When anorexia nervosa was first described by Richard Morton in 1689, as what he called “nervous consumption,” and later independently by Gull and Lasègue in 1873, there was little understanding of the causes behind the condition. Then, in the late 1960s and 1970, largely promoted by Hilde Bruch’s writings, including her famous book The Golden Cage, a psychodynamic model was adopted that saw the family as the origin and etiology of the problem, like it had been for schizophrenia and autism before. Only over the past three decades has research made tremendous progress in understanding the neurobiological underpinnings of eating and other psychiatric disorders. This has come on the heels of improved technology to study the living human brain, and the fields of neuroscience and psychology developing models to tie behavior with brain function in healthy individuals and test those models in individuals with eating disorders.
Review articles of the brain-imaging literature on anorexia nervosa have repeatedly implicated reward-processing circuits, aside from pathways involved in cognition or emotion processing; nevertheless, understanding the exact neurobiology of anorexia nervosa has been challenging. My lab has pursued the study of reward circuits in anorexia nervosa and specifically the dopamine-associated prediction error model. The dopamine prediction error is a learning signal important for food approach, and animal models have suggested that neuronal dopamine activation has a central role in food intake and restriction.
The dopamine neurotransmitter system has been intensively studied and is well-characterized. Its neurons’ cell bodies lie in the brain stem in the ventral tegmental area and substantia nigra, and from there distribute to the cortical and subcortical brain. The basal ganglia, especially the ventral striatum, which includes the nucleus accumbens, receives dopaminergic input and has been involved in the drive to approach rewarding stimuli. Those reward stimuli can be unconditioned (such as sweet tastes being preferred by babies at birth) or conditioned (learned later in and throughout life), just like in Pavlov’s famous conditioning paradigm.
A central feature of dopamine neuron response is that it is triggered by unexpectancy—i.e., a discrepancy between what one expects and what, in fact, happens. After receiving an unexpected reward such as food or money, a dopamine surge is elicited in the striatum and midbrain, called a positive prediction error response. When receiving this reward becomes a regular occurrence and can be associated with a specific predictor or conditioned stimulus, the dopamine signal is elicited by the conditioned stimulus that predicts the reward. However, the dopamine system does not respond when the actual reward is received, because the prediction matches the outcome. If the reward is predicted but not received (there is no food or money after expecting it), there is a dip in dopamine activity in the brain, which reflects the negative prediction error (unexpected omission). The beauty of this model lies in its applicability to real life. For instance, a colleague surprises a coworker by leaving a piece of cake on his desk, and when he gets to his desk and sees it, he has a surge in dopamine, because there is a reward that was not expected. If this colleague now puts a piece of cake on that person’s desk every Monday, he will learn that Monday is a day when he will find a piece of cake on his desk. Biologically what happens is that when the person gets up on Monday morning, he may think of the cake that he will later receive, and “Monday” will become a conditioned stimulus and he will have a dopamine surge. However, when he gets to his desk and finds the cake, there will be no dopamine surge, because the reward received and the reward expected were similar and there was no “error” in expectation or prediction. What happens if the friendly colleague is unexpectedly sick one Monday and cannot bring the cake? The person still had the expectation of getting cake, but since there is no cake and, thus, he is experiencing an unexpected “omission” of the reward, he may feel disappointed, and that is associated with a dip in dopamine neuron activity.
This dynamic can be studied in the living human brain with functional brain imaging during application of a Pavlovian conditioning paradigm: Participants learn to associate sweet tastes or monetary stimuli with pictures of colored shapes that become the conditioned stimulus and appear on the screen before money or sweet solution is delivered. Sometimes when the participants expect to get the reward, they will not get it; at other times, the reward is delivered unexpectedly.
Using this study paradigm, adults and adolescents with anorexia nervosa repeatedly showed an elevated response to the unexpected conditions in the insula and striatum, which suggests altered dopamine function. Basic science has found that in the process of food restriction, the dopamine system in the brain gets sensitized to stimulate food seeking. We interpreted this elevated activation as a normal response to food restriction to stimulate responsiveness to rewards in the environment. This brain activation, however, does not drive eating as it would in heathy individuals. In fact, it can often be observed in individuals with anorexia nervosa that despite weight loss, fear of weight gain worsens and there is no limit as to how low the weight will drop. In our most recent study, we proposed a model of how this drive to lose weight may be perpetuated and how the elevated prediction error response fits into this behavior.1 Our findings indicate that elevated brain response correlated positively with harm avoidance—a measure of trait anxiety—but negatively with weight gain during treatment. Harm avoidance was positively correlated with drive for thinness and body dissatisfaction. We propose that when a person who develops anorexia nervosa starts to lose weight, the dopamine system quickly gets sensitized. Weight loss leads to low blood sugar and changes in hormonal and neuropeptide levels, which signal to the hypothalamus that the organism should eat. However, this biological motivation and drive to eat disagrees with the conscious motivation to not eat and lose weight, which leads to high levels of anxiety. To avoid weight gain and driven by extreme anxiety, the person with anorexia eats even less, which further reduces weight, triggers more biological drive to eat, and further increases anxiety, thus setting off a vicious cycle that is difficult to break. We have recently published this model in the journal Physiology & Behavior(https://www.sciencedirect.com/science/article/pii/S0031938418309636),2available for free download.
Understanding what is causing an eating disorder is difficult. Models like the above can help provide patients and their families with a framework to better understand anorexia nervosa and other eating disorders, and also explore targets to develop novel treatments. In my clinical practice, I routinely draw figures of the brain and how brain function can be tied to behavior, such as in Figure 1. That helps reduce the stigma and mystery around anorexia nervosa. Furthermore, identifying biological mechanisms that drive eating disorder behaviors helps develop medical models for eating disorders. It is time that we accept eating disorders as problems that not only can be associated with a variety of psychosocial triggers, but also are rooted in genetic predisposition, altered brain function, and bodily changes, similar to other disorders that involve the central nervous system and the intersection of brain and behavior.
Figure 1. The fear of eating and weight gain conflicts with the body’s signals to stimulate eating, which increases anxiety and drives further food restriction.
About the author:
Dr. Guido Frank is a professor in the department of psychiatry at the University of California San Diego. He is board certified in adult as well as child and adolescent psychiatry. In addition, he received extensive formal training in biological brain research and psychotherapy. His research interest lies in bridging clinical presentation of eating disorders with brain research to develop more effective treatments. He has been funded through the National Institute of Mental Health since 2008. His combination of extensive clinical and research training gives him a unique perspective on psychiatric disorders and treatment, taking into account all aspects of past and current experience together with potential biological underpinnings. This fosters a neuroscience based approach to treatment.
Frank, G.K.W., DeGuzman, M.C., Shott, M.E., Laudenslager, M.L., Rossi, B., & Pryor, T. (2018). Association of Brain Reward Learning Response With Harm Avoidance, Weight Gain, and Hypothalamic Effective Connectivity in Adolescent Anorexia Nervosa.JAMA Psychiatry,75(10), 1071. doi: 10.1001/jamapsychiatry.2018.2151
Frank, G.K.W., DeGuzman, M.C., & Shott, M.E. (2019). Motivation to eat and not to eat – The psycho-biological conflict in anorexia nervosa. Physiology & Behavior, 206, 185-190. doi: 10.1016/j.physbeh.2019.04.007
Exploring Best Practices in the Treatment of Severe and Enduring Anorexia Nervosa: A Pilot Study
By Melinda Parisi Cummings, Ph.D., CEDS-S and Robbi Alexander, PhD, APN, PMHCNS-BC
A robust literature shows that despite treatment, a sizable group of patients with anorexia nervosa (AN)continue to experience symptoms over a prolonged period. Some will develop a persistent illness that becomes less responsive to treatment (Treasure et al., 2015), with limited recovery and a life-long course (Ciao et al., 2016; Steinhausen, 2002). Approximately 20-25% of those with AN develop this protracted form, increasingly termed severe and enduring AN (SE-AN; Ciao, et al., 2016). While the literature presently lacks a consistent definition of SE-AN, common markers include a long duration of illness (most frequently, seven or more years) and a history of unsuccessful treatment interventions (Broomfield, et al., 2017).
As in those with other chronic illnesses, it is well documented that individuals with SE-AN typically experience diminished quality of life and long-term impairment in several important areas of functioning (Ciao et al., 2016; Arkell & Robinson, 2008) while facing high mortality rates and often feeling burdensome to their family and other loved ones (Westmoreland & Mehler, 2016). In addition, individuals with SE-AN usually have a history of multiple treatment failures, placing them at risk for demoralization and an internalized sense of failure that may be manifested by rejection of additional treatment experiences (Conti et al., 2016), loss of hope (Robinson, et al., 2015), and increased suicidality (Smith et al., 2018). The burden of illness is so high that Westmoreland and Mehler (2016) noted that many patients with SE-AN consider whether a “compassionate death” (p. 313) would be preferable to an ongoing lifetime of serial treatments with little to no time in recovery.
Patients with SE-AN present with complex clinical challenges that are distressing not only to them, but often to the providers who treat them. As patients have frequently experienced multiple courses of treatment with limited sustained benefit, treatment rejection is a common theme. Clinicians who work with this population may experience anxiety, frustration, and even hopelessness when confronted with these realities (Parisi-Cummings & Erckert, 2020), complicating the relationship between patients and treatment providers. There is an urgent need to explore new models of care for this population.
There is increasing understanding that effective treatment of patients with SE-AN may require a different treatment paradigm that better suits their unique needs. For example, Treasure et al. (2015) have proposed a staging model for AN, with different treatment approaches suggested for different stages of illness. Treatment recommendations for those with SE-AN include widening treatment goals to include improvement in quality of life and psychosocial functioning, taking a more collaborative therapeutic stance, and focusing less explicitly on weight gain and symptom remission while maintaining clear safety parameters (Bamford et al., 2015; Touyz et al., 2016; Russell et al., 2019). Strategies that focus on enhancing motivation, reducing harm, identifying goals and instilling hope are thought to be particularly helpful (Touyz, et al., 2016). It is important to note, however, that most of the literature on treatment of SE-AN is conceptual rather than empirical. Outcome studies of high methodological quality are limited, with only one randomized-controlled study with this population (Touyz et al., 2016). Treatment recommendations generally remain theoretical rather than empirically supported (Kotilahti et al., 2020), and additional research in this area is vital.
In response to calls for a treatment approach more tailored to this population, we have developed an inpatient treatment protocol that addresses core components of treatment discussed in the SE-AN literature. The protocol espouses a harm reduction model (e.g., Russell et al., 2019), promoting improvement in medical and psychological safety, avoidance of further negative consequences of illness (including additional failure experiences), and improvement in quality of life, even though patients may remain at a weight that is below that of their ideal. Treatment includes an explicit focus on enhancing adaptive functioning and social adjustment, collaborative (vs. prescriptive) goal setting around weight gain, and an appreciation for the lived experience of those with SE-AN. Our aim is that a more collaborative therapeutic stance will result in increased motivation, treatment retention, hope, and long-term engagement that may ultimately result in improved weight restoration and symptom reduction over the long haul.
A pilot study is presently underway to evaluate the protocol. Patients will be eligible to participate in the study if they meet criteria for SE-AN as evidenced by
lack of sustained recovery despite receiving appropriate treatment (i.e., consistent with current practice guidelines; Yager, 2007)
severe impairment in multiple areas of functioning (Bamford & Mountford, 2012)
long-term maintenance of a malnourished state (Steinglass & Foerde, 2016)
low expressed motivation for full recovery (Bamford & Mountford, 2012), and
illness duration of at least seven years post-adulthood. Potential participants must therefore be at least age 25.
The last criterion was identified as an additional safeguard to ensure that patients without a significantly enduring course of illness were excluded and would therefore receive a traditional, full recovery-oriented treatment. Patients with SE-AN as defined above who receive recovery-oriented treatment-as-usual will be compared to patients with SE-AN receiving treatment under the new protocol at discharge and short-term follow-up (three and six months) intervals. Outcome measures include treatment retention, BMI, eating disorder symptoms, motivation, social adjustment, quality of life, and hope. In addition, each participating patient is interviewed to gather qualitative data about the lived experience of SE-AN and their response to treatment over the course of their illness. Lastly, in recognition of the need to partner with other clinicians to provide a continuum of care, providers from the eating disorder treatment community (physicians, therapists, and dietitians) were (and continue to be) invited to offer their perspectives on best practices for the treatment of SE-AN. It is our hope that information gained from the study of patients with SE-AN and the providers who treat them will add to the body of knowledge about how best to provide care and improve the quality of life for those with SE-AN.
If you are interested in learning more about the study or participating in a provider focus group around these issues, please contact Robbi Alexander at firstname.lastname@example.org.
About the authors:
Melinda Parisi Cummings, Ph.D., CEDS-S:
A licensed psychologist with over 20 years of eating disorders expertise, Dr. Parisi Cummings is currently an Assistant Professor at Holy Family University. Prior to her faculty appointment, she served for fifteen years as Program Director of the Princeton Center for Eating Disorders Care at Penn Medicine Princeton Medical Center. She remains a consultant to the program and is an affiliate member of the Penn Medicine Princeton medical staff. She has written and presented extensively on eating disorders, including their impact on families and ethical issues in providing care, and maintains a part-time psychotherapy, supervision, and consultation practice.
Assistant Professor Graduate Counseling Psychology, Holy Family University One Campus Drive Newtown, PA 18940 215-206-2180 email: email@example.com New Jersey Licensed Psychologist Pennsylvania Licensed Psychologist
Robbi Alexander, Ph.D., APN, PMHCNS-BC:
Dr. Alexander is a registered nurse whose entire career has been spent in psychiatric/mental health nursing, with 13 years devoted to the treatment of those with eating disorders. She is currently Director of the Princeton Center for Eating Disorders, Administrative Director of Psychiatry at Penn Medicine Princeton Health and an affiliate member of the Penn Medicine Princeton medical staff. Dr. Alexander is affiliated nursing faculty at the University of Delaware and graduate student preceptor for nurse practitioner students of University of Pennsylvania Nursing. Her research interests include nursing workforce diversity and best practices for treatment of those with eating disorders.
Director, Princeton Center for Eating Disorders, Administrative Director of Psychiatry Penn Medicine Princeton Health 1 Plainsboro Rd. Plainsboro, NJ 08536 609-462-0431 email: firstname.lastname@example.org Licensed RN/APN/CNS in NJ, PA, DE, MD
Arkell, J., & Robinson, P. (2008). A pilot case series using qualitative and quantitative methods: Biological, psychological and social outcome in severe and enduring eating disorder (anorexia nervosa). International Journal of Eating Disorders, 41, 650–656.
Bamford, B., Barras, C., Sly, R., Stiles-Shields, C., Touyz, S., LeGrange, D., Hay, P., Crosby, R., & Lacy, H. (2015). Eating disorder symptoms and quality of life: Where should clinicians place their focus in severe and enduring anorexia nervosa? International Journal of Eating Disorders, 48, 133-138.
Bamford, B. H., & Mountford, V. A. (2012). Cognitive behavioural therapy for individuals with longstanding anorexia nervosa: Adaptations, clinician survival and system issues. European Eating Disorders Review, 20, 49– 59.
Broomfield, C., Stedal, K., Touyz, S., & Rhodes, P. (2017). Labeling and defining severe and enduring anorexia nervosa: A systematic review and critical analysis. International Journal of Eating Disorders, 50, 611–623.
Ciao, A. C., Accurso, E. C., Wonderlich, S. A. (2016). What do we know about severe and enduring anorexia nervosa? In S. Touyz, D. Le Grange, J. H. Lacey, & P. Hay, (Eds), Managing severe and enduring anorexia nervosa: A clinician’s guide (pp. 1-12). Routledge/Taylor & Francis Group.
Conti, J., Rhodes, P., & Adams, H. (2016). Listening in the dark: why we need stories of people living with severe and enduring anorexia nervosa. Journal of Eating Disorders, 4, 1-7.
Kotilahti, E., West, M., Isomaa, R., Karhunen, L., Rocks, T., & Ruusunen, A. (2020). Treatment interventions for severe and enduring eating disorders: Systematic review. International Journal of Eating Disorders, 53, 1280-1302.
Parisi Cummings, M., & Erckert, I. M. (2020, September 25). Working with severe and enduring eating disorders: Managing treatment resistance and refusal [Webinar]. International Association of Eating Disorders Professionals Greater Philadelphia Chapter, Newtown, PA.
Robinson, P. H., Kukucska, R., Guidetti, G., & Leavey, G. (2015). Severe and Enduring Anorexia Nervosa (SEED-AN): A Qualitative Study of Patients with 20+ Years of Anorexia Nervosa. European Eating Disorders Review, 23, 318–326.
Russell, J., Mulvey, B., Bennett, H., Donnelly, B., & Frig, E. (2019). Harm minimization in severe and enduring anorexia nervosa. International Review of Psychiatry, 31(4), 391-402, DOI: 10.1080/09540261.2019.1601073
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Steinglass, J. E. & Foerde, K. (2016). How does anorexia nervosa become resistant to change? In S. Touyz, D. Le Grange, J. H. Lacey, & P. Hay, (Eds), Managing severe and enduring anorexia nervosa: A clinician’s guide (pp. 64-75). Routledge/Taylor & Francis Group.
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Dialectical Behavioral Therapy in the Treatment of Eating Disorders
By Anna M. Karam, Ph.D. and Tiffany Brown, Ph.D.
What is DBT for Eating Disorders & Why is it Used?
Both research and clinical experience suggest that eating disorders and challenging emotions go hand in hand. For example, anxiety or depressed mood may precede an episode of restriction or binge eating, and difficult emotions like guilt, anger, anxiety, and depression may pop up after eating or ruminating about one’s body image. Given this, researchers and clinicians have increasingly focused on targeting emotions in the treatment of eating disorders. One such treatment is dialectical behavior therapy (DBT), which was originally developed by Dr. Marsha Linehan to treat patients with Borderline Personality Disorder (BPD) and chronic suicidality (Linehan, 1991). The theoretical model underlying DBT is termed the skills deficits model, which proposes that individuals engage in harmful behaviors, such as self-harm, to reduce or avoid emotion dysregulation due to lack of knowledge of or mastery with more effective methods to regulate distressing emotions. Thus, DBT is a skills-based behavioral treatment with four modules: mindfulness, interpersonal effectiveness, emotion regulation, and distress tolerance. Full package DBT includes weekly individual therapy, skills groups, phone coaching, and therapist consultation (Linehan, 1991), although some have modified full DBT to only include some of these components.
DBT has been modified for treating eating disorders, and there are two major adaptations: The Stanford Model for Binge Eating Disorder (BED) and Bulimia Nervosa (BN) (i.e., DBT-BED/DBT-BN), and Multidiagnostic Eating Disorder-DBT (MED-DBT). For more details on these models, please see Ben-Porath et al. (2020). DBT-BED/DBT-BN formulates that, similar to the function of self-injurious behavior, eating disorder behaviors are thought to be a method used to attempt to regulate painful emotions. DBT-BED/DBT-BN helps patients learn and utilize more effective coping skills rather than engaging in eating disorder behaviors (Linehan & Chen, 2005). MED-DBT was adapted to treat patients with complex eating disorders either with comorbidities (substance use, BPD) and/or in higher levels of care settings (Federici, Wisniewski, & Ben-Porath, 2012).
DBT has also been adapted for adolescent populations in general and specifically for eating disorders. Generally, DBT adaptations for teens include family members, shortened treatment length, and materials with simplified language (Miller, Rathus, Linehan, Wetzler, & Leigh, 1997). Rathusand Miller (2015) published a 24-week treatment which includes individual therapy, multi-family skills groups, phone coaching for adolescent patients and their parents, family sessions as needed, and a supplementary skill training module called “walking the middle path” which teaches validation, behavioral principles, and dialectical dilemmas common to adolescent and family issues.
DBT for adolescents with eating disorders has been used both as the primary treatment intervention, and has also been used as a supplemental treatment. Family-Based Treatment is an evidence-based treatment for adolescents with Anorexia Nervosa (APA Presidential Task Force on Evidence-Based Practice, 2006), and has substantial research support backing its use across many eating disorder diagnoses (Gorrell, Loeb, & Le Grange, 2019). Thus, DBT for adolescents with eating disorders is commonly used as an adjunct treatment over the course of FBT to help the teen on a more individual level, while the focus of FBT is on empowering parents to refeed their child, monitor and help them eliminate compensatory behaviors, and normalize their pattern of eating (see Anderson et al., 2015 for more information on blended DBT-FBT).
Evidence for DBT in Adults and Adolescents with Eating Disorders
Research on DBT has been ongoing for the last 20 years. The following is a very brief summary of the evidence for DBT in treating eating disorders. For more specific details, please see comprehensive reviews on this topic for adults (Ben-Porath et al., 2020; Bankoff et al., 2012) and adolescents (Reilly et al., 2020).
Several studies in adults support that the Stanford model or DBT-BED/BN helps improve eating disorder symptoms in open or uncontrolled trials (Klein et al., 2012; Chen et al., 2008; Safer et al., 2002; Safer et al., 2001; Telch et al., 2000; Rahmani et al., 2018) and controlled trials (Chen et al., 2017; Safer et al., 2010). This has included improvements in body image and eating concerns, and binge eating and purging behaviors, with abstinence rates from binge eating rates ranging from 64% to 89% (Safer et al., 2010; Telch et al., 2001). To help make treatment more accessible to individuals who need it, recent research has also started to investigate DBT-based guided self-help interventions for patients with BED (Masson et al., 2013; Carter et al., 2020), with initial results supporting greater reductions in binge eating compared to control conditions at post-treatment and 6-month follow-up (Masson et al., 2013). Notably, most of these studies have examined outcomes for patients with BED, versus BN, so more research on DBT individuals diagnosed exclusively with BN are needed.
Within the DBT-MED model for adults, several studies support the utility of DBT for co-occurring eating disorders and BPD (Ben-Porath et al., 2009; Chen et al., 2008; Kröger et al., 2010; Palmer et al., 2003; Navarro-Haro et al., 2018), however, many of these studies have been limited by smaller sample sizes and so more research is needed. Research has also shown that individuals with ED and co-occurring substance use show improvements in their ability to regulate their emotions, improvements in emotional eating, and increased ability to resist substance use urges (Courbasson et al., 2012). Given the increased use of higher levels of care for eating disorder treatment, several recent studies have examined DBT-MED in higher levels of care (partial hospital programs, inpatient). These studies have demonstrated improvements in eating disorder symptoms (Federici & Wisniewski, 2013; Ben-Porath, et al., 2014; Brown et al., 2018), DBT skills use (Brown et al., 2019), emotion regulation (Ben-Porath et al., 2014; Brown et al., 2019), suicidal and self-injurious behaviors, therapy-interfering behaviors, psychiatric and medical hospitalizations, and clinician burnout (Federici & Wisniewski, 2013) post-treatment.
Overall, much less research has focused on DBT for adolescents with eating disorders. DBT for adolescents has been used as both a primary treatment (Salbach-Andrae et al., 2007; 2008; Safer et al., 2007; Fischer & Peterson, 2015) and as an adjunctive treatment for patients with eating disorders (Johnston et al., 2015; Murray et al., 2015; Pennell et al., 2019; Peterson et al., 2019; Reilly et al., 2020). Of those using DBT as a primary treatment, results demonstrate significant improvements in eating disorder behaviors, cognitive symptoms such as body image disturbance, and weight in inpatient samples (Salbach-Andrae et al., 2007) and eating disorder symptoms and general psychopathology in outpatient samples (Salbach-Andrae et al., 2008; Fischer & Peterson, 2015). Research examining DBT as an adjunct to FBT has demonstrated improvements in cognitive eating disorder symptoms and emotion regulation strategies for adolescents with BN (Murray et al., 2015) and improvements in weight (Reilly et al., 2020; Johnston et al., 2015; Pennell et al., 2019), adaptive skills use (Peterson et al, 2019), anxiety and depression (Reilly et al., 2020; Peterson et al., 2019), cognitive eating disorder symptoms (Reilly et al., 2020; Johnston et al., 2015; Peterson et al., 2019) and binge eating and purging behaviors (Reilly et al., 2020; Pennell et al., 2019) in mixed diagnostic samples.
What We Still Need to Know
Although the research on DBT for eating disorders has grown substantially in recent years, much is still unknown and should be the target of future research. Specifically, much of the research conducted on DBT for eating disorders to date has varied in rigor, setting, and treatment length. Relatedly, much of the research has occurred in naturalistic settings, and while this method may enhance generalizability of results, randomized controlled trials are needed for more conclusive evidence on the efficacy of all forms of DBT for eating disorders in samples of adults and youth. Moreover, research on moderators (who treatment works best for) and mediators (why treatments work) of DBT could help the field to better understand for whom DBT is most appropriate, and how DBT achieves its therapeutic effects. By better understanding moderators of DBT, clinicians could understand which patients (based on patient characteristics) or under what circumstances patients most benefit from DBT, which could guide clinicians to understand whether DBT is likely to benefit the patient or whether it would be in their best interest to be referred a different therapeutic modality. Treatment mediators help to uncover the mechanisms in which a treatment achieves its effects. Understanding this could help clinicians and researchers to understand the “active ingredients” of treatment. No published research to date has examined treatment mediators of DBT for eating disorders, however, authors are currently preparing a manuscript with results which showed that DBT skill usage 1 month into treatment mediated the relation between difficulties in emotion regulation at treatment admission and global eating disorder psychopathology at end-of-treatment among adults with eating disorders in a partial hospitalization program (Karam, Wierenga, Anderson, Kaye, & Brown, in preparation). This suggests that DBT skill use is a mechanism of how DBT works. Additional research on DBT treatment mediators could lead to clinicians and researchers using this treatment strategically to maximize efficacy.
In conclusion, substantial research highlights the benefits of DBT for eating disorders, and additional research will help the field of eating disorders to better understand its efficacy and how best to help patients reach eating disorder recovery.
About the authors:
Anna M. Karam, Ph.D. Dr. Anna Karam is a Postdoctoral Fellow at the UC San Diego Health’s Eating Disorders Center for Treatment and Research (EDC). Dr. Karam received her Bachelor’s in Psychology and Women’s and Gender Studies in 2013 from the University of North Carolina at Chapel Hill and received her PhD in Clinical Psychology from Washington University in St. Louis in 2020. She completed her predoctoral clinical internship at UCSD. Dr. Karam has received broad and comprehensive training in the evidence-based treatment of psychological disorders including eating disorders, anxiety disorders, and mood disorders, with an emphasis in the areas of eating and weight-related disorders. Her research interests include examining predictors, moderators, and mechanisms of evidence-based treatment for eating disorders, as well as the best methods for dissemination and implementation of evidence-based treatments for eating disorders, with the ultimate goal to enhance and increase access to eating disorder care. Dr. Karam is passionate about combining her research and clinical interests in the area of eating disorders.
Tiffany A. Brown, Ph.D.
Dr. Tiffany Brown is a licensed clinical psychologist and Assistant Project Scientist at the UCSD Eating Disorders Center. She graduated from Villanova University with her BA and from Florida State University with her PhD in Clinical Psychology. She has extensive clinical experience working with pediatric, adolescent, and adult patients with eating disorders using DBT, Cognitive Behavioral Therapy (CBT), Exposure and Response Prevention (EXRP), and Family Based Therapy (FBT) and enjoys working with patients from diverse backgrounds. In particular, she is an advocate for patients who have typically been underrepresented in the eating disorder field, including LGBTQ+ and male patients. Her research interests focus on eating disorder prevention in male and LGBTQ+ populations and treatments for body image and eating disorders, particularly those targeting altered interoception – the brain-body relationship – and anxiety about body sensations. Dr. Brown has received research funding from the National Institute of Minority Heath and Health Disparities, the Arlene and Michael Rosen Foundation, the Global Foundation for Eating Disorders, and the Academy for Eating Disorders. Her current research focuses on reducing eating disorder and muscle dysmorphia risk for LGBTQ+ and male populations, understanding factors related to treatment outcome across gender and sexual identity, the effectiveness of DBT for eating disorders, and how interoception and gastric specific anxiety can be targeted in eating disorder treatment (e.g., interoceptive exposure).
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