Week 4- eating disorders

Why are EDs often hard to treat?

"Often the eating disorder is wanted...it serves a purpose, so the individual doesn't want to change...even if they risk death"

Who argues that the traditional feminine role may be a protective factor?

- (Silverstein et al., 1986); Japan. Women as homemaker may be protective for eating disorders.

How many cases of eating disorders can be considered sub-threshold?

- 40-50% of cases do not fit neatly into diagnoses - Atypical cases (OSFED) are the largest group - many people move from one diagnosis to another: eg. move from anorexia to bulimia - Sub-threshold disorders are most common- rigid diagnoses- does not allow flexibility of the clinician to make sure that everyone can get the treatment and help if they need it

What is binge eating disorder?

- Recurrent episodes of eating significantly more food in a short period of time than most people would eat under similar circumstances; eating very fast in the absence of hunger. - Marked by feelings of loss of control and guilt, embarrassment, or disgust. - Bingeing happens once per week over at least 3 months -Binge eating episodes not followed by compensatory behaviours -Experience same loss of control, embarrassment and disgust as bulimia -Tend to be overweight- but not part of the criteria of diagnosis

Who coined the term superwoman syndrome?

- Superwoman Syndrome (Thornton et al., 1991) -conflicts around the expectations for women: eg. to be a mother, have a career, be beautiful etc.

What did Swinbourne et al. (2012) find in their study investigating the comorbidity of EDs and anxiety disorders?

- The prevalence of comorbidity was investigated from a sample of 152 women, which included 100 women presenting for treatment of an eating disorder and 52 women presenting for treatment of an anxiety disorder. • Of ED women, 65% also met criteria for at least one comorbid anxiety disorder; 69% of these reported the onset of the anxiety disorder to precede the onset of the eating disorder: social phobia (42%) post-traumatic stress disorder (26%) generalised anxiety disorder (23%) obsessive-compulsive disorder (5%) panic/agoraphobia (3%) specific phobia (2%) • 13.5% of women presenting for anxiety treatment also met criteria for a comorbid eating disorder. Furthermore, 71% (n = 5) reported the onset of the anxiety disorder to precede the onset of the eating disorder.

Evidence suggesting that remission rates of EDs are poor

- at 1-2 year follow up for AN, remission rates range from 13-50% (e.g., Brockmeyer et al., 2018); 30-40% in BN (Quadflieg & Fichter, 2019; Gorrell et al., 2020) - AN - if treatment efforts fail during adolescence, then at risk of "severe and enduring anorexia nervosa" (Wonderlich et al., 2020). -chronic version of anorexia that persists into adulthood. - Equivalent outcomes for males and females (e.g., Strobel et al., 2019) - Not a one size fits all for eating disorder treatments Lack good evidence of superiority for any therapies in: - multi-impulsive eating disorders - eating disorders characterised by exercise - most 'atypical' cases - the majority • And that is where the research is going...

What ages does AN, BN and BED usually onset?

-AN onset more likely to occur in 14-16- getting younger -Bulimia and BED more likely to onset a bit later- 18-20 -Don't have as good statistics for non western cultures and low SES countries -AN and bulimia tends to be most common in females- recent suggestions imply a 10:1 ratio -BED eating tends to be similar prevalence in males and females -More males now being identified and coming through to get support for eating disorders

What is the relationship between significant events and EDs?

-Around 30% of ED patients have experienced sexual abuse (Conners & Morse, 1993)-- but may be more significant in men -Childhood loss- has face validity, but not supported by evidence Fairburn and Harrison (2003): Others seem to predispose especially to bulimia nervosa—eg, childhood and parental obesity, early menarche, parental alcoholism—some of which could operate by sensitising the person to her or his shape, thereby encouraging dieting. This effect is most likely to be seen in women in view of the social pressure on them to be slim. Yet other risk factors are character traits, the two most prominent being low selfesteem and perfectionism, the latter being a particularly common antecedent of anorexia nervosa.

How does the criteria for bulimia nervosa differ between the DSM-4 and DSM-5?

-Binge eating: eating large amount of food in a short period of time, accompanied with a sense of a lack of control. Typically high fat and calories. Followed by some food of compensation- eg. vomiting, laxitives, excessive exercise behaviours -Reduced the frequency of which binging and compensation needs to occur- not difference in the severity of the disorder if individuals are binging and compensating once or twice a week. -Feelings of self worth tied with perceptions of body image -Binging and purging episodes nit simply a phase of anorexia- not a temporary phase in a broader cycle of restriction

What are the reasons why there is often a while between first spotting symptoms and starting treatment for an eating disorder?

-Denial that they have a problem, or that they need support to deal with that problem -Concern about stigma and shame -Waiting lists in the NHS- difficult to get help if they need- lag between referral and receiving support -Eating disorders can be functional for a person- may not want to give it up -Thresholds in place that make access to treatment difficult- eg. weight -Clinicians may misinterpret symptoms for other things Gilbert et al. (2012): The very large standard deviations in the current data indicate that access to services is not uniform and some individuals successfully accessed care after a short interval, whereas others had a more protracted journey. Barriers are likely to be patient‐based, clinician‐based and institutionally based, and all require exploration to ensure we strive for improved and equal access to services for all individuals. Means that a lot of people get worse before the get help- the longer symptoms go on for the harder it is to help a person.

What is the continuum model of eating disorder pathology?

-Eating behaviours exist on a continuum -We are not always on the same area of the continuum at all points of our lives -If you have disordered eating there is a high predictability that you will develop a clinical eating disorder -Disordered eating- attitudes towards eating and your body still having a significant impact on your daily lives, but not enough to meet clinical criteria

What are some criticisms associated with the different models of EDs?

-Not everyone that experiences significant life events experiences an eating disorder. More nuanced- eg -neural model: arguably more to do with cognitive factors. Problems distinguishing cause and effect- eg. did the disorder cause differences in serotonin or did differences in serotonin cause the disorder. -Hard to differentiate between environment and genes- often problems associated with the shared environment. Deterministic model. -cognitive behavioural model: explains multiple eating disorders- trans diagnostic. Lots of other models focus on AN. -Psychoanalytic model- unfalsifiable, simplistic- eg. this behaviour is associated with this thought, explanations of cognitions are usually focused on a certain sample- eg. adolescents, women rather than men. However still in favour for treatment.

According to Fairburn and Harrison (2003) what are the mechanisms underpinning EDs?

-propose that the restriction of food intake that characterises the onset of many eating disorders has two main origins, both of which may operate. -The first is a need to feel in control of life, which gets displaced onto controlling eating. The second is overevaluation of shape and weight in those who have been sensitised to their appearance. In both instances, the resulting dietary restriction is highly reinforcing. -in some patients one or more additional maintaining processes interact with the core eating disorder maintaining mechanisms (where an over evaluation of eating, shape and weight leads to dieting, which leads to binge eating, and evaluation of eating and shape again). These are severe perfectionism, core low self esteem, difficulty coping with intense emotional states and interpersonal difficulties. -Subsequently, other processes begin to operate-- eg. starvation, compensatory behaviours such as vomiting. There is increasing evidence that correction of these processes is necessary for recovery, especially in those with bulimia nervosa.

What standardised mortality ratio is associated with eating disorders?

5.4 --particularly those with low weight (self starvation caused 65% of deaths)

According to beat (2015) what percentage of individuals with eating disorders have symptoms before the age of 16?

62%

According to Fairburn and Harrison (2003) how does CBT explain binges in BN?

Cognitive behavioural theory suggests that binge eating is a product of the way patients restrict their eating (often very strict dietary rules), when individuals deviate even slightly from these rules, they interpret it as a lack of self control, and consequently abandon all efforts to control eating. Binging is usually a response to acute changes in mood, and they are often reinforced because they temporarily neutralise such emotional states

What eating disorders constitute "Eating Disorders Not Otherwise Specified"(DSM-5) (EDNOS)?

Eating Disorders Not Otherwise Specified; EDNOS; DSM-IV) • Atypical anorexia nervosa -meets all relevant criteria for AN but of normal weight • Low frequency bulimia nervosa -meet all other criteria other than frequency or duration of binging/purging • Low frequency binge eating disorder • Purging disorder -just the purging, but not in compensation for anything • Night eating syndrome -binging/ over eating at night but not other parts of the day

What did a meta analysis by Arcelus, Mitchell, Wales & Nielsen (2011) find in relation to eating disorders and premature death?

Elevated risk of death for all patients with eating disorders. • Significant increase for those with AN. • In practice: If I see 1000 patients with AN a year in my clinic, 5 will die and 1.3 will die of suicide • Patients with AN have nearly 6 times more chances of dying than people without AN • Older on assessment → higher mortality -Bulimia 1.7 deaths per 1,000 deaths -1.3 per 1,0000 deaths for (OSFED)

What did Devoe et al., 2022 find in their systematic review investigating the impact of covid on eating disorders?

Evidence to suggest that the pandemic led to: - increased diagnoses of EDs (↑15%); - increased hospital admissions for EDs (↑48%) - and increased ED symptoms. • Increased co-morbidity (e.g., anxiety, depression, suicidal ideation; Taquet et al., 2021) • Decreased access to care and treatment, changes to routine and loss of structure, social isolation

How does the criteria for anorexia nervosa differ between the DSM-4 and DSM-5?

Greater flexibility on the grounds of the clinician- no longer an arbitrary threshold for the specific weight a person has to be to be classified as anorexic -Two subtypes: restriction (restriction of energy intake- eg. cutting out certain food groups), binge-eating/ purging (restrict but occasionally binge eat and subsequently purging behaviours) -Tensions: binging and purging is characteristic of bulimia as well- if this is the core feature patients will be diagnosed with bulimia -Amenorrhea- absence of the menstrual cycle for 3-4 months. Been dropped: not relevant for males, pre-menarchal females, women on the oral contraceptive. Some people met all of the other criteria, but not this one.

Who highlights that the etiology of AN is unknown? And what are the implications of this?

Kaye et al. (2013) - A lack of understanding of the pathophysiology of these illnesses has hindered the development of effective treatments.

What is often the first line of treatment?

Medical treatments • Re-feeding for nutritional deficits- often first form of treatment - life-saving - mood stabilisation Inpatient care for the most unwell patients

How does the psychodynamic model explain EDs?

Way of understanding patients' experiences associated with people's disorders. Emphasise meanings attached to symptoms and function of them - Restriction = success / personal effectiveness / avoidance of sexuality (Bruch, 1974) - Vomiting = rid oneself of traumatic sexual experience or fantasy pregnancy - Hunger = greed (Dare & Crowther, 1995) Emphasise role of infancy and subsequent experiences in shaping a person. ➢ Control ➢ Avoidance of maturation (in adolescence) Critique? -focus on the unconscious- tries to explain why people have these symptoms

How does Pike and Dunne (2015) explain the Increase in eating disorders in the West in the mid- late 1960s?

an enormous body of literature emerged attributing this to the ultra-thin beauty ideal that was marketed to young women not only as the epitome of female beauty, but furthermore, as an attainable ideal towards which all women should aspire. In the West, the spread of the thin ideal has been accompanied by the acceptance of the notion of 'body instrumentality,' which promotes the idea that improvement of the physical body via diet and exercise provides a pathway through which an individual may attain a certain level of control that is somehow essential to achieving his or her ideal self

What is the average time it takes between first spotting symptoms and starting treatment for an eating disorder? beat: Hamilton et al. (2022): Gilbert et al. (2012):

beat: on average it takes 15 months between spotting symptoms and starting treatment Hamilton et al. (2022): found an average of 5.28 years between symptom onset and treatment in an Australian sample Gilbert et al. (2012): Found the average delay of 3 years and 3 months between developing concern and accessing specialist help: shows substantial delays between onset of the disorder and first treatment contact. --The longest latency was from disclosing to the GP, to accessing eating disorder services. This finding highlights the need for services and professionals to consider the ways in which they might contribute

According to Fairburn and Harrison (2003) how many individuals with BN would have met the criteria for AN at any given time?

in about a quarter of cases

When have eating disorders in Asia began to increase?

over the past 30 years

According to Caparrotta and Ghaffari (2006) what are eating disorders caused by? (psychodynamic account) --What implications does this have for the therapeutic relationship?

we believe that eating disorders represent various forms of selfimposed starvation and/or bingeing conveying vividly the struggle to thwart any attempts at separating and individuating from the intrusive and controlling mother. Food is thus perceived as bad and intrusive leading to passive surrender and loss of control --· Davies (2005) suggests, most clinicians have become aware of how patients suffering from eating disorders tend to fear, reject and destroy the therapeutic relationship which is unconsciously perceived as the controlling mother. The unconscious solution found by eating-disordered patients has to be understood within the complex interaction between early emotional and nourishing experiences, family dynamics and societal pressures.

According to beat (2015) how much do eating disorders cost the UK a year?

£15 billion

What did Jacobi et al. (2011) find to be risk factors for the development of EDs?

· A longitudinal cohort study over 3 years in a high-risk sample of 236 college-age women randomized to the control group of a prevention trial for Eds. At the 3-year follow-up, 11.2% of participants had developed a full or partial ED. Seven of 88 potential risk factors could be classified as independent risk factors, Critical comments about eating from teacher/coach/siblings and a history of depression were the most potent risk factors. The incidence for participants with either or both of these risk factors was 34.8% (16/46) compared to 4.2% (6/144) for participants without these risk factors. · Targeting preventive interventions at women with high weight and shape concerns, a history of critical comments about eating weight and shape, and a history of depression may reduce the risk for EDs.

According to Kaye et al. (2013) what are criticisms associated with the biological model of AN?

· A substantial limitation of neurotransmitter studies in humans is that only a few neuromodulatory components can be measured, and there are currently no means to measure or model the functional interactions of the many biochemical mechanisms that make up these complex systems. · As yet, there are no medications or other treatments that have been proven to reverse core symptoms in AN. · Causes and consequence remains unclear

According to Pike and Dunne (2015) how have accounts of westernisation previously explained the increase of EDs in Asia? -What evidence is there supporting this?

· According to this perspective, increasing exposure to 'the West' transmits a 'thin body ideal' and imparts Western notions of body instrumentality to non-Western societies, which in turn fosters growing body dissatisfaction, diet- ing, and eating disorders. --· There is evidence to support such explanations- e.g. studies on Fiji (which was isolated from Western influence until 1990s and where a more robust body type was considered the ideal) have found an increase in Eds after the introduction of TVs in the late 1990s. Definitions of female beauty standards and body ideals within the broader Fijian society were also reconfigured in the image of a more "Westernised" "thin ideal".

According to Fairburn and Harrison (2003) what is the cognitive -behavioural/ transdiagnostic model of EDs?

· Argue that BN and AN share the same core psychopathology: both groups of patients over-evaluating eating, shape and weight and their control, and this psychopathology is expressed in similar attitudes and behaviour. Thus patients with anorexia nervosa restrict their food intake in the same rigid way, and they may too use laxatives/ vomit. features. The major difference between the two disorders lies in the relative balance of the under- eating and over-eating, and its effect on body weight. · In our clinical experience rigid and extreme dietary restraint is prominent in most atypical eating disorders and sometimes it is accompanied by self-induced vomiting, over-exercising or laxative misuse. Binge eating (objective or subjective) is also a common feature, and in the majority of cases there is the over-evaluation of eating, shape and weight and their control that is the hallmark of the two prototypic eating disorders. · Severe perfectionism, core low self esteem, difficulty coping with intense emotional states and interpersonal difficulties can also be found in individuals with An and atypical eating disorders · Thus, common mechanisms are involved in the persistence of BN, AN and atypical eating disorders. · As with the comparison of anorexia nervosa and bulimia nervosa, cross-diagnostic commonalities become even more obvious when a longitudinal perspective is taken. For example, an atypical eating disorder is a common outcome of anorexia nervosa (e.g., Sullivan, Bulik, Fear & Pickering, 1998); bulimia nervosa typically starts as anorexia nervosa or an atypical eating disorder; and a particularly common outcome of bulimia nervosa is a chronic atypical eating disorder. The eating disorders of mid-adolescence typically take the form of anorexia nervosa or an anorexia nervosa-like state, whereas a bulimia nervosa-like picture is more typical of those of late adolescence or early adulthood.

What transdiagnostic treatment does Fairburn and Harrison (2003) propose?

· As they theorise that individuals with BN, AN and atypical eating disorders all tend to have a central cognitive disturbance characterised by over- evaluation eating, shape and weight and their control, and that in subgroups of these patients one or more of four additional mechanisms also serve to maintain the eating disorder (Severe perfectionism, core low self esteem, difficulty coping with intense emotional states and interpersonal difficulties), they propose a transdiagnostic treatment. · Suggest that if these 4 components are not addressed, treatment is not likely to result in full and lasting recovery as individuals are still feeding into the maintenance of these behaviours. An individuals type of eating disorder is therefore not considered relevant to the treatment.

What did Dingemans et al. (2002) find in their literature review of studies on BED?

· BED seems to be highly prevalent among subjects seeking weight loss treatment (1.3-30.1%). · Studies with compared BED, BN and obesity indicated that individuals with BED exhibit levels of psychopathology that fall somewhere between the high levels reported by individuals with BN and the low levels reported by obese individuals. Characteristics of BED seemed to bear a closer resemblance to those of BN than of those of obesity. · Dieting seems to play a role in the aetiology of BED, but research does not indicate that dieting is always a key factor in BED, as it seems to do in BN. · Obese patients with BED have less self-esteem and greater depressive symtomatology than obese persons without BED; they also have more comorbid psychiatric disorders, in particular affective disorders and personality disorders. · Individuals with BED compared to obese controls have a tendency to experience negative affect in response to perceived evaluation by others of weight-related behaviour. · A review of RCT's showed that presently cognitive behavioural treatment is the treatment of choice but interpersonal psychotherapy, self-help and SSRI's seem effective.

According to Kaye et al. (2013) what evidence is there to support the idea that individuals with AN have dysfunctions in their dopamine system?

· Brain studies that compare ill and recovered AN individuals with controls suggest that altered reward and interoceptive processing are traits characteristic of the disorder. E.g. insular neural activity has been correlated with pleasantness ratings for sucrose in control but not AN subjects. · findings from other studies suggest minimal insula response in AN to the tastes of food when hungry.

What protective factors did Langdon- Dally and Serpell (2017) find in their systematic review?

· Having a healthy family environment around eating (for example having frequent family meals and avoiding comments about weight) and other characteristics like high quality family relationships, may help to protect young people against problems with eating · Many of the potential protective factors identified, such as family support and connectedness, may be non-specific to eating difficulties, promoting general adaptive development and a range of positive development outcomes. Factors in the family environment around food, eating and weight, such as frequent family meals and avoiding comments about weight, may be more specific to ED and disordered eating.

According to Dingemans et al. (2002) why can IPT be particularly beneficial for individuals with BED?

· IPT uses techniques derived from psycho-dynamically oriented therapies, but the focus is on the patient's current circumstances and relationships. · It is based on the assumption that psychiatric disorders are intimately related to disturbances in social functioning, which, in turn, may be associated with the onset and/or maintenance of the disorder. IPT involves well-defined treatment strategies, techniques, and a therapeutic approach to the resolution of problems within four social domains: grief, interpersonal disputes, role transitions and interpersonal deficits. IPT is especially well-suited for BED patients because it teaches: (1) the requisite skills for developing and sustaining satisfying relationships; and (2) more effective strategies (than binge eating) for coping with social and interpersonal problems.

What treatment options do Fairburn and Harrison (2003) suggest for AN and atypical eating disorders?

· In view of the paucity of research on the treatment of anorexia nervosa, the following comments simply summarise mainstream opinion: · 1. The first is to help patients see that they need help and to maintain their motivation thereafter. · 2.Weight restoration · 3. The third aspect of management is addressing patients' overevaluation of shape and weight, their eating habits, and their general psychosocial functioning. There is no single way way to achieve this aim. One approach that has some research support is a family-based treatment,131 which seems to be of most help to younger patients132 and is thus mainly used with adolescents. · 4. The fourth aspect of management, use of compulsory treatment, is only relevant to a few cases. · No drug has been shown to be of clinical value in promoting weight regain,136,137 although preliminary findings suggest that fluoxetine might reduce the risk of relapse in those patients whose weight has recently been restored. · Atypical eating disorders: received almost no research attention, the only advice that can be given is for clinicians to follow the guidelines for treatment of bulimia nervosa in instances in which there is binge eating, and those for the treatment of anorexia nervosa in instances in which weight is low. · there is a pressing need for more treatment research, both in terms of developing more effective treatments and focusing on the full range of eating disorders. This research, and perhaps clinical

According to Fairburn et al. (2003) what is the evidence base for CBT- BN?

· Over 50 randomised controlled trials have been completed and there have been over 20 studies of CBT-BN. Although almost all of these studies have been "efficacy" rather than "effectiveness" trials, there are good reasons to think that their findings are relevant to everyday patient care. · CBT-BN has a substantial effect on the frequency of binge eating and purging, and the full range of the psychopathology of bulimia nervosa. Among treatment completers (typically 80 to 85%), between 40-50% cease binge eating and purging altogether. · CBT-BN is more effective than both delayed treatment and pharmacotherapy. · evidence that the most powerful and consistent predictors of CBT are the frequency of binge eating and purging at the start of treatment (the higher the frequency, the worse the prognosis) and, most especially, the extent of their reduction over the initial weeks of treatment. · However in CBT- BN only around half of all patients make a full and lasting response. · Suggest that the theory is currently too narrowly focused, and that there needs to be a reconceptualization of the processes that underpin BN- this should then inform therapy. -combining cognitive behaviour therapy with antidepressant drugs results in few consistent benefits over cognitive behaviour therapy alone few patients receive CBT-BN.

According to Caparrotta and Ghaffari (2006) what are the criticisms of the psychodynamic model?

· Overall most psychoanalytic publications were based on single case studies and concerned primarily with anorexia nervosa. No single model was identified, but a number of psychoanalytic ideas remain consistent throughout.

According to the DSM-5, how can eating disorders be defined?

· Severe, psychiatric disorders characterised by a dysfunctional relationship with food and distorted perceptions about the body, that significantly impairs physical health and/or psychosocial functioning. (APA, DSM-5) · Broad definition- doesn't detail what a distorted perception of the body is like or what characterises a dysfunctional relationship with food

What did Carpita et al. (2020) find in their review investigating the link between EDs and ASD?

· Studies have found higher rates of ASD amongst AN patients compared to controls · characteristics that are known to be typical of ASD and of OCD (such as perfectionism, rigidity, inflexibility, restrictive interests) were also key features of AN, although specifically oriented toward diet and eating habits · in patients with AN is detectable a specific neurocognitive phenotype (similar to that typically reported in subjects of the autism spectrum),which would feature rigidity in set-shifting tasks and in global processing as well as greater attention to details. -Moreover, social cognition and functioning seem to be altered in AN patients in a way that resemble that of ASD: in particular, AN patients show higher social anhedonia,94,100 alexithymia,100 impaired emotional intelligence,102-104 and emotional processing. -Even the Theory of Mind, whose impairment is one of the most relevant traits of ASD, seems to be compromised in AN, especially when advanced tasks are concerned -Data from neuroimaging studies reported amongst AN patients atypical neurostructural and functional alterations in specific areas of the social brain, such as amygdala, orbitofrontal cortex, and superior orbital sulcus, which are known to be significantly correlated with the presence of autistic traits -an increasing number of researchers hypothesized a conceptualization of AN as a female phenotype of ASD, on the basis of comorbidity, familiar aggregation, and significant neurocognitive and behavioral overlap between ASD and AN -· The conceptualization of AN as a gender-specific presentation of ASD may also provide an intriguing model for the opposite gender differences in ASD and AN prevalence FED could be considered as a possible psychopathological trajectory of a neurodevelopmental alteration, toward which female gender would act as one of many predisposing factors.

According to Pike and Dunne (2015) why may girls be particularly susceptible to the consequences associated with urbanisation and industrialisation?

· Suggests that changes associated with industrialisation and urbanisation have had a particularly transformative effect on women's lives. Specifically, Witcomb, Arcelus and Chen [101] suggest that the demands of an increasingly competitive environment in which women are expected to develop a new set of skills, may unavoidably expose them to greater criticism from peers, colleagues, and society, perhaps in turn prompting women to engage in more self- evaluation. Thus, physical appearance becomes one of several domains in which women 'measure' themselves against an aspirational ideal [101]. In Asia, the 'gendered' nature of societal transformation and globalization is especially striking due to the fact that economic development was initially driven by the growth in the manufacturing (specifically garment) industry, and later, the service industries, which resulted in a spike in demand for women's labor in particular [19]. · Silberstein and Rodin (1986) [131] suggest that girls, in particular, are very likely experiencing the stresses of these shifting roles and evolving expectations, which in turn, may place them at greater risk for overall psycho- logical distress [131]. Similarly, changes in male gender roles may be contributed to significantly higher rates of Eds in males.

What features of psychodynamic treatments do Abbate- Daga et al. (2016) suggest are clinically useful?

· That eating disorders are not just a constellation of eating symptoms: Before getting ill and sometimes for a long time, patients usually perceive loneliness, ineffectiveness, and fear of uncertainty and of others' opinions, often experienced as negative and humiliating. Moreover, patients commonly report that they could not recognize their bodily sensations and their emotions or relate certain inner feelings with external events. Relatedly, the drive for achievements somehow compensated for their confusion and fear, and the onset of the ED further disguises patients' emotions and ambivalence · The adaptive value of eating symptomatology; Psychodynamic models peculiarly consider symptoms on one hand as an expression of suffering (primary advantage), and on the other hand as an attempt to mitigate their pain (secondary advantage). Unfortunately, such a psychic functioning reinforces patients' symptoms generating resistance to treatments; as a result, patients affected by EDs highly value their illness as a strength. There is a large consensus on these concepts among clinicians who work in the ED field, independently of the approach (psychodynamic or not) adopted [106, 107]. However, psychodynamic psychotherapies consider in treatment not only pro-ED beliefs, but also the unconscious meanings of symptoms: it is crucial to help patients recognize those eating-related aspects that were covered by pain and shame. · The therapeutic relationship is essential for treatment: psychodynamic psychotherapies are not focused on interpretations, but rather on helping patient develop solid "feeling and thinking systems" [110, 111], fostering patients' self-trust and self-esteem in a relational context. In this process, the therapist's empathic comprehension represents the core of the encouraging process also given the current body of evidence on mirroring [36] and moments of meeting in psychotherapy [112]. Relatedly, also therapist's coping skills can become a sort of model for patients who often need to develop more adaptive coping strategies, also through intentional attunement [113]. Therefore, an intense therapeutic relationship is required to handle patients' relational difficulties, including those illness-related, and to improve. · Family experience: As previous authoritative literature has clearly stated [1], patients' family does not play any role in the ED onset; however, the family has a complex function on the psychosocial development in the first years of life and across the different stages of the disorder. · Patients' personality directs treatment: The way patients organize their interiority and relate with the environment is relevant to understand not only the relationship between patients and symptoms, but also the one existing between patient, treatment, and therapist. This is particularly true for EDs; in fact, the latter are psycho- and neurodevelopmental disorders [3] where the impairment related to personality traits is intertwined with the illness which compensates patients' identity problems · The difficulties in understanding and integrating internal states and emotions: Outstanding research showed that patients with EDs process interoceptive signals differently from healthy controls [123, 124] and that perception and awareness could be regulated by the same brain area [125]. Furthermore, the dysregulation of functional connectivity in the brain can contribute significantly to the illness [126, 127]. Notwithstanding, several emotional-focused approaches have been pioneered [99] and can influence prognosis [78]. Psychodynamic psychotherapies first generated such hypothesis and put conscious and unconscious emotions at the center of treatment.

According to Caparrotta and Ghaffari (2006) how have attachment theorists explained the onset of EDs?

· The advent of attachment theories and the self-psychology school have provided another perspective on the mother-infant relationship. The stages of development of attachment in the infant have led to increasing understanding of the arrest at different developmental levels of the self. Hence the anorexic solution - by maintaining a pre-pubertal body - thwarts any attempt at separating.

What did Abbate- Daga et al. (2016) find in their review of psychodynamic treatments for eating disorders?

· The body of literature on psychodynamic treatments is sparse and sometimes methodologically questionable; nevertheless, current data provide support to the effectiveness of these interventions, particularly for AN. · There can be many reasons for the lack of solid studies on psychodynamic treatments; importantly, no treatments with a solid level of evidence exist for AN [7, 9] denoting delays in clinical research in the field of EDs [7, 8] when compared with those of other psychiatric illnesses [91]. A sort of skepticism toward RCTs in AN could in part account for such a delay. In fact, it has been proposed that RCTs can be only partially representative of real-world patients [92] also because of high attrition [93] and dropout [94]. Moreover, some more specific difficulties should also be mentioned: psychodynamic interventions can be hardly manualized, require a long time to be completed, and are strongly tailored to each patient. Finally, outcome measures for psychodynamic treatments remain to date unclear [34, 95] contributing to both complexity and confusion around this topic.

According to Fairburn et al. (2003) what implications does cognitive theory have for the treatment of BN?

· The cognitive behavioural theory of the maintenance of bulimia nervosa has clear implications for treatment. Specifically, it suggests that the focus of treatment should not solely be on these patients' binge eating, despite the fact that binge eating is often their primary (and sometimes only) complaint. Rather, it suggests that to achieve a full and lasting response, these patients' dietary restraint also needs to be addressed, as does their response to adverse mood states and their over-evaluation of eating, shape and weight and their control.

According to Dingemans et al. (2002) how can CBT be used to help individuals with BED?

· The first is to identify the rationale underlying the cognitive-behavioural treatment approach, and the second is to replace binge eating with a stable pattern of regular eating. In stage two there is continuing emphasis on regular eating and the use of alternative behaviour, but in addition the focus broadens to address all forms of dieting, concerns about shape and weight, and more general cognitive distortions. The aim of the third and final stage is to ensure that progress is maintained in the future.

According to Fairburn and Harrison (2003) what factors complicate studies examining the prevalence of eating disorders?

· The general belief is that eating disorders have become more frequent over recent decades. · In the instance of bulimia nervosa, this notion could well be true but alternative explanations for the apparent increase in anorexia nervosa are plausible, including greater help-seeking and better detection than in the past, and changes in diagnostic practice. · The fact that many instances do not come to medical attention complicates research; for example, most individuals with bulimia nervosa are not in treatment,and the subgroup who are is biased in certain respects. · There has been little research done on the distribution of the atypical eating disorders, although they are frequently encountered in clinical practice. -The heterogeneity in course and outcome of AN is often neglected-- In some instances the disorder is short-lived and self-limiting, or only requires a brief intervention. In others, the disorder becomes entrenched and necessitates more intensive treatment

What problems with the concept of westernisation do Pike and Dunne (2015) highlight?

· The label ignores the diversity of the distinct cultures that characterize the region and is based largely on white, European-American stereotypical perceptions of homogeneity of individuals from the 'East.' · Given the enormous diversity within the geographic region of Asia, such gross terminology falls short in capturing the nuance of culture in the etiology of EDs in the region. · Significantly, the order by which EDs have spread among Asian countries closely tracks the so-called "Asian miracle" of economic transformation as it extends across the region [16, 19]. · It is important to recognise that there are ethnic differences within countries- e.g. studies in Malaysia suggest that women may internalise appearance- based media messages differently according to their ethnicity. Evidence from Thailand suggests that women from more developed, urban regions, place greater emphasis on body weight and shape in assessing physical appearance identity. · The danger of subsuming these respective phe- nomena under the umbrella of 'Westernization' is that it over-attributes the diverse changes and distinct develop- mental pathways of individual Asian societies, including the emergence of EDs, to the influence of the West. · One challenge researchers face is that measures and criteria typically used to assess eating dis- order psychopathology are based on Western models and have not been fully validated for use with non- Western samples.

What did Ringer and Crittenden (2007) find in their study investigating attachment and EDs?

· The results indicated that all women with an eating disorder were anxiously attached (62 young women- 19 with anorexia nervosa, 26 with bulimia nervosa and 17 with bulimic anorexia). About half used an extreme coercive Type C strategy while most of the others combined coercion with an extreme dismissing Type A strategy. The content of the AAIs suggested lack of resolution of trauma or loss among the mothers and also of hidden family conflict between the parents. This in turn elicited extreme strategies for generating parent-child contingency from the daughters

What are the biological explanations of AN that Kaye et al. (2013) propose?

· The traits associated with AN include anxiety, negative emotionality, perfectionism, inflexibility, HA, and obsessive behaviors (particularly with order, exactness, and symmetry). symmetry). This personality and behavioral profile may constitute an intermediate phenotype between genes and vulnerability to AN. E.g. studies have shown that AN subjects have high punishment sensitivity and low reward reactivity during both the ill and recovered states. An explanation is that individuals with AN have a disturbed interoceptive awareness and that this could be linked to alexithymia (difficulties in identifying emotions). This may result in difficulties interpreting hunger cues and in assessing emotional states. This has been suggested to be due to dysfunctions in serotonin and dopamine systems-- It has been proposed that 5-HT might play a role in altered satiety, impulse control, and mood, and that DA may be implicated in aberrant rewarding effects of food, motivation, or executive functions (inhibitory control, salience attribution, and de- cision-making). · Suggestion that for individuals with AN dietary restriction has an anxiety- reducing effect, whereas food consumption stimulates dysphoric mood. Suggests that for AN individuals excessive dopamine which is associated with food intake increases anxiety-- People with AN may enter a vicious cycle - which could account for the chronicity of this disorder - because eating exaggerates, and food refusal reduces, an anxious mood. Individuals with AN have an over-reliance on executive brain circuits involved in linking action to outcome may constitute an attempt at strategic (as opposed to hedonic) means of responding to reward stimuli

According to Fairburn and Harrison (2003) what evidence is there to support a trans diagnostic model of EDs?

· There seems to be cross-transmission between anorexia nervosa, bulimia nervosa, and the atypical eating disorders, suggesting a shared familial liability. -· Bulimia nervosa usually starts in much the same way as anorexia nervosa—indeed, in about a quarter of cases, the diagnostic criteria for anorexia nervosa are met for a time. Eventually, however, episodes of binge eating begin to interrupt the dietary restriction and, as a result, bodyweight rises to normal or near normal levels. The disorder tends to be self-perpetuating. Thus the average length of history at presentation is about 5 years, and even 5-10 years later on, between a third and a half of individuals still have an eating disorder of clinical severity, although in many it is atypical in form.

According to Kaye et al. (2013) what could be possible implications associated with a greater understanding of the origins of AN?

· These findings may help to identify drugs that act on 5-HT and/or DA neural processes that may be best suited to reduce HA behaviors in AN. · May explain why it is difficult to modify the core traits of ED in treatment settings. · Findings may inform the development of medications targeting the biology of AN that contributes to certain symptoms, such as anxiety. Although this may not be a cure for AN, it may substantially improve the ability to eat and maintain weight. · Second, they may guide the development of more effective psychotherapies to elicit behavioral changes that are educated by robust and neurally derived principles of the internal mechanisms of AN.

According to Dingemans et al. (2002) what are the weaknesses associated purely only with obesity therapy for BED?

· Treatment of obesity focuses on the reduction of energy intake, encourages a shift to a low-fat diet, addresses any medical contribution to the condition and initiates exercise. However, the underlying behavioural disturbances or the social and psychological consequences of obesity are often neglected. If the treatment of obese subjects with BED focuses only on reduction of bodyweight and does not address binge eating or underlying problems, binge eating continues or even worsens.

According to Dingemans et al. (2002) why are binging episodes for BED harder to operationalise compared to BN?

· episodes of binge eating are easier to define in BN because the binge eating is followed by compensatory behaviour like vomiting. In BED both the beginning and ending of an episode of binge eating are less clear.

What does Fairburn and Harrison (2003) conclude about the heritability of AN compared to BN?

· findings suggest a significant heritability of anorexia nervosa but not of bulimia nervosa. · Most importantly, the research must be targeted on the interaction of genetic and environmental processes, and this should be from a developmental perspective.

According to Fairburn and Harrison (2003) what is some evidence supporting/ refuting the neural model of EDs?

· some aspects of 5-HT function remain abnormal after recovery, leading to speculation that there is a trait monoamine abnormality that might predispose to the development of eating disorders or to associated characteristics such as perfectionism. · Furthermore, normal dieting in healthy women alters central 5-HT function, providing a potential mechanism by which eating disorders might be precipitated in women vulnerable for other reasons --cause and effect · Of the various central and peripheral abnormalities reported, many are likely to be secondary to the aberrant eating and associated weight loss. ---Kaye et al. (2013): · It has been controversial as to whether individuals with AN have a primary disturbance of appetite regulation or whether pathological feeding behavior is secondary to other phenomena, such as an obsessional preoccupation with body image.

According to Pike and Dunne (2015) why has there been an increase in EDs in Asia?

· suggest that the explanation of westernisation is too simplistic, and that countries in Asia are experiencing the processes of industrialisation and urbanisation independently, or in tandem, with Western influence. · E.g. recent findings suggest that body dissatisfaction and internalization of the thin ideal may, in fact, be more widespread in Korea than in the West. Rather than solely crediting Western beauty ideals for perpetuating an unhealthy 'thin' archetype, Jackson, Keel & Lee suggest that native Korean values may also promote eating disorders, owing to their emphasis on appearance rather than ability or talent as the factor crucial to a woman's success in marriage and in career [91]. · These transformations include fundamental shifts in population demographics, food supply, global economies, gender roles, and the traditional family structure. · Suggest that eating disorders are culturally reactive, rather than being culture bound: argue that certain cultural contexts results in social and environmental changes that increase risk of EDs. --important to acknowledge that many of the characteristics that have been ascribed to "Westernization" may, in fact, be more accurately associated with the processes of industrialization and urbanization, irrespective of countries of origin. While the "west" experienced industrialization and urbanization earlier in history, that process now unfolding throughout Asia may best be thought of as a new wave of industrialization and urbanization, moving be- yond the idea that the wholesale export of Western culture and influence, broadly defined, is the variable to which we should continue to devote primary attention when examin- ing cultural factors associated with the rise of EDs in Asia

How much do eating disorders cost the NHS?

• 60% of costs are for females under 24 yrs -most on inpatient support, normally associated with weight restoration • £510 per day per inpatient • Outpatient costs are about 40% of inpatient • GP visits • Treating associated problems (e.g., dental)

How does the neural model explain EDs?

• AN may have lower levels of chemicals in brain that might be involved in intake regulation, • I.e. Do not feel hungry and so do not eat. -Lower levels of serotonin that guide food behaviour- do not have the same hunger experiences- able to abstain from eating more easily

What are the rough prevalence rates of AN, BN and BED?

• Anorexia nervosa • 0.5-1.0% of teenage girls • Bulimia nervosa • 1-2% of women aged 16-35 • BED • Epidemiological studies are lacking. Extrapolation estimates are 3.6% of women and 2.1% of men aged 18-70. • OSFED • 2-3% of women aged 16-35

Why may prevalence/ incidence rates of eating disorders differ in the literature?

• Definitions used for diagnosis - DSM-IV vs 5. • Individual assessors / therapist opinion. • Sample - clinical cases only or self-reported. Lots of eating disorder questionnaires- but not as reliable as clinical disorders. • Other researcher variables e.g., new cases only, not re-referrals (which is common in eating disorders). • Across cultures; less ED? Less acceptable? Fewer treatment opportunities? -statistics don't reflect non westernised cultures

According to the Australian Institute of Health & Welfare where do EDs rank in terms of disability adjusted life years?

• EDs are 6th in terms of disability adjusted life years: from early mortality and reduced quality of life for ages 15-24. 1. Anxiety & depression 2. Asthma 3. Migraine 4. Genitourinary disease 5. Partner violence 6. Eating disorders 7. Road traffic accidents

Figures/ studies suggesting a genetic basis of EDs

• Eating disorders appear to run in families. • Strober et al (2000): female relatives of AN patient x11 more likely to develop AN. • Some specificity for ED type; but risk for all EDs is higher among first degree family members. • Heritability estimates up to 0.74 for AN • 55% identical twins concordant for AN. • Much weaker for BN (less is known about the genetic pathways for other EDs). • Significant genetic correlations between AN and other psychiatric disorders (e.g., schizophrenia). • Large genetic studies identified certain patterns of genes that seem to be important. -Less good evidence for bulimia- is AN more genetic or has there not just not been enough research on the genetic components of bulimia? -Not a single gene that has been identified that is associated with eating disorders -eg. Fairburn and Harrison (2003): Particular attention was drawn to the 5-HT2AR (HTR2A) gene after an association was reported between allelic variation in the promoter region (1438 A→G) and anorexia nervosa However, three of six studies, and a multicentre family-based study, have not been able to confirm this observation.

How does the sociocultural model explain eating disorders?

• Expression of social values • Culture-bound or ethnic disorder - Identity: child vs independent -reverting back to a child-like state= less stressful than the independence associated with adulthood - Strong but look tiny - Representations of beauty through unattainable levels of thinness. - Evidence to suggest increase in EDs when exposed to westernised ideals (e.g., introduction of TV in Fiji; Becker, 2004; social networking; Becker et al., 2011). -influence of social media on eating disorders

How do family systems accounts explain EDs?

• Family not the cause, but context in which ED is embedded (Eisler, 1995). Family is involved in treatments, particularly for adolescents. - Symptoms as communicative acts (eg. communication is not possible, ED becomes a way of communication, but which then actually prevents communication) - The homeostatic family (disrupts the homeostasis of the family) - Boundaries - Conflict avoidance

What are the other 3 eating disorders in the DSM?

• Pica -tendency to crave and consume things that are not food- eg. soil, mud, clay, straw, string, tissues- • Rumination Disorder -tendency to regurgitate food- self induced • Avoidant/Restrictive Food Intake Disorder -not associated with any body image concerns, associated with sensory components of food (eg. fears that occurs on exposure to certain foods), have a limited diet that requires nutritional supplements, may be of low weight

What comorbidities are associated with EDs?

• Self-harm • Anxiety disorders • Depression (and other mood disorders) • Substance use • Personality disorders • Temporal relationships are not always clear- don't understand which disorder occurred first.

What did Gilbert et al. (2012) find in their study on disclosure?

• Seventy‐one eating disorder service users interviewed using the Eating Disorder Disclosure Interview and the Eating Disorder Examination Questionnaire. • Faster access to services associated with being older at first disclosure and with disclosures that involved either a GP, an individual's partner or mother. • Patients' appraisals of 'other‐initiated' and 'volunteered' disclosures did not differ, although 'other‐initiated' disclosures were younger and accessed help more quickly than those who 'volunteered'. • The more positively disclosures were appraised, the quicker the subsequent help‐seeking. • Initiating a disclosure might lead to earlier access to treatment for individuals with eating disorders. --suggests that prompting disclosure could facilitate early access to treatment, and hence, better outcomes