, J., Schebendach, J., et al. (1995). Eating disorder in adolescents: A background paper. Journal of Adolescent Health, 16, 420437. Fisher, M., Pastore, D., Schneider, M., Pegler, C., & Napolitano, B. (1994). Eating attitudes in urban and suburban adolescents. International Journal of Eating Disorders, 6774.

121

Fisher, M., Schneider, M., Burns, J., Symons, H., & Mandel, F. S. (2001). Differences between adolescents and young adults at presentation to an eating disorders program. Journal of Adolescent Health, 28, 222227. Fisher, M., Schneider, M. Pegler, C., & Napolitano, B. (1991). Eating attitudes, health-risk behaviors, self-esteem, and anxiety among adolescent females in a suburban high school. Journal of Adolescent Health, 12(5), 377-384. Franko, D. L., Dorer, D. J., Keel, P. K., Jackson, S., Manzo, M. P., & Herzog, D. B. (2005). How do eating disorders and alcohol use disorder influence each other? International Journal of Eating Disorder, 38, 200207. Franko, D. L., Dorer, D. J., Keel, P. K., Jackson, S., Manzo, M. P. & Herzog, D. B. (2008). Interactions between eating disorders and drug abuse. Journal of Nerve Mental Disorder, 196(7), 556561. French, S. A., Perry, C. L., Leon, G. R., & Fulkerson, J. A. (1994). Food preferences, eating patterns, and physical activity among adolescents: Correlates of eating disorders symptoms. Journal of Adolescent Health, 15, 286294. French, S., Story, M., Downes, B., Resnick, M., & Blum, R. (1995). Frequent dieting among adolescents: Psychosocial and health behavior correlates. American Journal of Public Health, 85, 695701. French, S., Story, M., Neumark-Sztainer, D., Downes, B., Resnick, M., & Blum, R. (1997). Ethnic differences in psychosocial and health behavior correlates of dieting, purging, and binge eating in a population-based sample of adolescent females. International Journal of Eating Disorders, 22(3), 315322. Garber, A. K., Boyer, C. B., Pollack, L. M., Chang, Y. J. & Shafer, M. A. (2008). Body mass index and disordered eating behaviors are associated with weight dissatisfaction in adolescent and young adult female military recruits. Military Medicine, 173(2), 138145. Gardner, R. M. (1996). Methodological issues in assessment of the perceptual

122

component of body image disturbance. British Journal of Psychology, 87, 327337. Garfinkel, P. E., & Garner, D. M. (1982). Anorexia nervosa: a multidimensional perspective. New York: Bruner-Mazel. Garfinkel, P. E., Lin, E., Goering, P., Spegg, C., Goldbloom, D. S., Kennedy, S., et al. (1996). Should amenorrhea be necessary for the diagnosis of anorexia nervosa? British Journal of Psychiatry, 168, 500506. Garfinkel, P. E., & Newman, A. (2001). The eating attitudes test: Twenty-five years later. Eat Weight Disorders, 6(1), 124. Garner, D. M., (1993). Self-report measures for eating disorders. Current Contents, Social & Behavioral Sciences, 25(8), 8. Garner, D. M., & Garfinkel, P. E. (1979). The Eating Attitudes Test: An index of the symptoms of anorexia nervosa. Psychology Medicine, 9, 273279. Garner, D. M., & Garfinkel, P. E. (1980). Socio-cultural factors in the development of anorexia nervosa. Psychological Medicine, 10, 647656. Garner, D. M., & Garfinkel, P. E. (1981). Body image in anorexia nervosa: Measurement theory and clinical implications. International Journal of Psychiatry and Medicine, 2(11), 263284. Garry, J. P., Morrissey, S. L., & Whetstone, L. M. (2003). Substance abuse and weight loss tactics among middle school youth. International Journal of Eating Disorders, 33, 443457. Geist, R., Heinman, M., Stephens, D., Davis, R., & Katzman, D. K. (2000). Comparison of family therapy and family group psychoeducation in adolescents with anorexia nervosa. Canadian Journal of Psychiatry, 45, 173178. Gittleman-Klein, R. (1988). Adult anxiety disorders and childhood separation anxiety. In M. Roth, & R. Noyes (Eds.), Handbook of anxiety, volume 1: Biological and cultural perspectives (pp. 213229), New York: Elsevier.

123

Glasofer, D. R., Tanofsky-Kraff, M., Eddy, K. T., Yanovski, S. Z., Theim, K. R., Mirch, M. C., et al. (2007). Binge eating in overweight treatmentseeking adolescents. Journal of Pediatric Psychology. 32(1), 95105. Godart, N. T., Curt, F., Perdereau, F., Lang, F., Venisse, J. L., Halfon, O., et al. (2005). Is depressive disorder linked to anxiety disorder among anorexics and bulimics? Encephale, 31, 40311. Godart, N. T., Flament, M. F., Curt, F., Perdereau, F., Lang, F., Venisse, J. L., et al. (2003). Anxiety disorders in subjects seeking treatment for eating disorders: A DSM-IV controlled study. Psychiatry Res, 117, 245258. Godart, N. T., Flament, M. F., Lecrubier, Y., & Jaemmet, P. (2000). Anxiety disorders in anorexia nervosa and bulimia nervosa: co-morbidity and chronology of appearance. European Psychiatry, 15, 3845. Godart, N. T., Flament, M. F., Pereraeu, F., & Jeammet, P. (2002). Comorbidity between eating disorders and anxiety disorders: a review. International Journal of Eating Disorders, 32, 253270. Godart, N. T., Perdereau, F., Curt, F., Rein, Z., Lang, F., Venisse, J.L. et al. (2006). Is major depressive episode related to anxiety disorders in anorexics and bulimics? Comprehensive Psychiatry, 47, 9198. Godart, N. T., Perdereau, F., Jeammet, P., & Flament, M. F. (2005). Comorbidity between eating disorders and mood disorders: Review. Encephale, 31, 57587. Golan, M., & Weizman, A. (2001). Familial approach to the treatment of childhood obesity: Conceptual model. Journal of Nutrition Education & Behavior, 33(2), 102107. Golden, N. H. (2003). Osteopenia and osteoporosis in anorexia nervosa. Adolescent Medicine, 14, 97108. Golden, N. H., Jacobson, M. S., Schebendach, J., Solanto, M. V., Hertz, S. M., & Shenker, I. R. (1997). Resumption of menses in anorexia nervosa. Archives of Pediatrics and Adolescent Medicine, 151, 1621.

124

Goldschmidt, A. B., Aspen, V. P., Sinton, M. M., Tanofsky-Kraff, M., & Wilfley, D. E. (2008). Disordered eating attitudes and behaviors in overweight youth. Obesity, 16, 257264. Goldstein, D. J., Wilson, M. G., Thompson, V. L., Potvin, J. H., & Rampey, A. H. (1995). Fluoxetine Bulimia Nervosa Research Group. British Journal of Psychiatry, 166, 660666. Goldstein, D J., Wilson, M. G., Ascroft, R. C., al-Banna, M. (1999). Effectiveness of fluoxetine therapy in bulimia nervosa regardless of comorbid depression. International Journal of Eating Disorders, 25(1), 19 27. Goossens, L., Braet, C., & Decaluwe, V. (2007). Loss of control over eating in obese youngsters. Behavior Research and Therapy, 45(1), 19. Goossens, L., Braet, C., Vlierberghe, L. V. & Meis, S. (2009). Loss of control over eating in overweight youngsters: The role of anxiety, depression, and emotional eating. European Eating Disorders Review. 17, 6878. Gowers, S. G. & Shore, A. (2001). Development of weight and shape concerns in the etiology of eating disorders. British Journal of Psychiatry, 179, 236 242. Graber, J., Brooks-Gunn, J., Paikoff, R., & Warren, M. (1994). Prediction of eating problems: An 8-year study of adolescent girls. Developmental Psychology, 30, 823834. Grice, D. E., Halmi, K. A., Fichter, M. M., Strober, M., Woodside, D. M., Treasure, G., et al. (2002). Evidence of a susceptibility gene for anorexia nervosa on chromosome 1. American Journal Human Genetics, 70, 787 792. Grilo, C. M. (2004). Subtyping female adolescent psychiatric inpatients with features of eating disorders along dietary restraint and negative affect dimensions. Behavior Res Therapy, 42(1), 6778. Grilo, C. M., Masheb, R. M. & Wilson, G. T. (2001). Subtyping binge eating disorder. Journal of Consulting and Clinical Psychology, 69, 10661072.

125

Gross, H. A., Ebert, M. H., Faden, C. B., Goldberg, S. C., Nee, L. E., & Kaye, W. H. (1981). A double blind controlled trial of lithium carbonate in primary anorexia nervosa. Journal of Clinical Psychopharmacology, 1, 376 381. Grunbaum, J. A., Kann, L., Kinchen, S. A., Williams, B., Ross, J. G., Lowry, R., et al. (2002). Youth risk behavior surveillance: United States, 2001. Journal of School Health, 72, 313328. Guarda, A. S., Coughlin, J. W., Cummings, M. (2004). Chewing and spitting in eating disorders and its relationship to binge eating. Eating Behaviors, 5(3), 231239. Gual, P., Perez-Gaspar, M., Martinez-Gonzalez, M. A., Lahortiga, F., de IralaEstevez, J., & Cervera-Enguix, S. (2002) Self-esteem, personality, and eating disorders: Baseline assessment of a prospective populationbased cohort. International Journal of Eating Disorders, 31, 261273. Halmi, K. A., Eckert, E., LaDu, T .J., & Cohen, J. (1986). Anorexia nervosa: Treatment efficacy of cyproheptadine and amitriptyline. Archives of General Psychiatry, 43, 177181. Halmi, K. A., Stuess, A., & Goldberg, S. C. (1978). An investigation of weights in the parents of anorexia nervosa patients. Journal of Nervous and Mental Disease, 166, 358361. Hartman, D., Crisp, A., Rooney, B., Rackow, C., Atkinson, R., & Patel, S. (2000). Bone density of women who have recovered from anorexia nervosa. International Journal of Eating Disorders, 28, 107112. Hautala, L., Junnila, J., Helenius, H., Vaananeu, A. M., Liuksila, P. R., et al. (2008). Adolescents with fluctuating symptoms of eating disorders: a 1year prospective study. Journal of Adolescent Nursing, 62(6), 674680. Heesacker, R., & Neimeyer, G. (1990). Assessing object relations and social cognitive correlates of eating disorders. Journal of Counseling Psychology, 37, 419426.

126

Henry, J. D. & Crawford, J. R. (2005). The short-form version of the Depression Anxiety Stress Scales (DASS-21): Construct validity and normative data in a large non-clinical sample. British Journal of Clinical Psychology, 44, 227239. Hentherton, T. F., & Baumeister, R. F. (1991). Binge eating as escape from self awareness. Psychological Bulletin, 710, 86108. Herzog, D. B., Keller, N. B., Sacks, N. R., Yeh, C. J., & Lavori, P. W. (1992). Psychiatric co-morbidity in treatment-seeking anorexics and bulimics. Journal of the American Academy of Child & Adolescent Psychiatry, 31, 810 818. Hoek, H. W., & VanHoeken, D. (2003). Review of the prevalence of eating disorders. International Journal of Eating Disorders, 34(4), 383396. Hoek, H. W., vanHarten, P., vanHoeken, D., & Susser, E. (1998). Lack of relation between culture and anorexia nervosa: Results of an incidence study on Curacao. New England Journal of Medicine, 23, 12311232. Horesch, N., Apter, A., Lepkifer, E., Ratzoni, G., Weizman, R., & Tyano, S. (1995). Life events and severe anorexia nervosa in adolescence. Acta Psychiatrica Scandinavica, 91, 59. Hrabosky, J. I., & Grilo, C. M. (2007). Body image and eating disordered behavior in a community sample of Black and Hispanic women. Eating Behavior, 8(1), 106114. Isnard, P., Michel, G., & Frelut, M. L. (2003). Binge eating and psychopathology in severely obese adolescents. International Journal of Eating Disorders, 34, 235243. Isner, J. M., Roberts, W. C., Heymsfield, S. B., & Yager, J. (1985). Anorexia and sudden death. Annuals of Internal Medicine, 102, 4952. Jacobi, C., Hayward, C., deZwaan, M., Kraemer, H. C., & Agras, W. S. (2004). Coming to terms with risk factors for eating disorders: application of risk terminology and suggestions for a general taxonomy. Psychology Bulletin, 130(1), 1965.

127

Jaffe, S. L., & Simkin, D. R. (2002). Alcohol and drug abuse in children and adolescents. In M. Lewis (Ed.), Child and adolescent psychiatry: A comprehensive textbook (pp. 895911). Philadelphia: Lippincott, Williams, and Wilkins. Jaffe, S. L., & Solhkhah, R. (2004). Substance abuse disorder. In J. Wiener, & M. Dulcan (Eds.), Textbook of Child and Adolescent Psychiatry (pp. 795 812). Washington, DC: American Psychiatric Publishing, Inc. Jensen, P. S., & Hoagwood, K. (1997). The book of names: DSM IV in context. Development and Psychology, 9, 231249. Kandel, D. (2002). Stages and pathways of drug involvement. Examining the gateway hypothesis. Cambridge, UK: Cambridge University Press. Karwautz, A., Rabe-Hesketh, S., Hu, X., Zhao, J., Sham, P., Collier, D. A., et al. (2001). Individual-specific risk factors for anorexia nervosa: A pilot study using a discordant sister-pair design. Psychological Medicine, 31, 317329. Kay, T. (1990). Iron deficiency and sources of iron. British Journal of General Practice, 40(334), 217218. Kaye, W. H., Bulik, C. M., Thornton, L., Barburick, N., & Masters, K. (2004). Co-morbidity of anxiety disorders with anorexia and bulimia. American Journal of Psychiatry, 161(12), 22152221. Kaye, W. H., & Strober, M. (1999). Neurobiology of eating disorders. In D. Charney, E. Nestler, & B. Bunney (Eds.), Neurobiological Foundations of Mental Illness (pp. 891906). New York: Oxford University Press. Keel, P., Dorer, D., Eddy, K., Franko, D., Charatan, D., Herzog, D. (2003). Predictors of mortality in eating disorders. Archives of General Psychiatry, 60, 179183. Keel, P. K., Dorer, D. J., Franko, D. L., Jackson, S. C., & Herzog, D. D. (2005). Post remission predictors of relapse in women with eating disorders. American Journal of Psychiatry, 162, 22632268.

128

Kenardy, J., Arnow, B. & Agras, W. S. (1996). The adversiveness of specific emotional distress associated with binge eating in obese subjects. Australian New Zealand Journal of Psychiatry, 30, 839844. Kenny, M. E., & Hart, K. (1992). Relationship between parental attachment and eating disorders in an inpatient and a college sample. Journal of Counseling Psychology, 39, 521526. Khan, K., Green, R., Saul, A., Bennett, K, Crichton, K., Hopper, J., et al. (1996). Retired elite female ballet dancers and nonathletic controls have similar bone mineral density at weight bearing sites. Journal of Bone and Mineral Research, 11, 15661574. Killen, J. D., Taylor, C. B., Hayward, C., Haydel, K. F., Wilson, D. M., Hammer, L., et al. (1996). Weight concerns influence the development of eating disorders: A 4-year prospective study. Journal of Consulting Clinical Psychology, 64, 936940. King, R. D., Gaines, L. S., Lambert, E. W., Summerfelt, W. T., & Buckman, L. (2000). The co-occurrence of psychiatric substance use diagnosis in adolescents in different service systems: Frequency, recognition, cost, and outcomes. Journal of Behavioral Health Service Resources, 27, 417430. Kjelsas, E., Bjornstrom, C., & Gotestam, G. (2004). Prevalence of eating disorders in female and male adolescents (1415 years). Eating Behaviors, 5(1), 1325. Klump, K., Ringham, R., Marcus, M., & Kaye, W. (2001, November). A family history/family study approach to examining the nature of eating disorder risk in ballet dancers: Evidence for gene-environment combinations? Paper presented at the annual meeting of the Eating Disorder Research Society, Albuquerque, NM. Kotler, L. A., Devlin, M. J., Davies, M., & Walsh, B. T. (2003). An open trial of fluoxetine for adolescents with bulimia nervosa. Journal of Adolescent and Child Psychopharmacology, 13, 329335. Kovacs, M. (1996). Presentation and course of major depressive disorder

129

during childhood and later years of the lifespan. Journal of the American Academy of Child and Adolescent Psychiatry, 35, 705715. Kreipe, R. E, & Birndorf, D. O. (2000). Eating disorders in adolescents and young adults. Medical Clinics of North America, 84(4), 10271049. Lacy, J. H., & Crisp, A. H. (1980). Hunger, food intake, and weight: The impact of clomipramine on a refeeding anorexia nervosa population. Postgraduate Medical Journal, 56, 7985. Le Grange, D., Eisler, I., Dare, C., & Russell, G. F. M. (1992). Evaluation of family treatments in adolescent anorexia nervosa: A pilot study. International Journal of Eating Disorders, 10, 2240. Lewinsohn, P. M., Hops, H., Roberts, R. E., & Seeley, J. R. (1993). Adolescent psychopathology: I. Prevalence and incidence of depression and other DSM-III-R disorders in high school students. Journal of Abnormal Psychology, 102, 133144. Lewinsohn, P. M., Striegel-Moore, R. H., & Seeley, J. P. (2000). Epidemiology and natural course of eating disorders in young women from adolescence to young adulthood. Journal of the American Academy of Child and Adolescent Psychiatry, 39, 12841292. Lilenfeld, L., Kaye, W., Greeno, C., Merikangas, K., Plotnikovik, K., & Pollice, C. (1998). A controlled family study of restricting anorexia and bulimia nervosa: Co-morbidity in probands and disorders in first-degree relatives. Archives of General Psychiatry, 55, 603610. Lock, J. (1999). How clinical pathways can be useful: An example of a clinical pathway for the treatment of anorexia nervosa in adolescents. Journal of Clinical Child Psychology & Psychiatry, 4, 331. Lock, J. (2002). Treating adolescents with eating disorders in the family context: Empirical and theoretical considerations. Child & Adolescent Psychiatric Clinics of North America, 11(2), 331342. Lovibond, S. H. & Lovibond, P. F. (1995) Manual for the Depression, Anxiety, Stress Scales (2nd ed). Sydney: Psychology Foundation.

130

Lovibond, P. F., & Lovibond, S. H. (1994) The structure of negative emotional states: Comparison of the Depression Anxiety Stress Scales (DASS) with the Beck Depression and Anxiety Inventories. Behavior Research and Therapy, on line February 2000. Lowry, R., Galuska, D. A., Fulton, J. E., Wechsler, H., & Kann, L. (2002). Weight management goals and practices among U.S. high school students: Associations with physical activity, diet, and smoking. Journal of Adolescent Health, 31, 133144. Lucas, A. R., Beard, C. M., OFallon, W. M., & Kurland, L. T. (1988). Anorexia nervosa in Rochester, Minnesota: A 45-year study. Mayo Clinic Proceedings, 63, 433442. Lucas, A. R., Beard, C. M., OFallon, W. M., & Kurland, L. T. (1991). Fifty-year trends in the incidence of anorexia nervosa in Rochester, Minnesota: A population-based study. American Journal of Psychiatry, 148, 917922. Mahusmita, M., Soyka, L., Miller, K., Grinspoon, S., Levitsky, S. & Klibanski, L. (2003). Regional body composition in adolescents with anorexia nervosa and changes with weight recovery. American Journal of Clinical Nutrition, 77: 13611367. Martin, C. S., & Winters, K. C. (1998). Diagnosis and assessment of alcohol use disorders among adolescents. Alcohol Health and Research World, 22, 95 105. McKnight Investigators. (2003). Risk factors for the onset of eating disorders in adolescent girls: Results of the McKnight Longitudinal Risk Factor Study. American Journal of Psychiatry. 160, 248254. Mitchell, J., McConley, E., Burle, P. M., & Mass, S. J. (1988). Phenomenology of depression in children and adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 1, 1220. Mitchell, J. E., Raymond, N., Specker, S. (1993). A review of the controlled trials of pharmacotherapy and psychotherapy in the treatment of bulimia nervosa. International Journal of Eating Disorders, 14(3), 229247.

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Morgan, C. M., Yanovski, S. Z., Nguyen, T. T., McDuffie, J., Sebring, N. G., Jorge, M. R., et al. (2002). Loss of control over eating, adiposity, and psychopathology in overweight children. International Journal of Eating Disorders, 31(4), 4304330. National Center for Health Statistics. (2003). Overweight children and adolescents: United States, 19992000. Washington, DC: United States Government Printing Office. National Institute for Clinical Excellence. (2004). Eating disorders: Core intervention in the treatment and management of eating disorders in primary and secondary care. London: National Institute for Clinical Excellence. National Task Force on the Prevention and Treatment of Obesity. (2000). Dieting and the development of eating disorders in overweight and obese adults. Archives of Internal Medicine, 160, 25812589. Neumark-Sztainer, D., Eisenberg, M. E., Fulkerson, J. A., Story, M., & Larson, N. I. (2008). Family meals and disordered eating in adolescents: longitudinal findings from project EAT. Archives of Pediatric Medicine, 162(1), 1722. Neumark-Sztainer, D., Well, M., Guo, J., Story, M., Haines, J., et al. (2006). Author reply, Journal of American Dietetic Association, 106(9), 1360 1361. Nguyen-Rodriquez, S. T., Chou, C. P., Unger, J. B., & Spruijt-Metz, D. (2008). BMI as a moderator of perceived stress and emotional eating in adolescents. Eating Behavior, 9(2), 238246. OConnor, P., Lewis, R., Kirchner, E., & Cook, D. (1996). Eating disorder symptoms in former female college gymnasts: Relations with body composition. American Journal of Clinical Nutrition, 64, 840843. ODea, J. A., & Abraham, S. (2000). Improving the body image, eating attitudes, and behaviors of young male and female adolescents: a new educational approach that focuses on self-esteem. International Journal of Eating Disorders, 28(1), 4357.

132

Ogden, C. L., Carroll, M. D., Curtin, L. R., McDowell, M. A., Tabak, C. J., et al. (2006). Prevalence of overweight and obesity in the United States, 19992004. Journal of the American Medical Association, 295, 15491555. Ogren, F. P., Huerter, J. V., Pearson, P. H., Antonson, C. W., & Moore, G. F. (1987). Transient salivary gland hypertrophy in bulimics. Laryngoscope. 97, 951953.

Pastore, D. R., Fisher, M., & Friedman, S. B. (1996). Abnormalities in weight status, eating attitudes, and eating behaviors among urban high school students: correlations with self-esteem and anxiety. Journal of Adolescent Health, 18, 312319 Pine, D. S., Cohen, E., Gurley, D., Brook, J., & Ma, Y. (1998). The risk for early adulthood anxiety and depressive disorders in adolescents with anxiety and depressive disorders. Archives of General Psychiatry, 55, 5664. Powers, P. S., Santana, C. A., & Bannon, Y. S. (2002). Olanzapine in the treatment of anorexia nervosa: An open label trial. International Journal of Eating Disorders, 32, 146154. Powers, P. S., Simpson, H., & McCormack, T. (2005). Anorexia nervosa and psychosis. Primary Psychiatry, 12(4), 3945. Quay, H. C., & LaGreca, A. M. (1986). Disorders of anxiety, withdrawal, and dysphoria. In H. C. Quay, & J. S. Werry (Eds.), Psychopathological disorders of childhood (3rd ed., pp. 111155). New York: John Wiley & Sons. Raynor, H., Maier, D., Dietz, K., Kieras, M. A. (2006). What is the evidence of a causal relationship between dieting, obesity, and eating disorders in youth. Journal of the American Dietetic Association, 106(9), 135960. Robin, A. L., Siegel, P. T., Koepke, T. Moye, A. W., & Tice, S. (1994). Family therapy versus individual therapy for adolescent females with anorexia nervosa. Journal of Developmental and Behavioral Pediatrics, 15, 111116.

133

Robin, A. L., Siegel, P .T., Patricia, T., Moge, A. W., Gilroy, M., Dennis, A. B., et al., (1999). A controlled comparison of family versus individual therapy for adolescents with anorexia nervosa. Journal of the American Academy of Child and Adolescent Psychiatry, 38, 14821489. Robins, L. N., & McEvoy, L. (1990). Conduct problems as predictors of substance abuse. In L. Robins, & M. Ruller (Eds.), Straight and devious pathways from childhood to adulthood (pp. 182204). Cambridge, England: Cambridge University Press. Roerig, J. L., Mitchell, J. E., deZwann, M., Wonderlich, S. A., Kamran, S., Engbloom, S., et al. (2003). The eating disorder medicine cabinet revisited: a clinicians guide to appetite suppressants and diuretics. International Eating Disorders, 33, 443457. Rome, E. S., Ammerman, S., Rosen, D. S., Keller, R. J., Lock, J., Mammel, K. A., et al. (2003). Children and adolescents with eating disorders: The state of the art. Pediatrics, 111, 98108. Rosen, J. C., Jones, A., Ramirez, E., & Waxman, S. (1996). Body Shape Questionnaire: studies of validity and reliability. International Journal of Eating Disorders, 3, 315319. Rosenvinge, J. H., Borgen, J., & Borresen, R. (1999). The prevalence and psychological correlates of anorexia nervosa, bulimia nervosa, and binge eating among 15-year-old students: A controlled epidemiological study. European Eating Disorders Review, 7, 382391. Ruffolo, J. S., Phillips, K. A., Menard, W., Fay, C., & Weisberg, R. B. (2005). Co-morbidity of body dysmorphic disorder and eating disorders: Severity of psychopathology and body image disturbance. International Journal of Eating Disorders, 39, 1119. Russell, G. F. M., Szmukler, G. I., Dare, C., & Eislet, I. (1987). An evaluation of family therapy in anorexia nervosa and bulimia nervosa. Archives of General Psychiatry, 44, 10471056. Ryan, N. D., Puig-Antich, J., Ambrosini, P., Rabinovich, H., Robinson, D.,

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Nelson, B., et al. (1987). The clinical picture of major depression in children and adolescents. Archives of General Psychiatry, 44, 854861. Sands, R., Tricker, J., Sherman, C., Armatas, C., & Maschette, W. (1997). Disordered eating patterns, body image, self-esteem, and physical activity in preadolescent school children. International Journal of Eating Disorders, 21, 159166. Santos, M., Richards, C. S., & Bleckley, M. K. (2007). Comorbidity between depression and disordered eating in adolescents. Eating Behaviors, 8(4), 440449. Saporetti, G., Sancini, S., Bassoli, L., Castelli, B. & Pellai, A. (2004). Risk assessment for eating disorders in a high school: A study based on the Eating Attitudes Test 26. Minerva Pediatrics, 56(1), 8390. Schiff, R. J., Wurzel, C. L., Brunson, S. C., Kasloff, I., Nussbaum, M. P., & Frank, S. D. (1986). Death due to chronic syrup of ipecac use in a patient with bulimia. Pediatrics, 78, 412416. Schmidt, U., Tiller, J., & Treasure, J. (1993). Setting the scene for eating disorders: Childhood care, classification, and course of illness. Psychological Medicine, 23, 663672. Shamire, T., Golden, N. H., Arden, M., Filiberto, L., & Shenker, I. R. (2003). Resolution of vital sign instability: An objective measure of medical stability in anorexia nervosa. Journal of Adolescent Health, 32, 7377. Sharp, C. W., & Freeman, C. P. (1993). The medical complications of anorexia nervosa. British Journal of Psychiatry, 162, 452462. Shoebridge, P., & Gowers, S. (2000). Parental high concern and adolescentonset anorexia nervosa. British Journal of Psychiatry, 176, 132137. Silberg, J. L., & Bulik, C. M. (2005). The developmental association between eating disorders symptoms and symptoms of depression and anxiety in juvenile twin girls. Journal of Child Psychology and Psychiatry, 46, 1317 1326.

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Smolak, L., Murren, S. K., Ruble, A. E. (2000). Female athletes and eating problems: a meta-analysis. International Journal of Eating Disorders, 27(4), 371380. Sodersten, P., & Bergh, C. (2006). Letter to the Editor. American Journal of Psychiatry, 163, 327. Soo, K. L., Shariff, Z. M., Taib, M. N. & Samah, B. A. (2008). Eating behavior, body image, and self-esteem of adolescent girls in Mayaysia. Journal Perception Mot Skills, 106, 833844. Soyka, L. A., Grinspoon, S., Levitsky, L. L., Herzog, D. B., & Klibanski, A. (1999). The effects of anorexia nervosa on bone metabolism in female adolescents. Journal of Clinical Endocrinology & Metabolism, 84, 4489 4496. Soyka, L. A., Misra, M., Frenchman, A., Miller, K. K., Grinspoon, S., Schoenfeld, D.A., et al., (2001). Recovery from osteopenia in adolescent girls with anorexia nervosa. Postgraduate Medical Journal, 77(907), 305 311. Speranza, M., Corcos, M., Godart, N., Loas, G., Guilbaud, O., Jeammet, P., et al. (2001). Obsessive compulsive disorders in eating disorders. Eating Behavior, 2, 193207. Spindler, A. & Milos, G. (2007). Links between eating disorder symptom severity and psychiatric comorbidity. Eating Behavior, 8(3), 364373. Srinivasagam, N. M., Kaye, W. H., Plotnicov, K. H., Greeno, C., Weltzin, T. E., & Rao, R. (1995). Persistent perfectionism, symmetry, and exactness after long-term recovery from anorexia nervosa. American Journal of Psychiatry, 152, 16301634. Steiner, H., & Lock, L. (1998). Anorexia nervosa and bulimia nervosa in children and adolescents: A review of the past ten years. Journal of the American Academy of Child and Adolescent Psychiatry, 37(4), 352359. Steven, J. P. (2002). Applied multivariate statistics for the social sciences (4th ed.). Mahwah, NJ: Lawrence Erlbaum Associates.

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Stice, E. (2001). A prospective test in the dual pathway model of bulimia pathology: Mediating effects of dieting and negative affect. Journal of Abnormal Psychology, 110, 124135. Stice, E. (2002). Risk and maintenance factors for eating pathology: a meta analytic review. Psychological Bulletin, 128, 825848. Stice, E., & Agras, W. S. (1999). Subtyping bulimic women along dietary restraint and negative affect dimensions. Journal of Consulting and Clinical Psychology, 67, 460469. Stice, E., Haywood, C., Cameron, R. P., Killen, J. D., & Taylor, C. B. (2000). Body-image and eating disturbances predict onset of depression among female adolescents: a longitudinal study. Journal of Abnormal Psychology, 109, 438444. Stice, E., Maxfield, J., & Wells, T. (2003). Adverse effects of social pressure to be thin on young women: An experimental investigation of the effects of fat talk. International Journal of Eating Disorders, 34(1), 108117. Stice, E., Presnell, K., & Bearman, S. K. (2001). Relation of early menarche to depression, eating disorders, and comorbid substance abuse among adolescent girls. Developmental Psychology, 37, 608619. Stice, E., Presnell, K., Shaw, H., & Rohde, P. (2005). Psychological and behavioral risk factors for obesity onset in adolescent girls: A prospective study. Journal of Clinical Psychology. 73(2), 195202. Stice, E., Presnell, K., & Spangler, D. (2002). Risk factors for binge eating onset: A prospective investigation. Health Psychology, 21, 131138. Stice, E., Schupak-Neuberg, E., Shaw, H. E., & Stein, R. I. (1994). Relation of media exposure to eating disorder symptomology: An examination of mediating mechanisms. Journal of Abnormal Psychology, 103(4), 836840. Stice, E., & Whitenton, K. (2002). Risk factors for body dissatisfaction in adolescent girls: A longitudinal investigation. Developmental Psychology, 38, 669678.

137

Steiner, H., & Lock, L. (1998). Anorexia nervosa and bulimia nervosa in children and adolescents: A review of the past ten years. Journal of the American Academy of Child and Adolescent Psychiatry, 37(4), 352359. Striegel-Moore, R., & Franko, D. L. (2003). Epidemiology of binge eating disorder. International Journal of Eating Disorder, 34(suppl), 1929. Striegel-Moore, R., Silberstein, L., & Rodin, J. (1986). Toward an understanding of risk factors for bulimia. American Psychologist, 41, 246 263. Striegel-Moore, R., Silberstein, L., & Rodin, J. (1993). The social self in bulimia nervosa: Public self-consciousness, social anxiety, and perceived fraudulence. Journal of Abnormal Psychology, 102, 297303. Strober, M., Freemore, R., Lampert, C., Diamond, J. & Kaye, W. (2000). Controlled family study of anorexia nervosa and bulimia nervosa: Evidence of shared liability and transmission of partial syndromes. American Journal of Psychiatry, 157, 393401. Sullivan, P. F. (1995). Mortality in anorexia nervosa. American Journal of Psychiatry, 152, 10731074. Swinbourne, J. M., & Touyz, S. W. (2007). The co-morbidity of eating disorders and anxiety disorders: A review. European Eating Disorders Review. 15(4), 253274. Tanofsky-Kraff, M., Faden, D., Yanovski, S. Z., Wilfley, D. E., & Yanovski, J. A. (2005). The perceived onset of dieting and loss of control eating behaviors in overweight children. International Journal of Eating Disorders, 38, 112122. Tanofsky-Kraff, M., Theine, K. R., Yanovski, S. Z., Bassett, A. M., Burns, M. P., Ranzenhofer, L. M., et al. (2007). Validation of the emotional eating scale adapted for use in children and adolescents (EES-C). International Journal of Eating Disorders, 40, 232240. Tanofsky-Kraff, M., Yanovski, S. Z., Wilfley, D., Marmarosh, C., Morgan, C.

138

M., & Yanovski, J. A. (2004). Eating disordered behaviors, body fat, and psychopathology in overweight and normal-weight children. Journal of Consulting and Clinical Psychology, 72, 5361. Thaw, J. M., Williamson, D. A., & Martin, C. K. (2001). Impact of altering DSM IV criteria for anorexia and bulimia nervosa on the base rates of eating disorder diagnosis. Eating and Weight Disorders, 6, 121129. Thiels, C., & Patel, J. (2008). Survey of disordered eating and behaviour in children and adolescents. The Young Children, Psychiatry/Psychotherapy, 36(4), 265274. Twerski, A. J. (1999). The thin you within you. New York: St. Martins Press. Vandereycken, W. (1984). Neuroleptics in the short-term treatment of anorexia nervosa: A double-blind placebo-controlled study with sulpiride. British Journal of Psychiatry, 144, 288292. VonRanson, K. M., Kaye, W. H., Weltzin, T. E., Rao, R., & Matsunaga, H. (2001). Obsessive-compulsive disorder symptoms before and after recovery from bulimia nervosa. American Journal of Psychiatry, 158, 503 504. Walsh, B. T., Wilson, G. T., & Loeb, K. L. (1997). Medication and psychotherapy in the treatment of bulimia nervosa. American Journal of Psychiatry, 154, 523531. Walters, E. E., & Kendler, K. S. (1995). Anorexia nervosa and anorexia-like syndromes in a population-based female twin sample. American Journal of Psychiatry, 152, 6471. Weisz, J. R., Donnenberg, G. R., Han, S. S., & Kauneckis, D. (1995a). Child and adolescent psychotherapy outcomes in experiments versus clinics: Why the disparity? Journal of Abnormal Child Psychology, 23, 83106. Weisz, J. R., Donnenberg, G. R., Han, S. S. & Weiss, B. (1995b). Bridging the gap between laboratory and clinic in child and adolescent psychotherapy. Journal of Consulting and Clinical Psychology, 63, 688701.

139

Weisz, J. R., & Hawley, K. M. (2002). Developmental factors in the treatment of adolescents. Journal of Consulting and Clinical Psychiatry, 70, 2143. Werry, J. S. (1991). Overanxious disorder: A review of its taxonomic properties. Journal of the American Academy of Child and Adolescent Psychiatry, 30, 533544. White, M. A., & Grilo, C. M. (2005). Ethnic differences in the prediction of eating and body image disturbances among female adolescent psychiatric inpatients. International Journal of Eating Disorder, 38(1), 78 84. Wilson, G. T. (1999) Cognitive behavior therapy for eating disorder: Progress and problems. Behavior and Therapy, 37(suppl 1), S7995. Wittchen, H. U., Nelson, C. B., & Lanchner, G. (1998). Prevalence of mental disorders and psychosocial impairments in adolescents and young adults. Psychological Medicine, 28, 109128. Yaeger, J., Chair: Work Group on Eating Disorders (2006). American Psychiatric Association, Practice Guidelines for the treatment of patients with eating disorders. (3rd ed). American Journal of Psychiatry, 163, 7(suppl), 5. Yanez, A. M., Peix, M. A., Atseria, N., Aman, A., & Brug, J. (2007). Association of eating attitudes between teenage girls and their parents. International Journal of Social Psychiatry, 53(6), 507513.

APPENDIX

IRB Hospital Permission Subject Release & Subject Fliers Protocol for Obtaining Weight and Height Demographic Questionnaire Parent Letter EAT-26 BSQ-34 Permission from Dr. Garner DASS-21

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PROJECT TITLE:

PROJECT START DATE:

PROJECT END DATE:

The Presence of Eating Disorder Tendencies in Female Adolescent patients with Depression or Substance Abuse..Eating Attitudes and Body Image Disturbances.

Recruitment: hospitalized patients and community subjects inpatients with a diagnosis of depression or substance use disorder PRINCIPAL Name Student ID Degree(s)/Degree Sought School/College

Study: To identify if ED is co morbid with adolescent female

Phone No.

INVESTIGATOR:

Nadine King

ph0212019 PhD

Touro University International

901-763-0940

Mailing Address 6437 Massey Estates Cove Memphis, TN 38120

e-mail

nadinemsrd@juno.com
APPLICATION STATUS:

XX

New

Addendum

Renewal

Previous IRB number, if applicable:

BRIEF DESCRIPTION OF PROJECT:

This study will examine the prevalence of missed cases of adolescents at risk of developing an ED. The two groups will consist of an inpatient, female psychiatric group, and a group of middle and high school female students. They will all complete the same questionnaires. The scoring of the tests will indicate the prevalence of eating disorders in each group. The project will span the time necessary to recruit subjects and their completion of the questionnaires.

CAN THE RESEARCH BE DONE WITHOUT HUMAN SUBJECTS?

No, the research cannot be completed without human subjects.

DESCRIBE THE POOL OF SUBJECTS:

The subjects will be females, ages 12-17, DSM-IV primary Axis I psychiatric diagnosis of Depression or Substance Use Disorder. In the adolescent student group we will screen out those adolescents with an Axis I psychiatric disorder or ED, to the best of our knowledge.

HOW ARE SUBJECTS TO BE RECRUITED?

Subjects will be recruited through the designated psychiatric hospital and direct from community schools.

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DESCRIBE ANTICIPATED RISKS/DISCOMFORT TO THE SUBJECTS:

There are no anticipated risks. Discomforts for the subjects may include answering several of the questions in this study.

HOW IS PRIVACY AND CONFIDENTIALITY ENSURED?

Any information that is obtained in connection with this study and that can be identified with a subject will remain confidential and will be disclosed only with the permission of subject and legal guardian or if required by law. Results of tests are used for statistical analysis and no names are included. The researcher will enter the data into SPSS which will be maintained on a disc. This disc will be stored in a locker drawer in the researchers office.

DESCRIBE ANY DECEPTION TO BE USED WITH HUMAN SUBJECTS: There will be no deception used on the human subjects.

IF PROCEDURES ARE POTENTIALLY HARMFUL, DESCRIBE ARRANGEMENTS FOR MEDICAL REFERRAL OR OTHER ASSISTANCE:

The procedures used in this study are not harmful.

WHAT PROVISIONS HAVE BEEN MADE FOR CULTURAL OR LANGUAGE PROBLEMS, SHOULD THEY ARISE?

The investigator will research any unknown cultures should the need arise. Should a language barrier arise, the investigator will receive assistance from someone proficient in the language.

HAS CONSENT BEEN OBTAINED FROM AUTHORITIES IN A FOREIGN JURISDICTION?

No research will be conducted in a foreign country.

DOES THE INVESTIGATOR HAVE ANY FINANCIAL INTEREST IN THE RESEARCH? IF SO, BRIEFLY EXPLAIN AND ATTACH STATEMENT TO BE DISTRIBUTED TO SUBJECTS.

The researcher does not have any financial gain from the project

THE FOLLOWING SHOULD BE ATTACHED TO YOUR APPLICATION:

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1. 2. 3. 4. 5. 6.

INFORMED CONSENT (CERTIFIED TRANSLATION WHERE APPLICABLE) RESEARCH PROTOCOL AS SET FORTH IN THE APPLICANTS PROPOSAL SURVEYS, QUESTIONNAIRES, ETC CONTACT LETTERS, FLYERS, ADVERTISEMENTS, ETC USED TO RECRUIT SUBJECTS STATEMENT CONCERNING FINANCIAL INTERESTS OF INVESTIGATOR WRITTEN PROOF OF CONSENT OR COMPLIANCE WITH REQUIREMENTS OF FOREIGN JURISDICTIONS

INVESTIGATORS ASSURANCE

I certify that the information provided in this application is complete and correct. I understand that as Principal Investigator, I have ultimate responsibility for the conduct of the study, the ethical performance of the project, the protection of the rights and welfare of human subjects, and strict adherence to any stipulations imposed by the IRB. I agree to comply with all TUI policies and procedures, as well as with all applicable federal, State, and local laws regarding the protection of human subjects in research, including, but not limited to, the following: performing the project according to the approved protocol, implementing no changes in the approved protocol or consent form without prior IRB approval (except in an emergency, if necessary to safeguard the well-being of human subjects), obtaining the legally effective informed consent from human subjects or their legally responsible representative, and using only the currently approved, stamped consent form with human subjects,

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promptly reporting significant or untoward adverse effects to the IRB in writing within 5 working days of occurrence.

______________________________________________________________________________________________

Principal Investigator, TUIU

Date

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MEMO

DATE: February 15, 2007 TO: Touro University Dissertation Committee

FROM: Andrew Mayo, PhD Chief Executive Officer SUBJECT: Study On Co-Morbidity Of Eating Disorders And Psychiatric Disorders In Adolescent Females

Please be advised that the aforementioned study and review has been presented to, and approved by, both the Medical Executive Committee and the Board Of Governors of Parkwood Behavioral Health System. If you need any additional information, please do not hesitate to contact me at 662/893-7102. Thanks very much.

:ne

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CONSENT TO PARTICIPATE IN A RESEARCH PROJECT:

The Presence of Eating Disorder Tendencies in Female Adolescent Patients with Depression or Substance Use: Eating Attitudes and Body Image Disturbances You are asked to participate in a research study conducted by Nadine King, M.S., R.D., L.D.N., doctoral candidate from the Health Sciences department of Touro University International. The results of this study will contribute to a dissertation.

PURPOSE OF THE STUDY:

This study is designed to assess whether those girls ages 12-17 years also suffer from an unrecognized Eating Disorder.

PROCEDURES:
If you volunteer to participate in this study, you will do the following: As a subject participant, 1. You will be asked to complete four questionnaires and a demographic questionnaire given to you. 2. You will be asked about your age. Your height and weight will be

collected by a health care professional.

POTENTIAL RISKS AND DISCOMFORTS:

There are minimal risks, discomforts or inconveniences for this research project. The discomfort may be from some of the questions.

PAYMENT FOR PARTICIPATION:

There will be no payment for participation.

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CONFIDENTIALITY:
Any information that is obtained in connection with this study that can be identified with you will remain confidential and will be disclosed only with your permission or if required by law. Results of your BMI, EAT, and BSQ* will be included in reported statistics but names will not be included.

PARTICIPATION AND WITHDRAWAL:

Your participation is strictly voluntary and you have the right to withdraw at any time during the study period. You may refuse to answer any questions you dont want to answer and still remain in the study. The investigator may withdraw you from this research if circumstances arise which in the opinion of the researcher warrant it. Parental consent is required for those under the age of 18. IDENTIFICATION OF INVESTIGATORS: Principal Investigator-Nadine King, MS, RD 901-763-0940 (nadinemsrd@juno.com) Faculty Supervisor-S. Ghaddar, PhD (sghaddar@tuiu.edu) Institutional Review Board-A. Afrookhteh, JD, CHES RT (Ret) (aafrookhteh@tuiu.edu) SIGNATURE OF RESEARCH SUBJECT AND LEGAL REPRESENTATIVE: We understand the procedures and conditions of ______________participation described above. Questions have been answered to our satisfaction, and ___________agrees to participate in this study. We would like a copy of this form. Signature of Subject (Minor)_____________________________________________ Signature of Parent (Guardian) ___________________________________________

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In my judgment the subject and legal representative are voluntarily and knowingly giving informed consent and possess the legal capacity to give informed consent to participate in this research study. Signature of Investigator Date

BMI-Body Mass Index is a persons weight in relation to height EAT-Eating Attitudes Test is a persons perception of ingesting food BSQ-Body Shape Questionnaire is a persons idea of how their body appears

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YOUNG WOMEN NEEDED AGES 12 TO 17

TO PARTICIPATE IN A RESEARCH PROJECT THAT EXAMINES HEALTH PERCEPTIONS (how you see yourself) YOU AND YOUR GUARDIAN WILL SIGN A PERMISSION PAPER YOU WILL COMPLETE FOUR FORMS (ABOUT 20 MINUTES) THAT TALK ABOUT HEALTH PERCEPTIONS. (YOUR NAME WILL NOT APPEAR NEXT TO ANY PERSONAL INFORMATION IN THE RESEARCH) THE NURSE WILL MEASURE YOUR HEIGHT AND WEIGHT.

THANK YOU FOR YOUR HELP.

YOUR DOCTOR HAS GRANTED PERMISSION FOR THE STUDY TO BE CONDUCTED

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YOUNG WOMEN NEEDED AGES 12 TO 17

TO PARTICIPATE IN A RESEARCH PROJECT THAT EXAMINES HEALTH PERCEPTIONS (how you see yourself) YOU WILL NEED TO ASK YOUR PARENT FOR PERMISSION YOU WILL MEET WITH THE RESEARCHER FOR AN INFORMATION SESSION DURING SCHOOL COMPLETE 4 QUESTIONNAIRES (IN Class) ABOUT HEALTH PERCEPTIONS HAVE YOUR HEIGHT AND WEIGHT RECORDED, IN PRIVATE, BY THE RESEARCHER YOUR NAME WILL NOT APPEAR NEXT TO ANY PERSONAL INFORMATION IN THE RESEARCH THE PURPOSE OF THIS RESEARCH IS TO GATHER INFORMATION ABOUT HEALTH ATTITUDES AND PERCEPTIONS OF HEALTHY TEENAGE GIRLS VERSUS HOSPITALIZED TEENAGE GIRLS YOUR SCHOOL HAS GRANTED PERMISSION FOR THE STUDY TO BE CONDUCTED

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Protocol for Obtaining Height and Weight Have patient remove shoes and hat Weigh patient on provided scale (patient should be standing backwards) 1st weight_______ Have patient/student step off the scale then step back on for Reweigh ___________ Measure height with provided measure. (Hair to be flat and no hat) 1st height_______ Have patient/student step away then step back to Remeasure height ______

Patients initials (for identification)________ Patients date of birth__________ Patients Ethnicity____________

Thank you.

Patients BMI __________

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Demographics Questionnaire 1. Name___________________________________________ 2. Age_________________________________________ 1. education level: 1. 2. Elementary High School

2. Birthplace 1. Memphis Area 2. Olive Branch 3. Southaven 4. Tupelo Area 5. Other _____________ 3. Residence place 1. Memphis Area 2. Olive Branch 3. Southaven 4. Tupelo Area 5. Other_______________ 4. Family size: ___________________ total # of people living in a household 5. Smoking habit? 1. Never 2. Current smoking 3. Ex-smoking (stopped smoking<.) 1. Less than 6 months ago 2. Between 6 months and 1 year ago 3. More than 1 year ago 6. Alcohol habit? 1. Never

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2. 3.

Current drinker Ex-drinker

7. Do you have any tattoos/body piercing_______________ 8. How many days per week do you exercise? _______ 9. How many hours minutes do you exercise each session? ____ hours ____ minutes 10. How many hours minutes do you exercise per week? ___ hours ____ minutes 13. Do you study ballet? ___Yes ____No 14. Do any family members have an Eating Disorder_______ 1. Father 2. Mother 3. Sister 4. Brother 5. Other (specify)________________ 15. Do you consider your parents as: 6. very thin 7. thin 8. normal weight 9. Overweight 16. Do you suffer from Diabetes ______Yes ______No 17.Do you suffer from Cancer _______ Yes ______ No 18.Do you suffer from Lung disease _____ Yes _____No 19. Do you suffer from Kidney Disease ____Yes___ No 20.Do you suffer from Thyroid Disease ____Yes ___No

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21.Do you suffer from Cushing Syndrome ___Yes __No 22.Do suffer from Lupus ___ Yes ____ No 23. Do you take any pills for weight loss? 1. 2. Yes (specify) ________ No

24. Do you take any of the following medications? (check all that apply) 1. Diabetes (oral or insulin) 2. Hypertensive/ blood pressure 3. Lipid lowering medication 4. Steroids 5. Diuretics (water pills) Thank you for answering these personal questions

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Nadine King, MS, RD, LDN 6437 Massey Estates Cove Memphis, Tennessee 38120 901-763-0940 Dear Parent, My name is Nadine King and I am a Registered Dietitian seeking a PhD in Health Sciences. Your daughters school has been kind enough to allow me to do my research. The purpose of this research study is to examine the prevalence of unhealthy eating attitudes and perception of their body image. The study consists of your daughter completing three questionnaires: eating attitude questionnaire, perception of body image questionnaire and a brief demographic questionnaire. These questionnaires will take about 20 minutes to fill out. The researcher will administer them to your daughter during their school day without disruptions of their classes. The risk is quite minimal. The only anticipated risk that may be involved is your daughters discomfort in answering certain questions of the questionnaires. Confidentiality is ensured. Names are being used solely to match consent form with the questionnaire. Names are not being used in any portion of the study. Cumulative statistical data will be used. At the conclusion of the study we will share the results of the analysis with the school and hospital leadership. The data may provide information to increase the awareness of the leadership in schools and hospitals concerning teenage eating attitudes. We hope as a result of this study to help young women become more aware of possible unhealthy attitudes or perceptions that can have an impact on the young persons developing self esteem. Your daughter will gain new insights in how body perception affects eating and nutrition. None of the above can be accomplished without you and your daughter giving permission and signing the attached form.

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Please consider helping science. If you agree that your daughter participate in this research project, please sign this form and return it to school with your daughter in the next five school days. Sincerely, Member-Board of Trustees, CBHS

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Eating Attitudes Test (EAT-26)

The following screening questionnaire is designed to help you determine if your eating behaviors and attitudes warrant further evaluation. The questionnaire is not intended to provide a diagnosis. Rather, it identifies the presence of symptoms that are consistent with either a possible eating disorder. Answer the questions as honestly as you can, and then score the questions using the instructions at the end. Please mark a check to the right of each Always Usually Often Some Rarely
times

Never

Score

of the following statements:

1. 2. 3. 4. Am terrified about being overweight. Avoid eating when I am hungry. Find myself preoccupied with food. Have gone on eating binges where I feel that I may not be able to stop. 5. 6. 7. Cut my food into small pieces. Aware of the calorie content of foods that I eat. Particularly avoid food with a high carbohydrate content (i.e. bread, rice, potatoes, etc.) 8. 9. 10. 11. 12. Feel that others would prefer if I ate more. Vomit after I have eaten. Feel extremely guilty after eating. Am preoccupied with a desire to be thinner. Think about burning up calories when I exercise.

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13. 14.

Other people think that I am too thin. Am preoccupied with the thought of having fat on my body.

15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26.

Take longer than others to eat my meals. Avoid foods with sugar in them. Eat diet foods. Feel that food controls my life. Display self-control around food. Feel that others pressure me to eat. Give too much time and thought to food. Feel uncomfortable after eating sweets. Engage in dieting behavior. Like my stomach to be empty. Have the impulse to vomit after meals. Enjoy trying new rich foods.

Total Score=

1) Have you gone on eating binges where you feel that you may not be able to stop? (Eating much more than most people would eat under the same circumstances)

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No Yes How many times in the last 6 months? _________ 2) Have you ever made yourself sick (vomited) to control your weight or shape? No Yes How many times in the last 6 months? _________ 3) Have you ever used laxatives, diet pills or diuretics (water pills) to control your weight or shape? No Yes How many times in the last 6 months? _________ 4) Have you ever been treated for an eating disorder? No Yes When? ____________________

EAT-26 David M. Garner (1982)

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SCORING THE EATING ATTITUDES TEST (EAT-26) Follow the steps below:

EAT-26 ITEM SCORING: Score each item as indicated below and put score in box to the right of each item Items # 1-25: Always Usually Often Sometimes Rarely Never = = = = = = 3 2 1 0 0 0 = = = = = = Item #26 only: 0 0 0 1 2 2

Step 1

Step 2
Add item scores together for a Total EAT-26 score: Total =

Step 3

Determine if you are significantly underweight according to the table to the right

Step 4
If your EAT-26 score is 20 or more or if your weight is below the number on the weight chart to the right, we suggest that you discuss your results with your physician or therapist

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Significantly Underweight According to Height

(Body Mass Index of 18)* Height (inches) 58 58 59 59 60 60 61 61 62 62 63 63 64 64 65 65 66 66 67 67 Weight (pounds) 86 88 89 90 91 93 95 96 99 100 101 103 105 106 108 109 112 113 114 117 Height (inches) 68 68 69 69 70 70 71 71 72 72 73 73 74 74 75 75 76 76 77 77 Weight (pounds) 118 120 121 124 125 127 128 131 132 134 135 138 140 141 144 146 147 149 152 154

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* Note: The table above indicates the body weights for heights considered to be significantly underweight according to a Body Mass Index (BMI) of 18. BMI is a simple method of evaluating body weight taking height into consideration. It applies to both men and women. There is some controversy regarding whether or not BMI is the best method of determining relative body weight and it is important to recognize that it is possible for someone to be quite malnourished even though they are above the weight listed in the table. In order to determine if you are significantly underweight, locate your height (without shoes) on the table and see if the corresponding body weight (in light indoor clothing) is below that listed. If so, you are considered significantly underweight and should speak to your physician or therapist about your weight. To Calculate Body Mass Index (BMI) exactly: Weight (pounds) Divided by Height in Inches; Divide this again by Height in Inches and Multiply by 703. Formula: BMI = (lbs) (inches) (inches) X 703

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GRADING SCALE FOR THE BODY SHAPE QUESTIONNAIRE < 81 = Not worried 81110 = Slightly worried 111140 = Moderately worried > 141 = Extremely worried

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Dear Ms. King Thank you for your request for information on the Eating Attitudes Test (EAT). You have permission to copy EAT as well as to use it in your research and clinical work. There is no charge for this permission. When citing the EAT-26, please use the following credit line: Reproduced with permission by Dr. D. Garner (Garner et al., 1982. The eating attitudes test: Psychometric features and clinical correlates. Psychological Medicine, 12, 871-878). Further information on the EAT-26 can be obtained from: www.river-centre.org I would appreciate you providing me with a copy of any reports or publications in which this instrument is used since it may serve as a useful resource for other researchers and clinicians. Best wishes, David M. Garner, Ph.D. President and CEO, River Centre Clinic 5465 Main Street Sylvania, Ohio 43560 USA Phone: 419-885-8800 Fax: 419-885-8600 e-mail: garner@river-centre.org

From: nadinemsrd@juno.com [mailto:nadinemsrd@juno.com] Sent: Wednesday, September 14, 2005 11:55 AM To: Front Desk Subject: permission to use EAT in graduate research 9/14/05 Doctor Garner,

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DASS21
The rating scale is as follows: 0 1 2 3

Name:

Date:

Please read each statement and circle a number 0, 1, 2 or 3 which indicates how much the statement applied to you over the past week. There are no right or wrong answers. Do not spend too much time on any statement.

Did not apply to me at all Applied to me to some degree, or some of the time Applied to me to a considerable degree, or a good part of time Applied to me very much, or most of the time 1 2 3 4 5 6 7 8 9 I found it hard to wind down I was aware of dryness of my mouth I couldn't seem to experience any positive feeling at all I experienced breathing difficulty (eg, excessively rapid breathing, breathlessness in the absence of physical exertion) I found it difficult to work up the initiative to do things I tended to over-react to situations I experienced trembling (eg, in the hands) I felt that I was using a lot of nervous energy I was worried about situations in which I might panic and make a fool of myself I felt that I had nothing to look forward to I found myself getting agitated I found it difficult to relax I felt down-hearted and blue I was intolerant of anything that kept me from getting on with what I was doing I felt I was close to panic I was unable to become enthusiastic about anything I felt I wasn't worth much as a person I felt that I was rather touchy I was aware of the action of my heart in the absence of physical 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

10 11 12 13 14 15 16 17 18 19

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exertion (eg, sense of heart rate increase, heart missing a beat) 20 21 I felt scared without any good reason I felt that life was meaningless 0 0 1 1 2 2 3 3