New treatment approaches for severe and enduring eating disorders.

PHB-10901; No of Pages 10 Physiology & Behavior xxx (2015) xxx–xxx

Contents lists available at ScienceDirect

Physiology & Behavior journal homepage: www.elsevier.com/locate/phb

New treatment approaches for severe and enduring eating disorders

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Janet Treasure, Valentina Cardi, Jenni Leppanen, Robert Turton ⁎

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Section of Eating Disorders, Psychological Medicine, King's College London, Institute of Psychiatry, Psychology and Neuroscience, London, United Kingdom

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Keywords: Eating disorders Staging model Neuroprogressive changes Treatment targets Novel interventions

Objective: The aim of this paper is to map the possibility of new treatment approaches for eating disorders. Background: Eating disorders have a protracted trajectory with over 50% of cases developing a severe and enduring stage of illness. Although a good response to family-based interventions occurs in the early phase, once the illness has become severe and enduring there is less of a response to any form of treatment. Neuroprogressive changes brought about by poor nutrition and abnormal eating patterns contribute to this loss of treatment responsivity. Method: We have summarised the profile of symptoms at the various stages of illness and considered new treatments that might be applied. Results: In the enduring stage of illness in addition to problems with body image, food and eating, there are additional problems of low mood, high anxiety and compulsivity and problems in social functioning. This suggests that there are dysfunctions in circuits subsuming reward, punishment, decision-making and social processes. New approaches have been developed targeting these areas. Conclusion: New interventions targeting both the primary and secondary symptoms seen in the enduring stage of eating disorders may improve the response to treatment. © 2015 Published by Elsevier Inc.

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Article history: Received 28 February 2015 Received in revised form 22 May 2015 Accepted 4 June 2015 Available online xxxx

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1. The prevalence and characteristics of eating disorders

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Eating disorders have been described as being amongst the most difficult psychiatric conditions to treat [43,69]. It has been found that up to 0.3% of young women might develop Anorexia Nervosa (AN) and 1% Bulimia Nervosa (BN) across the lifespan [76]. For males a similar trend is reported although prevalence rates are lower than for females [153]. The Diagnostic and Statistical Manual of Mental Disorders—fifth edition (DSM-5; [6]) criteria for AN include significant weight loss (i.e., relative to an individual's sex, age and developmental trajectory) and an acute sense of fear associated with increasing weight. The criteria for BN are the presentation of binge eating (i.e., eating large amounts of food during a two-hour period associated with a sense of loss of control) and

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• We describe the development and progression of eating disorders. • Treatment approaches at the different stages of illness are outlined. • Possible change processes and novel treatment approaches are reviewed.

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⁎ Corresponding author at: Section of Eating Disorders, King's College London, Institute of Psychiatry, Psychology and Neuroscience, 103 Denmark Hill, London SE5 8AF, United Kingdom. E-mail addresses: [email protected] (J. Treasure), [email protected] (V. Cardi), [email protected] (J. Leppanen), [email protected] (R. Turton).

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compensatory behaviours such as self-induced vomiting and laxative abuse. A transdiagnostic concept across both illnesses is the overevaluation of shape and weight (i.e., extreme importance is given to shape and weight in defining the self). For many sufferers of eating disorders these life-threatening conditions run a protracted course; resulting in a profound impact upon an individual's health and psychosocial functioning.

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2. A staging model of eating disorders

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A unique longitudinal study from Sweden described the long-term trajectory of a cohort of AN cases ascertained early in the course of their illness (aged 15) [171]. The cohort was assessed at 16, 21, 24 and 32 years of age and compared to a group of healthy controls on a global assessment of functioning and the Morgan–Russell Outcome Assessment Schedule [119]. The mean duration of illness was found to be over 7 years for eating disorder psychopathology. The group with premorbid obsessive–compulsive personality disorder and autistic spectrum traits had a longer course (Anckarsater et al., 2012, [171]).

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http://dx.doi.org/10.1016/j.physbeh.2015.06.007 0031-9384/© 2015 Published by Elsevier Inc.

Please cite this article as: J. Treasure, et al., New treatment approaches for severe and enduring eating disorders, Physiol Behav (2015), http://dx. doi.org/10.1016/j.physbeh.2015.06.007

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3.1. Cognitive difficulties

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Clinically, individuals with AN present with rigid thoughts and behaviours relating to eating and weight. Inflexibility and poor central coherence have been found in patients with AN [97,131,144]. These difficulties are particularly strong in those with comorbid obsessive– compulsive disorder, obsessive–compulsive personality disorder or autistic traits. These traits have been associated with a poor response to treatment [4,8,33,172] and may underpin the compulsive nature of AN [60]. In contrast to over control in AN, impairments in inhibitory control have been found in a systematic review of BN (Wu et al., 2013c). These deficits were found to be particularly strong for disease-salient

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Individuals with eating disorders experience pervasive interpersonal difficulties, some of which predate illness onset and are associated with a poor outcome (Anckarsater et al., 2012, [171]). It has been suggested that abnormal eating behaviours might serve as a strategy to improve social acceptance [129] (Treasure and Schmidt, 2013). Problems in many aspects of social cognition were seen in a systematic review and meta-analysis of the literature [22]. A habitual tendency to interpret interpersonal encounters in a negative way might contribute to the maintenance of poor social adjustment, and in turn reinforce abnormal eating behaviours. Studies conducted by our group illustrate that patients have an attentional bias towards threatening faces, rather than neutral or compassionate expressions [23,24] and tend to interpret ambiguous social scenarios more negatively than healthy subjects (Cardi et al., submitted). Vigilance to social threat is attenuated in subjects who recovered from the illness [23], suggesting that it might be related to the secondary consequences of starvation. Neuroprogressive changes associated with dietary restriction, bingeing and purging may accentuate the impaired ability to relate to others.

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3.3. Emotional difficulties

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Negative emotional states also contribute to the maintenance of eating disorders. Studies employing daily assessments in naturalistic settings (i.e. ecological momentary assessments) indicate that negative emotional states are associated with binge episodes in patients with BN and Binge Eating Disorder (BED) [63,66] and with dietary restriction in patients with AN [41,99]. Laboratory-based studies have provided evidence for the impact of negative affective states such as anxiety on caloric intake (higher anxiety, lower intake; [148] and eating-disorders symptoms, such as feelings of fatness and urge to restrict [173] in AN. Interestingly, a recent study investigating the effects of eating on mood found that both patients with BN and AN reported increased negative affect during meal consumption [10]. In a recent meta-analysis conducted by our group we found that positive mood induction is positively associated with increased food intake on a test meal in patients with AN (Cardi et al., in preparation). A decrease in food consumption was found for patients with BN. These findings suggest that the use of strategies to disrupt the learned association between eating and negative emotions might help patients to develop a more positive attitude towards food and eating. This appears important as a recent systematic review of the literature found that although anxiety levels might decrease following treatment for AN they still remain above non-clinical norms [90].

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3.4. Neural substrates of cognitive, social and emotional difficulties

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Problems in the neural circuits of the limbic system are thought to explain some of the cognitive, social and emotional abnormalities found in eating disorders [56,84,102]. The circuits involved in these behaviours include frontal regions (medial prefrontal cortex, lateral prefrontal cortex and orbitofrontal cortex), the striatum (caudate and striatum) and the nucleus accumbens (Buckholtz and MeyerLindenberg, 2012) and the insula [123]. The evidence points to a hyper-responsive cortico-limbic-striatal circuit in response to food but in contrast, a hypo-responsive fear network in response to standard fear eliciting stimuli [181]. Decreased dopaminergic neurotransmission has been found in the mesolimbic reward system in recovered patients which supports general avoidance motivation, difficulties in cognitive flexibility and anhedonia in AN ([51]; 2015; [52]).

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The eating disorder phenotype is characterised by difficulties experienced in a range of different domains.

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stimuli including highly palatable foods, eating, and body weight related stimuli. This has led to suggestions that an impulsive/compulsive endophenotype might underlie the habitual nature of binge eating in BN [130,141].

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Only one patient did not meet the criteria for an affective disorder (i.e., depression) within the 18-year follow-up period (i.e., by 32 years of age). Thus, anhedonia, anxiety and autistic and obsessive–compulsive spectrum traits are features of late stage AN. This complexity may contribute to the loss of treatment responsivity in people with the severe and enduring form of illness. A recent retrospective cohort study found that over 50% of eating disorder cases develop a severe and enduring illness [151]. Gender comparisons revealed a 39% remission rate for females versus 59% for males after five years of illness duration. Moderating factors for the outcome of AN include illness duration, age of onset and presence of co-morbidities (Steinhausen, 2008). Based upon this evidence, a staging model of eating disorders has recently been formulated [162]. This framework incorporates the concept of a form of neuroprogression developing over time associated with the need to match treatment to the stage of illness. The staging model maps eating disorder psychopathology to the following stages: high risk, prodromal, full syndrome and severe and enduring. During childhood and adolescence individuals may become predisposed towards the development of an eating disorder due to the presence of high-risk markers. Shyness, social problems and obsessive–compulsive personality traits [8,58,171] seem to predate the onset of AN whereas, the traits that precede BN include a tendency to overeat [142] and problems with attention and impulsivity that may manifest as Attention Deficit Hyperactivity Disorder (ADHD) traits in childhood [116,138]. A significant amount of evidence has been found suggesting that childhood anxiety is also a high-risk marker for AN and BN [59,83]. These vulnerability factors can lead to a prodromal phase characterised by sub-clinical symptoms. During this early stage of illness symptoms can occasionally improve without engagement with clinical services and increased rates of diagnostic cross-over occur [162]. If prodromal symptoms do not remit, during early adulthood they may transition into the development of a ‘full-blown’ eating disorder. For AN, the time frame for this early stage of illness is currently outlined as being lower than three years in duration. In regard to BN, currently there is insufficient evidence to define time frames for the different stages of illness [162]. The final stage outlined by the model is the severe and enduring stage of illness, which may be defined as a prolonged illness of over seven years in duration [162]. It is hypothesised that neuroprogressive changes brought about by poor nutrition and/or abnormal eating patterns and diminished psychosocial resources lead to the complex profile of morbidity characteristic of this later stage. For instance, evidence has been found that in the severe and enduring stage of AN brain size is reduced particularly in the cerebellum and mesencephalon [50]. The atypical brain activation to illness relevant cues (for example salient body shape images) is more pronounced in adults than adolescents [47,48].

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4. Maintenance models of the phenotype

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4.1. Clinical maintenance models of AN

Once the illness has become severe and enduring there is less of a response to any form of treatment and there is uncertainty about clinical management [72,174]. Currently, there is no recommended first-line therapy for adults presenting with AN in the later stages of illness [71]. The limited evidence available for patients in the severe, enduring stage of illness suggests that remission rates are modest and treatment acceptability is poor [71]. Treatment drop-out can be high from outpatient treatment [36] and 26–41% of patients need additional in- or day-patient care, because of either a failure-to-improve or a deterioration of symptoms [43,182]. A focus on more of the psychosocial consequences of the illness may be of benefit for this stage delivered either individually [159] or through the family (Hibbs, submitted). Further exploration of treatment approaches for people who do not respond or who do not receive a timely first line effective intervention is needed. Many treatments for eating disorders have been adapted from those used to treat other conditions. It is possible that a more targeted approach to key eating disorder symptoms may improve outcomes. Translating from experimental medicine into clinical practice involves a variety of steps. The first is to build an accurate clinical profile of the various symptoms and model the underpinning psychopathology. The next stage is to consider possible techniques to foster change and to modify these dysfunctional systems. If we apply this construct to eating disorders then we are probably at the “drawing board” stage of model building especially for those in the severe enduring phase of illness.

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The maintenance of AN leading to an enduring form of illness has been described. The cognitive interpersonal model of Schmidt and Trea198 sure [136] describes how the visible aspects of AN which are relevant for 199 interpersonal processes add to the valued elements, such as feelings of 200 control and adherence to rules and channelling negative emotions and 201 lack of connection to others into food as a form of emotional regulation 202 Q12 ([136], Treasure and Schmidt, 2013). These behaviours, repeated over 203 time, become ingrained habits [60,169]. 204 These habits resemble those found in Obsessive Compulsive Disor205 ders, rather than in BN, in that they are formed from avoidant rather 206 than appetitive goals [57,130]. Interventions to break these unhelpful 207 habits might be of benefit in AN. 4.2. Clinical maintenance models of loss of control over eating

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5. Treatment approaches at the different stages of illness

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There is a paucity of evidence from high quality trials to answer questions in the enduring stage of illness about which treatments are 240 acceptable and how much benefit accrues. Much more is known about 241 the earlier stages of illness as can be seen in recent guidelines 242 (e.g., [71]). In the very early prodromal stage dissonance-induction 243 techniques and body acceptance interventions can prevent symptom 244 Q15 progression (Stice et al., 2007). In the early stage of AN family-based 245 therapies are helpful [46,71]. 246 Regarding the treatment of BN, guidelines have recommended that 247 Cognitive Behavioural Therapy (CBT), possibly in a self-help format, 248 should be the first line of therapy [71]. The failure of an early response 249 within the first 4 weeks may signal the need to switch to other forms 250 of treatment. Support for the use of specialist individual therapies, 251 such as an enhanced version of CBT [18,42] and interpersonal psycho252 therapy, has been found for patients with BN [12,28].

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6. The use of novel interventions to change the factors that maintain 277 the illness 278 The symptoms described above include several areas that can be targeted with new treatments. The new understanding about brain plasticity has led to the development of a wide variety of interventions that guide this malleable potential of the brain through training, drugs, transcranial magnetic stimulation and neurosurgical methods. These novel treatment approaches may be useful as adjunctive strategies to help improve the treatment outcomes for patients with severe and enduring eating disorders. An outline of the working models of AN (Fig. 1) and BN (Fig. 2) with possible treatment approaches matched onto it. Childhood anxiety, increased sensitivity to punishment, obsessive– compulsive and autistic traits and increased sensitivity to fear learning are some of the vulnerability factors which predispose to the onset of AN. Once the illness develops, core symptoms, such as restriction, weight loss and weight-, shape- and food-related preoccupations appear. With the illness progression, neuroprogressive secondary changes such as rigid eating habits; cognitive emotional and social difficulties and abnormalities in brain structure and function develop and in turn reinforce the illness. It is suggested that new treatment approaches could be used to target the neuroprogressive changes which occur in AN. Abnormalities in appetite regulation, childhood anxiety, reward sensitivity and inhibitory control are some of the vulnerability factors that predispose the onset of BN. Once the illness develops, core symptoms, such as cycles of restriction and loss of control over eating and weight-, shape- and food-related preoccupations appear. With illness progression, neuroprogressive secondary changes such as rigid eating habits and addictive-like changes; cognitive emotional and social difficulties and abnormalities in brain structure and function develop and in turn reinforce the illness. It is suggested that new treatment approaches could be used to target the neuroprogressive changes that occur in BN.

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6.1. Targeting cognitive functioning

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Abnormalities in the reward system might account for some of fea210 tures of the binge eating phenotype. In BN there appears to be decreased 211 responsiveness of the reward system, especially to taste reward. There 212 are two possibilities that may account for this. First, the reward defi213 ciency may be an innate vulnerability. He et al. [74] found that in 214 healthy subjects difficulties inhibiting the response to high calorie 215 food cues on the Go/No Go task were associated with increased activa216 tion to these stimuli in the right striatum (a circuit involved in habits). 217 These findings were stronger for participants with a higher body mass 218 Q13 index. Houben et al. (2011) found that participants with difficulties in 219 inhibitory control consumed greater amounts of highly palatable food 220 on a test meal than participants with strong inhibitory control. These 221 difficulties in inhibition may make individuals more prone to indulge 222 in highly palatable food due to the strong impulses they elicit (Houben 223 Q14 et al., 2011). The secondary consequences of impulsive/compulsive, 224 over control and loss of control over eating seen in BN and BED may 225 then lead to neuroadaptive changes in which a habitual addictive type 226 response to food develops. 227 The second possible explanation for the abnormalities in reward 228 sensitivity is that the reward system may be downregulated as a 229 neuroadaptive process to the over/under eating cycles. This latter mech230 anism may be relevant in obesity as adolescents at high risk for future 231 obesity have a hyper-responsive reward system [150]. Patients with 232 BN also exhibit impaired brain activation in the inhibitory control net233 work (fronto-striatal loops including the lateral prefrontal cortex, 234 precentral cortex, anterior cingulate cortex, and putamen [104,109, 235 110]). Interventions to increase inhibitory control and/or to moderate 236 the hedonic aspects of eating may be of value.

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Cognitive Remediation Therapy (CRT) is a novel form of therapy that 312 has been adapted for patients with eating disorders [156] from its initial 313 use for other disorders such as brain injury [29] and schizophrenia 314



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playful activities aimed at improving neurocognitive deficits in set shifting (thinking more flexibly) and central coherence (seeing the bigger picture as opposed to focusing on the details) and the enhancement

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of meta-cognitive skills [154]. Thus, CRT targets cognitive styles that are associated with obsessive–compulsive personality traits that are associated with a poor prognosis in AN [131]. Case studies and pilot studies have demonstrated that CRT is a feasible and acceptable form of treatment for adults [157] and children and adolescents [34] with AN. Studies have demonstrated that CRT can be

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Fig. 1. A model to describe the development of severe and enduring AN and new treatment approaches.

Fig. 2. A model to describe the development of severe and enduring and new treatment approaches.


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6.3. Targeting social difficulties

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In preliminary experimental medicine studies we have investigated the use of short video-clips including relaxing background music, pleasant images, and scripts to induce positive mood and motivation for recovery in patients with AN [26,27]. The development of these multicomponent video-clips is based on several theoretical frameworks. Namely, a number of authors have discussed the use of music therapy to positively affect physiological functioning [75,94]. Imagery has been proposed as a useful means to elicit specific cognitions, affects and behaviours related to food and it has been shown to modify behavioural eating patterns [82]. Finally, inducing positive emotions can restore self-regulation [158] and psychological and physical wellbeing [53,54]. Our recent findings in patients with AN indicate that the use of these video-clips is associated with increased calorie consumption during a test meal, reduced anxiety and higher levels of positive mood compared to a music only, control condition [25]. For patients with BN, the mood induction strategy was associated with a large reduction in their level of vigilance towards food stimuli [25]. These promising findings suggest that this approach may be beneficial as a strategy to help improve mealtimes on inpatient units. Further research may seek to examine whether personally tailored video scripts lead to enhanced treatment effects.

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In recent years, Cognitive Bias Modification (CBM) procedures have been developed with the purpose of modifying negative cognitive biases in interpretations and attention in a range of clinical populations 366 Q19 including: affective disorders [73] (Yang et al., in press), obsessive– 367 compulsive disorder [31] and substance abuse [139]. There are two 368 main variants of CBM procedures, both of which are computerised 369 [106]. One approach is targeted at changing negative biases in attention 370 through the use of a modified visual version of the dot-probe task [107]. 371 In this paradigm two stimuli appear onscreen; one of which is positively 372 valenced and the other negatively. A probe then appears onscreen for a 373 very brief period of time and patients must react to it as quickly as pos374 sible by pressing a computer key. In order to direct attention away from 375 the negative stimulus and towards the positive, this probe is repeatedly 376 presented onscreen in the space where the positive stimulus was posi377 tioned. The second CBM approach helps to remediate negative biases in 378 interpretation. This approach involves patients listening via head379 phones to ambiguous scenarios that have the risk for a negative inter380 pretation (e.g., you haven't spoken to a close friend in a while so you 381 message them to see how they have been. It's been several hours 382 since you messaged them but they haven't replied) but are given a pos383 itive resolution. 384 Quantitative data indicate that CBM can remediate negative atten385 tion and interpretation biases towards emotionally relevant stimuli 386 (e.g. facial expressions; emotionally valenced words) or anxiety- and 387 depression-specific stimuli with a moderate sized effect in clinical and 388 sub-clinical populations (g = 0.49; [68]. This effect was found to be

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6.4. Targeting eating behaviour habits and underlying processes

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6.4.1. Implementation intentions This goal-based approach to changing habits involves the planning of when and how an individual will perform the desired behaviour through an IF-THEN format. For instance, ‘if I feel like buying my ‘binge foods’ from my local store, then I will try going to a different supermarket’. This strategy to change behaviour has been tested as an approach to help individuals develop healthier eating patterns [3]. Clinically, implementation intentions have primarily been tested as a strategy to help develop healthier eating patterns and aid weightloss in obesity. Teaching overweight women how to form implementation intentions results in higher levels of weight-loss [105]. Furthermore, this approach has also been reported to increase adherence to meal-replacement programmes in overweight individuals leading to significant reductions in participants' BMI [180]. To date, no studies have examined the use of implementation intentions in AN or BN. They might be useful in the treatment of eating disorders when used alongside the use of self-monitoring techniques such as thought/food diaries that are often used as part of CBT interventions for eating disorders [121]. This may allow for the specific targeting of IF-THEN plans to eating disorder habits [98]. Troop [163] found that the effect of the formation of implementation intentions to increase greater fruit and vegetable consumption was moderated by participants' level of dietary restraint. It is therefore uncertain whether this approach can be applied to AN where levels of restraint are extreme.

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6.4.2. Exposure therapy Exposure therapy is based on the deliberate and planned systematic exposure to a feared stimulus, or representation of the stimulus, in a safe environment [128]. The aim is to confront (rather than avoid) the stimulus in order to: 1) learn that it does not signal danger; and 2) develop effective strategies of coping with the anxiety [128]. The approach has been found to be an effective treatment for a range of affective disorders that are often co-morbid with eating disorders such as social phobia [70] and obsessive–compulsive disorder [2]. Recent evidence-based theoretical models of AN confirm the pivotal role played by food-related anxiety in the onset and maintenance of the illness [143,147,152,160]. Therefore, researchers have suggested that exposure-based therapies maybe a useful adjunctive treatment for patients with AN [145,146]. A recent review highlighted the potential of in vivo gradual exposure to food stimuli to reduce food-related anxiety and increase caloric intake in AN [93]. However, previous research has not been conducted in patients in the severe and enduring stage of AN. We recently found that eight sessions of gradual and guided exposure to food stimuli can be helpful in reducing anxiety levels and eating-related fears in patients

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greater for remediating negative biases in interpretation (g = 0.81) than in attention (g = 0.29). Also, a recent meta-analysis found that benign interpretation training was associated with a significant increase in positive interpretation and decrease in negative mood in healthy controls, subclinical and clinical populations [115]. In a proof of concept study, a CBM intervention targeting negative self-beliefs was associated with a reduction in eating disorder symptoms in a subclinical sample [179]. Furthermore, a recent study from our group tested the use of 5 sessions of combined attentional and interpretation bias training in a sample of 28 inpatients with severe and enduring AN. Findings indicated that at the end of intervention participants showed a medium sized increase in attention to smiling faces and fewer negative interpretations of ambiguous social stimuli. Also, there was an increase in self-compassion and self-reported symptoms of anxiety (Cardi et al., submitted). These preliminary findings suggest that CBM might have a potential in targeting negative information processing in eating disorders. It remains to be tested whether such an approach modifies core symptoms such as eating behaviour.

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helpful for patients with AN in reducing cognitive rigidity [155], developing more global processing styles [49] and improving visual–spatial memory [34]. Randomised controlled trials have provided further evidence that CRT seems to be beneficial in lowering dropout rates from outpatient treatment [103], increasing patients' set-shifting abilities [21] and elevating patients' quality of life [37]. Although these findings are very promising, research in this area has predominantly focused on AN. Preliminary findings have indicated that CRT may be useful as a treatment enhancer for weight disorders such as obesity [127]. Therefore, adapting CRT further for other clinical populations such as patients with BN and BED appears a potential future direction for CRT [20] Further research to examine the stage of treatment that CRT is most effectively delivered (i.e., prevention, early-stage, severe and enduring, relapse prevention) would be of benefit.

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This neurosurgical technique uses electrical impulses to target dysfunctional brain circuits through the implantation of a brain pacemaker into the cortex. The procedure has been used across a range of disorders including treatment resistant depression [133,134], refractory obsessive–compulsive disorder [1], Parkinson's disease [17] and Tourette's syndrome (Visser-Vandewalle et al., 1999). This procedure is nonlesional and has been reported to be a safe treatment in both the short and long-term in the treatment of movement disorders [89]. It has been suggested that this approach may be a viable treatment option for patients in the severe and enduring stage of illness as a method to target the neurobiological mechanisms that underlie symptoms [124, 125]. A preliminary study from China with DBS of the nucleus accumbens in the early stage of AN reported benefits [176]. DBS in the subcallosal cingulate (an area implicated in treatment resistant depression) has also been used. A case report described DBS applied to this region as treatment for depression was found to also improve ED symptoms [80]. A recent prospective phase 1 trial from Canada noted that three of the six patients with severe enduring illness treated with DBS to the subcallosal cingulate region improved their physical status, matched with improvements in quality of life, at 9 months. Furthermore, there was improved mood, anxiety, affective regulation, and AN-related obsessions and compulsions in four patients and the harms (a fit (one case) and post-operative bleeding (one case) were not excessive [101]. Larger studies of DBS in patients with AN are required to clearly define the role of DBS for patients that have a severe and enduring illness.

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Barker, Jalinous and Freeston (1985) first described the therapeutic approach of rTMS which involves the magnetic stimulation of the cerebral cortex via the generation of an electromagnetic field from a coil. Research with animals has found that rTMS can be effective in increasing feeding behaviours [61], modulating serotonergic activity (Gur et al., 2000) and increasing brain derived neurotrophic factor [120]. Consequently, rTMS may represent a novel therapeutic approach for eating disorders due to its potential for changing eating behaviour and its regulation [164]. Case studies have demonstrated that 20 sessions of rTMS targeted at the Dorsolateral Prefrontal Cortex (DLPFC) can lead to improvements in eating disorder symptomatology and mood in patients with severe and enduring AN [81,114]. Promising findings have also been found when targeting the DMPFC in patients with treatment resistant BN [40]. In a recent pilot study including ten patients with AN, Van den Eynde et al. [165] found that one session of rTMS targeted at the left DLPFC reduced feelings of being fat, full and anxiousness. Further research is needed to clarify the optimal parameters of rTMS for the treatment of eating disorders.

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tDCS modulates neural excitability via the application of a low current to a targeted area of the cortex through the placement of electrodes onto the scalp [122]. Food cravings have been found to be reduced by tDCS targeted at the prefrontal cortex [55,62,113]. Kekic et al. [85] found that a 20-minute session of tDCS directed at the DLPFC led to temporary reductions in cravings for sweet rather than savoury foods. They also found that this effect was strongest for participants who were less impulsive on a temporal discounting task. Therefore, it may be

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6.4.4. Craving imagery disruptions Food craving has been identified as a precursor to binge eating in obese individuals [64,135] and in patients with BN [117,170]. Proof of concept studies have investigated whether imagery can disrupt food cravings [86,140]. The strength and frequency of cravings can be reduced [11], which has been found to lower craving-driven food consumption [88]. Recently, Hsu et al. [78] tested the effectiveness of a mobile-based application called iCrave, which prompts participants to complete a 10 second visualisation task when experiencing a food craving. Participants are then asked to record whether they consumed a healthy or unhealthy snack following the task or if their desire to eat was extinguished. The mobile-application was found to significantly reduce participants' snacking of unhealthy food items over a one-week period. Qualitative data suggested that participants reported that the intervention helped to increase their mood and their level of self-control over snacking behaviour [78]. Currently, there has been a limited amount of research examining the clinical application of approaches to disrupt craving imagery. To our knowledge, the only study to date [87] found that for overweight women on a prescribed weight-loss diet an imagery-based intervention was significantly more effective in lowering food cravings relative to thought-suppression. However, this study did not examine the impact of the intervention on actual food intake. Further proof of concept research is needed to establish whether disrupt craving imagery approaches are helpful for clinical populations.

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6.4.3. Inhibition training Targeting impulsive actions such as loss of control over eating 458 through strengthening inhibitory processes through training is poten459 tially another valuable technique. This may be a beneficial treatment 460 for patients with BN to help increase inhibitory control over the highly 461 palatable foods (e.g., deserts and snacks) that are typically consumed 462 during binge episodes [132]. The go/no go paradigm has been devel463 oped as a novel computerised approach to help train individuals to in464 hibit their automatic impulses towards highly palatable foods. This 465 technique involves the presentation of food stimuli onscreen that are 466 paired onscreen with a go/no go cue (e.g., an arrow pointing left or 467 right). No go cues are consistently matched with pictures of highly pal468 atable food and go cues linked with healthier food choices. Participants 469 are informed that they must withhold their response when a no go cue 470 is presented and to respond accurately meaning that the task uses a 471 choice reaction time method to train participants to increase their in472 Q22 hibitory control over highly palatable binge foods (Veiling et al., 2011). 473 Stop-Signal Training is a novel variant of the go/no go approach that 474 involves a variable delay between the presentation of the food stimulus 475 onscreen and the presentation of the stop-signal. This training approach 476 requires the inhibition of an already initiated motor response [178]. Re477 search has suggested that both of these approaches appear to be prom478 ising methods to help reduce the consumption of highly palatable foods 479 [100,167]. These approaches have been found to be effective in chronic 480 dieters [166] and in healthy participants with low levels of inhibitory 481 control [77]. Further research with clinical samples appears warranted 482 due to the potential for these approaches to help patients that habitually 483 overeat.

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cingulate-fronto-parietal network was found to be significantly lower in response to food stimuli post-treatment.

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adjustable and largely reversible means of altering brain circuitry. The 514 circuits involved in reward, mood regulation and inhibition have been 515 the targets of neuromodulation approaches for eating disorders. 516

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452 Q21 with a severe and enduring illness (Cardi et al., submitted). An examina453 tion of neural specific symptom changes showed that activity in the

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7. The use of brain stimulation (external and internal) to change the factors that maintain the illness Neuromodulation in the forms of Deep Brain Stimulation (DBS), repetitive Transcranial Magnetic Stimulation (rTMS) and transcranial Direct Current Stimulation (tDCS) has emerged as a non-destructive,


519 520 521 522 523 Q23 524 525 526 527 528 529 530 531 532 533 534 535 536 537 538 539 540 541 542 543 544

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8. The use of pharmacology to target the factors that maintain the illness

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8.1. Oxytocin

[13,14,16,32,38,39,44,45,67,96,137,149,161,168,175,177]

588

The role of oxytocin, a hormone, in social processes, such as parental ponding has been well established in animal research (e.g. [111]). Recently there has been increasing interest in investigating oxytocin as a 591 potential treatment enhancer in autism, schizophrenia and anxiety dis592 Q26 orders ([7,65], Feifel et al., 2010, [126]). Results so far have indicated 593 that oxytocin may be beneficial in promoting trust, improving identifi594 cation of social emotional communication and attenuating negative in595 Q27 terpretation bias ([9,15], Di Simplicio et al., 2008). As autistic traits have 596 been found to be a prognostic factor for the outcome of eating disorders 597 [171] and the inclusion of interpersonal difficulties in numerous main598 tenance models of eating disorders (e.g., [42]; Treasure and Schmidt, 599 Q28 2013) it appears warranted to examine the use of oxytocin as a treat600 ment enhancer [108]. 601 Proof of concept studies in AN have been undertaken with oxytocin 602 by examining the impact of single dose intranasal administration of 603 oxytocin. These studies found that the attentional bias towards food 604 and body image stimuli was reduced [91] as was the attentional bias to605 wards negative facial emotions (disgust, anger) [92]. These finding sug606 gest that oxytocin might moderate some of the fear processing and 607 avoidance associated with the maintenance of AN.

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Vyvanse is an amphetamine that works through stimulating the central nervous system. The drug has been used as a treatment for ADHD 611 Q29 ([19], Ditmann et al., 2013) and has recently been approved as a medi612 cation for the treatment of moderate to severe BED by the Food and 613 Drug Administration (FDA) in the United States. It is hypothesised that 614 the drug might help to regulate dysfunctional dopamine systems 615 [112]. A recent systematic review of the literature found that over an 616 11 week trial a 50 or 70 mg/day dosage of Vyvanse is effective in reduc617 ing binge eating episodes for moderate to severe patients relative to a 618 placebo [30]. However, this review highlighted that a long-term analysis 619 of the treatment efficacy and safety profile of the drug is needed. This 620 appears necessary due to the potential risk of severe adverse effects as621 sociated with amphetamines and the potential for drug dependence/ 622 abuse. 623

9. Conclusion

624

In line with a consideration of the staging categorisation of people with eating disorders it might seem necessary to develop a form of stepped care protocol for patients with eating disorders. In the case of people who are resistant to standard first line therapy it may be beneficial to use treatments that directly target some of the dysregulated circuits that maintain the disorder. These may circumvent the need to work only through top down processes, which are disabled by the neuroprogressive changes that ingrain in the habits and fears that

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This study was part funded by the National Institute for Health Research (NIHR) Mental Health Biomedical Research Centre at the South London and Maudsley NHS Foundation Trust and King's College London. Valentina Cardi is funded by the National Institute for Health Research (NIHR)'s Research for Patient Benefit Programme (Grant Reference Number RP-PG-0712-28041). Jenni Leppanen and Robert Turton receive studentships funded by the Psychiatry Research Trust (PRT) and by the Institute of Psychiatry, Psychology & Neuroscience (IOPPN)/Medical Research Council (MRC). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, IOPPN, MRC, PRT or the Department of Health. Potential conflict of interest: The author(s) declare having no conflict of interests in the writing of this paper.

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