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This is an intermediate-level course. Upon completing this course, mental health professionals will be able to:
This course introduces treatment providers to a new treatment approach that augments their current eating disorder treatment by filling in the biological bases of the illness and applies brain-based responses to treatment applications. As neurobiological research continues to emerge, and international research findings on TBT-S increase, treatment significance will continue to be refined. Risks could occur if clinicians present the research findings as absolute instead of comparing neurobiological findings with their clients’ experiences for the clients to better clarify what they are experiencing in their illness and why.
This course addresses a novel treatment approach for Eating Disorders, Temperament Based Therapy with Support, aka TBT-S. TBT-S has initially focused on eating disorders due to the high mortality rate and the lack of effective treatment over time. Yet TBT-S holds the potential to be studied and applied to all mental disorders that are trait based, such as anxiety or obsessive compulsive disorder.
This course is based on the book, Temperament Based Therapy with Support for Anorexia Nervosa: A Novel Treatment, by Hill, Peck and Wierenga (2022, Cambridge University Press, England). TBT-S is a treatment of doing. This course is as much about “trying on” neurobiological ideas and concepts as it is about reading about them. It introduces the reader to what this new treatment is and provides examples of TBT-S treatment tools and skills for clinicians, dietitians, medical professionals, and educators, and how it could be applied in various types of therapeutic and educational settings.
Eating disorders are one of the most misunderstood and yet deadly of all mental disorders. The diagnostic name, “Eating Disorder” (ED) reflects the little that was known when initially described in the DSM-III[1] in 1980. Treatments then and now focus primarily on symptoms, outward problematic expressions of thoughts, feelings, and behaviors.
However, eating is a requirement of life, not a disorder. Everyone eats, but not everyone has an eating disorder. The diagnostic name set the stage for people to either downplay an everyday requirement of life or distance themselves from the poorly understood illness. Misunderstanding of EDs became targeted against adolescent white girls who were described as being on a campaign to over-control their appearance. Social, cultural, family, and analytic theories abounded addressing outward symptoms. What was missing? The underlying biological causes of the illness, i.e. the genetic, neurobiological, and temperament bases.
It was not until after the genome was sequenced in 2000 and technology became more refined in the early 2000s that researchers could begin to look inside the brain in a 3-D functional way while activities were being studied, in order to observe brain response. Walter Kaye, at UCSD, led this research globally. His groundbreaking article in 2009 that identified brain circuits that fire significantly differently between those who had eating disorders and those who did not, indicated that there was much more going on in brain response than ever imagined. The last 20 years of research has continued to refine what is happening on the inside of the brain of those with EDs, while also identifying genetic differences and temperaments that set up ED vulnerability.
Temperament Based Therapy with Support, TBT-S, emerged out of the growing biological eating disorder research. It describes Eating Disorders as grounded in traits, which are genetically caused and neurobiologically defended. From the moment of conception, the genetic makeup of the ovum becomes the recipe for the brain to begin wiring to express inherited traits. This wiring is both biological, such as height, and temperament based, such as extroverted.
One’s temperament is the biological/“nature” side of personality and consists of traits. Character is the social or “nurture” side of personality. While the research community’s main population distanced themselves from being associated with eating disorders, clinicians have tended to distance themselves from genetic and neurobiologically based research into what has more recently been found to be the very nature of the illness. Many graduate programs still do not offer neurobiological mental health courses. This results in a huge gap in clinician understanding of EDs and perpetuates the sole use of past theories and symptom-focused therapies. The mental health world has remained flat, when in fact it is 3-D and round.
TBT-S is a treatment that integrates genetic, neurobiological, and temperament research into treatment applications to augment ongoing therapies. The TBT-S approach provides clinicians with a framework to apply other therapies. It provides the biological bases of the illness that offer direction signs for what intervention to apply and when.
If symptoms are the limbs of a tree, then traits are the roots. An evergreen tree can never be a deciduous tree, nor should it. There are many variations of any one type of tree, such as variations of oak or variations of spruce. Yet, mental health providers are often trained to approach clients with the same therapeutic expectations in spite of widely diverse traits. A person’s traits, drawn from their temperament, do not go away. While we work to reduce or eliminate symptoms, a person’s traits are with them for life. However, clinicians are often not taught the difference between symptoms and traits and may erroneously work with clients to eliminate their traits, or aspects of who they are, such as being impulsive, rather than working on their symptoms. This sets the client up to fail, lowers motivation, and increases treatment dropout.
TBT-S works with clients to identify their traits and use them as strengths. Traits are traditionally taught and viewed as pathological. TBT-S provides clinicians with a means to identify clients’ temperaments, and methods on how to reshape clients’ destructively expressed traits to be more productively expressed over time. For example, while an impulsive trait cannot be eliminated, shifting the impulsivity from destructive binges to impulsive writing and research “binges,” as one client did, can result in clients becoming a better version of themselves.
Scripts are in italics throughout the course. Clinicians are encouraged not to read the scripts verbatim but instead to learn the points and share them in their own voices.
The treatment name, Temperament Based Therapy with Support, uses the word “Support.” Adult clients with anorexia nervosa chose this word themselves. They shared that they did not want people to whom they turned for support to be labeled as “caregivers,” because they did not want to be “taken care of.” Adult clients requested that they be referred to as “Supports.” In many cases, these support persons extend far beyond their parents and family of origin. “Family” in family-based therapy is descriptive for adolescents with an eating disorder (ED). Adults with ED, however, reported they preferred a broader descriptor for people to whom they turn for support. They chose the word “Supports” to describe both the people and the actions they need from them. The word in the treatment title, Support, becomes a two-for-one term. “Supports” is capitalized throughout the course, referring to the persons to whom adult clients turn for support.
Regarding diversity, this course addresses the underlying biological aspects of eating disorders. Fundamentally and metaphorically, every race and culture has the same biological color. It is red, the color of blood. Basically, everyone has the same organs, blood types, bones, and brain structures regardless of culture or race. Skin color is a result of genetic inheritance and unto itself does not biologically contribute to eating disorders.
Environmental and cultural influences shape inherited traits. If a person of any race or culture inherits traits that are proving to increase vulnerability in developing an eating disorder, then that person may develop the illness, regardless of race or culture. Gender does impact Eating Disorders due to biological causes. Eating disorders are primarily a female illness due to biological, specifically hormonal/gonadal, responses interplaying with temperament. Our open trials included persons across the gender continuum.
In addition, persons who experience trauma and have traits that are vulnerable to eating disorder development, may develop an eating disorder after experiencing the trauma. The trauma appears to be the trigger that intensifies the person’s traits to become more extremely expressed, but the trauma is not the sole cause of the illness. As discussed in the book, while social pressures to be thin may vary across cultures, genetic researchers have found that social pressures are secondary to genetically triggered traits from adolescence through older adulthood. Genes override environment from one’s teens throughout life as is described in the sections below. It is how the inherited traits are shaped that matters. Environment, therapy, families, friends, and communities hold that role.
Each section that follows provides “bite-size” chunks of information concisely describing what practitioners and educators who have little neurobiological training or knowledge can learn and use to share with their clients or students. Each section is a module that could be offered in any one session or classroom, and integrated into ongoing therapy sessions or classroom lectures. Each section has bottom-line points that if nothing else is remembered, are “key points” for the reader to hold onto and use.
Just as the structural foundation of a house is critical in providing a firm and solid foundation for the rooms built upon it, so too is the research that grounds this treatment. TBT-S is grounded in research. Research is the vital component that creates the walls and structural bases of the treatment. That is why the references are provided. The reader is referred to references that repeatedly explored more deeply the genetic, neurobiological, and temperament factors of eating disorders that grounds TBT-S. We urge you to refer to the references for more depth.
Anorexia nervosa (AN) is a serious, life-threatening condition that has one of the highest death rates of all mental illnesses.[1–4] It is diagnostically defined as having extremely low body weight, an intense fear of weight gain, and disturbance in how one’s body weight and shape are experienced.[5] It occurs primarily in females,[6] usually taking form during puberty with the potential to develop acute and chronic impairment over one’s lifetime.[7] The illness places a considerable strain on families, friends, and work settings.
While progress has been made in understanding the psychosocial and behavioral mechanisms responsible for the development and maintenance of the illness, there is an urgent need to optimize treatment approaches to reduce chronicity and improve outcomes.[7] This necessitates new and innovative treatments that contribute to long-term symptom reduction and incorporate contemporary neurobiological findings such as those covered in TBT-S.
Key Point |
TBT-S has focused on AN because of its high mortality rate and low treatment efficacy over time. |
Temperament Based Therapy with Support (TBT-S) is an emerging neurobiologically informed treatment approach designed to augment existing treatments. This course describes how and why TBT-S has been developed for adults with AN, while recognizing that it has the capacity to be applied to other psychological disorders. TBT-S fills the gap between research and clinical practice by acknowledging and treating underlying brain-based factors. TBT-S recognizes that there is a biological basis to psychological illnesses that involves temperament and altered brain function. This affects the regulation of eating and emotion for those with AN. TBT-S applies neurobiological research findings to inform treatment targets.
TBT-S combines psychoeducation and experiential activities that emphasize the key role of neurobiological factors in the development and maintenance of AN to increase insight and recognize temperament patterns. Skills-based training is used to teach clients and Supports age-appropriate strategies to manage these neurobiological factors so as to reduce problem thoughts and behaviors. TBT-S treatment targets include common AN temperament traits (e.g., anxiety, cognitive inflexibility, harm avoidance) and related brain processes such as altered reward-and-punishment sensitivity, interoception, inhibitory control, and decision-making.
The focus of TBT-S is to work with clients who have AN and their Support persons to acknowledge, understand, and utilize their own temperament as a primary source for strength and change. Supports can include members of one’s family of origin (such as parents, siblings, grandparents, adult children) and of one’s “family of choice” (such as spouses, partners, friends, housemates, or colleagues). The TBT-S approach was developed and refined over a 10-year period, integrating AN research with ongoing client and Support feedback to assure the intervention strategies accurately reflect client experiences and temperaments.[8, 9] TBT-S was originally developed and studied in an intensive 5-day, 40-hour program with groups of clients and their Supports.[9]
Key Point |
Temperament Based Therapy with Support (TBT-S) is an emerging and novel neurobiologically based treatment that works with a client's temperament to motivate change and to manage and reduce symptoms. |
Temperament is the biological basis of our personality, influenced by genetics and brain circuit development and function over one’s life span. Character is the external shaping of one’s temperament. Temperament is to nature as character is to nurture (Figure 1).
Figure 1. Temperament in relation to personality and character.
Temperament has been studied for more than 70 years with a primary focus on children.[10] In the late 1980s Chess and Thomas led interventions for parents and educators to incorporate children’s “reactive patterns” into classroom and parenting responses.[11] They countered the trend that children were solely “products of the environment,” advocating that they bring their own tendencies to the picture. Subsequently, temperament researchers began to acknowledge that traits can be disadvantageous in one situation and advantageous in others.[11] Educational and parental interventions encouraged a “goodness of fit” framework for children.[12] However, therapeutic interventions that focus on shaping adults’ “natural” thoughts, feelings, and behaviors have been left off the therapeutic table in the area of eating disorders.[13, 14] Working with clients’ temperaments acknowledges who they are and what they bring of themselves to the therapeutic experience. (See Table 1.)
Table 1. What is Temperament? |
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Figure 2. Traits are distinguishing features of temperament that interact with environment
Temperament is expressed through traits, as shown in Figure 2, which affect our thoughts, feelings, and behaviors. Temperament traits are observed in infancy and are relatively preserved across the lifespan, suggesting that personality is hardwired and consistent throughout life. Importantly, temperament is strongly related to most psychopathologies, especially those involving anxiety and mood disturbance. People have varying levels of vulnerabilities to develop a psychological disorder based on the traits they inherit. In fact, growing evidence indicates that temperament traits are uniquely associated with specific brain systems linked to various psychopathologies, including those involved in Eating Disorders (ED).[15–19] This suggests that temperament traits are genetic, and brain-based, and have a powerful influence on ED, and thus should be included in treatment approaches. (See Figure 3.)
Figure 3. Current ED therapies focus on personality and character
Key Point |
Temperament is the biological foundation of personality and consists of traits that are fundamental expressions of each person. |
Accumulating behavioral and neuroimaging evidence points to a neurobiologically based AN temperament that increases risk and contributes to the development and maintenance of the disorder.[20–36] This AN temperament is characterized by anxiety, altered sensitivity to reward and punishment, altered interoceptive awareness, difficulty with decision-making, and cognitive inflexibility and rigidity.[30, 32, 37–42] Individuals with AN also tend to be high-achieving, perfectionistic, inhibited, and rule-abiding. These temperament and personality traits are related to altered insula and fronto-striatal neural circuit function, highlighting their neurobiological basis.[43–47] In addition to predating the disease, these traits often persist in a mild to modest degree after recovery, offering evidence they are biologically based traits and not behavioral symptom expressions.[30, 37–40, 48]
This AN temperament profile serves as a framework that identifies the neurobiological constructs and traits targeted in TBT-S and guides the interventions designed to address symptoms specific to AN. TBT-S has been developed to fill a gap in ED treatment. It features AN temperament, focusing on the traits that make a person vulnerable to AN, why AN symptoms emerge and are maintained, and how to shift trait expressions or construct environmental modifications to reduce symptoms and to impact positive change. (See Figure 4.)
Figure 4. TBT-S augments other treatments by focusing on temperament
Key Point |
AN has common traits creating a temperament profile that guides TBT-S interventions to work with client traits as natural resources for lifelong changes. |
The theoretical model of TBT-S approaches the illness from the inside out. It begins with genes. Environmental factors (such as life stresses, malnutrition, and trauma) can modify gene expression and temperament via epigenetic processes (e.g., gene x environment interactions), suggesting that although traits are relatively stable, they can be shaped by experience and treatment.[49] Figure 5 shows the relationship between temperament and environmental influences on symptoms. Genes, the center circle, code how the brain wires its circuits, impacting thoughts, perceptions, feelings, and actions. Traits develop from brain circuits structured by genes which are influenced by the environment. Persons with AN have specific alterations in the wiring of these brain circuits that contribute to destructive AN trait expressions.
Other circuits function normally, affording healthy and/or above-average productive trait expressions. Altered trait expressions impact the type of symptoms that develop. For example, elevated harm-avoidance is related to dietary restriction and reduced social interactions. TBT-S focuses on acknowledging and utilizing one’s trait expressions to modify, shape, and promote recovery. For example, TBT-S prescribes structure and routine, in alliance with a rule-bound trait, to reduce anxiety and intolerance of uncertainty around meals. The inside-out approach of TBT-S complements ongoing therapies that are grounded in environmental and behavioral models.
Figure 5. The relationship between traits and environmental influences on symptoms
Key Point |
The TBT-S theoretical model approaches treatment from the inside out, targeting traits and underlying biology that complement other treatment approaches which work from the outside in. |
TBT-S was designed to be administered to adult clients and their Supports. Thus, both clients and Supports participate with the clinical team. Conducting TBT-S with clients and their Supports is a powerful and effective way to ensure information is relayed, experienced, and processed similarly. We have focused our research and this course on adults with AN and their broad range of Supports in response to the higher chronicity and mortality within this subpopulation. The TBT-S focus is on improving client-Support relationships and communication to facilitate recovery. (See Table 2.)
Table 2. Temperament Based Therapy with Support (TBT-S) |
TBT-S is a treatment approach that:
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Key Point |
TBT-S endorses including Supports in the treatment of adults with anorexia nervosa to increase understanding of the illness and improve communication and continuity in care. |
TBT-S core principles and modules can be applied in (a) one-on-one, (b) client with Support person, and (c) client and/or Support group sessions either (d) virtually or face-to-face, or (e) ranging from outpatient through day-hospital levels of care. When TBT-S core principles are described in therapy sessions, clients learn about the neurobiological underpinnings of their temperament expressions and skills to help shape their traits. The therapeutic change process is enhanced when additional components include virtual or face-to-face: (a) Support person(s), and (b) the act of practicing the skills together. The learning and change process can be further enhanced by providing TBT-S interventions in group settings through the power of client and Support interactions.[183]
TBT-S was originally developed in a 5-day group intensive format to maximize efficacy, intensively build on skill development, minimize attrition, and provide a practical and accessible approach for adult clients and Supports to work together in a discrete amount of time. Increased treatment frequency and intensity are critical components needed to elicit behavior change.[50, 51] Treatment models for anxiety indicate that intense, repeated, and focused in vivo practice is key to altering biologically driven avoidance behaviors by maximizing learning through massed practice and allowing close monitoring of compliance.[52–59]
Intensive treatment formats also show an increase in initial efficacy.[60, 61] This appears to be critical in treating AN, as evidence suggests that adolescents with AN who gain weight in the first four sessions of family-based treatment (FBT) have significantly better outcomes than those who do not gain weight early in treatment.[62] An intensive treatment format offers several additional advantages, including reduced burden on the adult client and Support(s) of having to commit to treatment over long periods of time, thus likely improving accessibility, acceptability, and compliance. An initial intensive model may also be a cost-effective “jump-start” to shorten residential or partial hospital treatments and augment outpatient ED treatments.
In the studied TBT-S 5-day model, multiple adult clients and Supports are treated together in a group structure, commonly known as a multi-family group, in adolescent treatment. Group settings enable and facilitate peer-to-peer consultation, a powerful method of learning that can improve outcomes. Having multiple adult clients and their Supports together can improve participants’ understanding of the illness by allowing them to learn from similar and diverse perspectives during group activities. Working with groups of clients and Supports broadens viewpoints on effective ways to manage recovery and generates new ideas. The TBT-S focus is on improving client-Support relationships and communication to facilitate recovery.
Key Point |
TBT-S was studied in a 5-day group format to intensify treatment intervention, unify clients and Supports, and increase accessibility to treatment. |
TBT-S is implemented as a modular treatment, meaning that it has multiple, individual, complementary treatment interventions that have been studied in different combinations as part of the 5-day TBT-S program. TBT-S treatment modules were designed to target symptoms using a broad array of intervention strategies (e.g., psychoeducation, experiential learning, skills training, meal coaching and behavioral agreements) that include both the client and Supports. Each TBT-S treatment module is described and includes a variety of treatment activities. Clinicians can select activities from each module deemed to be most relevant depending on the clinical presentations and developmental stage of the clients and their Supports present in treatment.
Many clinicians may not have the infrastructure to deliver TBT-S in its tested 5-day format. Individual treatment modules or activities can be administered independently across multiple treatment settings, including outpatient through partial hospitalization settings, and in multiple formats, such as group, individual, or family therapy settings.
The TBT-S multi-day design has also been administered in shorter intensive formats over two to four days in outpatient and higher level of care settings in the United States, Canada, Norway, and Greece. Efforts to deliver the multi-day TBT-S program in a virtual format also appear promising. This course provides examples of how to structure and organize modules by treatment target or temperament trait in multiple treatment settings.
Key Point |
Clinicians can apply TBT-S flexibly, integrating its modular format with multiple treatment strategies to formulate unique stylized interventions. |
Two versions of TBT-S have been developed and tested to date, YA and SE-AN. Both versions uphold TBT-S core principles as central themes and adhere to the same structure, format of treatment, and level of Support involvement. They differ in how adults are approached when in young adult stages of life development compared to adults who have Severe-and-Enduring forms of AN.
The Young Adult model of TBT-S (YA TBT-S) is designed for clients with AN and other restrictive-type ED between the ages of 17 and 27 and their parents, who are automatically nominated as primary Supports. This highly focused version of TBT-S was designed to enhance treatment by integrating important developmental considerations since many seeking treatment for AN often fall within this age range. Naturally, young adults with AN are undergoing developmental changes and growth that are central to this age and often have a primary impact on treatment and recovery, both individually and within the context of their family system. YA TBT-S is tailored to provide education on neurobiology, skills training, and a model of family assistance that takes into account these important developmental considerations.
Emerging adulthood is a developmental window that has gained more attention in recent years, in part because the incidence of mental illness is highest in this developmental stage. Young adults do not squarely fit into either adult or child/adolescent services because most in this age category are embarking on the launch to independence (versus being fully independent) and, increasingly so, continue to be embedded in their family system in important ways. Young adults are adjusting to significant life transitions during this developmental stage, including separation from family of origin, increasing autonomy and individual responsibility, and more commonly in this modern era, interdependence within their family of origin.
Developmentally, young adults are striving to individuate from their family, learning to make their own decisions, and increasingly focusing on carving their own path in life. This developmental backdrop is significant and imposing in the life of a young adult and thus deserves consideration when working with clients with AN in this age range. YA TBT-S brings these developmental dilemmas to the forefront of treatment and addresses them within the context of recovery and treatment.
Themes touched on in treatment include: the capacity for change within the context of the temperament framework due to neurodevelopment; how to assist a YA in recovery from AN; how to make use of continued parental involvement to positively impact recovery; how to strike a balance of autonomous and family-focused recovery; and navigating an effective working relationship among YAs and their parents.
The SE-AN version of TBT-S is designed for all adults with AN across the life span who have chronic AN. It recognizes that traditional adult therapy focuses on individuation. In contrast, TBT-S integrates interdependence within a neurobiological framework. In this model, Supports may be anyone the client designates as a “support person.” The SE-AN version of TBT-S has been studied with clients of all ages, from newly graduated 18-year-old females and males to older clients in their 50s and 60s who have developed chronic AN tendencies. As SE-AN clients age, they tend to turn to a wider diversity of Support persons, with many of their primary family members having “burned out.”
Trait expressions continue throughout one’s lifetime. When TBT-S is offered in a group format, the expertise from older clients offers lived wisdom informing younger clients of symptoms that can become ingrained over time, while the younger clients resurrect hope and motivation in the older clients to reshape trait expressions. TBT-S presents neurobiological information that is congruent with AN temperament, increasing awareness that there are tools that those with AN can utilize that align with their own temperament.
Clients tend to enter treatment assuming they have little within themselves that can be a part of the solution. They report having tried many behavioral interventions, but some have failed over time. In a TBT-S approach, the adult client educates, coaches, and clarifies with their Supports their own experiences of what it is like to have AN traits, how symptoms allow relief and lower anxiety, and what helps and does not help. Clients actively explore how to utilize the same traits that have been expressed destructively in more productive ways.
The discovery that their authentic selves and their own temperament have worth and are a means toward health and well-being motivates change and empowers their strengths. The more SE-AN adult clients align with the biological bases of their personality, the sooner they can begin to identify how to use their own traits to impact change.
SE-AN adults have engrained, rule-bound rituals that have sustained their ED symptoms over years. TBT-S utilizes its trait-based approach to empower the rule-bound traits as solutions to step away from destructive tendencies, using tools to shift the same traits toward productive expressions.
Key Point |
There are two versions of TBT-S. YA TBT-S is designed for ages 17–27 and integrates important developmental considerations into the TBT-S model. SE-AN TBT-S is designed for those aged 18–60 who have chronic AN symptoms (more than five years of illness). Both versions interrupt and shift AN symptoms by teaching clients to identify their own trait-based behavioral solutions. |
Summary Key Points |
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TBT-S has five core principles derived from neurobiological research:
TBT-S is grounded in the temperament based neurobiological etiological model of anorexia nervosa (AN) initially developed by Kaye, et al.[35] and coined “When Good Traits Go Bad: Temperament and the Course of AN.” This model, as shown in Figure 6, recognizes AN as a heritable illness with a strong genetic component.[6, 27, 28, 33, 63–66] Heritable risk is conferred through temperament traits that increase susceptibility to developing AN and also serve to maintain the illness. This neurobiological model has been updated to integrate findings from brain imaging studies showing altered function in brain systems regulating food intake in AN.
Key Point |
Key Point: Temperament traits and altered brain responses inform the treatment targets of TBT-S, which include altered anxiety, interoception, reward and punishment sensitivity, decision-making, and cognitive or inhibitory control. |
The updated neurobiological model shown in Figure 6 depicts that good traits can go bad, and then become good again. This is the TBT-S philosophy.
Approaching AN from a temperament based neurobiological perspective provides a biological foundation and conceptual framework from which to view symptoms and the underlying mechanisms that drive behavior. Temperament informs targeted interventions directed at the cause of the behavior, rather than at the behavior itself. This is a paradigm shift for many. Treatment of AN has been thwarted by the lack of a mechanistic understanding of the disorder and recognition of the central role of temperament in its biological basis. This is similar to how treatments of medical illnesses (like diabetes) were ineffective until the underlying mechanisms (insulin production) were discovered. Similarly, by adopting a temperament based neurobiological and etiological model of AN, the treatment emphasis shifts away from attempts to understand how behaviors developed and toward a focus on their functional impact to guidestrategies to redirect trait expressions to achieve a reduction in eating disorder symptoms.
Figure 6. TBT-S neurobiological model of AN
Key Point |
TBT-S has emerged from a neurobiological model that identifies how “good” traits biologically shift to “bad” expressions and can become “good” again with trait-based intervention to promote recovery. |
Individuals with AN often exhibit characteristic temperament traits. (See Table 3.) Some AN traits are productive and serve as strengths throughout life. These traits can be utilized in the course of treatment to help clients manage destructive traits. For example, many persons with AN are highly achievement-oriented, which is needed to reduce ED symptoms and accomplish recovery. On the other hand, some AN traits result from genetically induced, altered neural circuit function that impacts the development and maintenance of the disorder.
As indicated in the TBT-S neurobiological model, ultimately, the same traits that increase vulnerability to AN can be shifted from destructive expressions that exacerbate ED symptoms to productive expressions that become strengths in overcoming and maintaining a healthier and more successful lifestyle.
Table 3. Common Eating Disorder Traits |
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It is important to note that not all people with AN will identify with all of the traits associated with AN. Rather, these traits are like a menu, where most people with AN identify with at least a few, if not many or all, of these traits (see Table 3). Rather than trying to change traits that are hardwired in the brain (e.g., it would be difficult for an introvert to naturally become an extrovert), the goal of “treat to the trait” is to identify and experientially explore how an individual’s traits could contribute to their strengths so as to reduce their ED symptoms. TBT-S focuses on adjusting destructively expressed traits to expressions of strength by: (a) clients experientially identifying their own trait-based productive responses; (b) teaching skills to endorse client solutions; and (c) drawing upon Supports’ strategies to compensate for inherent difficulties.
The philosophy of TBT-S is to utilize “traits as strengths.” Treatment modules and activities are specifically designed to target one or more of the destructive trait expressions and help clients realize how to shift them to strengths. This requires the clinician to adopt what may be a different framework for conceptualizing these traits as strengths. Table 4 provides an example of reconceptualizing traits as strengths and treatment strategies that are used when treating to the trait.
Table 4: Reconceptualizing traits as strengths and strategies to treat to the trait |
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Trait | Trait as strength (productively expressed) | TBT-S treatment strategy |
Uncertainty Intolerance |
Highly structured |
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Altered sensitivity to reward/punishment | Motivated by having options/ choices, planning, structure, and long-term goals |
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Obsessionality | High error-detection Attention to detail |
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Anxiety |
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Inhibition | Ability to delay gratification, cautious, and unlikely to impulsively enter into harmful situation |
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Key Point |
Traits can be expressed destructively or productively, and clients can be taught to utilize their own traits as strengths throughout life. |
In discussing temperament, it is important to clarify differences between traits and symptoms, highlighted in Table 5 and Figure 7. Symptoms are thoughts, feelings, and behaviors that have become problematic, dysfunctional, or harmful for persons and/or those around them. They are often influenced by traits. For example, a person with a strong impulsive trait is more likely to develop a substance use disorder or engage in binge eating than a person with an inhibited trait, who is more likely to avoid eating. ED symptoms, such as food restriction, binge eating, purging, or excessive exercise, are behaviors that can and should be eliminated. Temperament and traits, however, cannot be eliminated.
Table 5. How traits relate to symptoms |
Symptoms
Traits
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Figure 7. Example of trait impact on symptoms
Key Point |
Symptoms can be reduced or eliminated; traits are with us throughout life and vary in intensity. |
Drawing from a biological perspective, food is the natural and fundamental substance that “medicates” our bodies to be strong, healthy, and balanced. Food is energy. Like other ED treatments, TBT-S recognizes that appropriate nutrition and body composition stabilization are necessary and fundamental to recovery. To facilitate this, TBT-S includes comprehensive dietetic recommendations and meal plans “prescribed” by an ED dietitian.
The dietetic philosophy in TBT-S is that dosing energy for adults with AN is similar to dosing medicine. Clients and Supports attend dietary sessions and groups where they are “prescribed” foods and learn a meal plan tailored to the clients’ needs alongside other basic dietary information. Biological tenets of TBT-S are woven into the dietary philosophy by prescribing a dietary approach that acknowledges core personality and temperament traits and the biologically based function of recommended foods. TBT-S emphasizes a highly structured meal plan in an effort to prioritize nutritional and weight rehabilitation in a way that honors the AN client’s unique temperamental tendency toward structure and certainty. Meal plans are organized to prioritize predictability and consistency. This can include adherence to highly scheduled meal and snack times and predictable (and, importantly, calorically sufficient) meals and snacks, among other things. In this way, the treatment prioritizes structure and certainty over flexibility and variety to cater to the clients’ preferences for structure based on personality.
TBT-S continues to acknowledge the need for dietary expansion, which may include incorporating additional foods or expanding food horizons in a variety of different ways. However, even this therapeutic endeavor toward variety is approached in a structured manner.
Alongside Supports and the dietary team, clients learn to plan out challenge foods in a structured format and, importantly, are the key stakeholders in deciding how and when, and even if, this therapeutic endeavor is undertaken. As such, TBT-S is unwavering in the need for abstinence from restriction and ensures that clients adopt and practice a meal plan that is calorically sufficient, includes major macronutrient groups, and upholds a more flexible approach with regard to variety. This allowance stems from acknowledging that the need for sameness and routine-surroundings eating may be related to core personality styles and may in fact promote a more sustainable recovery practice in the long term. This structure and routine around meals compensates for altered interoception (e.g., altered hunger and/or satiety signaling that promotes food restriction or overeating, altered trust in body-related signals), decision-making (e.g., difficulty deciding what foods to eat), and reward sensitivity (e.g., reduced brain response for pleasure to motivate eating and affirm how much energy the body needs).
Key Point |
Food is framed as medicine for those with AN to integrate its biological purpose and “side effects,” and is “prescribed” in a structured format that schedules food variety based on client traits. |
TBT-S advocates that it is necessary to include Supports (spouses, parents, children of adult clients, roommates, partners, friends, colleagues, etc.) in the treatment process for adults of all ages. The term “Supports” was chosen at the request of clients participating in an open trial of TBT-S at The Center for Balanced Living, in Ohio, to reflect their preference for support rather than being cared for, which they believed the more common term “carer” connotes. TBT-S requires that a minimum of one Support person participate in treatment with each client in designated sessions. Family-based treatment (FBT) is the first-line treatment for adolescents with AN. It is effective because it teaches families strategies to understand, interact, and manage AN.[67–69] Similarly, TBT-S focuses on providing psychoeducation and skills training so that Supports learn about the causes of AN and effective ways to interact and manage symptoms.
Supports are appointed as part of the treatment team and are seen as an important asset to aid with recovery. The education, training, and practice that they receive in TBT-S sessions are intended to increase empathy and understanding by providing a biological understanding of AN and improving their ability to provide effective assistance. Supports in TBT-S sessions receive focused skills training on effective and age-appropriate assistance strategies that are practiced throughout the clients’ treatment.
TBT-S takes the perspective that Supports play a critical role in recovery by providing accountability, assistance, leverage, and the potential to compensate for traits that clients do not have. Supports learn tools that the client chooses as helpful to assist in the process of reducing ED symptoms. In addition to formal skills training, when TBT-S is offered in group settings, Supports also learn new skills by receiving feedback and consultation from both their loved one and other Supports, as part of the TBT-S group milieu. If TBT-S is offered in a 5-day program, upon completion Supports are armed with what the adult clients deem to be the best practices for providing assistance, in the context of a biological and temperament perspective of the illness. TBT-S views clients as the experts. Experts, however, do not work and function alone.
Key Point |
A Support is any person who offers support/assistance in a client’s life. Supports need the same information and tools as clients to offer consistency in reshaping altered trait expressions to promote recovery. |
TBT-S is a treatment of “doing.” The tendency to be physically active is one of the first traits to be identified historically and is considered the most essential trait of one’s temperament.[70] Behavioral change requires behavioral action. Learning occurs when “neurons that fire together , wire together.”[50] Thus, our brains are fluidly flexible to change throughout life. The brain rewires through extensive practice of new ways of expression and behaviors, and TBT-S capitalizes on this through guiding in vivo practice of new skills during treatment. Clients and their Supports identify and practice the same phrases and actions that they have identified as helpful toward achieving a healthier lifestyle.
Many of the TBT-S treatment interventions are movement-driven; clients “try them on” to explore new behaviors that bring them closer to their goals. Active interventions are helpful because the brain learns through actions. Individuals are more likely to repeat what they have practiced. In vivo activities allow clients to refine their verbal and behavioral responses through corrective feedback via their own experience or from that of others. This iterative method of corrective feedback serves to enhance building new skills.
Movement is also needed to shift cognitive sets. Many ED behaviors represent rituals that have become automatic. Many individuals with AN have a trait-based tendency that causes their thoughts to become stuck on one topic. Movement can be used to interrupt destructive thoughts and behaviors so as to shift and move on to more productive thoughts and behaviors. TBT-S utilizes movement as a core part of the change process.
Key Point |
TBT-S is an active intervention approach. |
Summary Key Point |
TBT-S has five core principles that draw from neurobiological research to inform and direct treatment. |
TBT-S utilizes multiple intervention strategies to apply TBT-S principles. These strategies have been developed and adapted over a 10-year period through iteratively integrating client and Support feedback in the treatment development process to increase accuracy and acceptability. Five strategies are described in this section. It can be helpful to provide visual aids, including some of the figures in this course (detailed handouts are also available in the Appendices of the book).
The primary goals of neurobiological psychoeducation are to educate clients and their Supports on relevant neurobiological constructs, temperament traits, and associated symptom expression and to provide a framework and rationale for TBT-S intervention strategies. In doing so, neurobiological psychoeducation serves as an intentional strategy to increase motivation for recovery and engagement in treatment, validate and reduce blame, and improve insight and awareness to inform skill-use and drive behavior change.
Psychoeducation materials include current genetic, neurobiological, and biological research findings that address causes of Anorexia Nervosa (AN) and introduce the neurobiologically based targets of treatment. These include the following temperament traits: anxiety, altered interoception, sensitivity to reward and punishment, inhibitory control, cognitive flexibility, and decision-making.
This course provides scripts to help clinicians communicate neurobiological research in a standardized manner without requiring that they independently become neuropsychologists. We describe relevant neurobiological information and key points for clinicians to share with clients and their Supports.
Key Point |
Interactive psychoeducation identifies AN neurobiological underliers and offers a rationale for targeted interventions in a format all clinicians can utilize. |
TBT-S is a treatment of doing. This is accomplished through carefully constructed experiential activities and in vivo practice, conducted with clients and Supports in various treatment formats. Learning by doing heightens retention of information and facilitates skill-building. Practicing new skills and behaviors during treatment, and developing solutions to problems rather than just talking about them, increases the likelihood that clients and their Supports will continue to utilize the new skills and solutions in their daily lives.
TBT-S includes a series of experiential activities that are designed to actively apply neurobiological information and elicit problem-solving strategies. They are intended to increase knowledge and empathy of Eating Disorder (ED) behaviors and motivate change. These clinician-led experiential TBT-S activities simulate AN experiences and temperament expressions through active metaphors to promote a better understanding of what it is like to live the illness, to experience and identify one’s own traits, and to help clients and Supports identify and use methods congruent to their temperaments to solve problems.
Using game-like approximations of their AN experiences is a less threatening and acceptable approach to help clients work through solutions and compensatory strategies that can be used to overcome and manage symptoms. Supports are included in the experiential activities sessions to learn about underlying causes and contributing factors of the illness at the same time as the clients. In addition, Supports are taught tools to develop skills that help their loved ones realize their potential outside of treatment and achieve success in symptom reduction.
Key Point |
Experiential treatment interventions provide frameworks for clients and their Supports to acknowledge and understand problems and explore solutions. |
The Young Adult version of TBT-S includes approaches based on multi-family therapy (MFT), where multiple clients and their families are treated simultaneously in a group format. MFT has been shown to improve outcomes over single-family therapy.[71] In adult AN, family therapy shows promise.[71] Additionally, considerable evidence suggests that family interventions in adult mental health can be enhanced by using a multi-family treatment format[73–75] and is feasible in adult AN.[76, 77] MFT is a powerful approach because it can enhance learning and change among clients and their attending Supports and because attendees have the benefit of learning from one another via sharing, feedback, modeling, and observation and comradery/group affiliation.
The Young Adult version of TBT-S considers the multi-family milieu as a powerful opportunity to enhance change and recovery. Multi-family activities are used to facilitate group cross-talk and sharing so that members have the opportunity to create a live assistance network consisting of others with lived experience. Exercises emphasize creating affiliation and relationships and, later, interfamily feedback and peer-to-peer consultation so that MFT group members have the opportunity to learn from one another.
Key Point |
Multi-family therapy is a powerful treatment format that can enhance outcomes. TBT-S has been applied and tested in a multi-family format. The Young Adult version of TBT-S includes a variety of multi-family therapy activities. |
Clients and Supports receive skills training to develop tools that can be used to reduce and manage symptoms and destructive or unhealthy trait expressions such as obsessive preoccupation with calories or food avoidance.
Client coping skills focus on constructive, temperament-congruent strategies targeting symptom reduction. These include a variety of skills borrowed from other treatment modalities such as dialectical behavior therapy (DBT), as well as skills developed to target primary neurobiological targets such as anxiety and altered reward sensitivity.
Supports receive training on effective tools to assist their loved one. These tools address a variety of factors that are common among Supports of individuals with AN, including tools that achieve a balance between providing emotional assistance and encouraging accountability. Support person skills also include a focus on developing effective communication, demonstrating client-identified effective responses to symptoms, reducing blame, increasing empathy, and managing Support burnout.
In the 5-day program, clients and Supports are separated for skills-training groups and receive training for effective management of ED symptoms in client-only or Support-only groups.
Key Point |
Clients and Supports receive focused skills training that integrate their own traits into skills development to manage and reduce client eating disorder symptoms. |
As noted in the core principles section, TBT-S emphasizes action as a central treatment component. Treatment encourages in vivo practice, including therapeutic meals in various treatment settings. Clients and Supports and/or TBT-S clinicians attend the meals throughout treatment. The dietitian provides feedback and coaching as necessary to navigate barriers to dietary success. The therapeutic meals may include the presence of ED behaviors such as restriction, skills deficits to manage anxiety and other challenging experiences, and/or client/Support conflict or ineffectiveness.
In vivo meal practice and observation are necessary and active treatment components. Clinicians and dietitians remain present to make an assessment of interventions and skills needed to increase success, and to observe client/Support patterns and any emerging problematic behaviors. The treatment team encourages clients and Supports to apply TBT-S skills learned during mealtimes, and intervenes as necessary to ensure that clients and Supports alike are being skillful.
Dietitians are also present to ensure that clients are practicing the prescribed meal plan. Clients are asked to make their meals and snacks, and dietitians “check off” on each meal and snack during treatment to ensure that they are adequate and to provide feedback as necessary. Supports observe clients receiving feedback from dietitians. Additionally, they practice providing learned TBT-S assistance strategies as necessary during designated meals and snack sessions.
Key Point |
Eating within structures with active coaching allows adult clients and Supports to practice taking their “medicines” in “doses” and combinations to meet individual needs. |
During TBT-S, clients and their Supports develop a written Behavioral Agreement (BA) that establishes a mutually agreed -upon framework for necessary action that the client has identified so as to achieve recovery. The Behavioral Agreement is a written document – a treatment plan – that includes daily commitments surrounding primary domains of recovery (such as eating or physical activity) and a detailed plan for Support involvement.
There are two versions of the BA, the Severe-and-Enduring Anorexia Nervosa (SE-AN) and Young Adult (YA) versions. They take slightly different approaches addressing differing developmental stages and levels of Support involvement. The BAs are fundamental, structured TBT-S clinician and client and Support tools to hold those with AN accountable and to develop and practice new client and Support skills. The BAs incorporate client temperaments to endorse congruence in client actions and client traits
Key Point |
Behavioral Agreements are structured frameworks for treatment plans developed to align with AN temperaments. |
Summary Key Point |
TBT-S structures its interventions around Behavioral Agreements for Young Adults (YA BA) and those with Severe-and-Enduring Anorexia Nervosa (SE-AN BA) that integrate experiential learning, meal planning/coaching, and skills training for clients and Supports. |
We now introduce the reader to two of the neurobiologically informed modules to “try on” what could be shared with clients when explaining anorexia nervosa and other eating disorders.
We have found that TBT-S could replace motivational treatments. Adult and adolescent clients have repeatedly reported to us that once they learn more details about the brain bases of their illness, guilt and oppressive self-evaluations decrease, and knowledge about why they experience what they do increases the desire to change. They report that they can picture what is happening in their brain, why it is painful and hard to change, and yet report a greater desire to change. TBT-S reflects and applies metaphoric parallels with Eating Disorder brain responses to help clients use tools that compensate for what they cannot do by themselves. This is not unlike wearing glasses. When retinal neuropathways do not align correctly, many people need external glasses to compensate for what cannot be seen clearly. TBT-S tools are clinical glasses to compensate for what cannot be sensed internally or registered clearly in the brain.
The purpose of the Neurobiology Psychoeducation Modules are to provide research evidence on anorexia nervosa (AN) as a neurobiological and brain-based disorder. This evidence provides the neurobiological foundation, framework, and rationale for the neurobiologically based intervention strategies that have evolved into a novel treatment approach called Temperament Based Therapy with Support (TBT-S).
Its specific goals follow:
The Neurobiology Psychoeducation Modules are organized by neurobiological and temperament targets that are specifically addressed with temperament based interventions. Clinicians can provide these modules whenever deemed appropriate.
These psychoeducation modules are designed to be shared with clients and/or their Supports in a range of settings – including outpatient individual and group settings through higher levels of care – to educate clients and/or their Supports on the neurobiological underpinnings of AN. Delivering psychoeducation in group settings offers the advantage of fostering discussion and sharing of experiences and knowledge among group members to facilitate communication and shared understanding.
Content for each module on specific neurobiological constructs and traits is provided in the following sections.
Several studies show benefits of providing psychoeducation to clients, their family members, and the community.[80–82] Importantly, this research suggests that psychoeducational messages emphasizing “malleable biology” and “cognitive-behavioral factors” tend to produce more optimism and self-efficacy in recovery, as well as perceived credibility of therapy compared with “biologically reductionist” messages that communicate that one’s psychological and emotional experience is nothing more than the result of brain or biological functions.[81–85] In anxious individuals, biologically based psychoeducation has also been shown to reduce self-blame.[86]
However, clinicians should also be aware that studies have identified factors associated with poor outcomes following psychoeducation. These include psychoeducation that takes an overly narrow and reductionist biological etiological stance, and psychoeducation that is delivered solely via written text or recorded videos, or involves assigning educational materials individually or online.[87, 88]
To maximize benefits, TBT-S psychoeducation is designed to be conducted by a clinician during a therapeutic session with clients and/or Supports, encouraging questions and discussion, generating real-life examples, and providing validation of the clients’ experiences. TBT-S emphasizes neurobiological malleability and neuroplasticity. The brain can be re-wired through behavioral practice and skill-use to manage AN traits and move toward recovery. As such, TBT-S psychoeducation modules are used to increase understanding and motivation for recovery, validate client experience when clinicians encourage clients to compare their own experiences with research evidence, reduce Support blame and criticism, and gain trust of and commitment to the TBT-S therapeutic interventions. Clients report this increases their motivation to change their eating disorder (ED) symptoms.
Neurobiological psychoeducation in TBT-S is designed to be delivered in an informal interactive lecture-style format. The content is included in the following sections. The clinician role is to engage discussions about individual experiences and knowledge in relation to the research findings.
This provides an opportunity for the clinician to correct misunderstandings about ED such as inaccurate beliefs about the causes of AN (e.g., AN is a choice, or the parents’ fault) and misattributions of the function of ED behaviors (e.g., food refusal is willful). This is best done by the clinician sharing the research findings objectively and validating client/Support experiences. The clinician can highlight the damage that misinformation causes (e.g., blame, stigma).
This also serves to position the client as expert (consistent with TBT-S philosophy) and facilitates open communication regarding knowledge and beliefs about AN to align understanding and improve the client-Support relationship.
Clinician techniques and scripts (in italics) that can be used with all psychoeducation modules follow:
1. Clinicians are encouraged to ask questions of the client and Support or group members to facilitate discussion and sharing of experiences.
- How do these findings compare with your own experience?
- Can you relate to these findings?
- How or what specifically resonates with your experience? What does not resonate for you?
- Is there an example in your life that reflects these findings?
2. Clinicians solicit questions to tailor information to the specific needs and interests of the clients/Supports.
- How does this make sense, or not make sense to you?
- Do you have any questions about what has been covered today?
- What is your take-home message of this information in relation to your experience?
3. Clinicians acknowledge when they do not know an answer to a question.
- Full transparency is modeled by clinician authenticity and scientific humility. This builds trust and fosters collaboration between clinicians and clients/Supports.
- Clinicians do not need to be experts in neurobiology to share neurobiological research findings. Research is constantly growing.
- This course provides basic neurobiological information informing the TBT-S approach. It is not exhaustive. If a clinician does not know an answer, then the answer is, “I will look into that and find out.”
- The reference list at the end of the course may be helpful for clinicians who would like to take a deeper dive into the scientific literature to share with clients/ Supports.
4. Clinicians are encouraged to acknowledge limits to existing research and validate when the study findings do not match with an individual’s experience. If the clinician is sharing research findings that they have read independently of the findings reported in this course, study limitations should be acknowledged. The findings described in this course take the limitations into account. Some common research limitations include the following:
- Results report averages across people in the study. It is expected that individual client experiences may vary from the average findings reported.
- Many studies include a small number of clients in a homogenous group that is not representative of the clients who are present for treatment. For example, many studies are expected to not include clients who have comorbid diagnoses, when in reality most clients have comorbid diagnoses such as depression, anxiety disorders, trauma history, or substance abuse.
- Some studies do not differentiate between AN-restricting type and AN–binge/purge type.
- Studies may address people at different states of illness (e.g., malnourished, weight-restored but symptomatic, recovered), which can impact results.
5. Clinicians use neurobiological research as a foundation to engender hope that recovery is possible.
- Clinicians validate that treatment is difficult, and that clients may feel counter to what they want to feel, due to their biological predisposition.
- You have to work harder than people who don’t have eating disorders to eat in a healthier way. It is counter to the way you are hardwired. Your brain signals are telling you not to eat, yet the best way to re-wire your brain is through the practice of eating specified foods. You are swimming upstream, and you are stronger by doing so.
Summary Key Points
- Research indicates that providing biologically informed psychoeducation is beneficial to clients and their families.
- Psychoeducation that communicates that biology both contributes to AN and that biology can change to promote recovery is more effective than messages that only focus on the causative role of biology.
- TBT-S uses interactive psychoeducation as an interventional strategy to increase motivation for treatment and recovery, validate client/Support experience, reduce stigma and blame, and raise awareness of the role of temperament and neurobiology in maintaining eating disorder symptoms.
Neurobiological and Trait Targets
The purpose of the Anxiety and Interoception Psychoeducation Module is to introduce clients and Supports to the scientific evidence addressing the role of anxiety and altered interoception in disordered eating behavior and other symptoms of AN. Interoception refers to disturbances in the experience of physical sensations inside one’s body. This module also provides the justification and rationale for intervention strategies aimed at managing anxiety and compensating for altered interoception by reducing reliance on internal (interoceptive) signaling to promote healthy eating behavior.
This module is provided early in treatment to set the stage for a trait-based approach. However, it can be provided whenever the clinician wishes to introduce this topic. In the studied 5-day TBT-S Programs, it was offered on the second day.
This module can be offered to clients only and/or Supports only, individually or in a group. It was tested in a 5-day, 40-hour format with a group of clients and their Supports to foster discussion and sharing of experiences among the group.
The following six talking points and additional evidence are offered for clinicians to share with clients and Supports. Clinician scripts (which can be said verbatim) and notes are provided to help guide discussion.
Clinician Scripts
Notes for the Clinician
It can be helpful to discuss what the patient quote communicates, including difficulty making sense of internal signals. Poor interoception leads to a sense of blindness or absence of guiding information. This makes it difficult to know what to expect of one’s self, and what the client needs from others (aka, Supports).
Notes for the Clinician
Figure 8. Insula
An example of a neural interoceptive prediction error is shown in Figure 9.
Figure 9. Example of a Neural Interoceptive Prediction Error
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Clinician Scripts
Notes for the Clinician
Figure 10. Decreased insula response to touch anticipation is associated with increased body dissatisfaction and harm avoidance in women remitted from anorexia nervosa
© The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Notes for the Clinician
If one cannot rely on internal body-state signals, then it is important for clinicians to use and encourage clients and Supports to:
Key Point |
|
The purpose of the Decision-Making and Inhibitory Control Psychoeducation Module is to introduce clients and Supports to the scientific evidence demonstrating the role of altered decision-making and inhibition in disordered eating behavior and other symptoms of anorexia nervosa (AN). This module also provides the basis for strategies aimed at managing difficulties in decision-making and emphasizing that cognitive control can be redirected to promote healthy eating behavior.
The module can be provided whenever the clinician wishes to introduce this topic. In the studied 5-day format, it was provided on the third day in one program and on the second day in another program.
This module can be offered to clients only and/or Supports only, individually or in a group. It was tested in a 5-day, 40-hour format with a group of clients and their Supports to foster discussion and sharing of experiences among the group.
The following six talking points, as well as additional evidence, are offered for clinicians to share with clients and Supports. Clinician scripts (which can be said verbatim) and notes are provided to help guide discussion.
Performance on cognitive tasks suggests AN is characterized by:
Figure 11. Inhibitory control circuit
Notes for the Clinician
Figure 12. Altered brain response during decision-making in AN: Money
From Wierenga CE, Bischoff-Grethe A, Melrose AJ et al. Hunger does not motivate reward in women remitted from anorexia nervosa. Biol Psychiatr. 2015;77(7):642–52; and Ely A, Berner LA, Wierenga CE, et al. Neurobiology of Eating Disorders: Clinical implications. Psychiatr Times. 2016;33(4).
Notes for the Clinician
(Script) Delay-discounting tasks are commonly used to assess someone’s decision-making style and whether they tend to be more impulsive or more inhibited/restrained.
In this task, individuals must choose between two options of monetary reward: a smaller-sooner reward or a larger-later reward. For instance, would you rather receive $31 today or $85 dollars in four weeks? Raise your hand if you would choose $31 today. Okay, now raise your hand if you would choose $85 in four weeks. Those of you who chose $31, what motivated that decision? Those of you who chose $85, what motivated that decision? What decision-making style do you think individuals with AN, who are more restrictive, tend to use?
Notes for the Clinician
It can be helpful to present Figure 13.
Figure 13. Altered brain response during decision-making in AN: Food
From Foerde K, Steinglass JE, Shohamy D, et al. Neural mechanisms supporting maladaptive food choices in anorexia nervosa. Nat Neurosci. 2015;18(11):1571–3.
Notes for the Clinician
Summary Key Point |
|
We strongly encourage the reader to “try on” the “Nondominant Hand” activity while reading about it. The ‘doing’ of it brings a life to the activity and allows enhanced comprehension for both the clinician and the client.
These traits could work against the client in this situation:
These traits could work for the client in this situation:
The Nondominant Hand was first published in the Family Eating Disorder Manual, by Hill, L. et al., 2012, The Center for Balanced Living, Columbus, Ohio. A variation of it was also published in Brain-Based Approach to Eating Disorder Treatment, by Hill, L., The Center for Balanced Living, Columbus, Ohio. 2017.
Key Point |
Reducing ED symptoms is a nondominant brain response. |
1. Clinician shares (does not read) the following instructions:
- I would like you to try on an experience that has you acting against your dominant responses that your brain is wired to do.
- Please take out a piece of paper and pencil/pen.
- There are four steps to this activity.
2. Everything you write is to be with your nondominant hand.
3. First, write down, with your nondominant hand the following: “I am writing with my nondominant hand.”
- When completed: “Now show your writing to the person next to you (or the clinician if one-on-one).”
- Allow a couple of minutes for each person to show what their writing looks like.
4. Now fill in the blank, your answer to this question, while writing with your nondominant hand: “I feel writing with my nondominant hand_________.”
- Wait while the client(s) and/or Supports write their “feeling words.
- No need to write the complete sentence.
5. Now turn to a person beside you as your partner (the partner would be the clinician in one-on-one settings). One person is to be the person who writes, the other person will be the “talker.”
When partners have identified their roles, present the following instructions:
- The person who is the talker is to speak to, interrupt, or disrupt in various ways the person who is writing. Pressure the person to write faster and get done sooner.
- The person who is the writer is to write with their nondominant hand, the following statement, “I am still trying to write with my nondominant hand!”
- You have 30 seconds to write the above statement. Now begin.
When completed, instruct everyone to answer the last question using their nondominant hand.
- The last question, still using your nondominant hand, is: “If I were to tell you that you had to write with your nondominant hand for the rest of your life, what would you do?” (Note: not feel, or think, but do.)
- Wait until everyone has completed their answers (about one minute).
Key Point |
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Clients are to practice an action and their own productive traits identified earlier for one week and report back.
This course introduces you to a new mental health treatment approach (TBT-S) that fills a significant gap by focusing on patients’ temperament traits, and research findings of underlying neurobiological irregularities that trigger symptoms. This approach holds the potential to be applied to other disorders that are trait based, such as anxiety or obsessive compulsive disorders. We have begun by focusing on eating disorders, specifically anorexia nervosa, due to the high rate of mortality and low rate of positive outcomes over time among adults.
TBT-S focuses on the root causes of an illness to augment ongoing therapies that concentrate primarily on symptoms. It treats from the inside out serving as the foundation for other treatments that treat from the outside in. Traits are central to who a person is and what their potentials are. TBT-S provides tools to help each client identify their own traits and how they are expressed on a continuum from productive to destructive. It provides tools to help clients use their productive traits to shift their destructively expressed traits to be the best of who they can be. It is critical for practitioners to know the difference between symptoms and traits since symptoms can be eliminated and traits are the means to manage and reduce symptoms throughout one’s life. TBT-S includes “Supports” in adult treatment integrating interdependence into treatment applications, ensuring that those who support the patient know the same information about the illness, have the same tools to use outside of treatment and learn when and how the client needs them for support.
TBT-S treats to the traits to manage symptoms with Supports for clients of all ages.
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1. Birmingham C, Su J, Hlynsky J, et al. The mortality rate from anorexia nervosa. Int J Eat Disord. 2005;38:143–6.2. Crow S, Petersen C, Swanson S, et al. Increased mortality in bulimia nervosa and other eating disorders. Am J Psychiatr. 2009;166:1342–6.
3. Foerde K, Steinglass J. Decreased feedback learning in anorexia nervosa persists after weight restoration. IntJEat Disord. 2017;50(4):415–23.
4. Udo T, Bitley S, Grilo C. Suicide attempts in US adults with lifetime DSM-5 eating disorders. BMC Med. 2019;17(1):120.
5. American Psychiatric Association. DSM-5 Development. www.dsm5.org/Proposed Revision/Pages/proposedrevision.aspx? rid=26; 2012.
6. Bulik C, Blake L, Austin J. Genetics of eating disorders: What the clinician needs to know. Psychiatr Clin North Am. 2019;42(1):59–73.
7. Zeeck A, Herpertz-Dahlmann B, Friederich H, et al. Psychotherapeutic treatment for anorexia nervosa: A systematic review and network meta-analysis. Front Psychiatr. 2018;9(158):1–14.
8. Hill L. Can Your Brain Cure Anorexia? A Brain-Based Approach to Eating Disorder Treatment Eating Disorders Catalogue. Carlsbad, CA: Gurze Books Publishing 2017.
9. Knatz Peck, S., Towne, T., Wierenga, C. E., Hill, L., Eisler, I., Brown, T., Han, E., Miller, M., Perry, T., & Kaye, W. (2021). Temperament-based treatment for young adults with eating disorders: acceptability and initial efficacy of an intensive, multifamily, parent-involved treatment. Journal of eating disorders, 9(1), 110. https:// doi.org/10.1186/s40337-021-00465-x
10. Rothbart M. Advances in temperament, history, concepts and measures. In Zentner M, Shiner RL (Eds.), Handbook of Temperament (p. 3). New York: Guilford Press; 2012.
11. Mervilde I, De Pauw S. Models of child temperament. In Zentner M, Shiner RL (Eds.), Handbook of Temperament (pp. 21–40). New York: Guilford Press; 2012.
12. Aron E. Temperament in psychotherapy: Reflections on clinical practice with the trait of sensitivity. In Zentner M, Shiner RL (Eds.), Handbook of Temperament (pp. 645–670). New York: Guilford Press; 2012.
13. Cole C. Infant temperament predicts personality more than 20 years later. Neuroscience News; 2020.
14. Mitchell K. Innate. Princeton, NJ: Princeton University Press;2018.
15. Whittle S, Allen N, Lubman D, et al. The neurobiological basis of temperament: Towards a better understanding of psychopathology. Neurosci Biobehav Rev. 2006;30(4):511–25.
16. Whittle S, Yucel M, Fornito A, et al. Neuroanatomical correlates of temperament in early adolescents. J Am Acad Child Adolesc Psychiatr. 2008;47(6):682–93.
17. Yucel M, Harrison BJ, Wood S, et al. State, trait and biochemical influences on human anterior cingulate function. Neuroimage. 2007;34(4):1766–73.
18. Hettema J, Bourdon J, Sawyers C, et al. Genetic and environmental risk structure of internalizing psychopathology in youth. Depress Anxiety . 2020;37(6):540–8.
19. Tang A, Crawford H, Morales S, et al. Infant behavioral inhibition predicts personality and social outcomes three decades later. Proc Natl Acad Sci USA. 2020;117(18):9800–7.
20. Kaye W, Bailer U. Understanding the neural circuitry of appetitive regulation in eating disorders. Biol Psych. 2011;70(8):704–5.
21. Kaye W, Wierenga C, Bailer U, et al. Nothing tastes as good as skinny feels: The neurobiology of anorexia nervosa. Trends Neurosci. 2013;36(2):110–20.
22. Kendler KS, MacLean C, Neale M, et al. The genetic epidemiology of bulimia nervosa. Am J Psychiatr. 1991;148 (12):1627–37.
23. Walters EE, Kendler KS. Anorexia nervosa and anorexic-like syndromes in a population-based female twin sample. Am J Psychiatr. 1995;152(1):64–71.
24. Lilenfeld L, Kaye W. Genetic studies of anorexia and bulimia nervosa. In Hoek HW, Treasure JL, Katzman MA (Eds.), Neurobiology in the Treatment of Eating Disorders (pp. 169–194). Hoboken, NJ: John Wiley; 1998.
25. Strober M, Freeman R, Lampert C, et al. Controlled family study of anorexia nervosa and bulimia nervosa: Evidence of shared liability and transmission of partial syndromes. Am J Psychiatr. 2000;157 (3):393–401.
26. Treasure J, CampbellI. The casefor biology in the aetiology of anorexia nervosa. Psychol Med. 1994;24(1):3–8.
27. Berrettini W. Genetics of psychiatric disease. Annu Rev Med. 2000;51:465–79.
28. Bulik C, Sullivan PF, Tozzi F, et al. Prevalence, heritability and prospective risk factors for anorexia nervosa. Arch Gen Psychiatr. 2006;63(3):305–12.
29. Steinglass JE, Walsh T. Psychopharmacology of anorexia nervosa, bulimia nervosa, and binge eating disorder. In Brewerton TD (Ed.), Clinical Handbook of Eating Disorders: An Integrated Approach (pp. 489–508). New York: Marcel Dekker; 2004.
30. Anderluh MB, Tchanturia K, Rabe-Hesketh S,etal. Childhood obsessive-compulsive personality traits in adult women with eating disorders: Defining a broader eating disorder phenotype. Am J Psychiatr. 2003;160(2):242–7.
31. Stice E. Risk and maintenance factors for eating pathology: A meta-analytic review. Pychopharmacol Bull. 2002;128:825–48.
32. Lilenfeld L, Wonderlich S, Riso LP, et al. Eating disorders and personality: Amethodological and empirical review. Clin Psychol Rev. 2006;26(3):299–320.
33. Bulik C, Breen G. Solving the eating disorders puzzle piece by piece. Biol Psychiatr. 2017;81(9):730–1.
34. Wadden T, Sternberg J, Letizia K, et al. Treatment of obesity by very low calorie diet, behavior therapy, and their combination: A five-year perspective. Int J Obes. 1989;30(Suppl 2):39–46.
35. Kaye W, Fudge J, Paulus M. New insights into symptoms and neurocircuit function of anorexia nervosa. Nat Rev Neurosci. 2009;10(8):573–84.
36. Kaye W, Wierenga C, Bailer U, et al. Does a shared neurobiology for foods and drugs of abuse contribute to extremes of food ingestion in anorexia and bulimia nervosa? Biol Psychiatr. 2013;73(9):836–42.
37. Kaye W, Bulik C, Thornton L, et al. Comorbidity of anxiety disorders with anorexia and bulimia nervosa. Am J Psychiatr. 2004;161(12):2215–21.
38. Cassin S, von Ranson K. Personality and eating disorders: A decade in review. Clin Psycho Rev. 2005;25(7):895.
39. Wagner A, Barbarich N, Frank G, et al. Personality traits after recovery from eating disorders: Do subtypes differ? Int J Eat Disord. 2006;39(4):276–84.
40. Lilenfeld L. Personality and temperament. Curr Top Behav Neurosci. 2011;6:3.
41. Fassino S, Piero A, Gramaglia C, et al. Clinical, psychopathological and personality correlates of interoceptive awareness in anorexia nervosa, bulimia nervosa and obesity. Psychopathology. 2004;37(4):168–74.
42. Harrison A, O’Brien N, Lopez C, et al. Sensitivity to reward and punishment in eating disorders. Psy Res. 2010;177 (1–2):1–11.
43. BernerL, Crosby RD, Cao, L, et al. Temporal associations between affective instability and dysregulated eating behavior in bulimia nervosa. J Psychiatr Res. 2017;92:183–90.
44. DeGuzman M, Shott M, Yang T, et al. Association of elevatedreward prediction error response with weight gain in adolescent anorexia nervosa. Am J Psychiatr . 2017;174(6):557–65.
45. Kerr K, Moseman S, Avery J, et al. Altered insula activity during visceral interoception in weight-restored patients with anorexia nervosa Neuropsychopharmacology. 2016;41 (2):521–8.
46. Oberndorfer T, Frank G, Fudge J, et al. Altered insula response to sweet taste processing after recovery from anorexia and bulimianervosa. Am J Psychiatr. 2013;214(2):132–41.
47. Wierenga C, Bischoff-Grethe A, Melrose A, et al. Hunger does not motivate reward in women remitted from anorexia nervosa. Biol Psychiatr. 2015;77(7):642–52.
48. Atiye M, Miettunen J, Raevuori-Helkamaa A. A meta-analysis of temperament in eating disorders. Eur Eat DisordRev. 2015;23(2):89–99.
49. Steiger H, Booij L. Eating disorders, heredity and environmental activation: Getting epigenetic concepts into practice. J Clin Med. 2020;9(5):E1332.
50. Hebb D. The Organization of Behavior. New York: McGraw-Hill; 1949.
51. Kolb B. Brain Plasticity and Recovery of Function in Adulthood. Mahwah, NJ: Lawrence Erlbaum Associates; 1995.
52. Abramowitz J, Foa E, Franklin M. Exposure and ritual prevention for obsessive-compulsive disorder: Effects of intensive versus twice-weekly sessions. J Consult Clin Psychol. 2003;71(2):394–8.
53. Deacon B, Abramowitz J. A pilot study of two-day cognitive-behavioral therapy for panic disorder. Behav Res Ther.2006;44 (6):807–17.
54. Gallo K, Chan P, Buzzell B, et al. The impact of an eight-day intensive treatment for adolescent panic disorder and agoraphobia on comorbid diagnosis. Behav Ther. 2012;43:153–9.
55. Ollendick T, Ost L, Reyuterskiold L, et al. One-session treatment of specific phobias in youth: A randomized clinical trial in the United States and Sweden. J Consult Clin Psychol. 2009;77:504–16.
56. Santucci L, Ehrenreich J, Trosper S, et al. Development and preliminary evaluation of a one-week summer treatment program for separation anxiety disorder. Cogn Behav Pract. 2009;16:317–31.
57. Schmidt R, Bjork R. New conceptualizations of practice: Common principles in three paradigms suggest new concepts for training. Psychol Sci. 1992;3 (4):207–17.
58. Storch E, Geffken G, Merlo L,et al. Family-based cognitive-behavioral therapy for pediatric obsessive-compulsive disorder: Comparison of intensive and weekly approaches. J Am Acad Child Adolesc Psychiatr. 2007;26:469–78.
59. Whiteside S, Jacobsen A. Anun controlled examination of a 5-day intensive treatment for pediatric OCD. Behav Ther. 2010;41:414–22.
60. Fernandez M, Storch E, Lewin A, et al. The principles of extinction and differential reinforcement of other behaviors in the intensive cognitive-behavioral treatment of primarily obsessional pediatric OCD. Clin Case Stud. 2006;12:511–21.
61. Storch E, Merlo L, Lehmkuhl L, et al. Cognitive-behavioral therapy for obsessive-compulsive disorder: A non-randomized comparison of intensive and weekly approaches. J Anxiety Disord. 2008;22(7):1146–58.
62. Doyle P, Le Grange D, Loeb K, et al. Early response to family-based treatment for adolescent anorexia nervosa. Int J Eat Disord. 2010;43(7):659–62.
63. Bulik C M, Devlin B, Bacanu S A, et al. Significant linkage on chromosome 10p in families with bulimia nervosa. Am J Hum Genet. 2003;72(1):200–7.
64. Bulik C M, Sullivan PF, Kendler KS. Heritability of binge-eating and broadly defined bulimia nervosa. Biol Psychiatr. 1998;44(12):1210–8.
65. Duncan L, Yilma Z, Gaspar H, et al. Significant locus and metabolic genetic correlations revealed in genome wide association study of anorexia nervosa. Am J Psychiatr. 2017;174(9):850–8.
66. Hinney A, Kesselmeier M, Jall S, et al. Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index. MolPsychiatr. 2017;22 (2):321–2.
67. Lock J, Le Grange D. Can family-based treatment of anorexia nervosa be manualized? J Psychother Pract Res. 2001;10(4):253–61.
68. Lock J, le Grange D. Family-based treatment of eating disorders. Int J Eat Disord. 2005;37(Suppl):S64–S7.
69. LoebK, LeGrange D. Family-based treatment for adolescent eating disorders: Current status, new applications and future directions. Int J Child Adolesc Health. 2009;2(2):243–54.
70. Strelau J, Zawadzki B. Activity as a temperament trait. In Zentner M & Shiner RL (Eds.), Handbook of Temperament (pp. 83–104). New York: Guilford Press; 2012.
71. Eisler I, Simic M, Hodsoll J, et al. A pragmatic randomised multi-centre trial of multifamily and single family therapy for adolescent anorexia nervosa. BMC Psychiatr. 2016;16(1):422.
72. Dare C, Eisler I, Russell G, et al. Psychological therapies for adults with anorexia nervosa: Randomised controlled trial of out-patient treatments. BR J Psychiatr. 2001;178:216–21.
73. Lemmens G, Eisler I, Buysse A, et al. The effects on mood of adjunctive single family and multi-family group therapy in the treatment of hospitalised patients with major depression: An RCT and 15 months follow-up study. Psychother Psychosom. 2009;78:98–105.
74. McFarlane W. Family interventions for schizophrenia and the psychoses: A review. Fam Process. 2016;55(3):460–82.
75. Miller I, Solomon CE, Keitner G. Does adjunctive family therapy enhance recovery from bipolar I mood episodes? J Affect Disord. 2004;82(3):431–6.
76. Dimitropoulos G, Farquhar J, Freeman V, et al. Pilot study comparing multi-family therapy to single family therapy for adults with anorexia nervosa in an intensive eating disorder program. Eur Eat Disord Rev. 2015;23(4):294–303.
77. Tantillo M. A relational approach to eating disorders multifamily therapygroup: Moving from difference and disconnection to mutual connection. Families Syst Health. 2006;24(1):82–102.
78. Kaye W, Wierenga C, Knatz S, et al. Temperament-based treatment for anorexia nervosa. Eur EatDisordRev. 2015;23(1):12–18.
79. Hill L, Peck S, Wierenga C, et al. Applying neurobiology to the treatment of adults with anorexia nervosa. JEat Disord. 2016;4:31.
80. Crisafulli M, Von Holle A, Bulik C. Attitudes towards anorexia nervosa: The impact of framing on blame and stigma. Int J Eat Disord. 2008;41(4):333–9.
81. Wiesjahn M, Jung E, Kremser J, et al. The potential of continuum versus biogenetic beliefs in reducing stigmatization against persons with schizophrenia: An experimental study. JBehav TherExp Psychiatr. 2016;50:231–7.
82. Hod Y. Psychoducation des patients et de leurs proches dans les pisodes psychotiques [Psychoeducation of patients and their family members during episode psychosis]. Encephale. 2013;39(Suppl 2): S110–S4.
83. Farrell N, Lee A, Deacon B. Biological or psychological? Effects of eating disorder psychoeducation on self-blame and recovery expectations among symptomatic individuals. Behav Res Ther. 2015;74:32–7.
84. Lebowitz M, Ahn W. Emphasizing malleability in the biology of depression: Durable effects on perceived agency and prognostic pessimism. Behav Res Ther. 2015;7:125–30.
85. Han D, Chen S.Reducing the stigma of depression through neurobiology-based psychoeducation: A randomized controlled trial. Psychiatr Clin Neurosci. 2014;68(9):666–73.
86. Lebowitz, M S, Pyun, J J., Ahn, W.K. Biological explanations of generalized anxiety disorder: effects on beliefs about prognosis and responsibility. Psychiatr Serv. 2014;65(4):498–503.
87. Lebowitz M, Ahn W, Nolen-Hoeksema S. Fixable or fate? Perceptions of the biology of depression. J Consult Clin Psychol. 2013;81(3):518–27.
88. Zimmermann M, Papa A. Causal explanations of depression and treatment credibility in adults with untreated depression: Examining attribution theory. Psychol Psychother. 2020;93(3):537–54.
89. Lilenfeld LR, Kaye WH, Greeno CG, et al. A controlled family study of anorexia nervosa and bulimia nervosa: Psychiatric disorders in first-degree relatives and effects of proband comorbidity. Arch Gen Psychiatr. 1998;55(7):603–10.
90. Bulik C, Slof-Op’t Landt M, van Furth E, et al. The genetics of anorexia nervosa. Ann Rev Nutr. 2007;27:263–75.
91. Watson H, Yilmaz Z, Thornton LH, et al. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa. Nat Genet. 2019;51(8):1207–14.
92. Klump K, Strober M, Johnson C, et al. Personality characteristics of women before and after recovery from an eating disorder. Psych Med. 2004;34(8):1407–18.
93. Jacobs M, Roesch S, Wonderlich S, et al. Anorexia nervosatrios: Behavioral profiles of individuals with anorexia nervosa and their parents. Psychol Med. 2009;39(3):451–61.
94. Woodside DB, Bulik CM, Halmi KA, et al. Personality, perfectionism, and attitudes toward eating in parents of individuals with eating disorders. Int J Eat Disord. 2002;31(3):290–9.
95. Harrison A, Sullivan S, Tchanturia K, et al. Attentional bias, emotion recognition and emotion regulation in anorexia: State or trait? Biol Psych. 2010;68(8):755–61.
96. Klump K, Keel P, Racine S, et al.The interactive effects of estrogen and progesterone on changes in emotional eating across the menstrual cycle [Errata]. J Abnorm Psychol. 2013 Feb;122(1):137.
97. Klump K, Fowler N, Mayhall L, et al. Estrogen moderates genetic influences on binge eating during puberty: Disruption of normative processes? J Abnorm Psychol. 2018;127(5):458–70.
98. Berthoud H, Lenard N, Shin A. Food reward, hyperphagia, and obesity. AM J Physiol Regul IntegrComp Physiol. 2011;300(6):R1266–R77.
99. Cowdrey F, Park R, Harmer C, et al. Increased neural processing of rewarding and aversive food stimuli in recovered anorexia nervosa. Biol Psych. 2011;70 (8):736–43.
100. Frank G, Reynolds J, Shott M, et al. Anorexia nervosa and obesity are associated with opposite brain reward response. Neuropsychopharmacology. 2012;37(9):2031–46.
101. Lock J, Garrett A, Beenhakker J, et al. Aberrant brain activation during a response inhibition task in adolescent eating disorder subtypes. Am J Psychiatr. 2011;168(1):55–64.
102. Foerde K, Steinglass J, Shohamy D, et al. Neural mechanisms supporting maladaptive food choices in anorexia nervosa. Nat Neurosci. 2015;18(11):1571–3.
103. Ehrlich S, Geisler D, Ritschel F, et al. Elevated cognitive control over reward processing in recovered female patients with anorexia nervosa. JPsychiatr Neurosci. 2015;40(5):307–15.
104. Dellava J, Thornton L, Hamer RS, et al. Childhood anxiety associated with low BMI in women with anorexia nervosa. Behav Res Ther. 2010;48(1):60–7.
105. Bischoff-Grethe A, Wierenga C, Berner L, etal.Neural hypersensitivity to pleasant touch in women remitted from anorexia nervosa. Transl Psychiatr. 2018;8(1):161.
106. Holsen L, LawsonE, Blum K, et al.Food motivation circuitry hypoactivation related to hedonic and nonhedonic aspects of hunger and satiety in women with active anorexia nervosa and weight-restored women with anorexia nervosa. J Psychiatr Neurosci. 2012;37(5):322–32.
107. Kaye W, Wierenga C, Bischoff-Grethe A, et al. Neural insensitivity to the effects of hunger in women remitted from anorexia nervosa. Am J Psychiatr. 2020;177 (7):601–10.
108. Bischoff-Grethe A, McCurdy D, Grenesko-Stevens E, et al. Altered brain response to reward and punishment in adolescents with anorexia nervosa. Psychiatr Res. 2013;214 (3):331–40.
109. Frank G, Collier S, Shott M, et al. Prediction error and somatosensory insula activation in women recovered from anorexia nervosa. J Psychiatr Neurosci. 2016;41(2):304–11.
110. Roberts M, Tchanturia K, Stahl D, et al. A systematic review and meta-analysis of set-shifting ability in eating disorders. Psychol Med. 2007;37(8):1075–84.
111. Smith K, Mason T, Johnson J, et al. A systematic review of reviews of neurocognitive functioning in eating disorders: The state-of-the-literature and future directions. Int J Eat Disord. 2018;51 (8):798–821.
112. Wu M, Brockmeyer T, Hartmann M, et al. Set-shifting ability across the spectrum of eating disorders and in overweight and obesity: A systematic review and meta-analysis. Psychol Med. 2014;44 (16):3365–85.
113. Berner L, RomeroE, Reilly EE, et al. Task-switching inefficiencies in currently ill, but not remitted anorexia nervosa. Int J Eat Disord. 2019;52 (11):1316–21.
114. Decker J, Figner B, Steinglass J. On weight and waiting: Delay discounting in anorexia nervosa pretreatment and post-treatment. Biol Psychol. 2015;78 (9):606–14.
115. Steward T, Mestre-Bach G, Vintro-Alcaraz C, et al. Delay discounting of reward and impulsivity in eating disorders: From anorexia nervosa to binge eating disorder. Eur Eat Disord Rev. 2017;25(6):601–6.
116. Wierenga C, Ely A, Bischoff-Grethe A, et al. Are extremes of consumption in eating disorders related to an altered balance between reward and inhibition? Front Behav Neurosci. 2014;9(8):410.
117. BrownT, VanzhulaI, Reilly E, et al. Body mistrust bridges interoceptive awareness and eating disorder symptoms. J Abnorm Psychol. 2020;129(5):445–56.
118. Strigo I, Matthews S, Simmons A, et al. Altered insula activation during pain anticipation in individuals recovered from anorexia nervosa: Evidence of interoceptive dysregulation. Int J Eat Disord. 2013;46:23–33.
119. Berner L, Simmons A, Wierenga C, et al. Altered interoceptive activation before, during, and after aversive breathing load in women remitted from anorexia nervosa. Psychol Med. 2018;48(1):142–54.
120. Oberndorfer T, Simmons A, McCurdy D, et al. Greater anterior insula activation during anticipation of food images in women recovered from anorexia nervosa versus controls. Psychiatr Res. 2013 214 (2):132–41.
121. Bailer U, Narendran R, Frank W, et al. Amphetamine induced dopamine release increases anxiety in individuals recovered from anorexia nervosa. Int J Eat Disord. 2012;45(2):263–71.
122. Frank G, Bailer UF, Henry S, et al. Increased dopamine D2/D3 receptor binding after recovery from anorexia nervosa measured by positron emission tomography and [11C]raclopride. Biol Psychiatr. 2005;58(11):908–12.
123. Wagner A, Aizenstein H, Venkatraman M, et al. Altered reward processing in women recovered from anorexia nervosa. Am J Psychiatr. 2007;164(12):1842–9.
124. Arnett J. The Oxford Handbook of Emerging Adulthood. Arnett J (Ed.). Oxford: Oxford University Press; 2015.
125. Gustavson K, Knudsen A, Nesvag R, et al. Prevalence and stability of mental disorders among young adults: Findings from a longitudinal study.BMCPsychiatr. 2018;18(1):65.
126. US Department of Health and Human Services. National Survey of Drug Use and Health (NSDUH). www.samhsa.gov/data/ release/2019-national-survey-drug-use-and-health-nsduh-releases; 2019.
127. Twenge JM, Cooper AB, Joiner T, et al. Age, period, and cohort trends in mood disorder indicators and suicide-related outcomes in a nationally representative dataset, 2005–2017. J Abnorm Psychol. 2019;128(3):185–99.
128. Volpe U, Tortorella A, Manchia M, et al. Eating disorders: What age at onset? Psychiatr Res. 2016;30(238):225–7.
129. Mitrofan O, Petkova H, Janssens A, et al. Care experiences of young people with eating disorders and their parents: Qualitative study. BJPsych Open. 2019;5 (1):e6.
130. Dimitropoulos G, Landers A, Freeman V, et al. Open trial of family-based treatment of anorexia nervosa for transition age youth. J Can Acad Child Adolesc Psychiatr. 2018;27(1):50–61.
131. Dimitroupoulos G, Freeman V, Allemang B, et al. Family-based treatment with transition age youth with anorexia nervosa: A qualitative summary of application in clinical practice. J Eat Disord. 2015;3(1):1–13.
132. Asen E, Scholz M. Multi-family Therapy: Concepts and Techniques. New York: Routledge; 2010.
133. Simic M, Eisler I. Multi-family therapy. In Loeb K, LeGrange D (Eds.), Family Therapy for Adolescent Eating and Weight Disorders: New Applications (pp. 110–38). New York: Routledge; 2015.
134. Linehan M. DBT Skills Training Manual (2nd ed.). New York: Guilford Press; 2015.
135. Linehan M. Dialectical Behavior Therapy in Clinical Practice. New York: Guilford Press; 2020.
136. Zuckerman M. Models of adult temperament. In Handbook of Temperament (Chapter 3). New York: Guilford Press; 2012.
137. Hill L. A brain-based approach to eating disorder treatment. www.brainbasedeatingdisorders.org/; 2017.
138. Hodgekiss A. Trying to lose weight? Try the HAND DIET: Measure food portions using just your fingers, thumbs and palm. Daily Mail; 2014.
139. Squire L, Kandel E. Memory, from Mind to Molecules (2nd ed.). Boulder, CO: Roberts; 2009.
140. Cross-Disorder Group of Psychiatric Genomics Consortium. Genomic relationships, novel loci, and pleiotropic mechanisms across eight psychiatric disorders. 2019.
141. Bulik C, Flatt R, Abbaspour A, et al. Reconceptualizing anorexia nervosa. Psychiatr Clin Neurosci. 2019;73 (9):518–25.
142. Liu P, Peng G, Zhang N, et al. Crosstalk between the gut microbiota and the brain: An update on neuroimaging findings. Front Neurol. 2019;10:833.
143. Hubel C, Yilmaz Z, Schaumberg K, et al. Body composition in anorexia nervosa: Meta-analysis and meta-regression of cross-sectional and longitudinal studies. Int J Eat Disord. 2019;52(11):1205–23.
144. AkkermannK, Paaver M, Nordquist N, et al. Association of 5-HTT gene polymorphism, platelet MAO activity, and drive for thinness in a population-based sample of adolescent girls. International Journal of Eating Disorders. 2008;41(5):399–404.
145. Danner U, Sanders N, Smeets P, et al. Neuropsychological weaknesses in anorexia nervosa: Set-shifting, central coherence, and decision making in currently ill and recovered women. Int J Eat Disord. 2012;45(5):685–94.
146. Frank G, Kaye W. Current status of functional imaging in eating disorders. Int J Eat Disord. 2012;45(6):723–36.
147. Klump K. Puberty as a critical risk period for eating disorders: A review of human and animal studies. Horm Behav. 2013;64 (2):399–410.
148. Ma R, Mikhail M, Fowler N, et al. The role of puberty and ovarian hormones in the genetic diathesis of eating disorders in females. Child Adolesc Psychiatr Clin N Am. 2019;28(4):617–28.
149. Simmons W, Avery J, Barcalow J, et al. Keeping the body in mind: Insula functional organization and functional connectivity integrate interoceptive, exteroceptive, and emotional awareness. HumBrainMapp. 2013;34(11):2944–58.
150. Ehrlich S, Lord A, Geisler D, et al. Reduced functional connectivity in the thalamo-insular subnetwork in patients with acute anorexia nervosa. Hum Brain Mapp. 2015;36(5):1772–81.
151. Treasure J, Zipfel S, Micali N, et al. Anorexia nervosa. Nature Rev Dis Primers. 2015;1:15074.
152. Nunn K, Frampton I, Gordon I, et al. The fault is not in her parents but in her insula – a neurobiological hypothesis of anorexia nervosa. Eur Eat Disord Rev. 2008;16 (5):355–60.
153. Nunn K, Frampton I, Lask B, et al. Anorexia nervosa and theinsula. Med Hypotheses . 2011;76(3):353–7.
154. FrankG, Shott M, Keffer C, et al. Extremes of eating are associated with reduced neural taste discrimination. Int J Eat Disord. 2016;49(6):603–12.
155. Szalavitz M. The currency of desire. Sci Am Mind. 2017;28:48–53.
156. Sullivan PF. Mortality in anorexia nervosa. Am J Psychiatr. 1995;152(7):1073–4.
157. Ackard D, Richter S, Egan A, et al. Poor outcome and death among youth, young adults, and midlife adults with eating disorders: An investigation of risk factors by age at assessment. Int J EatDisord. 2014;47(7):825–35.
158. Arcelus J, Mitchell A, Wales J, et al. Mortality rates in patients with anorexia nervosa and other eating disorders. Arch Gen Psychiatr. 2011;68(7):724–31.
159. Compan V, Walsh B, Kaye W, et al. How does the brain implement adaptive decision making to eat? JNeurosci. 2015;35(41):13868–78.
160. Brainstorm Consortium. Analysis of shared heritability in common disorders of the brain. Science. 2018;360:6395.
161. Mahon P, Hildebrandt T, Burdick K. New genetic discoveries in anorexia nervosa: Implications for the field. Am J Pschiatr. 2017;174(9):821–2.
162. Simone M, Askew A, Lust K, et al. Disparities in self-reported eating disorders and academic impairment in sexual and gender minority college students relative to their heterosexual and cisgender peers. IntJ Eat Disord . 2020;53(4):513–24.
163. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-V, 5th ed.). Washington, DC: American Psychiatric Association; 2013.
164. Yau W-Y, Bischoff-Grethe A, Theilmann R,et al. Alterations in white matter microstructure in women recovered from anorexia nervosa. Int J Eat Disord. 2013;46(7):701–98.
165. Stiles-Shields C, Bamford B, Lock J, et al. The effect of driven exercise on treatment outcomes for adolescents with anorexia and bulimia nervosa.IntJ Eat Disord. 2015;48(8):392–6.
166. Zerwas S, Lund B, Von Holle A, et al. Factors associated with recovery from anorexia nervosa. J Psychiatr Pract. 2013;47(7):972–9.
167. Levinson C, Zerwas SC, Brosof LC, et al. Associations between dimensions of anorexia nervosa and obsessive-compulsive disorder: An examination of personality and psychological factors in patients with anorexia nervosa. Eur Eat Disord Rev. 2018;27(2):161–72.
168. Klump K, Burt S, Spanos A, et al. Age differences in genetic and environmental influences on weight and shape concerns. Int J Eat Disord. 2010;43(8):679–88.
169. Klump K, Culbert K, O’Connor S, et al. The significant effects of puberty on the genetic diathesis of binge eating in girls. Int J Eat Disord. 2017;50(8):984–9.
170. Hubel C, Gaspar H, Coleman J, et al. Genetic correlations of psychiatric traits with body composition and glycemic traits are sex- and age-dependent Nat Commun. 2019;10(1):5765.
171. McAdams C, Jeon-Slaughter H, Evans S, et al. Neural differences in self-perception; Oberndorfer T, Kaye W, Simmons A, et al. Demand-specific alteration of nmedial prefrontal cortex response during an inhibition task in recovered anorexic women. Int J Eat Disord. 2011;44(1):1–8.
174. Linehan M. Cognitive-Behavioral Treatment of Borderline Personality Disorder. New York: Guilford Press; 1993.
175. Pruis T, Keel P, Janowsky J. Recovery from anorexia nervosa includes neural compensation for negative body image. Int J Eat Disord. 2012;45:919–31.
176. McCormick L, Keel P, Brumm M, et al. Implications of starvation-induced change in right dorsal anterior cingulate volume in anorexia nervosa. Int J Eat Disord. 2008;41(7):602–10.
177. Bergen A, Yeager M, Welch R, et al. Association of multiple DRD2 polymorphisms with anorexia nervosa. Neuropsychopharmacology. 2005;30 (9):1703–10.
178. Frieling H, Romer K, Scholz S, et al. Epigenetic dysregulation of dopaminergic genes in eating disorders. IntJ Eat Disord. 2010;43(7):577–83.
179. Richmond B, Liu Z, Shidara M. Predicting future rewards. Science. 2003;301:179–80.
180. Robinson P, Kukucska R, Guidetti G, et al. Severe and enduring anorexia nervosa (SEE-AN): A qualitative study of patients mindful eating vs. distraction during food exposure. International Journal of Eating Disorders 2013;46(6):582–85.
185. Hill L. The wood burning stove: A metaphor for dietary regulation for persons with eating disorders. In Eating Disorders Treatment and Prevention, Vol. 1 (2) New York: Brunner/Mazel; 1993.
186. Kaye WH, Barbarich NC, Putnam K, Gendall KA, Fernstrom J, Fernstrom M, et al. Anxiolytic effects of acute tryptophan depletion in anorexia nervosa. Int J Eat Disord 2003;33:257–67.
187. Fairburn CG, Beglin SJ. Eating Disorder Examination Questionnaire (EDE-Q) [Database record]. APA PsycTests;1994.
188. Schebendach J, Mayer LES, Devlin MJ, Attia E, Walsh, BT. Dietary energy density and diet variety as risk factors for relapse in anorexia nervosa: A replication. Int. J. Eat. Disord. 2012; 45:79–84. doi: 10.1002/eat.20922
189. Gianini, LM, Walsh BT, Steinglass J, Mayer L. Long-term weight loss maintenance in obesity: Possible insights from anorexia nervosa? International Journal of Eating Disorders, 2017;50:341– 42. doi: 10.1002/eat.22685
190. Jewell, T., Blessitt, E., Stewart, C., Simic, M., & Eisler, I. (2016). Family therapy for child and adolescent eating disorders: a critical review. Family Process, 55(3), 577–594.
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