Michael J Devlin Stephen A Wonderlich B Timothy Walsh and James E Mitchell

The following dialogue takes place in an eating disorders clinic at an academic medical center, in the present time. The telephone rings.

Research

Assistant: Hello, Eating Disorders Treatment Research Program, RA speaking.

Caller: Hello, this is C. I've been struggling for more than 20 years with a terrible binge eating problem. You may remember me - I called your clinic back in 1990, and you had nothing to offer me. I'm still having exactly the same problems that I was having back then. Has anything gotten better in the meantime?

RA: I'm glad you called back, C, and I'm sorry you've been suffering for so long. I'm happy to say that the situation has indeed improved. For starters, we now have a name for what you have. It's called binge eating disorder, or BED, and we've developed a number of different treatment approaches, including different forms of psychotherapy, medication, and even self-help approaches. We'll need to meet with you to find out exactly what your goals are and what type of approach would be most helpful.

C: I'm glad I'm not the only person who has this problem.

RA: Far from it. Many people have had and continue to have similar problems. It's taken us a long time for us to realize what many of our colleagues in clinical practice have known for decades: that BED is a distinct problem and individuals with BED deserve help that is tailored to their particular struggles.

C: I wish I could say that I'd been able to figure out a way to get myself better in all this time, but I haven't. Why has this been such a difficult problem for me?

RA: Well, there are a lot of elements that can contribute in any given person - genetic risk factors, your individual experience, and the world we live in all play a role. The one thing I want to emphasize is that it's not due to a lack of will power.

C: That's a relief. I feel like I have a lot of will power in general, but this is something I just haven't been able to beat. So there are really other people out there with these kinds of problems? RA: You bet, and there are organizations that bring together researchers who are interested in BED with people who have suffered or are currently suffering with the problem, family members, clinicians, and anyone who wants to make the make the world a place where we can all lead healthier lives and feel better about ourselves and each other.

C: That's great, because I'm not just interested in getting help. I'm interested in helping. I want to get better and I also want to make sure that others don't have to go through this. When can I come in? Thanks to this conversation I feel like, at last, I'm ready to start.

Like the dialogue that opened the book, this is not taken verbatim from an actual conversation, but is representative of the sorts of conversations that, given the past two decades of research, growing clinical experience, and advocacy, we are now able to have. In addition, it is intended to convey the generosity of spirit of many of the patients with whom we've worked who truly are interested not only in obtaining relief from their own suffering, but in helping one another and in bringing about lasting change in the community so that those who come after us can lead lives that are healthy, productive, and free from the suffering associated with BED.

The chapters in this volume have ably reviewed the many developments in our field that have taken place over the past two decades. In closing, we will share some thoughts regarding what lies ahead in four areas: (1) psychopathology and diagnosis; (2) pathophysiologic mechanisms, particularly the question of addiction (3) treatment, and (4) advocacy and community-level change.

Psychopathology and diagnosis of BED

Studies of the psychopathology characterizing BED have significantly clarified the nature of this relatively new eating disorder. We have acquired a clearer understanding of the nature of binge eating, the importance of loss of control of eating, and the distress surrounding binge eating episodes in individuals suffering from BED. We believe that several psychopathological concepts will continue to generate significant empirical research in the near future: 1) loss of control over eating; 2) overvaluation of shape and weight; 3) heterogeneity within the BED diagnosis and the possibility of subtypes; and 4) bio-behavioral dimensions or traits associated with BED.

As the chapters in this book have highlighted, loss of control (LOC) eating is an important aspect of the BED diagnosis which is associated with levels of current distress, comorbid psychopathology, and also appears predictive of negative medical and psychiatric outcomes in several populations. However, there remain significant issues regarding LOC eating which are not well understood. Is

LOC eating simply a loss of control over eating or is this phenomenon part of a larger construct of loss of control over various other behaviors? For example, is LOC related to loss of control over spending, substance use, gambling, or other behaviors reflecting general disinhibition? What is the relationship of LOC eating to various personality traits (e.g., impulsivity, affect regulation)? What profiles of psychiatric symptoms display the strongest association to LOC eating? All of these issues raise questions about the inherent nature of LOC eating, particularly discriminant validity. Clarifying whether LOC eating represents a construct that is specific to eating versus other behaviors will help clarify our understanding of this aspect of BED and inform future studies of eating behavior in BED.

Another feature of BED psychopathology that has recently emerged in the scientific literature is overvaluation of shape and weight. The absence of this cognitive feature in the diagnostic criteria set for DSM-IV and DSM-5 differentiates BED from the other eating disorders. Evidence for the clinical utility of overvaluation of shape and weight also continues to accumulate as this trait seems tied to clinical severity of BED and also predicts response to common treatments for BED. Although overvaluation of shape and weight has been considered as a diagnostic criterion for BED, this would potentially prohibit individuals with significant binge eating problems who lack such overvaluation from being diagnosed and receiving treatment. Consequently, researchers have alternatively suggested that overvaluation of shape and weight be considered as a specifier for the BED diagnosis, which would allow useful clinical information associated with this aspect of psychopathology to inform diagnostic and clinical decision making. As the relationship of BED and overvaluation of shape and weight is more fully understood across the eating disorder research community, this cognitive feature may ultimately enhance the diagnostic framework of BED, which could further hone targets for clinical interventions.

Additionally, within-diagnosis heterogeneity in psychopathology is likely to characterize BED in the same manner that it has bulimia nervosa (BN) and anorexia nervosa (AN). An accumulating number of empirical studies document several (often three) subtypes within the diagnoses of AN and BN. Furthermore, these subtypes differ in terms of clinical features, response to treatment, and longitudinal course. The diagnosis of BED has already been characterized as having clinically useful heterogeneity related to dietary restraint and mood disturbance. Such a model suggests that one type is characterized by high levels of dietary restraint and mood disturbance while another type is characterized by high levels of dietary restraint without mood disturbance. As noted previously, considerable variability is also associated with overvaluation of shape and weight within the BED construct and future studies may effectively identify other subtypes within BED, perhaps based on personality or cognitive traits. Clarifying such heterogeneity may enhance clinical interventions by targeting subtype specific psychopathology among people with BED.

Finally, such heterogeneity within the BED diagnosis raises the issues of variability along key underlying behavioral traits or dimensions associated with BED.

Dimensional approaches to understanding AN and BN have been considered for decades. Dimensional thinking has also been seen in the growing interest in endophenotypic traits associated with the eating disorders such as cognitive set shifting, central coherence, and impulsive disinhibition. Recently the role of traits and dimensions in all areas of psychopathology has been stimulated by the Research Domain Criteria (RDoC) initiative at the National Institute of Mental Health (NIMH) in the United States. The RDoC project was initiated to implement the NIMH strategic goal to develop, for research purposes, new ways of classifying mental disorders based on behavioral and neurobiological dimensions. RDoC is a dimensional classification system which does not rely on typical diagnostic categories and attempts to measure dimensions in terms of behavioral, genetic, brain circuitry, physiologic, and self-report assessment strategies. By studying behavioral dimensions associated with BED (e.g., negative emotionality or cognitive control), which not only characterize BED, but also are linked to other forms of psychopathology, we may learn how BED, and other eating disorders are situated in the broader range of psychopathology. Also, RDoC may ultimately help to identify dimensions of behavior which are specific to the eating disorders, and perhaps even specific to BED. Clearly, although RDoC is currently designed for research purposes, it does introduce a new way of thinking about psychopathology which differs from the category based system associated with the DSM and could ultimately inform clinical perspectives.

Mechanisms underlying BED: the question of addiction

There has been significant progress in identifying factors that contribute to the development and persistence of BED. As reviewed in Chapter 3, we now know that BED tends to run in families in patterns that suggest there is a genetic component, although no specific gene has been clearly identified and replicated. The occurrence of BED is clearly associated with that of obesity, but the nature of the association - what is cart and what is horse - has not yet been elucidated. There appears to be an increased frequency of substance use disorders among those with BED, and, as referenced in the Foreword, there have been reports that more than half of individuals with BED meet criteria for "food addiction". Indeed, there are striking parallels between the symptoms of people with BED and of those who abuse substances, including excessive consumption of, and craving for, food or the abused drug, respectively. It is very likely that this overlap of symptoms reflects the involvement of some of the same neural pathways in BED and in substance use disorders. Specifically, for example, dopamine is released in the ventral striatum (nucleus accumbens) in response to the intake of palatable food and in response to the administration of drugs of abuse. The activation of these and other reward centers is positively reinforcing and leads to increased and eventually repeated attempts to acquire palatable foods and drugs of abuse. The fact that both palatable foods and substances that are abused activate similar areas of the brain is virtually certain to account for the parallels in the clinical presentations and some of the difficulties faced by individuals with BED and those who abuse drugs.

Yet, it is critical to emphasize major differences. Drugs that are abused are substances that are not required to sustain life; people can abstain from cocaine, nicotine and alcohol with no adverse consequences, and, often, with an improvement in their general state of well-being. Needless to say, the consumption of food is required to sustain life. It has been argued that people with BED are "addicted" only to certain foods, such as highly palatable sweet foods. However, objective data from meals observed in a laboratory setting indicate that the foods preferred by people with BED are not significantly different from those preferred by comparable people without BED, and, while people with BED do, indeed, consume greater amounts of food, the pattern of food consumption does not appear disturbed. That is, there does not appear to be compelling evidence that a particular food or food component constitutes for people with BED the single substance that is abused - a significant difference from people who abuse substances.

Finally, successful treatment does not require that people with BED cease consuming foods that they prefer. Rather, a number of interventions documented to be successful encourage them to consume non-binge amounts of foods that were previously problematic. This approach is distinctly different from the typical approach recommended for people with substance abuse.

For these reasons, while it is critical to understand underlying disturbances in neural circuits that are likely to be similar in BED and in substance use disorders, it is important not to over-emphasize the parallels between these disorders. Viewing individuals with BED simply as being "addicted" is likely to do more harm than good.

Treatment of BED

As reviewed in this volume, there has been considerable progress in developing effective treatment approaches for patients with BED. These include pharmacological strategies, psychotherapeutic strategies, and combinations of these approaches. With an eye toward the future, we ask: Where are we heading with regard to psychotherapy and pharmacotherapy for BED? What are the next important questions to ask regarding treatment for BED, and how should we go about asking these questions? The comments that follow, while focused on BED, reflect the broader challenges of overall effectiveness, treatment matching, and availability in the community that exist across eating disorders and psychiatric disorders in general.

What lies ahead for psychotherapy?

As detailed above, a number of treatment approaches have been devised and studied which clearly impact on the course of BED. The literature has grown dramatically since the late 1990s. Cognitive behavioral therapy (CBT) remains the best established therapy. There is also strong evidence supporting the utility of interpersonal therapy (IPT) and there are suggestions that other sorts of therapy may be effective as well, including dialectic behavior therapy (DBT), therapies targeting eating awareness and mindfulness, and some recent modifications to CBT, including enhanced cognitive behavior therapy (CBT-E) and integrative cognitive affective therapy (ICAT). So, the field is making progress. However, a number of problems remain that we hope will be addressed soon:

1 We still have not developed effective ways to match patients to the optimal specific treatments. Unfortunately, so far in most of the psychotherapy literature, the obvious matching choices have not always turned out to be best. Part of this reflects the questions that have been asked, but much of the problem reflects the fact that most of the sample sizes in the available trials have made it impossible to parse the variables necessary to adequately examine this.

2 We still have very little knowledge about predictors of response to specific therapies or parts of therapies, or how therapies actually work. Prediction, mediation and moderation must be meaningfully examined to understand mechanisms. These are difficult issues to address because of sample size, cost, and the statistical methodologies involved, in that the process of studying such variables is still evolving. Therefore it is difficult to move forward with therapeutic techniques, except on a theoretical basis. This will continue until we actually know what changes mediate and moderate the effects of therapy and what variables predict response.

3 As has been widely recognized in recent years, clinical trials have demonstrated the efficacy of therapies for a variety of disorders including BED, yet these are not routinely employed in clinical practice. While some practitioners espouse a particular therapeutic orientation, many use amalgams of techniques acquired through professional training, continuing education workshops, and reading, and very rarely use manual-based therapies in the form in which they were studied. There are a number of reasons for this. First is the tension between tailoring treatment to the individual patient using familiar practices vs. employing a manual-based treatment in the form in which its efficacy has been demonstrated. Second, training is expensive and time consuming, and many existing psychotherapy training programs across disciplines do not yet include these approaches. The barriers to collaboration between clinical research and general practice communities must be understood and overcome. Fortunately, as detailed in the Introduction to Section 2, such efforts are underway.

4 Another major problem is the limited number of therapists, even in areas where the therapy network is well developed and practitioners are available. In many parts of the world, therapy is not available even to those with insurance or ability to pay out of pocket. There is a growing gulf between what we know to work and what is actually available to patients. This cannot be addressed simply by training in available therapies but must additionally entail the implementation of methods of delivery of therapy that are far more cost effective and less dependent on the availability of individual practitioners. Such methods may include everything from telemedicine-based approaches, where therapy needs to be delivered to a distal area, to an increased utilization of group approaches, to manual- or computer-based self-help. The literature suggests that this is a growing yet largely untapped area where our expertise and our research have not caught up with the demand. To be able to meet the needs of our patients, not just now but in the future, we increasingly need to think about not only what we deliver but also how we can deliver therapy more widely and cost effectively.

What lies ahead for pharmacotherapy?

Although we posit specific linkages between given drugs and given illnesses, most of the psychopharmacological agents that we have currently are nonspecific in their effects, and not uncommonly used for a variety of psychiatric diagnoses. often there are several theoretical reasons for applying drugs developed for one condition to the treatment of other conditions for which new pharmacotherapy approaches are desirable. Sometimes this proves successful, and sometimes not. The pattern holds true for BED in that several previously available agents have been tried, with generally encouraging results. In particular the serotonin reuptake inhibitors may impact substantially on binge eating behavior, although their benefits for weight loss are modest at best. There also has been a great deal of interest in drugs that target not only on binge eating but also weight. These include topiramate and zonisamide which are not currently and never will be approved by the Food and Drug Administration in the United States for BED because they are available as generic agents. Nonetheless they have significant effect on binge eating frequency and on weight. Several other drug classes, reflecting other theoretical mechanisms, have been studied, and some appear promising. These include GABA agonists, agents that antagonize the endogenous opioid system such as naloxone and naltrexone, and combinations of drugs targeting obesity that may also suppress binge eating, several of which are in the pipeline. However, a major problem remains: drugs that suppress binge eating for the most part have minimal effects on weight and vice versa. The exceptions to this rule, i.e. the weight-reducing drugs that also suppress binge eating, are at times difficult to use and can result in significant side effects and toxicity.

So how does one achieve substantial and prolonged weight loss and at the same time suppress or eliminate binge eating behavior? one avenue of investigation stems from our growing knowledge of the psychobiology of the control of eating and appetite, including overeating and binge eating. We have learned much the past ten years about both the central and peripheral mechanisms of appetite and weight regulation. We know now that there are separate but interconnected systems in the central nervous system, the peripheral nervous system, and the gut, and the number of chemical transmitters involved, in particular peptidergic substances which have been found to play important roles, continues to multiply. Our knowledge of these factors and how to manipulate them will contribute to effective and, ideally, specific pharmacological approaches to the treatment of binge eating disorder and obesity. Additionally, there has been a growing interest in the genetics of obesity and of binge eating and, despite the complexity, progress is being made.

Ultimately, the development of treatments for BED will rely on the confluence of scientific knowledge and clinical experience. This spans our psychosocial understanding of the disorder and the ways in which we can help patients achieve healthy change in their attitudes and behaviors, along with our biological knowledge of BED and its strong genetic and psychobiological components, perhaps modifiable through pharmacologicalor other means. The end result may be a combination of approaches. Despite the complexities involves this is an exciting time with potentially rewarding opportunities for more concerted and aggressive development of new treatment approaches.

The community response to BED

As reviewed above, we have witnessed, in a relatively short time, impressive progress in our understanding of BED, including its pathophysiology, diagnosis, and treatment, and we look forward to major advances, perhaps even significant reappraisals of our current understanding, in the years ahead. Yet, regardless of advances in our understanding, those affected by BED, including patients, carers, and clinicians, will only be served to the degree to which we as a community embrace the challenge of eradicating BED and promoting both healthy lifestyles and healthy attitudes toward our bodies. The phenomenal efforts in this direction by and on behalf of those affected by BED have been well described in this volume. In closing, we wish to highlight a few hallmarks of advocacy that serve both as indicators of how far we have come and as reminders of how far we still need to go.

Advocacy is recognizing need

A real advance in the past two decades has been the sophistication with which we are able to recognize the suffering of those who seek help for binge eating. Recognition goes beyond mere acknowledgement. As reflected in the opening dialogue in the Foreword, well-meaning acknowledgement falls short of the informed empathic understanding that we as clinicians must provide in order to be most effective in helping those in need. Even prior to treatment per se, recognition and expert diagnosis can be extremely therapeutic in its own right. The challenge for us in the years ahead, as clinicians and as a society, is to provide more refined and accurate recognition for those suffering with BED as a first step toward helping. While this may sound rather abstract, it is a capability that is based on extensive and in-depth communication among patients, clinicians, researchers, and the public, and the infrastructure for this is still in its early stages of development.

Advocacy is speaking with courage and listening with humility

We tend to think of advocacy as speaking - loudly and to whoever will listen. Indeed, the courage of our convictions is essential to effective advocacy, and much has been achieved by remaining on message with regard to the central principles reflected in the preceding chapters: that BED is a serious eating disorder that deserves recognition and treatment, that BED and obesity must not be conflated, that weight stigmatization cannot be tolerated. At the same time, a willingness to question our assumptions and to listen carefully is equally essential. As suggested in the dialogues that open and close this volume, it has only been through careful listening to one another on the part of researchers, patients, and clinicians that the BED diagnosis has been recognized and codified.

We are at a point at which our community is faced with a large and rising burden of illness resulting from unhealthy weight gain-promoting lifestyles, and at the same time tremendous distress and dysfunction stemming from weight stigmatization. The eating disorders community is sensitized to the adverse effects of naming obesity as the problem, of assuming that body size or shape necessarily reflects lifestyle, and of conflating disordered eating with body type. Along with conveying this understanding to our colleagues engaged in battling what has come to be known as the obesity epidemic, we are also challenged to listen carefully to their experience and their concerns, and to embrace them as ours. We have made progress in the past two decades in bringing the eating disorders and obesity communities together and, as reviewed in Chapter 7, in developing approaches to prevention that promote both psychological and physiological health; indeed, the two are undoubtedly synergistic. Much remains to be accomplished and the well-coordinated efforts of all concerned are required to substantially elevate the level well-being in our community, recognizing that medical and psychological dimensions are inextricably intertwined.

Advocacy is sharing knowledge and skills

Words are important. As well reviewed in the Introduction to Section 2, seemingly straightforward efforts such as "dissemination" of empirically-based treatments may be undercut by the implication, intended or not, of top-down uni-directional knowledge flow. Just as motivational interviewing has taught us that motivation exists in the dyad, so our efforts at fostering expertise must be based on not simply the appearance of sharing but rather the genuine sharing of knowledge and skills, recognizing that expertise comes in many forms and, in its most highly developed form, exists in the space between researcher, clinician, patient and carers. The "virtuous cycle" model introduced herein provides a valuable framework, and its application to all areas of endeavor, including etiology, diagnosis, treatment, and prevention, will be a major challenge in the years ahead.

Advocacy is engendering the collective will to change

Ultimately, what is true for the individual is true for the community: motivation is essential for change. Unfortunately, change is expensive, consuming time, energy and money. And, of course, attempts at unilateral motivation are no more successful in the community than at the individual level. Effective motivation requires engagement and, while many strides have been made toward community engagement, much greater unity and broader involvement is possible. It is our hope that this volume represents a step in the direction of engagement of clinicians, researchers, patients, carers, policy makers, and members of the community in a joint endeavor to eliminate BED. To the degree that it promotes conversation among all of us whose lives are touched by BED, its purpose will have been well served.

Index

Page numbers in bold refer to tables.

5HTT gene 31

5HTTLPR gene 31-2

12-item Medical Outcomes Study Short

Form (SF-12) 73 24-hour phone consultation in dialectical behavior therapy 129, 134 36-item Medical Outcomes Study Short

Form (SF-36) 72, 73 196G/A (val66met) polymorphism of the BDNF gene 33

Academy for Eating Disorders (AED) 104, 245; Research-Practice Integration Initiative 104-8 active gene-environment correlation 33, 34

addiction and BED 250-1 Addiction Transfer Model 187-9 addiction treatment models 102 adolescents; anxiety in 45; in behavioral weight loss programs 170; binge eating in 42-8, 118-19; body dissatisfaction in 45, 223; body mass index in 171; depression in 45, 222; development of body image disturbance 82; dietary restraint in 46, 47; family-based therapy for anorexia nervosa 100; loss of control eating in 42-8, 119, 148, 156-7, 170-8; low self-esteem in 171, 172, 222; and negative affect 82, 171, 172; obese 43, 224; overweight 45, 47, 170, 171, 220, 224; parental influences on 36-7, 82, 177, 222; prevalence of BED 16, 18, 44; prevention of BED in 223, 224; psychosocial impairment in 43, 45, 223; risk factors for BED 94, 219, 220, 221,

222; shape and weight concern in 6, 47, 171, 172; substance abuse in 45 Adverse Childhood Experiences (ACE) study 58

advocacy for BED 229-37, 254-6 affect regulation model 47, 48, 125 affective attunement to "other" 205 affective disorders 31, 69, 71 African Americans; body mass index in 18, 19, 21; comorbidity in 16; factors influencing development of BED 18, 19; gender differences in BED 17; loss of control eating in children and adolescents 45; overweight and obese 5, 200; prevalence of BED 6, 14, 16; psychotherapy for 156; relationship between BED and obesity 20; risk factors for BED 222 age and BED 5, 17, 18 alcohol abuse 69, 187-9 see also substance abuse alternate rebellion (dialectical behavior therapy) 132, 133 American Medical Association (AMA) 245

ancillary treatment for dialectical behavior therapy 127, 129-31 anorexia nervosa (AN); and the 5HTTPR gene 31; and BED 113, 115; blame in 95; body checking and avoidance behaviors 81; body image disturbance as a diagnostic criterion 79; and childhood trauma 57; cognitive behavioral body image therapy for 84, 85, 87; dieting as a "gateway" to 206; family-based therapy for 100; gender differences in 5, 17; misconceptions about 242; overvaluation of shape and weight in 6, 80; prevalence of 5, 15, 218; resources and support for 241; shape and weight concern in 79; stigma associated with 242-3; subtypes 249 antidepressants 163-4 anxiety 45, 69, 86, 92, 232, 233 anxiety disorders; and childhood trauma 54; as a comorbid factor in BED 7, 59, 60, 69, 71; pharmacologic treatment for 162, 163, 167; in racial and ethnic groups 19 "Apparently Irrelevant Behaviors"

(dialectical behavior therapy) 131 appetite 253-4

Asian Americans 14, 16, 17, 18, 20 Asian Indian Americans 17 assessment of BED: clinical interviews for 112, 114-17; and failure to adequately identify the illness 6, 20; special considerations in 117-19; structured assessment tools for 112, 119-20 see also DSM-IV; DSM-IV-TR: DSM-5 assessment of childhood trauma 57 association studies in genetics 31 atomoxetine 164 attachment styles 205 attachment theory 103 Australian research on eating disorders 69 avoidance behavior 78, 79, 81, 82, 84, 85, 87

avoidant personality disorder (APD) 60

bariatric surgery 58, 59, 61, 182-9, 194 behavior modification 102 behavioral; activation strategies 61; component of body image 81, 85; problems 45, 69; skills 127; traits 249-50

behavioral weight loss (BWL): for children and adolescents 170; compared with interpersonal psychotherapy 148; description of 196-8; effectiveness of 8-9, 104, 137, 196; future directions 199-200; guided self-help 200; short-term and long-term outcomes 198-9

Behavioural Tech. LLC 134 Biggest Loser, The (ABC TV) 240 binge eating, definition xxiv,184, 194 Binge Eating Disorder Association (BEDA) 103, 229, 231-2, 234, 235, 236, 237 Binge Eating Disorder Task Force (NEDA) 244

binge eating in children and adolescents

42-8, 118-19 Binge Eating Scale (BES) 120 biosocial theory 125, 132 blacks see African Americans; Caribbean blacks blame: in anorexia nervosa 95; in BED 36, 37, 94, 95

body checking 78, 79, 81, 82, 84, 85, 87 body dissatisfaction: and body image disturbance 78; and childhood trauma 59; in children and adolescents 45, 82, 223; compared in BED, obesity without BED, and bulimia nervosa 79-80; and depression 79, 82; and the dual pathway model of binge eating 47; and low self-esteem 82; in obesity 79; as a risk factor for BED 221 body dysmorphic disorder (BDD) 79 body image, definition 78 body image disturbance: in anorexia nervosa 79; cognitive model of 81, 81-2; definition 78-9; development in children and adolescents 82; as a maintaining factor of BED 83, 83-4; as a risk factor for BED 82; three components of 79-81; treatments for 84-6, 129, 197 body image in racial and ethnic groups 19 body mass index (BMI): and body dissatisfaction 79; in Caucasians 18, 21; and childhood trauma 58, 59; in children and adolescents 171; considered acceptable in places of employment and colleges 243; and eating breakfast 94; in intuitive eaters 207; in obesity 68-9; as a predictor of later body dissatisfaction 82; and psychotherapy treatment 104; in racial and ethnic groups 18, 19, 20, 21; and regular meal patterns 8; report cards on in schools 244, 245; and shape and weight concern 80, 221 Body Project, The 223 borderline personality disorder (BPD) 7,

59-60, 123, 124 Boutelle, K.N. 176 boys 45, 56, 219, 221-2. see also adolescents; children brain derived neurotrophic factor (BDNF) 32-3

brain functioning 32, 250 breakfast 94

bulimia nervosa (BN): and the 5HTTPR gene 31; and BED 113, 115; body checking and avoidance behaviors 81; body image disturbance as a diagnostic criterion 79; and childhood trauma 57, 61; and comorbidity in BED 68; compared with BED xxiv; dieting as a "gateway" to 206; gender differences in 5; overlap in binge eating behavior between BED and 103; overvaluation of shape and weight in 6, 79, 80; prevalence of 5, 15, 20, 218; purging and non-purging forms 71; resources and support for 241; and serotonin functioning 31; shape and weight concern in 80; stigma associated with 242-3; subtypes 249; symptoms retained after treatment 124; treatments for 84, 85, 87, 93, 100, 124 "Burning Bridges" (dialectical behavior therapy) 133

caloric restriction in behavioral weight loss 8, 9

candidate gene association studies 31, 33 "Capitulating" (dialectical behavior therapy) 131 Caribbean blacks 16

case control association studies in genetics 30

case studies and experiments, importance of communicating 107 Casebook of Interpersonal Psychotherapy

(Markowitz and Weissman) 157 Caucasians: age and BED 18; body mass index in 18, 21; comorbidity in women 16; factors influencing development of BED 18, 19; gender differences in BED 17; loss of control eating in children and adolescents 45; obesity in 5, 200; overweight 200; prevalence of BED 6, 15; relationship between BED and obesity 20; risk factors for BED 222; shape and weight concern in 21 Celiac disease 207, 208 chain analysis in dialectical behavior therapy 127, 128, 132 childhood; emotional abuse (CEA) 55, 56, 59, 60, 82; emotional neglect (CEN) 58, 59; neglect (CN) 55-6; physical abuse (CPA) 55, 56, 58, 60; physical neglect (CPN) 58, 59, 60; sexual abuse (CSA) 54, 55, 58, 59, 60, 61, 82; trauma 54-61

Childhood Trauma Interview (CTI) 57 Childhood Trauma Questionnaire (CTQ) 57, 58

children: anxiety in 45; in behavioral weight loss programs 170; binge eating in 42-8, 118-19; body dissatisfaction in 45; body mass index in 171; depression in 45; development of body image disturbance 82; dietary restraint in

46, 47; loss of control eating in 42-8, 119, 156-7, 170-8; low self-esteem in 171, 172; and negative affect 82, 171, 172; obese 43; overweight 45, 47, 170, 171, 220; parental influences on 36-7, 82, 177, 222; prevalence of BED 44; psychosocial impairment in 43, 45; shape and weight concern in 6, 47, 171, 172; substance abuse by 45; weight-related bullying and stigma 213

Children's Appetite Awareness Training

(CAAT) program 176, 177 Chinese Americans 17 citalopram 164

clinical interviews to assess BED 112, 114-17

cognitive behavioral body image therapy 84-6, 87

cognitive behavioral model of binge eating

cognitive behavioral therapy (CBT): for bulimia nervosa 100, 124; for loss of control and binge eating in children and adolescents 171; manualized form of delivery 100-1; specialist training required for 9 cognitive behavioral therapy (CBT) for BED: compared with other treatments 125, 137, 148; description of 93; enhanced (CBT-E) 252; evidence-based nature of 103-4, 124, 156; as the gold-standard treatment 195, 252; guided self-help (CBTgsh) 103-4, 148, 200; implementing 139-46; integrative cognitive affective therapy (ICAT) 252; for racial and ethnic groups 21; rationale for modifying CBT for BED 138-9; weight loss in 8, 144, 171, 195, 196

Cognitive-Behavioural Treatment of BPD

(Linehan) 134 cognitive; distortions 93; emotional component of body image 79-80, 85; model of body image disturbance 81,

81-2; narrowing 118; restructuring 84, 85, 86, 139, 141-2, 197 collapses in binge eating 146 college attendance and student body mass index 243 commitment in dialectical behavior therapy 132 community response to BED 254-6 comorbidity, definition 67 comorbidity in BED: and dialectical behavior therapy 124; epidemiological perspective on 67-8; pharmacologic treatment for 162, 163, 167; prevalence of 7, 16; types and extent of 68-74; psychiatric disorders 5, 54, 59-61, 71, 125, 194 comorbidity in obesity 187 compensatory behaviors xxiv, 8, 115, 184 complex trauma 56 compulsive eating 102 constipation after bariatric surgery 184 costs of BED 235-6 costs of obesity to the community 4 cravings 47, 133, 176, 177, 197 Cuban Americans 17 cue reactivity model of binge eating 47 culturally diverse groups see racial and ethnic groups d-fentluramine 164, 165 D2 gene 32

daily food records in cognitive behavioral therapy 140, 141 DAT1 gene 32

depression in BED: and body dissatisfaction 79, 82; and childhood trauma 56, 60; in children and adolescents 45, 222; psychotherapy for 93, 103; in racial and ethnic groups 16, 18, 19; and shape and weight concern 7, 80 desipramine 164 diabetes 207-8, 241

diagnostic criteria for BED see DSM-IV;

DSM-IV-TR; DSM-5 dialectical abstinence 130, 132 dialectical behavior therapy (DBT) for BED: compared with cognitive behavioral therapy 125; description of

123-4; effectiveness of 103, 195, 252; rationale for modifying DBT for BED

124-5; standard DBT 126-31, 134; Stanford DBT Model 124-5, 131-4

dialectical behavior therapy for substance use disorders (DBT-SUD) 132, 133 Dialectical Behaviour Therapy for Binge

Eating and Bulimia (Safer et al.) 134 dialectical strategies 130 diary cards in dialectical behavior therapy

126,132 diet industry 207, 234 diet paradigms 208-9 dietary restraint and dieting: as a "gateway" to anorexia nervosa and bulimia nervosa 206; after bariatric surgery 184; BED patients' beliefs about 207, 233; in behavioral weight loss 104; binge eating ascribed to 46, 47; and childhood trauma 59; in children and adolescents 46, 47; and cognitive behavioral therapy for BED 139; and dialectical behavior therapy 128; patient history of and current strategies 8; as a predictor of later body dissatisfaction 82; in the restraint model of binge eating 138; as a risk factor for BED 18, 220, 224

disease-specific measures of quality of life 73

disinhibited eating 7, 48, 171, 175 dissemination and implementation research 156, 177 dissociative behavior 118, 205 distress as a criterion for diagnosing BED 71

distress tolerance 128, 132 dopamine 32, 233, 250 "double dose" of risk 34 DSM-IV: BED as a diagnostic concept in 14, 44, 73, 74; diagnostic criteria: BED 71; eating disorders not otherwise specified 102; overvaluation of shape and weight 70, 249; shape and weight concern 44, 71 DSM-IV-TR: BED categorized under eating disorders not otherwise specified 113; diagnostic criteria: BED 30; body image disturbance 79; underweight 115

DSM-5: BED included as a diagnosis 33, 100, 102, 113, 184, 231, 245; diagnostic criteria: BED 5, 33, 44; overvaluation of shape and weight 249; underweight 115 dual pathway model of binge eating 47 dumping after bariatric surgery 184 dysfunctional body-related thoughts see negative (dysfunctional) body-related cognitions dysphagia after bariatric surgery 184 dysthymia 60

early intervention in BED 244-5 Eating Disorder Diagnostic Scale (EDDS) 120

Eating Disorder Examination (EDE)

119-20, 149 Eating Disorder Examination-Questionnaire (EDE-Q) 120 eating disorder screening 245 eating disorders not otherwise specified (EDNOS): BED categorized as 99, 102, 113; cognitive behavioral body image therapy for 84-5, 87; prevalence of 243; resources and support for 241; stigma associated with 242 eating in the absence of hunger 175, 176-7 eating patterns, regular 7-8, 9, 94, 138, 139 eating rapidly 5

emotion dysregulation: and dialectical behavior therapy 123, 125, 128, 130, 132, 133; and maintenance of BED 84 emotional eating 48, 102, 175, 177, 229 Emotional Eating Scale 149 employment and body mass index 243 endogenous opioid system 253 endophenotypic traits 250 enhanced cognitive behavior therapy

(CBT-E) 252 environment and genetics of BED 29,

33-4, 36 escitalopram 164

ethnicity see racial and ethnic groups evidence-based (empirically supported)

treatments (EBTs) 92, 100, 101-2 evocative gene-environment correlation 33, 34

exercise: in behavioral weight loss 196, 198; in The Body Project 223; in cognitive behavioural therapy 195; and intuitive eating 208, 209, 214 exposure therapy 61, 84, 85 eye movement desensitization and reprocessing (EMDR) 103

family-based therapy (FBT) 100 family environments 18, 36-7, 177 family studies of BED 28-9, 33 fat intake 7

fathers and weight-related teasing 222

Filipino Americans 17

financial strain and eating disorders 18-19

flexible restraint 138, 141

fluoxetine 163-4

fluvoxamine 164

food: "addiction" 250, 251; cravings 47, 133, 176, 177, 197; "forbidden" 139, 142, 207, 208, 210; objectively large amounts xxiv, 44, 114-15, 119, 170, 183, 184; variety in 141, 207 "Food Preoccupation" (dialectical behavior therapy) 131 FTo gene 220 fullness 212-13

functional impairment in racial and ethnic groups 16 funding for BED research 230

GABA agonists 253 gastric banding surgery 188 gender: differences in anorexia nervosa 5, 17; differences in BED 5, 17; differences in bulimia nervosa 5; differences in obesity 5; as a risk factor for BED 219 gene-environment interactions 34 generalized anxiety disorder (GAD) 60, 71 generic measures of quality of life 73 genes and obesity 220 genetics of BED: and blame 94; clinical implications 34-7; and environment

29, 33-4, 36; family studies 28-9, 33; genetic studies 30-3; growing interest in 250; serotonin 31-2; twin studies 29-30, 33

genomewide association studies (GWAS)

30, 31, 33 ghrelin gene 32, 33

girls: loss of control eating in 45; physical abuse of 56; prevention programs for 223; risk factors for BED 94, 219, 220, 221-2. see also adolescents; children goals in interpersonal psychotherapy 153

Goffman, Erving 231 grief (interpersonal psychotherapy) 148, 153, 173

group therapy: in behavioral weight loss 196, 198; in cognitive behavioral therapy 139; in dialectical behavior therapy 128-9, 131-2, 134; in interpersonal psychotherapy 148, 172, 173

Growing Up Today Study (GUTS) 221 guided self-help: behavioral weight loss 200; cognitive behavioral therapy (CBTgsh) 103-4, 148, 200

health, definition 233 Health at Every Size (HAES) 103 health complications in obesity and BED 4-5

health-related quality of life 72 healthy weight intervention 223 heritability of BED 28, 29-30 Hispanics see Latinos (Hispanics) histrionic personality disorder (HPD) 60 human genome 30, 31 hypothalamus 32

impulsivity 31, 59, 124 India 156

individual therapy: in behavioral weight loss 198; in cognitive behavioral therapy 139; in dialectical behavior therapy 126, 131-2, 134; in interpersonal psychotherapy 148 integrated prevention of BED and obesity 224

integrative cognitive affective therapy

(ICAT) 252 internal-external theory of hunger 176

Internalized Weight Bias (IWB) in Obese

Patients with BED 232 International Society for Interpersonal

Psychotherapy 157 interpersonal deficits (interpersonal psychotherapy) 148, 153, 173; formulation 152; functioning 84, 128, 172; inventories 152, 172-3; model of binge eating 147, 147; interpersonal psychotherapy (IPT): for Adolescent Skills Training 172; for BED; for African Americans 156; effectiveness of 93-4, 103-4, 124, 137, 156, 195, 252; implementing 148-55; rationale for modifying IPT for BED 146-8; for bulimia nervosa 93, 100, 124; compared with other treatments 125, 148; conditions treated with 93; for loss of control eating in adolescents 171-3; for the Prevention of Excessive Weight Gain (IPT-WG) 171-2, 173 Interpersonal Psychotherapy for Group (Wilfley) 157

interpersonal relationships and behavioral weight loss 197 interpersonal role disputes (interpersonal psychotherapy) 148, 153, 173 intuitive eating 102, 206-7 Intuitive Eating and Movement (IEM): development of 206-8; tenets of and clinical implications 208-15 invalidating environments 125 Inventory of Eating Problems 149 irregular meal patterns 5, 7. see also regular meal patterns

Japanese Americans 17 Jung, Carl 206

Kessler Psychological Distress Scale

(K-10) 73 King, Nancy 208-9 Korean Americans 17

lapses in binge eating 146 Latinos (Hispanics): age and BED 18; body mass index in 18, 20; bulimia nervosa in 20; emphasis on interdependence and family 198; ethnicity as a risk factor for BED 219; factors influencing development of BED 18-19; functional impairment in 16; gender differences in BED 17; loss of control eating in children and adolescents 45; obesity in 5, 200; overweight 200; prevalence of BED 6, 14-15, 16-17, 20; relationship between BED and obesity 20; shape and weight concern in 21 LEARN Program for Weight Management

9, 196, 197 learning and respecting fullness (Intuitive

Eating and Movement) 212-13 learning theory 47, 176 Leu72Met polymorphism of the ghrelin gene 33

life charts in interpersonal psychotherapy

150-1, 152 life-threatening behaviors 127, 129 lifestyle plans for managing binge eating and weight 144-6, 145 Linehan, M.M. 123, 134 linkage studies in genetics 30-1 Longitudinal Assessment of Bariatric

Surgery Consortium 188 loss of control (LOC) eating: and assessment for bariatric surgery 183, 184; in children and adolescents 42-8, 119, 148, 156-7, 170-8; considered in BED assessment 114, 115, 248-9; as a key feature of BED xxiv; and quality of life impairment 74 low-calorie diets 197 low educational achievement and BED 18, 156

low self-esteem: associated with body dissatisfaction 82; and childhood trauma 60; in children and adolescents 171, 172, 222; and the cognitive-behavioral model of binge eating 47; as a maintaining factor for BED 84, 141; and weight-based stigma 232

maintaining factors in BED 83, 83-4, 87, 141

major depressive disorder (MDD) 60, 71 making peace with food and challenging the "food police" (Intuitive Eating and Movement) 210-11 Markowitz, J.C. 157 meal skipping 7

medical costs associated with obesity 4 melanoncortin 4 receptor gene (MC4R) 32, 220

men: anorexia nervosa and bulimia nervosa 5; Australian 69; mental health impairment in 69, 70; obesity in 5; prevalence of BED 5, 17, 71, 218, 224, 243; quality of life impairment in 74; risk factors for BED 219, 222; and the Stanford Model of dialectical behavior therapy 124 mental health impairment 69-72 metabolic abnormalities 5 metabolic syndrome 45 methylphenidate 32 Mexican Americans 17, 20 Mid-Treatment Evaluation Questionnaire in cognitive behavioral therapy 143, 144

Mid-treatment Goal Reflection in interpersonal psychotherapy 153, 154 mindfulness: in dialectical behavior therapy 123, 128, 129; during eating 132-3, 207, 212; training 103 "Mindless Eating" (dialectical behavior therapy) 131 minimization of BED symptoms 117-18 mirror exposure 85-6

misconceptions about anorexia nervosa 242

misconceptions about BED 35, 229-31, 245

molecular genetics studies 30 mood disorders 54, 59, 92, 167 motivational interviewing 223, 255 movement 214-15

naloxone 253

National Alliance on Mental Illness (US) 36

National Comorbidity Survey-Replication

Study (US) 73, 222 National Eating Disorders Association

(NEDA) 239, 240, 243, 244-5 National Health and Nutrition

Examination Survey (US, 2007-2008) 4 National Institute of Mental Health (US) 15, 250

National Latino and Asian American Study

(NLAAS) 16 National NEDA Navigator Program 244 National Survey of American Life (NSAL) 16

National Weight Control Registry (US) 94 Native Americans 200 Native Hawaiian/Pacific Islanders 200 negative affect: binge eating ascribed to 46-7, 118, 147; and The Body Project 223; and children and adolescents 82, 171, 172; as a risk factor for BED 222 negative body-related cognitions 80, 81-2,

85, 93, 139, 141-2, 163, 171 nibbling 7 nocturnal eating 7

non-binge eating obesity see obesity

(non-binge eating) Norwegian twin studies 30 Nottingham Health Profile 73 nucleus accumbens 250

obesity (non-binge eating): and assessment for bariatric surgery 183; body image disturbance in 79, 80-1, 85; body mass index in 68-9; gender differences in 5; and genes 220; and loss of control eating in children and adolescents 170, 171; medical costs associated with 4; and mental health impairment 69; misconceptions about 230, 231; prevalence of: in Caucasians 5, 200; in children and adolescents 43, 224;

in men 5; in racial and ethnic groups 5-6, 200; in the United States 4, 68, 224, 241; in women 5; worldwide 4; prevention of 224, 240, 241, 243; and psychological trauma 58; as a risk factor for BED 220-1; treatments for 8, 85, 87, 167, 234 obesity and BED: compared with non-binge eating obesity, 5-8 194-5; epidemiology of 5-6; health complications associated with 4-5; relationship between 20-1, 68-9, 250 "obesity epidemic" 239, 240, 255 objective binge eating xxiv, 44, 130 objective overeating 44 objectively (unambiguously) large amounts of food xxiv, 44, 114-15, 119, 170, 183, 184 obsessive compulsive personality disorder

(OCPD) 60 orlistat 164, 165, 167 over-exercising 128 overeating 44, 229, 230 overvaluation of shape and weight: in anorexia nervosa 6, 80; in BED 6-7, 79, 80-1, 87, 249; in bulimia nervosa 6, 79, 80; in racial and ethnic groups 19, 21; as a risk factor for BED 82; treatment for 84. see also shape and weight concern overweight: Caucasians 200; children and adolescents 45, 47, 170, 171, 220, 224; racial and ethnic groups 5, 200; in the United States 4, 220, 224

parents of binge eating children and adolescents 36-7, 82, 177, 222 passive gene-environment correlation 33-4

perceptual component of body image

80-1, 85 perfectionism 82, 84 personal costs of BED 235-6 personality disorders 7, 54, 59-60 pharmacologic treatments for BED 9, 61,

104, 137, 161-7, 199, 253-4 pharmokinetic changes in alcohol after bariatric surgery 188, 189 phone consultation in dialectical behavior therapy 129, 134 photo distortion technique 80-1 physical health impairment 68-9 picking at food 7

"Planning for the Future" worksheet 134 play in Intuitive Eating and Movement 215

plugging after bariatric surgery 184 positive body-related activities 85, 86 post-traumatic stress disorder (PTSD) 56,

57, 60, 93, 222 Post Traumatic Stress Disorder Reaction

Index (UCLA-PTSD RI) 57 prevention of BED: information on genetics used for 37; programs for 222-4; and risk factors for BED 218-22 problem-solving therapy 199 Project EAT 221

protective mechanism of BED 205 psychiatric comorbidity 5, 54, 59-61, 71, 125,194

psychodynamic psychotherapy 103 psychoeducation 84, 85, 92, 93, 101, 128, 177

psychological functioning in BED 6-7 psychological trauma and BED 57-9 psychopathology and BED diagnosis 248-50

psychosocial impairment 5, 43, 45, 194, 223

psychotherapy for BED 251-3. see also behavioral weight loss (BWL); cognitive behavioral therapy (CBT); dialectical behavior therapy (DBT); interpersonal psychotherapy (IPT) psychotropic medications 125, 195 puberty 94

public education programs for BED 245 Puerto Rican Americans 17 purging 8, 54, 71, 74, 244

quality of life impairment 72-4, 194 quality-of-life interfering behaviors 127, 128, 131

racial and ethnic groups: age and BED 17, 18; anorexia nervosa in 15; assessment of BED in 119; body image in 19; body mass index in 18, 19, 20, 21; bulimia nervosa in 15, 20; comorbidity in 16; depression in 16, 18, 19; factors influencing development of BED 17, 18-20; functional impairment in 16; gender differences in BED 17; loss of control eating in children and adolescents 45; obesity in 5-6, 200; overvaluation of shape and weight in

19, 21; overweight in 200; prevalence of BED 6, 14-16; race/ethnicity as a risk factor for BED 219-20; relationship between BED and obesity 20-1; socioeconomic status 18, 19, 20; treatment of BED 15, 21-2; within-group differences 16-17 rapid eating 5

recall biases in BED assessment 118 reclaiming movement (Intuitive Eating and

Movement) 214-15 recovery from BED 93, 94 regular meal patterns 7-8, 9, 94, 138, 139 Regulation of Cues (ROC) program 176-7

relapse prevention: in behavioral weight loss 198; in cognitive behavioral therapy 85, 139, 144, 146; in dialectical behavior therapy 132, 134; in interpersonal psychotherapy 155 relapses in binge eating 84, 93, 146, 163 relational boundaries 205 relearning hunger (Intuitive Eating and

Movement) 209-10 Resch, Elyse 206

Research Domain Criteria (RDoC) 250 research funding for BED 230 research-practice gap in BED 99-108, 199-200

respect your body's true shape and size (Intuitive Eating and Movement) 213-14 response prevention tasks 85 restaurant meals 7

restraint model of binge eating 138, 138

Restraint Theory 47

reward system of the brain 32

risk factors for BED 82, 94, 218-22;

"double dose" 34 role transitions (interpersonal psychotherapy) 148, 153, 173 Roux-en-Y gastric bypass surgery 188

satiety and satisfaction (Intuitive Eating and Movement) 211-12 science and BED 91-5 screening for binge eating 114 screening tools for detecting eating disorders 245 selective serotonin reuptake inhibitors

(SSRIs) 163-4, 167, 253 Self 206, 207, 209, 214, 215

self-blame in BED 36. see also blame in BED

self-esteem 45, 78, 197 self-injury 124, 125, 127, 131 self-monitoring in treatment 84, 138, 141, 197

self-stigma associated with BED 36 serotonin 31-2 sertraline 164

sex as a risk factor for BED 219 shame associated with weight 103, 118,

125, 130, 206, 241, 242, 243 shape and weight concern: in African American women 19; in anorexia nervosa 79; in BED 6, 7, 80, 87, 194; and body image disturbance 78; and body mass index 80, 221; in bulimia nervosa 80; in Caucasians 21; in children and adolescents 6, 47, 171, 172; in Latinos 21; and mental health impairment 69, 70-1; and quality of life impairment 74; as a risk factor for BED 221; treatments for 103, 171. see also overvaluation of shape and weight sibutramine 164, 165 silhouette technique 79-80 Skills Training Manual for Treating BPD

(Linehan) 134 skipping meals 7 slips in binge eating 146 snacking 7, 44, 139 social anxiety (phobia) 60, 127 socio-economic status of racial and ethnic groups 18, 19, 20 somatic disconnection 205-6 Stanford Model of dialectical behavior therapy 124-5, 131-4 Statistical Manual for the Use of

Institutions for the Insane (1918) 71 stimulus control 197 stress and BED 46, 93, 139, 222 structured assessment tools for BED 112, 119-20

stylistic strategies in dialectical behavior therapy 130-1 subjective binge eating xxiv, 44 subjective quality of life 72, 73 substance abuse: after bariatric surgery 187-9; alcohol 69, 187-9; and childhood trauma 54, 56, 60; in children and adolescents 45; as a comorbid factor in BED 59, 69; dialectical behavior therapy for 132, 133; and symptoms of BED 250-1 subtypes within BED 249 suicidal behavior and risk 45, 123, 124,

127, 131, 187 supportive psychotherapy 125 suppressed affect 147 symptoms of BED xxiii; 250-1;

minimized by patients 117-18 syndrome of BED xxiii-xxiv, xxiv talk therapy 234

target hierarchy in dialectical behavior therapy 126-8, 132 technologies enabling access to treatment

telephone consultation in dialectical behavior therapy 129, 134 therapist consultation team in dialectical behavior therapy 129 therapy-interfering behaviors 127 thin ideal 47, 82, 205, 207, 221, 223 timeline follow-back procedure use in

BED assessment 118 topiramate 164, 165, 167, 253 transdiagnostic model of eating disorders 83-4

trauma and BED 60-1, 103, 205, 222 Trauma Symptom Checklist for Children 57 treatment: advocating for effective 233-5; availability of not known about 6; evidence-based (empirically supported) 92, 100, 101-2; future directions 251-4; influence of comorbidity and trauma on 60-1; technologies enabling access to 156-7; types 93-4. see also behavioral weight loss (BWL); cognitive behavioral therapy (CBT); dialectical behavior therapy (DBT); interpersonal psychotherapy (IPT); pharmacologic treatments for BED; psychotherapy for BED

"treatment as usual" and evidence-based treatments 101 treatment contracts 152 treatment targets in dialectical behavior therapy 132 Tribole, Evelyn 206 twin studies of BED 29-30, 33

UCLA PTSD Reaction Index 57 Uganda 156

underweight, definition 115 United States: BED in 92; childhood trauma in 54, 55; National Comorbidity Survey-Replication Study 73, 222; obesity in 4, 68, 224, 234, 241; overweight in 4, 220, 224; twin study 30. see also racial and ethnic groups urge surfing (dialectical behavior therapy) 132, 133

validation strategies in dialectical behavior therapy 130 variety in food 141, 207 ventral striatum 250 video feedback exposure 85, 86 Vietnamese Americans 17 Virtuous Cycle model for research-practice integration 105, 105-7, 108, 256

Weigh to Eat 223-4

weight as an indicator of eating disorders 241

weight cycling 103, 195, 207, 240 weight loss: BED treatment sought for 93; and behavioral weight loss 8-9, 104, 170, 198-9; and cognitive behavioral therapy 8, 144, 171, 196; and dialectical behavior therapy 127; and pharmacologic treatment 104, 162, 163, 164, 165, 167, 195 weight outcomes after bariatric surgery

185, 185-6, 186, 187 Weight Stigma Awareness Week 231 weight-related bullying 205, 213, 232, 244

weight-related discrimination 82, 232, 240, 244

weight-related stigma: effects of 47, 70, 82, 103, 205, 213-14, 231-2, 240; reducing 36, 95, 242-3, 245 weight-related teasing 82, 125, 172,

221-2, 224 weight tolerant attitudes 19 Weissman, M.M. 157 Western influence on development of BED

in racial and ethnic groups 17, 20 whites see Caucasians Whole Foods 243 Wilfley, D.E. 157 Winfrey, oprah 187 women: anorexia nervosa and bulimia nervosa in 5; Australian 69; comorbidity in 16; emotion dysregulation in 123;

mental health impairment in 69, 70; obesity in 5; prevalence of BED 5, 17, 218, 224; quality of life impairment in 74; racial and ethnic factors in development of BED 18, 19; risk factors for BED 219, 220-1, 222; treatment of 85, 123, 124, 125 World Health Organization Brief Quality of Life Assessment (WHOQOL-BREF) 72-3

zonisamide 253

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