anorexia nervosa research paper pdf

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• Published: 30 May 2023

Eating disorder outcomes: findings from a rapid review of over a decade of research

• Jane Miskovic-Wheatley 1 , 2 ,
• Emma Bryant 1 , 2 ,
• Shu Hwa Ong 1 , 2 ,
• Sabina Vatter 1 , 2 ,
• Anvi Le 3 ,
• National Eating Disorder Research Consortium ,
• Stephen Touyz 1 , 2 &
• Sarah Maguire 1 , 2  

Journal of Eating Disorders volume  11 , Article number:  85 ( 2023 ) Cite this article

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Eating disorders (ED), especially Anorexia Nervosa (AN), are internationally reported to have amongst the highest mortality and suicide rates in mental health. With limited evidence for current pharmacological and/or psychological treatments, there is a grave responsibility within health research to better understand outcomes for people with a lived experience of ED, factors and interventions that may reduce the detrimental impact of illness and to optimise recovery. This paper aims to synthesise the literature on outcomes for people with ED, including rates of remission, recovery and relapse, diagnostic crossover, and mortality.

This paper forms part of a Rapid Review series scoping the evidence for the field of ED, conducted to inform the Australian National Eating Disorders Research and Translation Strategy 2021–2031, funded and released by the Australian Government. ScienceDirect, PubMed and Ovid/MEDLINE were searched for studies published between 2009 and 2022 in English. High-level evidence such as meta-analyses, large population studies and Randomised Controlled Trials were prioritised through purposive sampling. Data from selected studies relating to outcomes for people with ED were synthesised and are disseminated in the current review.

Of the over 1320 studies included in the Rapid Review, the proportion of articles focused on outcomes in ED was relatively small, under 9%. Most evidence was focused on the diagnostic categories of AN, Bulimia Nervosa and Binge Eating Disorder, with limited outcome studies in other ED diagnostic groups. Factors such as age at presentation, gender, quality of life, the presence of co-occurring psychiatric and/or medical conditions, engagement in treatment and access to relapse prevention programs were associated with outcomes across diagnoses, including mortality rates.

Results are difficult to interpret due to inconsistent study definitions of remission, recovery and relapse, lack of longer-term follow-up and the potential for diagnostic crossover. Overall, there is evidence of low rates of remission and high risk of mortality, despite evidence-based treatments, especially for AN. It is strongly recommended that research in long-term outcomes, and the factors that influence better outcomes, using more consistent variables and methodologies, is prioritised for people with ED.

Plain English summary

Eating disorders are complex psychiatric conditions that can seriously impact a person’s physical health. Whilst they are consistently associated with high mortality rates and significant psychosocial difficulties, lack of agreement on definitions of recovery, remission and relapse, as well as variations in methodology used to assess for standardised mortality and disability burden, means clear outcomes can be difficult to report. The current review is part of a larger Rapid Review series conducted to inform the development of Australia’s National Eating Disorders Research and Translation Strategy 2021–2031. A Rapid Review is designed to comprehensively summarise a body of literature in a short timeframe to guide policymaking and address urgent health concerns. This Rapid Review synthesises the current evidence-base for outcomes for people with eating disorders and identifies gaps in research and treatment to guide decision making and future clinical research. A critical overview of the scientific literature relating to outcomes in Western healthcare systems that may inform health policy and research in an Australian context is provided in this paper. This includes remission, recovery and relapse rates, diagnostic cross-over, the impact of relapse prevention programs, factors associated with outcomes, and findings related to mortality.

Introduction

Eating disorders (ED), especially Anorexia Nervosa (AN), have amongst the highest mortality and suicide rates in mental health. While there has been significant research into causal and maintaining factors, early identification efforts and evidence-based treatment approaches, global incidence rates have increased from 3.4% calculated between 2000 and 2006 to 7.8% between 2013 and 2018 [ 1 ]. While historically seen as a female illness, poorer outcomes are increasingly seen in other genders, including males [ 2 ].

Over 3.3 million healthy life years are lost worldwide due to ED each year, and many more lost to disability due to medical and psychiatric complications [ 3 ]. Suicide accounts for approximately 20% of non-natural deaths among people with ED [ 4 ]. As this loss of healthy life is preventable, there is a grave responsibility to better understand outcomes for people with ED, including factors which may minimise the detrimental impact they have on individuals, carers, and communities, as well as to optimise recovery.

There has been considerable debate within the clinical, scientific and lived experience (i.e., patient, consumer, carer) communities about the definition and measurement of key outcomes in ED, including ‘remission’ from illness (a period of relief from symptoms), ‘relapse’ (a resumption of symptoms) and ‘recovery’ (cessation of illness) [ 5 , 6 ], which can compromise outcome comparisons. Disparities include outcome variables relating to eating behaviours as well as medical, psychological, social and quality of life factors. There is increasing awareness in the literature of the elevated likelihood of diagnostic crossover [ 7 ]; research examining specific diagnostic profiles potentially misses outcomes where symptom experience transforms rather than alleviates. Methodological approaches in outcomes research are varied, the most significant being length of time to follow up, compromising direct study comparisons.

The aim of this Rapid Review (RR) is to synthesise the literature on outcomes for people with ED, including rates of remission, recovery and relapse, diagnostic crossover, and mortality. Factors influencing outcomes were summarised including demographic, illness, treatment, co-morbidities, co-occurring health conditions, societal factors, and impact of relapse prevention programs. This RR forms one of a series of reviews scoping the field of ED commissioned to inform the Australian National Eating Disorders Research and Translation Strategy 2021–2031 [ 8 ]. The objective is to evaluate the current literature in ED outcomes to identify areas of consensus, knowledge gaps and suggestions for future research.

The Australian Government Commonwealth Department of Health funded the InsideOut Institute for Eating Disorders (IOI) to develop the Australian Eating Disorders Research and Translation Strategy 2021–2031 [ 8 ] under the Psych Services for Hard to Reach Groups initiative (ID 4-8MSSLE). The strategy was developed in partnership with state and national stakeholders including clinicians, service providers, researchers, and experts by lived experience (including consumers and families/carers). Developed through a 2 year national consultation and collaboration process, the strategy provides the roadmap to establishing ED as a national research priority and is the first disorder-specific strategy to be developed in consultation with the National Mental Health Commission. To inform the strategy, IOI commissioned Healthcare Management Advisors (HMA) to conduct a series of RRs to broadly assess all available peer-reviewed literature on the six DSM-V [ 9 ] listed ED. RR’s were conducted in the following domains: (1) population, prevalence, disease burden, Quality of Life in Western developed countries; (2) risk factors; (3) co-occurring conditions and medical complications; (4) screening and diagnosis; (5) prevention and early intervention; (6) psychotherapies and relapse prevention; (7) models of care; (8) pharmacotherapies, alternative and adjunctive therapies; and (9) outcomes (including mortality) (current RR), with every identified paper allocated to only one of the above domains from abstract analysis by two investigators. Each RR was submitted for independent peer review to the Journal of Eating Disorders special edition, “Improving the future by understanding the present: evidence reviews for the field of eating disorders”.

A RR Protocol [ 10 ] was utilised to swiftly synthesise evidence to guide public policy and decision-making [ 11 ]. This approach has been adopted by several leading health organisations, including the World Health Organization [ 12 ] and the Canadian Agency for Drugs and Technologies in Health Rapid Response Service [ 13 ], to build a strong evidence base in a timely and accelerated manner, without compromising quality. RR was chosen as the most suitable design as it is conducted with broader search terms and inclusion criteria allowing to gain a better understanding of a specific field, returning a larger number of search results and providing a snapshot of key findings detailing the current state of a field at study [ 10 ]. A RR is not designed to be as comprehensive as a systematic review—it is purposive rather than exhaustive and provides actionable evidence to guide health policy [ 14 ].

The RR is a narrative synthesis adhering to the PRISMA guidelines [ 15 ]. It is divided by topic area and presented as a series of papers. Three research databases were searched: ScienceDirect, PubMed and Ovid/MEDLINE. To establish a broad understanding of the progress made in the field of eating disorders, and to capture the largest evidence base on the past 13 years (originally 2009–2019, but expanded to include the preceding two years), the eligibility criteria for included studies into the RR were kept broad. Therefore, included studies were published between 2009 and 2022, in English, and conducted within Western healthcare systems or health systems comparable to Australia in terms of structure and resourcing. The initial search and review process was conducted by three reviewers between 5 December 2019 and 16 January 2020. The re-run for the years 2020–2021 was conducted by two reviewers at the end of May 2021 and a final run for 2022 conducted in January 2023 to ensure the most up to date publications were included prior to publication.

The RR had a translational research focus with the objective of identifying evidence relevant to developing optimal care pathways. Searches, therefore, used a Population, Intervention, Comparison, Outcome (PICO) approach to identify literature relating to population impact, prevention and early intervention, treatment, and long-term outcomes. Purposive sampling focused on high-level evidence studies such as: meta-analyses; systematic reviews; moderately sized randomised controlled trials (RCTs) ( n  > 50); moderately sized controlled-cohort studies ( n  > 50), or population studies ( n  > 500). However, the diagnoses Avoidant Restrictive Food Intake Disorder (ARFID), Eating Disorder Not Otherwise Specified (EDNOS), Other Specified Feeding or Eating Disorder (OSFED) and Unspecified Feeding or Eating Disorder (UFED) necessitated a less stringent eligibility criterion due to a paucity of published articles. As these diagnoses are newly captured in the DSM-V [ 9 ] (released in 2013, within the allocated search timeframe), the evidence base is emerging, and fewer studies have been conducted. Thus, smaller studies ( n  ≤ 20) and narrative reviews were also considered and included. Grey literature, such as clinical or practice guidelines, protocol papers (without results) and Masters’ theses or dissertations, was excluded.

Full methodological details including eligibility criteria, search strategy and terms and data analysis are published in a separate protocol paper [ 10 ]. The full RR included a total of over 1320 studies (see Additional file 1 : Fig. S1). Data from included studies relating to outcomes for eating disorders were synthesised and are presented in the current review.

Of the 1320 articles included in the RR, the proportion of articles focused on outcomes in ED was relatively small, just less than 9% ( n  = 116) (see Additional file 2 : Table S1). Studies typically examined outcomes in AN, Bulimia Nervosa (BN) and Binge Eating Disorder (BED), with limited research in other diagnostic groups. Whereas most outcome studies reported recovery, remission and relapse rates, others explored factors impacting outcomes, such as quality of life, co-occurring conditions, and outcomes from relapse prevention programs.

ED, particularly AN, have long been associated with an increased risk of mortality. The current review summarises best available evidence exploring this association. Several factors complicate these findings including a lack of consensus on definitions of remission, recovery and relapse, widely varying treatment protocols and research methodologies, and limited transdiagnostic outcome studies or syntheses such as meta-analyses. Table 1 provides a summary of outcomes reported by studies identified in this review. There is considerable heterogeneity in the reported measures.

Overall outcomes

A good outcome for a person experiencing ED symptomatology is commonly defined as either remission or no longer meeting diagnostic criteria, as well as improved levels of psychosocial functioning and quality of life [ 28 , 29 ]. However, such a comprehensive approach is rarely considered, and there is no consensus on a definition for recovery, remission, or relapse for any of the ED diagnoses [ 30 , 31 ]. To contextualise this variation, definitions and determinants for these terms are presented in Table 2 .

The terms ‘remission’ and ‘recovery’ appear to be used interchangeably in the literature. Whilst ‘remission’ is usually defined by an absence of diagnostic symptomatology, and ‘recovery’ an improvement in overall functioning, the period in which an individual must be symptom-free to be considered ‘remitted’ or ‘recovered’ varies greatly between studies, follow-up (FU) time periods are inconsistent, and very few studies examine return to psychosocial function and quality of life (QoL) after alleviation of symptoms. The current review uses the terms adopted by the original studies. ‘Relapse’ is typically defined by a return of symptoms after a period of symptom relief. The reviewed studies report a variety of symptom determinants including scores on standardised psychological and behavioural interviews or questionnaires, weight criteria [including Body Mass Index (BMI) or %Expected Body Weight (%EBW)], clinical assessment by a multidisciplinary team, self-reported ED behaviours, meeting diagnostic criteria, or a combination of the above.

Remission, recovery, and relapse

In a global overview of all studies reviewed, remission or recovery rates were reported for around half of the cohort, regardless of diagnostic group. For example, a 30 month FU study of a transdiagnostic cohort of patients found 42% obtained full and 72% partial remission, with no difference between diagnostic groups for younger people; however, bulimic symptoms emerged frequently during FU, regardless of initial diagnosis [ 44 ]. A 6 year study following the course of a large clinical sample ( n  = 793) reported overall recovery rates of 52% for AN, 50–52% for BN, 57% for EDNOS-Anorectic type (EDNOS-A), 60–64% for BED and 64–80% for EDNOS-Bulimic type (EDNOS-B) [ 7 ]. Of those who recorded full remission at end of treatment (EOT), relapse was highest for AN (26%), followed by BN (18%), and EDNOS-B (16%). Relapse was less common for individuals with BED (11–12%), and EDNOS-A (4%). Change in diagnosis (e.g., from AN to BN) was also seen within the relapse group [ 7 ].

Longer-term FU studies may more accurately reflect the high rates of relapse and diagnostic crossover associated with ED. A 17 year outcome study of ED in adult patients found only 29% remained fully recovered, with 21% partially recovered and half (50%) remaining ill [ 52 ], noting the protracted nature of illness for adults with longstanding ED. Relapse is observed at high rates (over 30%) among people with AN and BN at 22 year FU [ 61 ]. In a large clinical study using predictive statistical modelling, full remission was more likely for people with BED (47.4%) and AN (43.9%) compared to BN (25.2%) and OSFED (23.2%) [ 41 ]. This result is distinct from other studies citing AN to have the worst clinical outcomes within the diagnostic profiles [ 52 ]. The cut‐off points for the duration of illness associated with decreased likelihood of remission were 6–8 years for OSFED, 12–14 years for AN/BN and 20–21 years for BED [ 41 ]. As with recovery rates, reported rates of relapse are highly variable due to differing definitions and study methodologies used by researchers in FU studies [ 35 , 61 ].

Evidence from a meta-analysis of 16 studies found four factor clusters that significantly contributed to relapse; however, also noted a substantial variability in procedures and measures compromising study comparison [ 62 ]. Factors contributing to heightened risk of relapse included severity of ED symptoms at pre- and post-treatment, presence and persistence of co-occurring conditions, higher age at onset and presentation to assessment, and longer duration of illness. Process treatment variables contributing to higher risk included longer duration of treatment, previous engagement in psychiatric and medical treatment (including specialist ED treatment) and having received inpatient treatment. These variables may indicate more significant illness factors necessitating a higher intensity of treatment.

Importantly, full recovery is possible, with research showing fully recovered people may be indistinguishable from healthy controls (HCs) on all physical, behavioural, and psychological domains (as evaluated by a battery of standardised assessment measures), except for anxiety (those who have fully recovered may have higher general anxiety levels than HCs) [ 29 ].

Diagnostic crossover

Most studies reported outcomes associated with specific ED diagnoses; however, given a significant proportion of individuals will move between ED diagnoses over time, it can be challenging to determine diagnosis-specific outcomes. Results from a 6 year FU study indicated that overall individuals with ED crossed over to other ED diagnoses during the FU observational period, most commonly AN to BN (23–27%), then BN to BED (8–11%), BN to AN (8–9%) and BED to BN (7–8%) [ 7 ]. Even higher crossover trends were observed in the subgroup reporting relapse during the FU period, with 61.5% of individuals originally diagnosed with AN developing BN, 27.2% and 18.1% of individuals originally diagnosed with BN developing AN and BED respectively, and 18.7% of people with a previous diagnosis of BED developing BN [ 7 ].

A review of 79 studies also showed a significant number of individuals with BN (22.5%) crossed over to other diagnostic groups (mostly OSFED) at FU [ 63 ]. A large prospective study of female adolescents and young adults in the United States ( n  = 9031) indicated that 12.9% of patients with BN later developed purging disorder and between 20 and 40% of individuals with subthreshold disorders progressed to full threshold disorders [ 64 ]. Progression from subthreshold to threshold eating disorders was higher for BN and BED (32% and 28%) than for AN (0%), with researchers suggesting higher risk for binge eating [ 66 ]. Progression from subthreshold to full threshold BN and BED was also common in adolescent females over the course of an 8 year observational study [ 33 ]. Some researchers contend that such diagnostic ‘instability’ demonstrates a need for ‘dimensional’ approaches to research and treatment which have greater focus on the severity rather than type of symptoms [ 7 ]. Diagnostic crossover is common and should be considered in the long-term management and monitoring of people with an ED.

Anorexia nervosa (AN)

People with restrictive-type ED have the poorest prognosis compared to the other diagnostic groups, particularly individuals displaying severe AN symptomatology (including lower weights and higher body image concerns) [ 44 ]. There is a paucity of effective pharmacological and/or psychological treatments for AN [ 65 ]. Reported rates of recovery vary and include 18% [ 56 ] to 52% at 6 year FU [ 7 ] to 60.3% at 13 year FU [ 20 ] and 62.8% at 22 year-FU [ 61 ]. Reported relapse rates in AN also vary, for example, 41.0% at 1 year post inpatient/day program treatment [ 35 ] to 30% at 22 year FU [ 61 ]. Average length of illness across the reviewed studies also varies from 6.5 years [ 56 ] to 14 years [ 41 ].

A variety of reported outcomes from treatment studies is likely due to the breadth of treatments under investigation, diverse study protocols and cohorts. For example, in a mixed cohort of female adult patients with AN and Atypical AN (A-AN), 33% were found to have made a full recovery at 3 year FU after treatment with cognitive behavioural therapy (CBT) [ 57 ], while 6.4% had a bad outcome and 6.4% a severe outcome. However, in a 5–10 year FU study of paediatric inpatients (mean age 12.5 years) approximately 41% had a good outcome, while 35% had intermediate and 24% poor outcome [ 66 ]. Multimodal treatment approaches including psychiatric, nutritional, and psychological rehabilitation have been found to be most efficacious for moderate to severe and enduring AN but noting a discrete rate of improvement [ 67 ].

Very few factors were able to predict outcomes in AN. Higher baseline BMI was consistently found to be the strongest predictor of recovery, and better outcomes were associated with shorter duration of illness [ 7 , 55 , 61 , 66 ]. Earlier age of illness onset [ 59 , 68 , 69 ] and older age at presentation to treatment [ 30 ] were related to chronicity of illness and associated with poorer outcome.

There was a consensus across a variety of studies that engagement in binge/purge behaviours (Anorexia Nervosa Binge/Purge subtype; AN-BP) was associated with a poorer prognosis [ 20 , 56 , 70 ]. Similarly, individuals with severe and enduring AN restrictive sub-type (AN-R) are likely to have a better outcome than individuals with AN-BP. AN-BP was associated with a two-fold greater risk of relapse compared to AN-R [ 30 , 35 ]. Some studies, however, were unable to find an association between AN subtype and outcome [ 55 ]. Other factors leading to poorer outcome and higher probability of relapse were combined ED presentations, such as combined AN/BN [ 35 ], higher shape concern [ 57 ], lower desired weight/BMI [ 44 ], more ED psychopathology at EOT, low or decreasing motivation to recover, and comorbid depression [ 35 , 61 ].

Preliminary genetic work has found associations between a single nucleotide polymorphism (SNP) in a ghrelin production gene (TT genotype at 3056 T-C) and recovery from AN-R [ 71 ], and the S-allele of the 5-HTTLPR genotype increasing the risk susceptibility for both depressive comorbidity and diagnostic crossover at FU of AN patients [ 72 ]. These studies, however, need to be interpreted with caution as they were conducted over a decade ago and have not since been replicated. Research in eating disorder genetics is a rapidly emerging area with potential clinical implications for assessment and treatment.

Bulimia nervosa (BN)

Overall, studies pertaining to a diagnostic profile of BN report remission recovery rates of around 40–60%, depending on criteria and FU period, as detailed below. Less than 40% of people achieved full symptom abstinence [ 73 ] and relapse occurred in around 30% of individuals [ 61 ]. A meta-analysis of 79 case series studies reported rates of recovery for BN at 45.0% for full recovery and 27.0% for partial remission, with 23.0% experiencing a chronic course and high rates of treatment dropout [ 63 ]. At 11 year FU, 38.0% reported remission in BN patients, increasing to 42.0% at 21 year [ 45 ]. At 22 year FU, 68.2% with BN were reported to have recovered [ 41 ]. Higher frequency of both objective binge episodes and self-induced vomiting factors influencing poorer outcomes [ 44 ].

Considering impact of treatment, analysis of engagement in self-induced vomiting as a predictor for outcome indicated there were no differences between groups in treatment dropout or response to CBT among a sample of 152 patients with various types of EDs (AN-BP, BN, EDNOS) at EOT [ 74 ]. Meta-analysis of results from 45 RCTs on psychotherapies for BN found 35.4% of treatment completers achieved symptom abstinence [ 73 ] with other studies indicating similar rates of recovery (around 52–59% depending on DSM criteria) [ 7 ].

Studies delivering CBT or other behavioural therapies reported the best outcomes for BN [ 73 ]. Specifically, early treatment progression, elimination of dietary restraint and normalisation of eating behaviour resulted in more positive outcomes [ 22 ]. These findings are supported by results from a study comparing outcomes of CBT and integrative cognitive-affective therapy (ICAT) [ 75 ]. Additional moderating effects were shown at FU (but not EOT), with greater improvements for those with less baseline depression, higher stimulus seeking (the need for excitement and stimulation) and affective lability (the experience of overly intense and unstable emotions) in the ICAT-BN group and lower stimulus seeking in the Enhanced Cognitive Behavioural Therapy (CBT-E) group. Lower affective lability showed improvements in both treatment groups [ 75 ]. Such findings indicate personality factors may deem one treatment approach more suitable to an individual than another.

A review of 4 RCTs of psychotherapy treatments for BN in adolescents (including FBT and CBT) reported overall psychological symptom improvement by EOT predicting better outcomes at 12 months, which underscored the need for not only behavioural but psychological improvement during 6 month treatment [ 31 ]. Other factors leading to poorer outcomes included less engagement in treatment, higher drive for thinness, less global functioning, and older age at presentation [ 45 ]. More research is needed into consistent predictors, mediators and moderators focused on treatment engagement and outcomes [ 22 ].

While many studies combine findings for BN and BED, one study specifically considered different emotions associated with binge eating within the two diagnostic profiles [ 60 ]. At baseline, binge eating was associated with anger/frustration for BN and depression for BED. At FU, objective binge eating (OBE) reduction in frequency (a measure of recovery) was associated with lower impulsivity and shape concern for BN but lower emotional eating and depressive symptoms for BED. These differences may provide approaches for effective intervention targets for differing presentations; however, how these may play out within a transdiagnostic approach requires further enquiry.

Binge eating disorder (BED)

BED is estimated to affect 1.5% of women and 0.3% of men worldwide, with higher prevalence (but more transient) in adolescents. Most adults report longstanding symptoms, 94% lifetime mental health conditions and 23% had attempted suicide, yet only half were in recognised healthcare or treatment [ 76 ].

Compared with AN and BN, long-term outcomes, and treatment success for individuals with BED were more favourable. Meta-analysis of BED abstinence rates suggests available psychotherapy and behavioural interventions are more effective for this population [ 77 ]. Additionally, stimulant medication (i.e., Vyvanse) has been found to be particularly effective to reduce binge eating [see [ 78 ] for full review]. Results from a study of people who received 12 months of CBT for BED indicated high rates of treatment response and favourable outcomes, maintained to 4 year FU. Significant improvements were observed with binge abstinence increasing from 30.0% at post-treatment to 67.0% at FU [ 79 ]. A meta-analysis reviewing psychological or behavioural treatments found Interpersonal Therapy (IPT) to be the treatment producing the greatest abstinence rates [ 73 ]. In a comparative study of IPT and CBT, people receiving CBT experienced increased ED symptoms between treatment and 4 year FU, while those who received IPT improved during the same period. Rates of remission at 4 year FU were also higher for IPT (76.7%) versus CBT (52.0%) [ 80 ].

One study specifically explored clinical differences between ED subtypes with and without lifetime obesity over 10 years. Prevalence of lifetime obesity in ED was 28.8% (ranging from 5% in AN to 87% in BED), with a threefold increase in lifetime obesity observed over the previous decade. Observed with temporal changes, people with ED and obesity had higher levels of childhood and family obesity, older-age onset, longer ED duration, higher levels of ED (particularly BED and BN) and poorer general psychopathology than those who were not in the obese weight range [ 81 ], suggesting greater clinical severity and poorer outcomes for people of higher weight.

Comparison of 6 year treatment outcomes between CBT and Behavioural Weight Loss Treatment (BWLT) found CBT more effective at post-treatment but fading effectiveness over time, with remission rates for both interventions lower than other reported studies (37%) [ 82 ]. A meta-analytic evaluation of 114 published and unpublished psychological and medical treatments found psychological treatments, structured self-help, and a combination of the two were all effective at EOT and 12 month FU but noted a wide variation in study design and quality, and the need for longer term FU. Efficacy and FU data for pharmacological and surgical weight loss treatments were lacking [ 77 ].

Whilst high weight and associated interventions (such as bariatric surgery) can be associated with any ED, they are frequently studied in relation to BED. A significant proportion of individuals seeking bariatric surgery (up to 42%) displayed binge eating symptomatology [ 83 ], yet little is known about the effect of these interventions on ED psychopathology and whether this differs by type of intervention. A systematic review of 23 studies of changes in ED behaviour following three different bariatric procedures found no specific procedure led to long term changes in ED profiles or behaviours [ 84 ]; however, another study investigating the placement of an intragastric balloon in obese patients found post-surgical reductions in grazing behaviours, emotional eating and EDNOS scores [ 85 ]. Bariatric surgery in general is associated with a reduction in ED, binge eating and depressive symptoms [ 86 ].

Outcomes among patients receiving bariatric surgery with and without BED were assessed where weight loss was comparable between the groups at 1 year FU. However, compared with participants receiving a BWLT-based lifestyle modification intervention instead of surgery, bariatric surgery patients lost significantly less weight at a 10.3% difference between groups. There was no significant difference between lifestyle modification and surgery groups in BED remission rates [ 87 ]. These results indicate that BLWT-type interventions are more effective than surgery at promoting weight loss in individuals with BED over a 1 year FU period, and people with BED and higher BMI were able to maintain weight loss in response to psychotherapy (CBT) at up to 5 year FU [ 88 ]. In analysis of health-related quality of life (HRQoL) in people with BED who received various levels of CBT (therapist-led, therapist-assisted and self-help), evaluation indicated that all modalities resulted in improvements to HRQoL. Poorer outcomes were associated with obesity and ED symptom severity at presentation, stressing the importance of early detection and intervention measures [ 89 ]. Research into the role of CBT in strengthening the effect of bariatric surgery for obesity is ongoing but promising [ 90 ].

EDNOS, OSFED and UFED

Similarly to BED, a diagnosis of DSM-IV EDNOS (now OSFED) was associated with a more favourable outcome than AN or BN, including shorter time to remission. One study reported remission rates for both EDNOS and BED at 4 year FU of approximately 80% [ 21 ]. The researchers suggested that an ‘otherwise specified’ diagnostic group might be comprised of individuals transitioning into or out of an ED rather than between diagnostic categories; however, more work is needed in this area to fully understand this diagnostic profile. The reported recovery rate from EDNOS-A has been found to be much lower at 57% than for EDNOS-B at 80% (DSM-V). One factor suggested leading to poorer outcomes for EDNOS-A was a higher association with a co-occurring condition of major depression and/or dysthymia not found in other EDNOS subtypes [ 7 ]. Another study found purging occurred in 6.7% from total (cross-diagnostic) ED referrals, but this subtype did not have different post-treatment remission rates or completion rates compared to non-purging profiles [ 91 ], so results are mixed.

Acknowledging the scarcity of research within these diagnostic groups, remission rates for adolescents including those with a diagnosis of Other Specified Feeding or Eating Disorder (OSFED) and Unspecified Feeding or Eating Disorder (UFED) was reported to be 23% at 12 month FU in the one study reviewed, but no detail was provided on recovery rates by diagnosis [ 26 ]. No available evidence was identified specifically for the DSM-V disorders OSFED or UFED for adults.

Avoidant/Restrictive Food Intake Disorder (ARFID)

Research into outcomes for people with ARFID is lacking, with only three studies meeting criteria for the review [ 23 , 24 , 25 ]. While, like AN, recovery for people with ARFID is usually measured by weight gain targets, one of the three studies [ 63 ] identified by this review instead reported on outcomes in terms of meeting a psychiatric diagnosis, making comparison between the studies difficult.

In a cross-diagnostic inpatient study, individuals presenting with ARFID were younger, had fewer reported ED behaviours and co-occurring conditions, less weight loss and were less likely to be bradycardic than individuals presenting with AN [ 25 ]. Although both groups received similar caloric intakes, ARFID patients relied on more enteral nutrition and required longer hospitalisations but had higher rates of remission and fewer readmissions than AN patients at 12 months. This study highlights the need for further investigation into inpatient treatment optimisation for different diagnostic profiles.

People with ARFID who had achieved remission post-treatment were able to maintain remission until 2.5 year FU, with most continuing to use outpatient treatment services [ 23 ]. In a 1 year FU study assessing ARFID, 62.0% of patients had achieved remission as defined by weight recovery and no longer meeting DSM-V criteria [ 25 ]. In a study following children treated for ARFID to a mean FU of 16 years post-treatment (age at FU 16.5–29.9 years), 26.3% continued to meet diagnostic criteria for ARFID with no diagnostic crossover, suggesting symptom stability [ 24 ]. Rates of recovery for ARFID patients in this study were not significantly different to the comparison group who had childhood onset AN, indicating similar prognoses for these disorders. No predictors of outcome for patients with ARFID were identified by the articles reviewed [ 63 ].

Community outcomes

While most outcome studies derive from health care settings, two studies were identified exploring outcomes of ED within the community. The first reported the 8 year prevalence, incidence, impairment, duration, and trajectory of ED via annual diagnostic interview of 496 adolescent females. Controlling for age, lifetime prevalence was 7.0% for BN/subthreshold BN, 6.6% for BED/subthreshold BED, 3.4% for purging disorder, 3.6% for AN/atypical AN, and 11.5% for feeding and eating disorders not otherwise classified. Peak onset age across the ED diagnostic profiles was 16–20 years with an average episode duration ranging from 3 months for BN to a year for AN; researchers noted that these episodes were shorter than the average duration estimates reported in similar research and may be representative of the transient nature of illness rather than longer term prognosis. ED were associated with greater functional impairment, distress, suicidality, and increased use of mental health treatment [ 27 ].

A second study followed 70 young people (mean age of 14 years at study commencement) meeting DSM-IV criteria for a binge eating or purging ED and found 44% no longer met criteria at ages 17 or 20, while 25% still met criteria at age 20 (the latter individuals were more likely to have externalising behaviour problems and purging behaviour at age 17). Those who experienced a persistent ED were less likely to complete secondary education and report higher depressive and anxiety symptoms at age 20, indicating the ongoing impacts of ED on education and quality of life [ 92 ]. These studies provide information about the course and outcome of early onset ED at the population level with indicators of predictive and maintaining factors.

Factors relating to outcomes

Several factors relating to outcomes have been studied across ED presentations and in specific diagnostic profiles. These include predictors of outcome, moderators or mediators of outcome, and illness reinforcers, considering age of presentation and duration of illness, ED symptomatology, presence of co-occurring medical and psychiatric conditions, and treatment characteristics.

Age of presentation

Age of presentation to treatment has been shown to have a significant impact on outcome in all diagnoses. One study considering ED in general (including AN, BN and EDNOS) showed presentation at mid-life drastically decreased chances of achieving a good outcome in response to treatment (“good” outcome defined as BMI ≥ 18.5, 3 month remission of symptoms and Eating Disorder Examination Questionnaire (EDE-Q) scores within or better than normal range). Six percent of mid-life (≥ 40 years) presentations achieved a good outcome post-treatment compared to 14% of young adults (18–39 years) and 28% of younger people (< 18 years) [ 28 ]. This finding has also been seen in research comparing 22 year outcomes of AN and BN [ 61 ].

People presenting in mid-life often have more complex medical and psychiatric profiles as well as life circumstances. They are also far more likely to have a sustained length of illness by the time of initial presentation: 27.8 years compared with 1.2 years for youths [ 28 ]. Longer duration of illness is associated with greater increase in self-reported clinical impairment [ 93 ]; however, illness duration does not necessarily influence treatment outcome, though wide variation in study protocol and quality limit the interpretability of these findings [ 37 , 94 ]. The disparity in rates of favourable outcome between age groups highlights the importance of prevention, screening, awareness of ED in primary care settings and early intervention programs, as well as targeted programs for those presenting with more complex psychosocial and life challenges.

Clinical features and co-occurring conditions

A systematic review assessed the average duration of untreated illness duration in help-seeking populations at first contact to treatment services at 29.9 months for AN, 53.0 months for BN and 67.4 months for BED [ 69 ]. ED clinical factors significantly influence outcomes, with poorer prognosis in those with time of untreated illness, primary diagnosis of AN [ 95 ], lower BMI at presentation [ 93 ], and presence of binge/purge symptomatology [ 20 , 56 ]. Certain ED behaviours and cognitions at intake predict better outcome such as lower rates of purging behaviour, higher rates of body image flexibility [ 96 ], and lower EDE-Q scores at baseline [ 97 ].

There is strong evidence for the presence of co-occurring medical and psychiatric conditions as a predictor of outcome in ED. At 22 year FU, the presence of co-occurring psychiatric conditions including Major Depressive Disorder (MDD) and Substance Use Disorder (SUD) were negatively correlated with recovery, with those who had recovered from an ED being 2.17 times less likely to have MDD and 5.33 times less likely to have SUD [ 98 ]. Co-occurring mood disorders consistently lead to poorer outcomes [ 47 , 51 , 55 , 99 ] and greater chance of moving between ED diagnoses [ 7 ]. In one study, presence of a mood disorder was the strongest predictor of classification of AN-R (but not AN-BP) [ 61 ]. Comorbid personality disorder was found in several studies to be the most common predictor of poorer outcome in ED [ 20 , 41 , 44 , 67 ].

In an adolescent sample, 39% of individuals with AN met criteria for at least one other psychiatric disorder and poorer prognosis was associated with co-occurring diagnoses of Obsessive Compulsive Disorder (OCD) and autistic traits [ 59 ]. In a large community childhood health longitudinal study, presence of any ED profile was predictive of later anxiety and mood disorders. AN was prospectively associated with long term low weight, while BN and BED with obesity, drug use and deliberate self-harm compared to age-matched children who did not have an ED profile [ 100 ].

Personality traits have also been found to be associated with poorer outcomes such as low persistence and harm avoidance in AN, lower self-directedness (BN) and reward dependence (BED) [ 41 ]. Higher perfectionism at intake predicted a lower likelihood of remission at 12 months in an adolescent sample [ 26 ], a finding consistent with previous research in adult cohorts [ 41 ].

Medical comorbidities such as malnutrition [ 72 ], concurrent type 1 diabetes [ 39 , 42 ], bodily pain [ 55 ] and viral infections [ 72 ] have been identified as risk factors for poorer outcomes and increased rates of relapse. Other co-occurring factors associated with poorer outcomes for people with ED include anxiety [ 47 , 56 , 93 ], dissociative experiences [ 101 ], impulsivity [ 56 ], adjustment disorder [ 95 ], use of psychotropic medications [ 30 ], and autistic traits have been associated with greater use of ED treatment [ 102 ].

Psychosocial, environmental and health factors

A large United States community study found positive correlation between higher rates of smoking behaviour and ED in women [ 99 ]. The same study also reported birth-related outcomes in women with ED including having a later first birth, pregnancy health concerns, experience of miscarriage or abortion [ 99 ], and women with ED may have increased experience of adverse pregnancy and neonatal outcomes, and lower numbers of children [ 3 ]. For women with a history of ED, ED symptoms tend to alleviate during pregnancy; however, they commonly resurface during the postnatal period, and up to a third of women with ED report postnatal depression [ 103 , 104 ].

Demographic factors leading to poorer prognosis include being male [ 72 ], of the LGBTQIA + community [ 105 ], being from a non-white ethnic background, low family education levels [ 99 ], lower socioeconomic status, living in a remote or rural area [ 72 ], poor employment and social adjustment [ 30 ], functional impairment [ 47 ], and having a family member with an ED [ 99 ]. Complicating prognosis are additional factors such as financial stress (individuals with ED face yearly health care costs 48% higher than the general population, while the presence of co-occurring psychiatric conditions is associated with 48% lower yearly earnings [ 3 ]. These financial challenges limit ability to access evidence-based treatments (especially in countries lacking in publicly funded health care) which may prolong illness.

There is strong evidence to suggest QoL is reduced in people with an ED [ 3 , 106 ]. It is important to consider associations between QoL, ED symptomatology and treatment outcome. Evidence-based treatments have demonstrated positive effects on QoL in addition to reduction in ED symptomatology, for example, improvements in QoL and psychological functioning and well-being were seen in response to CBT in a cross-diagnostic sample [ 43 ]. However, a meta-analysis of ED outcome studies found that the QoL of recovered ED patients remained lower than in healthy populations, highlighting the importance of prevention efforts [ 107 ] and restoration of QoL in relapse prevention. These studies highlight the high public health and clinical burden of eating disorders and the need to consider co-occurring medical and psychiatric conditions during comprehensive assessment history-taking, treatment planning and provision.

Treatment factors

Early progression in treatment can provide indication of treatment outcomes. In an RCT comparing Family Based Treatment (FBT) and Adolescent Focused Therapy (AFT) for adolescents with AN, most people who achieved remission at 1 year FU maintained recovery to 4 years FU regardless of treatment arm with remission rates tended to remain stable after 1 year [ 108 ]. The First Episode Rapid Early Intervention for Eating Disorders (FREED) service model for young adults with AN reported significant and rapid clinical improvements in over 53.2% of people compared to 17.9% TAU and also reported more cost-effective treatment [ 109 ]. In a transdiagnostic study comparing inpatient vs outpatient settings, rapid response to treatment (defined here as a clinically meaningful reduction in disorder-specific symptoms within the first ten sessions) was the only outcome predictor accounting for 45.6% of variance in ED symptoms, suggesting future work should evaluate mediators and moderators of rapid response [ 37 ]. A systematic review of outcome predictors and mediators in response to CBT indicated that early behavioural and cognitive change was associated with positive outcomes across ED diagnoses [ 22 ]. Similarly, a recent systematic review and meta-analysis of 20 years of accumulated evidence concluded early response to treatment the most robust predictor of better treatment outcomes, however, only half of people investigated across numerous studies showed early change, and more research was needed to determine outcome predictors [ 110 ]. Ongoing assessment to identify individuals who do not show early response to treatment (defined by healthy weight and absence of ED behaviours at 12 month FU), as well as provision of targeted engagement approaches, may improve outcomes [ 47 ].

Due to the frequent need for medical stabilisation in the early and acute stages of AN, the role of hospitalisation needs to be considered in the evaluation of treatment outcomes. In a large patient cohort study ( n  = 7505) with 5 year FU, a clear trend was observed with the per-patient 5 year cumulated number of inpatient days decreasing by 6% per annum after adjustment for age at diagnosis, parental mental health, and household income. The number of hospital admissions decreased by 2% per year, although there was no change in outpatient visits [ 111 ]. Factors contributing to better outcomes were not identified in this study, but in other research, early change in %EBW and ED psychopathology in adolescent inpatients predicted later change in the same ED variables [ 18 ]. Another study showed longer first admission predicted increased use of the health system in young adults [ 112 ].

In a multicentre RCT there was no difference between higher or lower calorie refeeding on clinical remission or medical hospitalisation to 12 month FU [ 113 ]. A systematic scoping review of 49 studies found adolescent day programs (intensive treatment programmes that do not involve an overnight stay at the treatment facility) can be an effective alternative to inpatient hospitalisation or step up/down in treatment intensity and are generally associated with weight gain and improvements in ED and comorbid psychopathology [ 114 ]. Outcomes in the review were sustained from 3 months to 2 years from EOT; however, due to large variability in the content, structure and theoretical underpinnings of reviewed programs, findings should be interpreted with caution.

Difficulties with emotion regulation are also associated with poor outcome across diagnostic profiles. There is evidence to suggest emotion-focused treatment is beneficial both to emotional functioning and mood as well as ED severity for people with elevated emotion regulation issues at baseline with positive effects lasting up to 5 years FU [ 115 ].

Self-esteem, self-compassion, and motivation

There is little conclusive evidence regarding predictors of poor response to evidence-based treatments [ 22 , 58 ]; however, low self-esteem has been implicated across all ED diagnoses [ 98 , 101 ], particularly AN [ 55 ]. A meta-analysis exploring the role of self-esteem on treatment outcomes indicated that while self-esteem did not predict remission or long-term weight related outcomes, it did mediate progression during inpatient treatment (greater increase in self-esteem during inpatient treatment was associated with higher remission and lower relapse rates at FU) [ 116 ]. Relatedly, high fear of self-compassion was associated with greater severity of ED symptoms in individuals with an active ED, suggesting that a fearful unwillingness to become more self-compassionate, rather than the absence of self-compassion, may lead to more detrimental outcomes [ 117 ].

Greater pre-treatment motivation has also been associated with ED symptom improvement and management of co-occurring anxiety and depression, in a systematic review and meta-analysis of 42 longitudinal studies [ 118 ]. Therapeutic interventions that include enhancement of motivation, self-esteem and self-compassion have been shown across studies to improve treatment outcomes across diagnostic profiles [ 117 ].

Relapse prevention programs

Whilst the role of treatment is crucial in the alleviation of symptoms and restoration of wellbeing, active provision of evidence-based post-treatment recovery care may be an important determining factor in relapse prevention. Research suggests the period in which individuals are at greatest risk of relapse is between four and nine-months following discharge [ 35 ], with between 31 and 41% relapsing at one to two years post-discharge [ 62 ].

To reduce readmission among a group of females receiving inpatient treatment for AN at an Australian specialist child and adolescent ED service, a 10 week transition ‘day’ program was developed and evaluated. The delivered program allowed for a ‘step down’ option and was found to have significant benefit for participants, who achieved an average weight gain of over 1 BMI point and decreased ED symptomatology at six-month FU [ 65 ]. Promising findings were also seen in a 6-session post-(inpatient and/or outpatient) treatment relapse prevention program designed by clinicians, parents, and patients in the Netherlands, which included a take-home workbook and appointments up to 18 months (frequency dependent on patient progress). Evaluated with young people with AN-R and AN-BP, 70% maintained post-discharge recovery to the end of the study period [ 36 ]. Such programs were evaluated in the context of a comprehensive specialist service with no control group comparison to measure the impact of the specific intervention, and there was no FU assessment following conclusion of the intervention to assess maintenance. Although more work is needed, these studies indicate the value of targeted relapse prevention programs.

Online relapse prevention programs

There is emerging evidence to support the safety and efficacy of internet-based relapse prevention programs aimed at preventing readmission to intensive ED treatment following discharge. These programs have the potential to be widely disseminated to individuals who may otherwise disengage from ongoing support due to access issues (e.g., living in an underserviced area, financial burden) or personal reasons such as stigma or shame [ 119 , 120 ].

A 9-session (1/month) CBT-based online relapse prevention program for women with AN discharged from inpatient treatment (baseline BMI x̄  = 17.7) found participants who completed the program had significant gains in BMI at end of program ( x̄  = 19.1) while the treatment as usual (TAU) control group did not ( x̄  = 17.7). Of note, participants who were 1–2 sessions short of completing the program maintained a higher BMI ( x̄  = 18.0) than the TAU group, whereas participants with less than 50% completion had a significantly lower BMI than any group including TAU ( x̄  = 17.0) [ 121 ]. A similar CBT-based online program targeted toward women discharged from inpatient treatment for BN found that the intervention group reported 46.0% fewer vomiting episodes compared to TAU, with some improvement in symptom abstinence (intervention group: 21.4%, TAU control = 18.9%), although this finding was not statistically significant [ 122 ].

In Hungary, an internet-based aftercare support program for individuals who had received inpatient or outpatient treatment for BN or related EDNOS in the 12 months prior to the study included information and support offered via 30 min chat sessions with peers and clinicians. Results showed 40.6% of the intervention group reported improvement compared to TAU waitlist controls (24.4%), although this difference was not statistically significant. The study noted that, although on the waitlist for the internet-based aftercare support program, the TAU group could still access additional treatment if so required. Evaluation findings report the program was feasible and well accepted [ 123 ].

Text messaging-based interventions have also been trialled to maintain engagement post-treatment, whereby participants send regular symptom reports to the clinical team with feedback provided. A 12 week ‘mobile therapy’ study with a group of women exiting CBT treatment for BN resulted in significant improvement in binge/purge frequency, ED and depressive symptoms from baseline to FU, with high rates of protocol adherence (87.0%), although there was no control group comparison [ 124 ]. Further evidence was provided in a 16 week weekly symptom report study of women with BN following inpatient discharge, with a significantly larger proportion of the intervention group achieving remission (51%) compared with TAU (36%) at 8 months FU. There was no significant difference between groups in terms of outpatient service use [ 125 ]. Results from these studies conflict with evidence from a systematic review of 15 studies, which was unable to support the effectiveness of text messaging-based programs for people with ED as either a sole or adjunctive component of the intervention [ 126 ]; however, this review noted the lack of a common evaluation framework making comparison difficult.

Despite advances in awareness and treatment, ED, particularly AN, continue to be associated with increased risk of mortality [ 4 ]. Studies identified that focus on the assessment of ED mortality, as well as data from the Global Burden of Disease Study 2016 are discussed in this section. Importantly, there are several different metrics used to report mortality. These include the Standardised Mortality Ratio (SMR), or the number of observed deaths in a cohort versus the number of expected deaths in a reference population (where a rate greater than one is interpreted as excess mortality); Weighted Mortality Ratio (WMR), or the weighted average of age-specific mortality rates per 100,000 persons; Crude Mortality Rate (CMR) , or the number of deaths in a given period divided by the population exposed to risk of death in that period; and Years of Life Lost (YLL), a summary measure of premature mortality calculated by subtracting the age at death from the standard life expectancy in a reference population.

Standardised, weighted, and crude mortality

AN is consistently described as having the highest mortality rate of the ED, but actual rate difference varies between studies. A summary of Standardised Mortality Ratios across studies is presented in Table 3 . SMRs from a meta-analysis suggest that measured mortality of AN is approximately three times as high as for other ED diagnoses, and in a UK study of ED patients ( n  = 1892) accessing services between 1992 and 2004, the SMR for AN was almost five times higher than other ED [ 127 ]. This is consistent with other research (a meta-analysis summarising 41 studies) reporting people with AN were 5.2 [3.7–7.5] times more likely to die prematurely from any cause [ 128 ]. A longitudinal study ( n  = 246) found SMR of AN to be only twice as high compared to BN, but still 6.5 times the rate expected in the general population [ 49 ].

Some studies did not report higher SMR for AN compared to other ED, however, methodological differences need to be considered. For example, some studies reported comparable SMR for AN to other ED, but subthreshold AN cases were included (previously catagorised as EDNOS) which may have reduced the calculated AN SMR [ 104 , 108 ]. In a British study using English National Hospital Episodes Statistics (2001–2009) comparing AN and BN, little difference in SMRs was reported [ 132 ]. The diagnosis of BN was less likely than other diagnosis to be recorded as the primary diagnosis and may not have been representative.

In a 22 year trial FU of a large sample of inpatients treated for BN, 2.4% had died [ 45 ]; the CMR for BN was 0.32% [ 63 ] and in severely malnourished patients, the crude mortality rate rose to 11.5% with SMR 15.9 [CI 95% (11.6–21.4)], just over 5 years post-treatment [ 137 ]. WMR has been found to be 5.1 for AN, 1.7 for BN, and 3.3 for EDNOS. SMRs were 5.86 for AN, 1.93 for BN, 1.92 for EDNOS [ 4 ] and 1.5–1.8 for BED [ 76 ].

Mortality rates in AN were highest during the first year after admission to treatment, while in BN it is in the first two years [ 134 ], with a higher risk in adolescence [ 140 ]. In AN, peak age of risk of death has been reported to be 15 years of age, BN 22 years and EDNOS 18–22 years [ 141 ]. Substance use disorders (including alcohol and/or cannabis) increased mortality in people with eating disorders across the diagnostic profiles [ 142 ].

In ED, peak age of risk for males may be earlier than females [ 141 ]. SMRs are higher for males (SMR = 7.24; 95% CI 6.58–7.96) relative to females (SMR = 4.59; 95% CI 4.34–4.85) overall, and in all age groups [ 131 ]. This may be due to the lower likelihood of males to self-identify or be identified with ED resulting in treatment delays and higher severity of illness when finally seeking help [ 131 ]. In mortality research conducted with a male-only sample, similarly high SMRs for males with BN and particularly AN as in majority female samples [ 2 ] were reported; however, mortality rates of EDNOS in males were considerably higher than those reported in female-dominant or female-only samples. Moreover, a case-controlled study found there was a sex difference across all diagnostic categories in CMR, with male to female being 15–5% in AN, 8–3% in BN, and 4–3% in EDNOS, but there were no significant sex differences in SMR for any diagnostic group, with males showing a shorter survival time after onset [ 2 ]. Researchers have suggested that increased mortality in males could be due to several factors, including reluctance to seek treatment and current treatment approaches being less effective in males [ 138 ]. Further research in males with ED is required to better understand the impact and response in male patients. Regardless of the mortality metric used, these studies indicate the vital importance of considering elevated mortality risk across the range of ED diagnoses.

Years of life lost/years lived with disability

The Global Burden of Disease Study 2016 reported that YLL due to premature death attributable to AN was 0.4 per 100,000. No YLL were attributed to BN; however, cause-specific mortality (CSM)—where each death is attributed to a single underlying cause—was, per thousand, 0.5 for AN (with a 2.9% increase from 1980 to 2016) and 0.1 for BN (21.8% increase from 1980 to 2016) [ 143 ]. The 2019 extension advocated for the inclusion of BED and OSFED in the Global Burden of Disease Study, previously excluded, as both diagnostic groups accounted for the majority of global ED cases and accounted for an unrepresented 41.9 million people living with ED [ 144 ].

Estimates are that over 3.3 million healthy life years are lost per year worldwide due to eating disorders. Years lived with a disability (YLDs) have increased from 2007 to 2017 for both AN (6.2% increase) and BN (10.3%), a higher rate than other mental disorders (− 0.1%). ED outcomes include reduced self-reported quality of life and estimated health care costs at 48% higher than for the general population [ 3 ].

Risk factors

Little is known about specific risk factors for mortality, although some variables have been reported in the literature. People who receive inpatient treatment for AN have more than five to seven times mortality risk when matched to age and gender and compared to other ED diagnoses [ 3 , 131 , 133 ]. For individuals receiving AN or BN treatment in outpatient settings, the risk is still twice that of controls [ 3 ]. Older age of presentation is a significant risk; adult presentations are associated with much higher mortality rates than adolescent presentations likely due to longer duration of illness at presentation, higher rates of medical and psychiatric complications and less engagement in treatment [ 4 , 28 , 68 , 137 , 139 ]. Higher mortality rates (especially in AN) are associated with lower BMI, longer duration of illness at service presentation [ 4 , 49 , 68 , 137 , 139 ], diuretic use [ 68 ], and occurrence of an in-hospital suicide attempt [ 68 , 137 ]. Certain treatment factors may be associated with higher risk of mortality, including transfer to medical intensive care unit, discharge against medical advice, and shorter hospital stays [ 137 ]. Other factors associated with increased risk of mortality include poor psychosocial functioning, substance use [ 28 , 49 ] and absence of family ED history [ 28 ].

Cause of death

Results from a large prospective 20 year (1985–2005) longitudinal study of individuals admitted to inpatient services in Germany ( n  = 5839) showed people with AN were likely to die from health issues caused by their disorder, most commonly circulatory failure, cachexia, and multiple organ failure [ 133 ]. Other studies have identified somatic risk factors including anaemia, dysnatremia, infection, cardiac complications and haematological comorbidities [ 137 ]. A 2021 study reported rates of medical complications for severe AN, which included anaemia (79%), neutropenia (53.9%), hypertransaminasemia (53.7%), osteoporosis (46.3%), hypokalemia (39.5%), hypophosphatemia (26%), hypoglycaemia (13.8%), infectious complications (24.3%), cardiac dysfunction (7.1%), and proven gelatinous bone marrow transformation (6.5%). Five (1.4%) of the patients in this study died of the following causes: septic shock of pulmonary origin ( n  = 1), septic shock of urinary origin ( n  = 1) and suicide ( n  = 3) [ 145 ].

Suicide is the most common non-natural cause of death in people with AN, BN, BED and EDNOS [ 133 ]. High rates of suicidality were reported in a meta-analysis of 36 studies published between 1966 and 2010 with data showing one in five individuals who died from an ED did so by suicide [ 4 ]. Risk of suicide may be particularly elevated in AN [Hazard Ratio (HR) 5.07; 95% CI 1.37–18.84] and BN (HR 6.07; 95% CI 2.47–14.89) even when specialised treatments are available [ 134 ]: people with AN are 18.1 [11.5–28.7] times more likely to die by suicide than 15–34 year old females in the general population [ 128 ]. This is supported by results from a meta-review exploring risk of all-cause and suicide across major mental disorders. 1.7 million patients and over a quarter of a million deaths were examined, finding all mental health disorders had an increased mortality rate to the general population; however, substance use and AN were the highest, translating into 10–20 year reductions in life expectancy, with borderline personality disorder, AN, depression and bipolar disorder having the highest suicide risk [ 146 ].

This rapid review, which synthesised the available literature on ED remission, relapse and recovery rates including associated moderating and mediating variables such as psychosocial and treatment characteristics, highlighted significant challenges of synthesising outcome literature. This includes a wide variety of ways in which key outcomes ‘remission’, ‘relapse’ and ‘recovery’ are not only defined but also how they are measured and analysed. There is no consensus among clinical or research communities on these definitions for any of the ED diagnoses [ 30 , 31 , 94 ]; thus, comparison between studies is challenging.

As EDs have amongst the highest rates of mortality of the mental health disorders, including one in five deaths caused by suicide, research into preventable causes of death, mitigatable risk, prevention and treatment efficacy is of paramount importance. It is noteworthy that current reported YLL and YLD for ED are likely an underestimate due to lack of robust epidemiological data, methodological limitations of burden of disease studies, absence of the illness group from national surveys and underreporting of mortality [ 147 ].

‘Relapse’ is typically defined by a return of symptoms after a period of reduced symptomatology; however, reviewed studies report a variety of methods to measure this, including multidisciplinary healthcare team assessment, scores on standardised psychological and behavioural interviews or questionnaires, weight criteria (including BMI or %EBW), reported eating disorder behaviours, meeting DSM (IV or V) diagnostic criteria, or a combination of the above. More difficult is determining if there is a difference between ‘remission’ and ‘recovery’, with remission usually determined by an absence of diagnostic symptomatology (again, characterised by a variety of methods), and recovery an improvement in overall functioning. Many studies report remission and recovery interchangeably, and very few incorporate returns to psychosocial functioning and QoL post alleviation of symptoms [ 29 ]. More standardised definitions may progress research [ 148 ] by allowing direct comparison between outcome studies, improving the ability of future investigations to predict and report relapse versus recovery rates and to comprehensively evaluate intervention and relapse prevention approaches.

An additional challenge across studies is a highly variable period between initial assessment or baseline and the time at which ‘outcome’ is assessed—ranging from as little as one week up to 25 years. As rates of relapse increase with illness progression, relatively short FU periods may compromise the understanding of true long-term outcomes. Longer-term FU studies are crucial to understand optimised models of care for sustained recovery and wellbeing.

Along with illness progression over time in individuals, the shift of diagnostic profiles among the individual may differ the definition of relapse or remission and thus impacts on outcome measures. Most research protocols adopt a firm inclusion/exclusion criterion, focusing on specific diagnostic profiles; however, findings from this review suggest considering a transdiagnostic approach in outcomes research which may better reflect the potentially transient nature of ED symptomatology [ 44 ]. This may have implications for diagnoses such as OSFED, potentially a transient category [ 21 ], rather than categorisation in or out of full ED diagnostic syndromes. Identification and consideration of transdiagnostic profiles, combined ED presentations and co-occurring mental health conditions should be considered in the long-term management and monitoring of individuals.

Studies within this review reported on cohorts of individuals with a formal diagnosis and research conducted within treatment settings. However, previous research has suggested that incidence rates within the community are considerable, and yet help-seeking of any type for a problem related to ED symptoms is uncommon, ranging between 22 and 40% [ 106 ] and there can be a significant time delay from first symptom experience [ 69 ]. A recent large community survey of the impact of COVID-19 on people with ED reported up to 70% of people who experienced ED symptoms were not in treatment [ 149 ] suggesting a significant proportion of people with an ED are not captured within this outcome review. Outcomes for this population are largely unknown [ 150 ] but preliminary research suggests they may be less favourable [ 151 , 152 ].

Improved QoL has been shown to be a significant predictor of positive outcome and is an opportunity for broader scope interventions for people with ED [ 107 ], and yet consistent and more wholistic markers of life quality are rarely integrated into research or clinical decision making [ 153 , 154 ]. It is also noted that outcome determinants in the reviewed studies are predominantly biometric (e.g., weight) and ED symptom related, whereas qualitative lived experience evidence suggests a broader range of person-centred metrics should be used to measure outcome. These include supportive relationships (e.g., receiving support, advice and encouragement from others, including family, friends, and/or professional carers), sense of hope, identity, meaning and purpose, feelings of empowerment and self-compassion [ 155 ]. Involvement of those to whom the work pertains (i.e., individuals with lived experience) is essential in future outcomes research to add richness and utility to theoretical frameworks, methodological approaches and conclusions [ 156 ].

Key findings

ED frequently take a chronic course, with less than half of individuals achieving recovery at long-term FU [ 41 , 44 , 52 ]. Between 30 and 41% of people will relapse within two years of receiving treatment [ 35 , 61 ], and between 20 and 61% will experience more than one type of eating disorder [ 7 , 63 , 64 ]. As with much of the extant ED literature, most outcome research has been conducted in AN. Restrictive ED are consistently associated with the poorest prognosis. This review identified recovery rates in the range of 18–60% for AN and an average length of illness of between 6.5 and 14 years [ 41 , 56 ]. Binge/purge symptomatology within AN is associated with worse outcome [ 20 , 56 ]. Recovery rates for BN are slightly more optimistic at 35–59% [ 7 , 45 , 63 , 157 ], and similarly for BED at 37–77% [ 79 , 80 , 82 ]. There is limited data available on outcomes in ARFID, OSFED, and UFED.

Factors associated with a more positive long-term outcome include lower age of presentation [ 28 , 61 ], shorter duration of illness at first presentation [ 69 , 93 , 94 ], higher pre-treatment motivation to recover [ 116 ], and demonstrated early response to treatment [ 18 , 75 , 110 , 112 ]. Factors associated with poorer outcome are lower BMI at presentation [ 93 ], presence of binge/purge symptomatology [ 20 , 30 , 44 , 56 ], and presence of comorbid psychiatric condition/s such as depression, anxiety, or personality disorder [ 44 , 47 , 51 , 55 , 67 , 98 , 99 ]. Males, LGBTQIA + community [ 104 , 105 ], neurodiversity [ 102 ], individuals from non-white/ethnic backgrounds, and those from lower socioeconomic brackets or rural/remote communities are also more likely to experience a poor outcome [ 18 , 72 , 76 , 77 ].

Relapse following ED treatment is common [ 11 , 35 , 36 , 62 , 148 ] and is most likely to occur 4–9 months post discharge [ 35 ]. Up to 41% of individuals will relapse by the second-year post-discharge [ 62 ]. Aftercare relapse prevention programs, including online and face-to-face initiatives such as text-message based interventions, daily feedback to clinicians and intensive day programs have been shown to increase chance of maintaining recovery [ 121 , 123 – 125 ]. The implementation of such programs may be key to improving long-term recovery rates particularly for those individuals who may otherwise disengage from treatment for access reasons (such as living in an underserviced area) or because of the stigma of engaging with mental health care [ 119 , 120 ]. There is emerging evidence in the effectiveness of online intervention for preventing relapse and promoting treatment gains when individuals are motivated to change; however, evidence is not conclusive potentially due to the high variability of the interventions and evaluations of such programs.

ED are associated with unacceptably high mortality rates, and particularly high risk of suicide [ 128 , 133 ]. Of the ED, AN carries the highest mortality risk [ 49 , 127 , 128 ]. Standardised mortality ratios (SMRs) identified by this review ranged between 1.2 and 15.9 for AN; 1.4 and 4.8 for BN; 1.01 and 3.3 for BED; and 1.3 to 4.7 for EDNOS/OSFED [ 2 , 4 , 20 , 121 , 127 , 128 , 132 , 134 , 135 , 137 , 139 ]. Factors associated with increased risk of mortality include having received inpatient treatment [ 3 , 131 , 133 ], longer duration of untreated illness [ 4 , 28 , 68 , 68 , 137 , 139 ] and lower BMI at presentation [ 4 , 49 , 68 , 137 , 139 ]. Males are at higher risk of death than females [ 2 ].

Strengths and limitations

This rapid review has several strengths inherent to the methodological approach of the series, conducted to inform the Australian Eating Disorders Research and Translation Strategy 2021–2031 [ 1 ]. The RR process broadly assessed all available high-level evidence peer-reviewed literature swiftly [ 24 ], included all diagnostic categories covering transdiagnostic continuums, considered the full demographic range available and reported a variety of methodological designs including clinical trials (across a variety of settings), systematic reviews, meta-analyses, and population-level research. It aimed to provide the most comprehensive and current review possible with coordination of complex findings into a more cohesive structure. It was noted where applicable the limitations of conclusions drawn from this review, such as the widely disparate definitions and measurements for key outcome data (i.e., remission, relapse, and recovery rates), crossover from DSM-IV to DSM-V criteria (due to timeframe of search), vastly different periods of follow up impacting findings, and conflicting evidence. As with the series of rapid reviews, the inclusion criteria of evidence may have potentially excluded relevant evidence, and it is noted that evidence is always emerging.

This RR of outcomes in ED identified several gaps in current knowledge and provides direction for future strategic research directives, specifically, defining the key outcomes of remission, recovery, and relapse, with consensus of determinants and inclusion of broader QoL measures and lived experience. Identifying and refining risk factors, mediating and moderating factors that may influence outcomes is ongoing, with longer-term FU research needed to track remission versus relapse, diagnostic crossover and optimisation of treatment engagement and recovery. Regarding mortality literature, this review noted considerable gaps [ 146 ], with variety reporting methods, a paucity of research between population level reporting and small hospital outcome studies, and minimal investigation into life circumstances relating to death, especially as many of these deaths may be preventable. With low rates of remission despite evidence-based care and high risk of mortality, especially for AN, it is strongly recommended that focused, long-term follow-up research is prioritised for people with ED.

Availability of data and materials

Not applicable—all citations provided.

Abbreviations

Atypical anorexia nervosa

Adolescent focused therapy

• Anorexia nervosa

Anorexia nervosa binge/purge subtype

Anorexia nervosa restricting subtype

Avoidant restrictive food intake disorder

• Binge eating disorder

Body mass index

• Bulimia nervosa

Behavioural weight loss therapy

Cognitive behaviour therapy

Enhanced cognitive behavioural therapy

Crude mortality rate

Diagnostic and statistical manual of mental disorders

Expected body weight

• Eating disorders

Eating disorder examination questionnaire

Eating disorder not otherwise specified

Eating disorder not otherwise specified-anorectic type

Eating disorder not otherwise specified-bulimic type

End of treatment

Family-based therapy

Healthcare management advisors

Health related quality of life

Integrative cognitive-affective therapy

InsideOut Institute

Interpersonal therapy

Major depressive disorder

Objective binge eating

Obsessive compulsive disorder

Other specified feeding or eating disorder

Quality of life

Randomised controlled trial

National eating disorder research & translation strategy rapid review

Standardised mortality ratio

Substance use disorder

Treatment as usual

Unspecified feeding or eating disorder

Weighted mortality ratio

Years of life lost

Years lived with a disability

Galmiche M, Déchelotte P, Lambert G, Tavolacci MP. Prevalence of eating disorders over the 2000–2018 period: a systematic literature review. Am J Clin Nutr. 2019;109(5):1402–13.

Article   PubMed   Google Scholar  

Fichter MM, Naab S, Voderholzer U, Quadflieg N. Mortality in males as compared to females treated for an eating disorder: a large prospective controlled study. Eat Weight Disord. 2021;26(5):1627–37.

van Hoeken D, Hoek HW. Review of the burden of eating disorders: mortality, disability, costs, quality of life, and family burden. Curr Opin Psychiatr. 2020;33(6):521–7.

Article   Google Scholar  

Arcelus J, Mitchell AJ, Wales J, Nielsen S. Mortality rates in patients with anorexia nervosa and other eating disorders: a meta-analysis of 36 studies. Arch Gen Psychiatr. 2011;68(7):724.

Bardone-Cone AM, Hunt RA, Watson HJ. An overview of conceptualizations of eating disorder recovery, recent findings, and future directions. Curr Psychiatr Rep. 2018;20(9):79.

Noordenbos G, Seubring A. Criteria for recovery from eating disorders according to patients and therapists. Eat Disord. 2006;14(1):41–54.

Castellini G, Lo Sauro C, Mannucci E, Ravaldi C, Rotella CM, Faravelli C, et al. Diagnostic crossover and outcome predictors in eating disorders according to DSM-IV and DSM-V proposed criteria: a 6-year follow-up study. Psychosom Med. 2011;73(3):270–9.

InsideOut Institute for Eating Disorders. Australian Eating Disorders Research and Translation Strategy 2021–2031. 2021.

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders [Internet]. Fifth Edition. American Psychiatric Association; 2013 [cited 2022 Mar 15]. Available from: https://psychiatryonline.org/doi/book/ https://doi.org/10.1176/appi.books.9780890425596 .

Aouad P, Bryant E, Maloney D, Marks P, Le A, Russell H, et al. Informing the development of Australia’s national eating disorders research and translation strategy: a rapid review methodology. J Eat Disord. 2022;10(1):31.

Article   PubMed   PubMed Central   Google Scholar  

Grilo CM, Pagano ME, Stout RL, Markowitz JC, Ansell EB, Pinto A, et al. Stressful life events predict eating disorder relapse following remission: six-year prospective outcomes. Int J Eat Disord. 2012;45(2):185–92.

Brooks SK, Webster RK, Smith LE, Woodland L, Wessely S, Greenberg N, et al. The psychological impact of quarantine and how to reduce it: rapid review of the evidence. Lancet. 2020;395(10227):912–20.

Canadian Agency for Drugs and Technologies in Health. About the Rapid Response Service [Internet]. [Cited 2021 Jun 19]. Available from: https://www.cadth.ca/about-cadth/what-we-do/products-services/rapid-response-service .

Hamel C, Michaud A, Thuku M, Skidmore B, Stevens A, Nussbaumer-Streit B, et al. Defining rapid reviews: a systematic scoping review and thematic analysis of definitions and defining characteristics of rapid reviews. J Clin Epidemiol. 2021;129:74–85.

Page MJ, Moher D, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. PRISMA 2020 explanation and elaboration: updated guidance and exemplars for reporting systematic reviews. BMJ. 2021;372: n160.

Le Grange D, Hughes EK, Court A, Yeo M, Crosby RD, Sawyer SM. Randomized clinical trial of parent-focused treatment and family-based treatment for adolescent anorexia nervosa. J Am Acad Child Adolesc Psychiatr. 2016;55(8):683–92.

Guarda AS, Cooper M, Pletch A, Laddaran L, Redgrave GW, Schreyer CC. Acceptability and tolerability of a meal-based, rapid refeeding, behavioral weight restoration protocol for anorexia nervosa. Int J Eat Disord. 2020;53(12):2032–7.

Brown TA, Murray SB, Anderson LK, Kaye WH. Early predictors of treatment outcome in a partial hospital program for adolescent anorexia nervosa. Int J Eat Disord. 2020;53(9):1550–5.

Fichter MM, Quadflieg N, Lindner S. Internet-based relapse prevention for anorexia nervosa: nine-month follow-up. J Eat Disord. 2013;1(1):23.

Rigaud D, Pennacchio H, Bizeul C, Reveillard V, Vergès B. Outcome in AN adult patients: a 13-year follow-up in 484 patients. Diabetes Metab. 2011;37(4):305–11.

Agras WS, Crow S, Mitchell JE, Halmi KA, Bryson S. A 4-year prospective study of eating disorder NOS compared with full eating disorder syndromes. Int J Eat Disord. 2009;42(6):565–70.

Linardon J, de la Piedad GX, Brennan L. Predictors, moderators, and mediators of treatment outcome following manualised cognitive-behavioural therapy for eating disorders: a systematic review: predictors, moderators, and mediators of outcome for eating disorders. Eur Eat Disorders Rev. 2017;25(1):3–12.

Bryson AE, Scipioni AM, Essayli JH, Mahoney JR, Ornstein RM. Outcomes of low-weight patients with avoidant/restrictive food intake disorder and anorexia nervosa at long-term follow-up after treatment in a partial hospitalization program for eating disorders. Int J Eat Disord. 2018;51(5):470–4.

Lange CRA, Ekedahl Fjertorp H, Holmer R, Wijk E, Wallin U. Long-term follow-up study of low-weight avoidant restrictive food intake disorder compared with childhood-onset anorexia nervosa: psychiatric and occupational outcome in 56 patients. Int J Eat Disord. 2019;52(4):435–8.

Strandjord SE, Sieke EH, Richmond M, Rome ES. Avoidant/restrictive food intake disorder: Illness and hospital course in patients hospitalized for nutritional insufficiency. J Adolesc Health. 2015;57(6):673–8.

Johnston J, Shu CY, Hoiles KJ, Clarke PJF, Watson HJ, Dunlop PD, et al. Perfectionism is associated with higher eating disorder symptoms and lower remission in children and adolescents diagnosed with eating disorders. Eat Behav. 2018;30:55–60.

Stice E, Marti CN, Rohde P. Prevalence, incidence, impairment, and course of the proposed DSM-5 eating disorder diagnoses in an 8-year prospective community study of young women. J Abnorm Psychol. 2013;122(2):445–57.

Ackard DM, Richter S, Egan A, Cronemeyer C. Poor outcome and death among youth, young adults, and midlife adults with eating disorders: an investigation of risk factors by age at assessment: poor outcome and death. Int J Eat Disord. 2014;47(7):825–35.

Bardone-Cone AM, Harney MB, Maldonado CR, Lawson MA, Robinson DP, Smith R, et al. Defining recovery from an eating disorder: conceptualization, validation, and examination of psychosocial functioning and psychiatric comorbidity. Behav Res Ther. 2010;48(3):194–202.

Le Grange D, Fitzsimmons-Craft EE, Crosby RD, Hay P, Lacey H, Bamford B, et al. Predictors and moderators of outcome for severe and enduring anorexia nervosa. Behav Res Ther. 2014;56:91–8.

Gorrell S, Matheson BE, Lock J, Le Grange D. Remission in adolescents with bulimia nervosa: empirical evaluation of current conceptual models. Eur Eat Disorders Rev. 2020;28(4):445–53.

Keel PK, Dorer DJ, Franko DL, Jackson SC, Herzog DB. Postremission predictors of relapse in women with eating disorders. AJP. 2005;162(12):2263–8.

Stice E, Marti CN, Shaw H, Jaconis M. An 8-year longitudinal study of the natural history of threshold, subthreshold, and partial eating disorders from a community sample of adolescents. J Abnorm Psychol. 2009;118(3):587–97.

Agras WS, Walsh BT, Fairburn CG, Wilson GT, Kraemer HC. A multicenter comparison of cognitive-behavioral therapy and interpersonal psychotherapy for bulimia nervosa. Arch Gen Psychiatr. 2000;57(5):459.

Carter JC, Mercer-Lynn KB, Norwood SJ, Bewell-Weiss CV, Crosby RD, Woodside DB, et al. A prospective study of predictors of relapse in anorexia nervosa: implications for relapse prevention. Psychiatr Res. 2012;200(2–3):518–23.

Berends T, van Meijel B, Nugteren W, Deen M, Danner UN, Hoek HW, et al. Rate, timing and predictors of relapse in patients with anorexia nervosa following a relapse prevention program: a cohort study. BMC Psychiatr. 2016;16(1):316.

Walker DC, Donahue JM, Heiss S, Gorrell S, Anderson LM, Brooks JM, et al. Rapid response is predictive of treatment outcomes in a transdiagnostic intensive outpatient eating disorder sample: a replication of prior research in a real-world setting. Eat Weight Disord. 2021;26(5):1345–56.

Taylor MB, Daiss S, Krietsch K. Associations among self-compassion, mindful eating, eating disorder symptomatology, and body mass index in college students. Transl Issues Psychol Sci. 2015;1(3):229–38.

Custal N, Arcelus J, Agüera Z, Bove FI, Wales J, Granero R, et al. Treatment outcome of patients with comorbid type 1 diabetes and eating disorders. BMC Psychiatr. 2014;14(1):140.

Agüera Z, Riesco N, Jiménez-Murcia S, Islam MA, Granero R, Vicente E, et al. Cognitive behaviour therapy response and dropout rate across purging and nonpurging bulimia nervosa and binge eating disorder: DSM-5 implications. BMC Psychiatr. 2013;13(1):285.

Fernández-Aranda F, Treasure J, Paslakis G, Agüera Z, Giménez M, Granero R, et al. The impact of duration of illness on treatment nonresponse and drop-out: exploring the relevance of enduring eating disorder concept. Eur Eat Disorders Rev. 2021;29(3):499–513.

Colton PA, Olmsted MP, Daneman D, Farquhar JC, Wong H, Muskat S, et al. Eating disorders in girls and women with type 1 diabetes: a longitudinal study of prevalence, onset, remission, and recurrence. Diabetes Care. 2015;38(7):1212–7.

Tomba E, Tecuta L, Schumann R, Ballardini D. Does psychological well-being change following treatment? An exploratory study on outpatients with eating disorders. Compr Psychiatr. 2017;74:61–9.

Helverskov JL, Clausen L, Mors O, Frydenberg M, Thomsen PH, Rokkedal K. Trans-diagnostic outcome of eating disorders: a 30-month follow-up study of 629 patients. Eur Eat Disorders Rev. 2010;18(6):453–63.

Quadflieg N, Fichter MM. Long-term outcome of inpatients with bulimia nervosa—results from the Christina Barz study. Int J Eat Disord. 2019;52(7):834–45.

Carter JC, Stewart DA, Fairburn CG. Eating disorder examination questionnaire: norms for young adolescent girls. Behav Res Ther. 2001;39(5):625–32.

Wade T, Ambwani S, Cardi V, Albano G, Treasure J. Outcomes for adults with anorexia nervosa who do not respond early to outpatient treatment. Int J Eat Disord. 2021;54(7):1278–82.

Mond JM, Hay PJ, Rodgers B, Owen C, Beumont PJV. Validity of the eating disorder examination questionnaire (EDE-Q) in screening for eating disorders in community samples. Behav Res Ther. 2004;42(5):551–67.

Franko DL, Keshaviah A, Eddy KT, Krishna M, Davis MC, Keel PK, et al. A longitudinal investigation of mortality in anorexia nervosa and bulimia nervosa. AJP. 2013;170(8):917–25.

Eddy KT, Tabri N, Thomas JJ, Murray HB, Keshaviah A, Hastings E, et al. Recovery from anorexia nervosa and bulimia nervosa at 22-year follow-up. J Clin Psychiatr. 2017;78(02):184–9.

Lydecker JA, Grilo CM. Psychiatric comorbidity as predictor and moderator of binge-eating disorder treatment outcomes: an analysis of aggregated randomized controlled trials. Psychol Med. 2021;52(16):4085–93.

Eielsen HP, Vrabel K, Hoffart A, Rø Ø, Rosenvinge JH. The 17-year outcome of 62 adult patients with longstanding eating disorders—a prospective study. Int J Eat Disord. 2021;54(5):841–50.

Dare C, Eisler I, Russell G, Treasure J, Dodge L. Psychological therapies for adults with anorexia nervosa: randomised controlled trial of out-patient treatments. Br J Psychiatr. 2001;178(3):216–21.

Kordy H, Krämer B, Palmer RL, Papezova H, Pellet J, Richard M, et al. Remission, recovery, relapse, and recurrence in eating disorders: conceptualization and illustration of a validation strategy. J Clin Psychol. 2002;58(7):833–46.

Wild B, Friederich HC, Zipfel S, Resmark G, Giel K, Teufel M, et al. Predictors of outcomes in outpatients with anorexia nervosa—results from the ANTOP study. Psychiatr Res. 2016;244:45–50.

Zerwas S, Lund BC, Von Holle A, Thornton LM, Berrettini WH, Brandt H, et al. Factors associated with recovery from anorexia nervosa. J Psychiatr Res. 2013;47(7):972–9.

Ricca V, Castellini G, Lo Sauro C, Mannucci E, Ravaldi C, Rotella F, et al. Cognitive-behavioral therapy for threshold and subthreshold anorexia nervosa: a three-year follow-up study. Psychother Psychosom. 2010;79(4):238–48.

Winkler LAD, Bilenberg N, Hørder K, Støving RK. Does specialization of treatment influence mortality in eating disorders?—A comparison of two retrospective cohorts. Psychiatr Res. 2015;230(2):165–71.

Wentz E, Gillberg IC, Anckarsäter H, Gillberg C, Råstam M. Adolescent-onset anorexia nervosa: 18-year outcome. Br J Psychiatr. 2009;194(2):168–74.

Castellini G, Mannucci E, Lo Sauro C, Benni L, Lazzeretti L, Ravaldi C, et al. Different moderators of cognitive-behavioral therapy on subjective and objective binge eating in bulimia nervosa and binge eating disorder: a three-year follow-up study. Psychother Psychosom. 2012;81(1):11–20.

Franko DL, Tabri N, Keshaviah A, Murray HB, Herzog DB, Thomas JJ, et al. Predictors of long-term recovery in anorexia nervosa and bulimia nervosa: data from a 22-year longitudinal study. J Psychiatr Res. 2018;96:183–8.

Berends T, Boonstra N, van Elburg A. Relapse in anorexia nervosa: a systematic review and meta-analysis. Curr Opin Psychiatr. 2018;31(6):445–55.

Steinhausen HC, Weber S. The outcome of bulimia nervosa: findings from one-quarter century of research. AJP. 2009;166(12):1331–41.

Glazer KB, Sonneville KR, Micali N, Swanson SA, Crosby R, Horton NJ, et al. The course of eating disorders involving bingeing and purging among adolescent girls: prevalence, stability, and transitions. J Adolesc Health. 2019;64(2):165–71.

Goldstein M, Peters L, Baillie A, McVeagh P, Minshall G, Fitzjames D. The effectiveness of a day program for the treatment of adolescent anorexia nervosa. Int J Eat Disord. 2011;44(1):29–38.

Herpertz-Dahlmann B, Dempfle A, Egberts KM, Kappel V, Konrad K, Vloet JA, et al. Outcome of childhood anorexia nervosa-the results of a five- to ten-year follow-up study. Int J Eat Disord. 2018;51(4):295–304.

Amianto F, Spalatro A, Ottone L, Abbate Daga G, Fassino S. Naturalistic follow-up of subjects affected with anorexia nervosa 8 years after multimodal treatment: personality and psychopathology changes and predictors of outcome. Eur psychiatr. 2017;45:198–206.

Huas C, Caille A, Godart N, Foulon C, Pham-Scottez A, Divac S, et al. Factors predictive of ten-year mortality in severe anorexia nervosa patients: mortality in severe anorexia nervosa patients. Acta Psychiatr Scand. 2011;123(1):62–70.

Austin A, Flynn M, Richards K, Hodsoll J, Duarte TA, Robinson P, et al. Duration of untreated eating disorder and relationship to outcomes: a systematic review of the literature. Eur Eat Disorders Rev. 2021;29(3):329–45.

Dechartres A, Huas C, Godart N, Pousset M, Pham A, Divac SM, Rouillon F, Falissard B. Outcomes of empirical eating disorder phenotypes in a clinical female sample: results from a latent class analysis. Psychopathology. 2011;44:12–20.

Ando T, Komaki G, Nishimura H, Naruo T, Okabe K, Kawai K, et al. A ghrelin gene variant may predict crossover rate from restricting-type anorexia nervosa to other phenotypes of eating disorders: a retrospective survival analysis. Psychiatr Genet. 2010;20(4):153–9.

Castellini G, Ricca V, Lelli L, Bagnoli S, Lucenteforte E, Faravelli C, et al. Association between serotonin transporter gene polymorphism and eating disorders outcome: a 6-year follow-up study. Am J Med Genet. 2012;159B(5):491–500.

Linardon J. Rates of abstinence following psychological or behavioral treatments for binge-eating disorder: meta-analysis. Int J Eat Disord. 2018;51(8):785–97.

Dalle Grave R, Calugi S, Marchesini G. Self-induced vomiting in eating disorders: associated features and treatment outcome. Behav Res Ther. 2009;47(8):680–4.

Accurso EC, Wonderlich SA, Crosby RD, Smith TL, Klein MH, Mitchell JE, et al. Predictors and moderators of treatment outcome in a randomized clinical trial for adults with symptoms of bulimia nervosa. J Consult Clin Psychol. 2016;84(2):178–84.

Keski-Rahkonen A. Epidemiology of binge eating disorder: prevalence, course, comorbidity, and risk factors. Curr Opin Psychiatr. 2021;34(6):525–31.

Hilbert A, Petroff D, Herpertz S, Pietrowsky R, Tuschen-Caffier B, Vocks S, et al. Meta-analysis on the long-term effectiveness of psychological and medical treatments for binge-eating disorder. Int J Eat Disord. 2020;53(9):1353–76.

Rodan S, Bryant E, Le A, Maloney D, National Eating Disorders Collaboration, Touyz S, et al. Pharmacotherapy, adjunctive and alternative therapies: findings from a rapid review. J Eat Disord. (Under Review).

Fischer S, Meyer AH, Dremmel D, Schlup B, Munsch S. Short-term cognitive-behavioral therapy for binge eating disorder: long-term efficacy and predictors of long-term treatment success. Behav Res Ther. 2014;58:36–42.

Hilbert A, Bishop ME, Stein RI, Tanofsky-Kraff M, Swenson AK, Welch RR, et al. Long-term efficacy of psychological treatments for binge eating disorder. Br J Psychiatr. 2012;200(3):232–7.

Villarejo C, Fernández-Aranda F, Jiménez-Murcia S, Peñas-Lledó E, Granero R, Penelo E, et al. Lifetime obesity in patients with eating disorders: increasing prevalence, clinical and personality correlates. Eur Eat Disorders Rev. 2012;20(3):250–4.

Munsch S, Meyer AH, Biedert E. Efficacy and predictors of long-term treatment success for cognitive-behavioral treatment and behavioral weight-loss-treatment in overweight individuals with binge eating disorder. Behav Res Ther. 2012;50(12):775–85.

Opolski M, Chur-Hansen A, Wittert G. The eating-related behaviours, disorders and expectations of candidates for bariatric surgery: eating in bariatric surgery candidates. Clin Obes. 2015;5(4):165–97.

Opozda M, Chur-Hansen A, Wittert G. Changes in problematic and disordered eating after gastric bypass, adjustable gastric banding and vertical sleeve gastrectomy: a systematic review of pre-post studies: problematic/disordered eating in bariatric surgeries. Obes Rev. 2016;17(8):770–92.

Genco A, Maselli R, Frangella F, Cipriano M, Paone E, Meuti V, et al. Effect of consecutive intragastric balloon (BIB®) plus diet versus single BIB® plus diet on eating disorders not otherwise specified (EDNOS) in obese patients. Obes Surg. 2013;23(12):2075–9.

Ferreira Pinto T, Carvalhedo de Bruin PF, Sales de Bruin VM, Ney Lemos F, Azevedo Lopes FH, Marcos Lopes P. Effects of bariatric surgery on night eating and depressive symptoms: a prospective study. Surg Obes Relat Dis. 2017;13(6):1057–62.

Wadden TA, Faulconbridge LF, Jones-Corneille LR, Sarwer DB, Fabricatore AN, Thomas JG, et al. Binge eating disorder and the outcome of bariatric surgery at one year: a prospective, observational study. Obesity. 2011;19(6):1220–8.

Calugi S, Ruocco A, El Ghoch M, Andrea C, Geccherle E, Sartori F, et al. Residential cognitive-behavioral weight-loss intervention for obesity with and without binge-eating disorder: a prospective case-control study with five-year follow-up: treatment for obesity with binge-eating disorder. Int J Eat Disord. 2016;49(7):723–30.

Mason TB, Crosby RD, Kolotkin RL, Grilo CM, Mitchell JE, Wonderlich SA, et al. Correlates of weight-related quality of life among individuals with binge eating disorder before and after cognitive behavioral therapy. Eat Behav. 2017;27:1–6.

Paul L, van Rongen S, van Hoeken D, Deen M, Klaassen R, Biter LU, et al. Does cognitive behavioral therapy strengthen the effect of bariatric surgery for obesity? Design and methods of a randomized and controlled study. Contemp Clin Trials. 2015;42:252–6.

Tasca GA, Maxwell H, Bone M, Trinneer A, Balfour L, Bissada H. Purging disorder: psychopathology and treatment outcomes. Int J Eat Disord. 2012;45(1):36–42.

Allen KL, Byrne SM, Oddy WH, Crosby RD. Early onset binge eating and purging eating disorders: course and outcome in a population-based study of adolescents. J Abnorm Child Psychol. 2013;41(7):1083–96.

Glasofer DR, Muratore AF, Attia E, Wu P, Wang Y, Minkoff H, et al. Predictors of illness course and health maintenance following inpatient treatment among patients with anorexia nervosa. J Eat Disord. 2020;8(1):69.

Radunz M, Keegan E, Osenk I, Wade TD. Relationship between eating disorder duration and treatment outcome: systematic review and meta-analysis. Int J Eat Disord. 2020;53(11):1761–73.

Li A, Cunich M, Miskovic-Wheatley J, Maloney D, Madden S, Wallis A, et al. Factors related to length of stay, referral on discharge and hospital readmission for children and adolescents with anorexia nervosa. Int J Eat Disord. 2021;54(3):409–21.

Bluett EJ, Lee EB, Simone M, Lockhart G, Twohig MP, Lensegrav-Benson T, et al. The role of body image psychological flexibility on the treatment of eating disorders in a residential facility. Eat Behav. 2016;23:150–5.

Wade TD, Hart LM, Mitchison D, Hay P. Driving better intervention outcomes in eating disorders: a systematic synthesis of research priority setting and the involvement of consumer input. Eur Eat Disorders Rev. 2021;29(3):346–54.

Keshishian AC, Tabri N, Becker KR, Franko DL, Herzog DB, Thomas JJ, et al. Eating disorder recovery is associated with absence of major depressive disorder and substance use disorders at 22-year longitudinal follow-up. Compr Psychiatr. 2019;90:49–51.

O’Brien KM, Whelan DR, Sandler DP, Hall JE, Weinberg CR. Predictors and long-term health outcomes of eating disorders. PLoS ONE. 2017;12(7):e0181104.

Micali N, Solmi F, Horton NJ, Crosby RD, Eddy KT, Calzo JP, et al. Adolescent eating disorders predict psychiatric, high-risk behaviors and weight outcomes in young adulthood. J Am Acad Child Adolesc Psychiatry. 2015;54(8):652-659.e1.

La Mela C, Maglietta M, Lucarelli S, Mori S, Sassaroli S. Pretreatment outcome indicators in an eating disorder outpatient group: the effects of self-esteem, personality disorders and dissociation. Compr Psychiatr. 2013;54(7):933–42.

Li Z, Halls D, Byford S, Tchanturia K. Autistic characteristics in eating disorders: treatment adaptations and impact on clinical outcomes. Euro Eat Disord Rev. 2022;30(5):671–90.

Bye A, Martini MG, Micali N. Eating disorders, pregnancy and the postnatal period: a review of the recent literature. Curr Opin Psychiatr. 2021;34(6):563–8.

Sollid C, Clausen L, Maimburg RD. The first 20 weeks of pregnancy is a high-risk period for eating disorder relapse. Intl J Eat Disord. 2021;54(12):2132–42.

Grammer AC, Vázquez MM, Fitzsimmons-Craft EE, Fowler LA, Rackoff GN, Schvey NA, et al. Characterizing eating disorder diagnosis and related outcomes by sexual orientation and gender identity in a national sample of college students. Eat Behav. 2021;42: 101528.

Hay PJ, Buettner P, Mond J, Paxton SJ, Quirk F, Rodgers B. A community-based study of enduring eating features in young women. Nutrients. 2012;4(5):413–24.

Winkler LA. Funen anorexia nervosa study—a follow-up study on outcome, mortality, quality of life and body composition. Danish Med J. 2017;64(6):B5380.

Google Scholar  

Le Grange D, Lock J, Accurso EC, Agras WS, Darcy A, Forsberg S, et al. Relapse from remission at two- to four-year follow-up in two treatments for adolescent anorexia nervosa. J Am Acad Child Adolesc Psychiatr. 2014;53(11):1162–7.

Austin A, Flynn M, Shearer J, Long M, Allen K, Mountford VA, et al. The first episode rapid early intervention for eating disorders-upscaled study: clinical outcomes. Early Interv Psychiatr. 2022;16(1):97–105.

Chang PGRY, Delgadillo J, Waller G. Early response to psychological treatment for eating disorders: a systematic review and meta-analysis. Clin Psychol Rev. 2021;86: 102032.

Støving RK, Larsen PV, Winkler LA, Bilenberg N, Røder ME, Steinhausen H. Time trends in treatment modes of anorexia nervosa in a nationwide cohort with free and equal access to treatment. Int J Eat Disord. 2020;53(12):1952–9.

McClelland J, Simic M, Schmidt U, Koskina A, Stewart C. Defining and predicting service utilisation in young adulthood following childhood treatment of an eating disorder. BJPsych open. 2020;6(3): e37.

Golden NH, Cheng J, Kapphahn CJ, Buckelew SM, Machen VI, Kreiter A, et al. Higher-calorie refeeding in anorexia nervosa: 1-year outcomes from a randomized controlled trial. Pediatrics. 2021;147(4): e2020037135.

Baudinet J, Simic M. Adolescent eating disorder day programme treatment models and outcomes: a systematic scoping review. Front Psychiatr. 2021;12: 652604.

Thompson-Brenner H, Singh S, Gardner T, Brooks GE, Smith M, Lowe M, et al. The Renfrew unified treatment for eating disorders and comorbidity: long-term effects of an evidence-based practice implementation in residential treatment. Front Psychiatr. 2021;12:641601.

Kästner D, Löwe B, Gumz A. The role of self-esteem in the treatment of patients with anorexia nervosa—a systematic review and meta-analysis. Int J Eat Disord. 2019;52(2):101–16.

Kelly AC, Vimalakanthan K, Carter JC. Understanding the roles of self-esteem, self-compassion, and fear of self-compassion in eating disorder pathology: an examination of female students and eating disorder patients. Eat Behav. 2014;15(3):388–91.

Sansfaçon J, Booij L, Gauvin L, Fletcher É, Islam F, Israël M, et al. Pretreatment motivation and therapy outcomes in eating disorders: a systematic review and meta-analysis. Int J Eat Disord. 2020;53(12):1879–900.

Griffiths S, Mond JM, Li Z, Gunatilake S, Murray SB, Sheffield J, et al. Self-stigma of seeking treatment and being male predict an increased likelihood of having an undiagnosed eating disorder: predicting undiagnosed eating disorders. Int J Eat Disord. 2015;48(6):775–8.

Foran A, O’Donnell AT, Muldoon OT. Stigma of eating disorders and recovery-related outcomes: a systematic review. Eur Eat Disord Rev. 2020;28(4):385–97.

Fichter MM, Quadflieg N, Nisslmüller K, Lindner S, Osen B, Huber T, et al. Does internet-based prevention reduce the risk of relapse for anorexia nervosa? Behav Res Ther. 2012;50(3):180–90.

Jacobi C, Beintner I, Fittig E, Trockel M, Braks K, Schade-Brittinger C, et al. Web-based aftercare for women with bulimia nervosa following inpatient treatment: randomized controlled efficacy trial. J Med Internet Res. 2017;19(9): e321.

Gulec H, Moessner M, Túry F, Fiedler P, Mezei A, Bauer S. A randomized controlled trial of an internet-based posttreatment care for patients with eating disorders. Telemed e-Health. 2014;20(10):916–22.

Shapiro J, Bauer S, Andrews E, Pisetsky E, Bulik-Sullivan B, Hamer R, et al. Mobile therapy: use of text-messaging in the treatment of bulimia nervosa. Int J Eat Disord. 2010;43(6):513–9.

Bauer S, Okon E, Meermann R, Kordy H. Technology-enhanced maintenance of treatment gains in eating disorders: efficacy of an intervention delivered via text messaging. J Consult Clin Psychol. 2012;80(4):700–6.

Anastasiadou D, Folkvord F, Lupiañez-Villanueva F. A systematic review of mHealth interventions for the support of eating disorders. Eur Eat Disord Rev. 2018;26(5):394–416.

Button EJ, Chadalavada B, Palmer RL. Mortality and predictors of death in a cohort of patients presenting to an eating disorders service. Int J Eat Disord. 2010;43(5):387–92.

PubMed   Google Scholar  

Keshaviah A, Edkins K, Hastings ER, Krishna M, Franko DL, Herzog DB, et al. Re-examining premature mortality in anorexia nervosa: a meta-analysis redux. Compr Psychiatr. 2014;55(8):1773–84.

Ward ZJ, Rodriguez P, Wright DR, Austin SB, Long MW. Estimation of eating disorders prevalence by age and associations with mortality in a simulated nationally representative US cohort. JAMA Netw Open. 2019;2(10): e1912925.

Nielsen S, Vilmar JW. What can we learn about eating disorder mortality from eating disorder diagnoses at initial assessment? A Danish nationwide register follow-up study using record linkage, encompassing 45 years (1970–2014). Psychiatr Res. 2021;303: 114091.

Iwajomo T, Bondy SJ, de Oliveira C, Colton P, Trottier K, Kurdyak P. Excess mortality associated with eating disorders: population-based cohort study. Br J Psychiatr. 2021;219(3):487–93.

Hoang U, Goldacre M, James A. Mortality following hospital discharge with a diagnosis of eating disorder: national record linkage study, England, 2001–2009: mortality following a diagnosis of eating disorder. Int J Eat Disord. 2014;47(5):507–15.

Fichter MM, Quadflieg N. Mortality in eating disorders—results of a large prospective clinical longitudinal study: mortality in eating disorders. Int J Eat Disord. 2016;49(4):391–401.

Suokas JT, Suvisaari JM, Gissler M, Löfman R, Linna MS, Raevuori A, et al. Mortality in eating disorders: a follow-up study of adult eating disorder patients treated in tertiary care, 1995–2010. Psychiatr Res. 2013;210(3):1101–6.

Crow SJ, Peterson CB, Swanson SA, Raymond NC, Specker S, Eckert ED, et al. Increased mortality in bulimia nervosa and other eating disorders. AJP. 2009;166(12):1342–6.

Castellini G, Caini S, Cassioli E, Rossi E, Marchesoni G, Rotella F, et al. Mortality and care of eating disorders. Acta Psychiatr Scand. 2023;147(2):122–33.

Guinhut M, Godart N, Benadjaoud M, Melchior J, Hanachi M. Five-year mortality of severely malnourished patients with chronic anorexia nervosa admitted to a medical unit. Acta Psychiatr Scand. 2021;143(2):130–40.

Quadflieg N, Strobel C, Naab S, Voderholzer U, Fichter MM. Mortality in males treated for an eating disorder—a large prospective study. Int J Eat Disord. 2019;52(12):1365–9.

Rosling AM, Sparén P, Norring C, von Knorring AL. Mortality of eating disorders: a follow-up study of treatment in a specialist unit 1974–2000. Int J Eat Disord. 2011;44(4):304–10.

Crow SJ, Swanson SA, le Grange D, Feig EH, Merikangas KR. Suicidal behavior in adolescents and adults with bulimia nervosa. Compr Psychiatr. 2014;55(7):1534–9.

Zerwas S, Larsen JT, Petersen L, Thornton LM, Mortensen PB, Bulik CM. The incidence of eating disorders in a Danish register study: associations with suicide risk and mortality. J Psychiatr Res. 2015;65:16–22.

Mellentin AI, Mejldal A, Guala MM, Støving RK, Eriksen LS, Stenager E, et al. The impact of alcohol and other substance use disorders on mortality in patients with eating disorders: a nationwide register-based retrospective cohort study. AJP. 2021;179(1):46–57.

Naghavi M, Abajobir AA, Abbafati C, Abbas KM, Abd-Allah F, Abera SF, et al. Global, regional, and national age-sex specific mortality for 264 causes of death, 1980–2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet. 2017;390(10100):1151–210.

Santomauro DF, Melen S, Mitchison D, Vos T, Whiteford H, Ferrari AJ. The hidden burden of eating disorders: an extension of estimates from the Global Burden of Disease Study 2019. Lancet Psychiatr. 2021;8(4):320–8.

Guinhut M, Melchior JC, Godart N, Hanachi M. Extremely severe anorexia nervosa: hospital course of 354 adult patients in a clinical nutrition-eating disorders-unit. Clin Nutr. 2021;40(4):1954–65.

Chesney E, Goodwin GM, Fazel S. Risks of all-cause and suicide mortality in mental disorders: a meta-review. World Psychiatr. 2014;13(2):153–60.

Bryant E, Koemel N, Martenstyn J, Marks P, Hickie I, Maguire S. Mortality and mental health funding—when the dollars don’t add up: a portfolio analysis of eating disorder research funding in Australia 2009–2021. Lancet Regional Health (Western Pacific).

Khalsa SS, Portnoff LC, McCurdy-McKinnon D, Feusner JD. What happens after treatment? A systematic review of relapse, remission, and recovery in anorexia nervosa. J Eat Disord. 2017;5(1):20.

Miskovic-Wheatley J, Koreshe E, Kim M, Simeone R, Maguire S. The impact of the COVID-19 pandemic and associated public health response on people with eating disorder symptomatology: an Australian study. J Eat Disord. 2022;10(1):9.

Smink FRE, van Hoeken D, Hoek HW. Epidemiology, course, and outcome of eating disorders. Curr Opin Psychiatr. 2013;26(6):543–8.

Vinchenzo C, McCombie C, Lawrence V. The experience of patient dropout from eating disorders treatment: a systematic review and qualitative synthesis. BJPsych open. 2021;7(S1):S299–S299.

Article   PubMed Central   Google Scholar  

Björk T, Björck C, Clinton D, Sohlberg S, Norring C. What happened to the ones who dropped out? Outcome in eating disorder patients who complete or prematurely terminate treatment. Eur Eat Disorders Rev. 2009;17(2):109–19.

Jenkins PE, Hoste RR, Meyer C, Blissett JM. Eating disorders and quality of life: a review of the literature. Clin Psychol Rev. 2011;31(1):113–21.

Calvete E, Las Hayas C, Gómezdel Barrio A. Longitudinal associations between resilience and quality of life in eating disorders. Psychiatr Res. 2018;259:470–5.

Wetzler S, Hackmann C, Peryer G, Clayman K, Friedman D, Saffran K, et al. A framework to conceptualize personal recovery from eating disorders: a systematic review and qualitative meta-synthesis of perspectives from individuals with lived experience. Int J Eat Disord. 2020;53(8):1188–203.

Musić S, Elwyn R, Fountas G, Gnatt I, Jenkins ZM, Malcolm A, et al. Valuing the voice of lived experience of eating disorders in the research process: benefits and considerations. Aust N Z J Psychiatr. 2022;56(3):216–8.

Linardon J, Wade TD. How many individuals achieve symptom abstinence following psychological treatments for bulimia nervosa? A meta-analytic review. Int J Eat Disord. 2018;51(4):287–94.

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Acknowledgements

The InsideOut Institute is a collaboration between the University of Sydney and Sydney Local Health District. We thank all the staff from the Institution for their support of this significant project. The authors would like to thank and acknowledge the hard work of Healthcare Management Advisors (HMA) who were commissioned to undertake the Rapid Review. Additionally, the authors would like to thank all members of the consortium and consultation committees for their advice, input, and considerations during the development process. Further, a special thank you to the carers, consumers and lived experience consultants that provided input to the development of the Rapid Review and wider national Eating Disorders Research & Translation Strategy. Finally, thank you to the Australian Government—Department of Health for their support of the current project. National Eating Disorder Research Consortium Members (alphabetical order of surname): *indicates named authors. Phillip Aouad InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Sarah Barakat InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Robert Boakes School of Psychology, Faculty of Science, University of Sydney, NSW Australia. Leah Brennan School of Psychology and Public Health, La Trobe University, Victoria, Australia. Emma Bryant* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Susan Byrne School of Psychology, Western Australia, Perth, Australia. Belinda Caldwell Eating Disorders Victoria, Victoria, Australia. Shannon Calvert Perth, Western Australia, Australia. Bronny Carroll InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. David Castle Medicine, Dentistry and Health Sciences, University of Melbourne, Victoria, Australia. Ian Caterson School of Life and Environmental Sciences, University of Sydney, Sydney, New South Wales, Australia. Belinda Chelius Eating Disorders Queensland, Brisbane, Queensland, Australia. Lyn Chiem Sydney Local Health District, New South Wales Health, Sydney, Australia. Simon Clarke Westmead Hospital, Sydney, New South Wales, Australia. Janet Conti Translational Health Research Institute, Western Sydney University, Sydney NSW Australia. Lexi Crouch Brisbane, Queensland, Australia. Genevieve Dammery InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Natasha Dzajkovski InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Jasmine Fardouly School of Psychology, University of New South Wales, Sydney, New South Wales, Australia. John Feneley New South Wales Health, New South Wales, Australia. Amber-Marie Firriolo University of Sydney, NSW Australia. Nasim Foroughi Translational Health Research Institute, Western Sydney University, Sydney NSW Australia. Mathew Fuller-Tyszkiewicz School of Psychology, Faculty of Health, Deakin University, Victoria, Australia. Anthea Fursland School of Population Health, Faculty of Health Sciences, Curtain University, Perth, Australia. Veronica Gonzalez-Arce InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Bethanie Gouldthorp Hollywood Clinic, Ramsay Health Care, Perth, Australia. Kelly Griffin InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Scott Griffiths Melbourne School of Psychological Sciences, University of Melbourne, Victoria, Australia. Ashlea Hambleton InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Amy Hannigan Queensland Eating Disorder Service, Brisbane, Queensland, Australia. Mel Hart Hunter New England Local Health District, New South Wales, Australia. Susan Hart St Vincent’s Hospital Network Local Health District, Sydney, New South Wales, Australia. Phillipa Hay Translational Health Research Institute, Western Sydney University, Sydney NSW Australia. Ian Hickie Brain and Mind Centre, University of Sydney, Sydney, Australia. Francis Kay-Lambkin School of Medicine and Public Health, University of Newcastle, New South Wales, Australia. Ross King School of Psychology, Faculty of Health, Deakin University, Victoria, Australia. Michael Kohn Paediatrics & Child Health, Children's Hospital, Westmead, Sydney, Australia. Eyza Koreshe InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Isabel Krug Melbourne School of Psychological Sciences, University of Melbourne, Victoria, Australia. Jake Linardon School of Psychology, Faculty of Health, Deakin University, Victoria, Australia. Randall Long College of Medicine and Public Health, Flinders University, South Australia, Australia. Amanda Long Exchange Consultancy, Redlynch, New South Wales, Australia. Sloane Madden Eating Disorders Service, Children’s Hospital at Westmead, Sydney, New South Wales, Australia. Sarah Maguire* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Danielle Maloney InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Peta Marks InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Sian McLean The Bouverie Centre, School of Psychology and Public Health, La Trobe University, Victoria, Australia. Thy Meddick Clinical Excellence Queensland, Mental Health Alcohol and Other Drugs Branch, Brisbane, Queensland, Australia. Jane Miskovic-Wheatley* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Deborah Mitchison Translational Health Research Institute, Western Sydney University, Sydney NSW Australia. Richard O’Kearney College of Health & Medicine, Australian National University, Australian Capital Territory, Australia. Shu Hwa Ong* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Roger Paterson ADHD and BED Integrated Clinic, Melbourne, Victoria, Australia. Susan Paxton La Trobe University, Department of Psychology and Counselling, Victoria, Australia. Melissa Pehlivan InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Genevieve Pepin School of Health & Social Development, Faculty of Health, Deakin University, Geelong, Victoria, Australia. Andrea Phillipou Swinburne Anorexia Nervosa (SWAN) Research Group, Centre for Mental Health, School of Health Sciences, Swinburne University, Victoria, Australia. Judith Piccone Children's Health Queensland Hospital and Health Service, Brisbane, Queensland, Australia. Rebecca Pinkus School of Psychology, Faculty of Science, University of Sydney, NSW Australia. Bronwyn Raykos Centre for Clinical Interventions, Western Australia Health, Perth, Western Australia, Australia. Paul Rhodes School of Psychology, Faculty of Science, University of Sydney, NSW Australia. Elizabeth Rieger College of Health & Medicine, Australian National University, Australian Capital Territory, Australia. Karen Rockett New South Wales Health, New South Wales, Australia. Sarah-Catherine Rodan InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Janice Russell Central Clinical School Brain & Mind Research Institute, University of Sydney, New South Wales, Sydney. Haley Russell InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Fiona Salter Ramsay Health Care, Perth, Australia. Susan Sawyer Department of Paediatrics, The University of Melbourne, Australia. Beth Shelton National Eating Disorders Collaboration, Victoria, Australia. Urvashnee Singh The Hollywood Clinic Hollywood Private Hospital, Ramsey Health, Perth, Australia. Sophie Smith Sydney, New South Wales, Australia. Evelyn Smith Translational Health Research Institute, Western Sydney University, Sydney NSW Australia. Karen Spielman InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Sarah Squire The Butterfly Foundation, Sydney, Australia. Juliette Thomson The Butterfly Foundation, Sydney, Australia. Stephen Touyz* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Ranjani Utpala The Butterfly Foundation, Sydney, Australia. Lenny Vartanian School of Psychology, University of New South Wales, Sydney, New South Wales, Australia. Sabina Vatter* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Andrew Wallis Eating Disorder Service, The Sydney Children’s Hospital Network, Westmead Campus, Sydney, Australia. Warren Ward Department of Psychiatry, University of Queensland, Brisbane, Australia. Sarah Wells University of Tasmania, Tasmania, Australia. Eleanor Wertheim School of Psychology and Public Health, La Trobe University, Victoria, Australia. Simon Wilksch College of Education, Psychology and Social Work, Flinders University, South Australia, Australia. Michelle Williams Royal Hobart, Tasmanian Health Service, Tasmania, Australia.

The RR was in-part funded by the Australian Government Department of Health in partnership with other national and jurisdictional stakeholders. As the organisation responsible for overseeing the National Eating Disorder Research & Translation Strategy, InsideOut Institute commissioned Healthcare Management Advisors to undertake the RR as part of a larger, ongoing, project. Role of Funder: The funder was not directly involved in informing the development of the current review.

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Faculty of Medicine and Health, InsideOut Institute for Eating Disorders, University of Sydney, Level 2, Charles Perkins Centre (D17), Sydney, NSW, 2006, Australia

Jane Miskovic-Wheatley, Emma Bryant, Shu Hwa Ong, Sabina Vatter, Phillip Aouad, Sarah Barakat, Emma Bryant, Bronny Carroll, Genevieve Dammery, Natasha Dzajkovski, Veronica Gonzalez-Arce, Kelly Griffin, Ashlea Hambleton, Eyza Koreshe, Sarah Maguire, Danielle Maloney, Peta Marks, Jane Miskovic-Wheatley, Shu Hwa Ong, Melissa Pehlivan, Sarah-Catherine Rodan, Haley Russell, Karen Spielman, Stephen Touyz, Sabina Vatter, Stephen Touyz & Sarah Maguire

Sydney Local Health District, Sydney, Australia

Healthcare Management Advisors, Melbourne, Australia

School of Psychology, Faculty of Science, University of Sydney, Sydney, NSW, Australia

Robert Boakes, Rebecca Pinkus & Paul Rhodes

School of Psychology and Public Health, La Trobe University, Victoria, Australia

Leah Brennan & Eleanor Wertheim

School of Psychology, Perth, Western Australia, Australia

Susan Byrne

Eating Disorders Victoria, Victoria, Australia

Belinda Caldwell

Perth, Australia

Shannon Calvert

Medicine, Dentistry and Health Sciences, University of Melbourne, Victoria, Australia

David Castle

School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, Australia

Ian Caterson

Eating Disorders Queensland, Brisbane, QLD, Australia

Belinda Chelius

Sydney Local Health District, New South Wales Health, Sydney, Australia

Westmead Hospital, Sydney, NSW, Australia

Simon Clarke

Translational Health Research Institute, Western Sydney University, Sydney, NSW, Australia

Janet Conti, Nasim Foroughi, Phillipa Hay, Deborah Mitchison & Evelyn Smith

Brisbane, Australia

Lexi Crouch

School of Psychology, University of New South Wales, Sydney, NSW, Australia

Jasmine Fardouly & Lenny Vartanian

University of Sydney, Sydney, NSW, Australia

Carmen Felicia & Amber-Marie Firriolo

New South Wales Health, Sydney, NSW, Australia

John Feneley & Karen Rockett

School of Psychology, Faculty of Health, Deakin University, Victoria, Australia

Mathew Fuller-Tyszkiewicz & Ross King

School of Population Health, Faculty of Health Sciences, Curtain University, Perth, Australia

Anthea Fursland

Hollywood Clinic, Ramsay Health Care, Perth, Australia

Bethanie Gouldthorp & Jake Linardon

Melbourne School of Psychological Sciences, University of Melbourne, Victoria, Australia

Scott Griffiths & Isabel Krug

Queensland Eating Disorder Service, Brisbane, QLD, Australia

Amy Hannigan

Hunter New England Local Health District, New Lambton, NSW, Australia

St Vincent’s Hospital Network Local Health District, Sydney, NSW, Australia

Brain and Mind Centre, University of Sydney, Sydney, Australia

School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia

Francis Kay-Lambkin

Westmead Hospital, Sydney, Australia

Michael Kohn

College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia

Randall Long

Exchange Consultancy, Redlynch, NSW, Australia

Amanda Long

Eating Disorders Service, Children’s Hospital at Westmead, Sydney, NSW, Australia

Sloane Madden

The Bouverie Centre, School of Psychology and Public Health, La Trobe University, Victoria, Australia

Sian McLean

Clinical Excellence Queensland, Mental Health Alcohol and Other Drugs Branch, Brisbane, QLD, Australia

Thy Meddick

College of Health and Medicine, Australian National University, Canberra, ACT, Australia

Richard O’Kearney & Elizabeth Rieger

ADHD and BED Integrated Clinic, Melbourne, VIC, Australia

Roger Paterson

Department of Psychology and Counselling, La Trobe University, Victoria, Australia

Susan Paxton

School of Health and Social Development, Faculty of Health, Deakin University, Geelong, VIC, Australia

Genevieve Pepin

Swinburne Anorexia Nervosa (SWAN) Research Group, Centre for Mental Health, School of Health Sciences, Swinburne University, Victoria, Australia

Andrea Phillipou

Children’s Health Queensland Hospital and Health Service, Brisbane, QLD, Australia

Judith Piccone

Centre for Clinical Interventions, Western Australia Health, Perth, WA, Australia

Bronwyn Raykos

Central Clinical School Brain & Mind Research Institute, University of Sydney, Sydney, NSW, Australia

Janice Russell

Ramsay Health Care, Perth, Australia

Fiona Salter

Department of Paediatrics, The University of Melbourne, Parkville, Australia

Susan Sawyer

National Eating Disorders Collaboration, Victoria, Australia

Beth Shelton

The Hollywood Clinic Hollywood Private Hospital, Ramsey Health, Perth, Australia

Urvashnee Singh

Sydney, Australia

Sophie Smith

The Butterfly Foundation, Sydney, Australia

Sarah Squire, Juliette Thomson & Ranjani Utpala

Eating Disorder Service, The Sydney Children’s Hospital Network, Westmead Campus, Sydney, Australia

Andrew Wallis

Department of Psychiatry, University of Queensland, Brisbane, Australia

Warren Ward

University of Tasmania, Hobart, TAS, Australia

Sarah Wells

College of Education, Psychology and Social Work, Flinders University, Adelaide, SA, Australia

Simon Wilksch

Royal Hobart, Tasmanian Health Service, Hobart, TAS, Australia

Michelle Williams

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National Eating Disorder Research Consortium

• Phillip Aouad
• , Sarah Barakat
• , Robert Boakes
• , Leah Brennan
• , Emma Bryant
• , Susan Byrne
• , Belinda Caldwell
• , Shannon Calvert
• , Bronny Carroll
• , David Castle
• , Ian Caterson
• , Belinda Chelius
• , Lyn Chiem
• , Simon Clarke
• , Janet Conti
• , Lexi Crouch
• , Genevieve Dammery
• , Natasha Dzajkovski
• , Jasmine Fardouly
• , Carmen Felicia
• , John Feneley
• , Amber-Marie Firriolo
• , Nasim Foroughi
• , Mathew Fuller-Tyszkiewicz
• , Anthea Fursland
• , Veronica Gonzalez-Arce
• , Bethanie Gouldthorp
• , Kelly Griffin
• , Scott Griffiths
• , Ashlea Hambleton
• , Amy Hannigan
• , Susan Hart
• , Phillipa Hay
• , Ian Hickie
• , Francis Kay-Lambkin
• , Ross King
• , Michael Kohn
• , Eyza Koreshe
• , Isabel Krug
• , Jake Linardon
• , Randall Long
• , Amanda Long
• , Sloane Madden
• , Sarah Maguire
• , Danielle Maloney
• , Peta Marks
• , Sian McLean
• , Thy Meddick
• , Jane Miskovic-Wheatley
• , Deborah Mitchison
• , Richard O’Kearney
• , Shu Hwa Ong
• , Roger Paterson
• , Susan Paxton
• , Melissa Pehlivan
• , Genevieve Pepin
• , Andrea Phillipou
• , Judith Piccone
• , Rebecca Pinkus
• , Bronwyn Raykos
• , Paul Rhodes
• , Elizabeth Rieger
• , Sarah-Catherine Rodan
• , Karen Rockett
• , Janice Russell
• , Haley Russell
• , Fiona Salter
• , Susan Sawyer
• , Beth Shelton
• , Urvashnee Singh
• , Sophie Smith
• , Evelyn Smith
• , Karen Spielman
• , Sarah Squire
• , Juliette Thomson
• , Stephen Touyz
• , Ranjani Utpala
• , Lenny Vartanian
• , Sabina Vatter
• , Andrew Wallis
• , Warren Ward
• , Sarah Wells
• , Eleanor Wertheim
• , Simon Wilksch
•  & Michelle Williams

Contributions

AL carried out and wrote the initial review from the first search; JMW conducted subsequent reviews, analysed results, wrote the first manuscript and the final edit; EB, SHO and SV contributed to specific sections, detailed tables and figures, responded to review comments and contributed to ongoing drafts to manuscript completion; the National Eating Disorder Research Consortium reviewed and provided expert feedback; ST and SM provided project direction, methodological design, comprehensively reviewed the manuscript and provided overall supervision and leadership. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Jane Miskovic-Wheatley .

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Not applicable.

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Competing interests.

ST receives royalties from Hogrefe and Huber, McGraw Hill and Taylor and Francis for published books/book chapters. He has received honoraria from the Takeda Group of Companies for consultative work, public speaking engagements and commissioned reports. He has chaired their Clinical Advisory Committee for Binge Eating Disorder. He is the Editor in Chief of the Journal of Eating Disorders. He is a committee member of the National Eating Disorders Collaboration as well as the Technical Advisory Group for Eating Disorders. AL undertook work on this RR while employed by HMA. JMW and SM are guest editors of the special issue “Improving the future by understanding the present: evidence reviews for the field of eating disorders.”

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Supplementary Information

Additional file 1: fig. s1..

PRISMA flow diagram.

Additional file 2: Table S1.

Studies included in the Rapid Review.

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Miskovic-Wheatley, J., Bryant, E., Ong, S.H. et al. Eating disorder outcomes: findings from a rapid review of over a decade of research. J Eat Disord 11 , 85 (2023). https://doi.org/10.1186/s40337-023-00801-3

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Assessment of anorexia nervosa: an overview of universal issues and contextual challenges

Lois j surgenor, sarah maguire.

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Received 2012 Dec 2; Accepted 2013 Jun 3; Collection date 2013.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Anorexia Nervosa (AN) is a complex and clinically challenging syndrome. Intended for specialist audiences, this narrative review aims to summarise the available literature related to assessment in the adult patient context, synthesising both research evidence and clinical consensus guidelines.

We provide a review of the available literature on specialist assessment of AN focusing on common trajectories into assessment, obstacles accessing assessment, common presenting issues and barriers to the assessment process, the necessary scope of assessment, and tools and techniques. It describes the further step of synthesising assessment information in ways that can inform resultant care plans.

In addition to assessment of core behaviours and diagnostic skills, considerations for the expert assessor include the functions of primary care, systemic and personal barriers, knowledge of current assessment tools and research pertaining to comorbid pathology in AN, assessing severity of illness, role of family at assessment, as well as medical, nutritional and compulsory elements of assessment.

Comprehensive assessment of AN in the current healthcare context still remains largely the remit of the specialist ED clinician. Assessment should remain an on-going process, paying particular attention to available empirical evidence, thereby reducing the gap between research and practice.

Keywords: Anorexia nervosa, Assessment, Eating disorders

Introduction

Most health workers recognise that anorexia nervosa (AN) is a serious disorder that results in significant disability and impaired quality of life. Unfortunately for some, this disorder becomes a chronic or life-shortening illness. It is well-established that AN has the highest mortality rate of all psychiatric disorders [ 1 ]; compared with their peers without the illness the risk of premature death is approximately ten-fold in a person with AN [ 2 ]. Health consequences are widespread, both in terms of direct physical and mental health effects and economic costs to society overall; a recent Australian analysis placed the total yearly direct health system costs of AN at $59.8 million [ 3 ]. This means that although AN and AN-like conditions are relatively rare, severe and enduring forms of AN have impairment outcomes comparable to people with moderately severe depression and schizophrenia [ 3 ].

Assessment and a resulting early diagnosis become a vital task for the health system and current research continues to suggest that, although primary care is the context of most presentation [ 4 ] areas with specialist services have more than double the number of diagnosable eating disorder (ED) cases, suggesting a sizeable proportion of diagnoses do not occur until the specialist service level [ 5 ]. What this means for both settings is worth discussion, but regardless, assessment skills and knowledge of the evidence base pertaining to diagnoses remain an important part of the skill set of the specialist clinician.

Regardless of the setting and complexity, there are descriptions of ‘ideal practice’ in the assessment of the disorder and associated health difficulties. However, assessment approaches do vary, along with models of service delivery, admission thresholds and the resources available in specialist settings [ 5 ]. Such factors will influence the composition of a multidisciplinary assessment team. There are suggestions about what constitutes an ‘ideal’ assessment team, but rarely will services have all recommended components, and multiple tasks may fall to ‘mini teams’ [ 6 ]. There is however areas of general consensus about many necessary and desirable tasks of assessment and given the above constraints it often falls to the specialist clinician working in relative isolation to be well versed in all factors pertinent to a comprehensive assessment. Focusing primarily on adult populations, this paper aims to reduce the gap between research and practice (as it relates to assessment of AN) by firstly providing a comprehensive review of the current literature relating to assessment pathways, barriers to assessment, diagnostic issues, instruments for assessment of illness and severity, role of the family at assessment, comorbid presentations relevant to assessment, medical, nutritional and compulsory assessment practises. Secondly, it discusses the process of synthesising information gathered at assessment for the purposes of formulation and ultimately to direct treatment.

Pathways to assessment

Links with primary care providers.

Given the scarcity of specialist ED services, most people with AN will not be seen by a specialist service in the first instance, and for a significant number, specialist assessment may not occur at any stage. Half of those with an ED are first diagnosed by their primary care physician, although of concern a sizeable minority may go through life without any help whether this is for AN or other emotional problems [ 4 ]. General practitioners (GPs) and other primary health care providers are best placed to be the health practitioners first involved in conducting preliminary assessments, providing initial triage, and thereafter sharing case management with other clinicians [ 7 ]. This is partly because people with eating disorders attend GPs and other medical speciality services more frequently than their peer group, albeit often for conditions seemingly unrelated to the disorder. The presence of an ED also increases the rate of presentations to Emergency Departments [ 4 ]. In terms of accuracy of diagnosis, AN is the ED most often accurately diagnosed by primary care physicians [ 8 ]. Atypical cases, or those who do not present with all diagnostic criteria, can be misdiagnosed [ 9 ] or considered ‘less serious’ despite clearly having a clinically significant disorder that squarely sits within the AN spectrum.

A number of obstacles arise for primary care health professionals in their attempt to detect AN and refer on to ED services. Setting obstacles include the limited consultation time available and relatively limited exposure to AN. Clinical obstacles include patient minimisation of behavioural and psychological symptoms, the diversity of symptom expression, and well-hidden symptoms [ 7 ]. Further, there may be difficulty in determining which symptoms are most important in assessing medical acuity or how severe the condition has become.

Systemic issues also contribute to rates of diagnosis and their accuracy. GP education about risk factors and early warning signs as well as screening instruments like the SCOFF [ 10 ] can assist detection and management, particularly where GPs are expected to coordinate and manage concurrent medical and psychiatric conditions. Close and regular liaison with ED specialists may encourage more regular enquiry about eating difficulties in those who frequently present with emotional and/or physical problems. GPs are referral “gatekeepers” (whether intended or otherwise), and ED clinicians have a role in supporting and educating their colleagues about frontline assessment practices and referral thresholds. In the regions where there are specialist services, GPs are likely to have greater awareness of eating disorders and in turn refer to specialist services more frequently [ 6 ]. In any event, presentation to primary care or emergency services should always be used as an opportunity to introduce, or re-engage with an ED clinician or ED service if one is available.

Facilitating assessment following referral

Early identification and treatment of AN is consistently argued as a means to reduce the duration of AN [ 11 , 12 ]. A systematic review of treatment seeking has recently estimated that the median delay from onset to treatment for AN is 15 years [ 13 ]. Identifying the barriers between these two time points becomes pivotal, and will likely vary. A significant minority of people referred for ED problems fail to attend an initial assessment [ 14 ], and further significant attrition occurs between assessment and providing and/or completing treatment. The following sections discuss common obstacles and possible solutions.

System and resource barriers

There are extensive system factors contributing to delays in accessing assessment. The shortage of services often results in prolonged waiting lists for assessment, meaning that by the time of assessment, patients may be demotivated or otherwise less likely to engage in what is offered. Tatham et al. [ 15 ] trialled an active ‘opt in’ waitlist management strategy for an ED clinic, whereby following initial assessment patients were required to actively select to remain on the waitlist for treatment. While ‘opting in’ letters may reduce the waiting time for an assessment [ 16 ], this triage approach is not without significant risk. Specifically, those most in need of assessment may be the least able or willing to ‘opt in’.

Long assessment waiting lists are likely to pose a barrier to engaging in any subsequent assessment - just as these do in many other health settings. It has been reported by patients that this can send a distorted message that the disorder is not serious enough. World-wide, services are caught in the ethical dilemma of setting priorities for how scarce resources should be allocated and prioritised. As these decisions have major clinical implications, resource priority-setting should be reviewed at regular intervals. Suggested strategies that have been shown to increase the likelihood of a valid referral resulting in an assessment include direct phone contact with the patient [ 14 ] accurate written knowledge services and, where appropriate, steps to engage significant others (for example, family) in the assessment process [ 11 ].

Barriers of ambivalence and motivation

There are multiple psychological reasons why people with AN may be reluctant to present for assessment or are guarded during an assessment. The disorder itself, at best, presents genuine ambiguity for many who suffer from it. As one woman described it, “I want to get rid of the disorder but not the body shape (of AN)…I want the best of both worlds” [ 17 ], page 29. AN has been demonstrated to serve more pivotal functions of affect numbing or identity and the individual may see no reason to alter it at all or, as is most common, the patient may move between wanting to address it and not seeing it as a problem. This ambivalence is complex and may shift even in the preliminary assessment interview. The interview may be infused with ‘bargaining points’ or requests for ‘conditional’ or no treatment at all. With these dynamics at play, careful clinical skills are required. It is important that such bargaining is not seen as ‘manipulation’ with the negative connotations of that concept. Rather, it represents a genuine struggle with symptoms that are both controlling and out of control, and at times deeply confusing for the person. It can be very validating to the client, and move the process of assessment along smoothly, to express understanding for the two seemingly opposite positions that can be held within the one person, and to not dismiss or invalidate the part of the client that wants to retain the illness. Family and carers may be equally conflicted about the need for treatment, with parents sometimes caught between loyalty for their offspring and wanting to heed professional advice. Assessment of family functioning is discussed later in this paper.

Although overlapping with ambivalence, motivation is a wider construct involving cognitive, behavioural, and biological systems. Appraising motivation for treatment and ability to change is an important component of any initial assessment: it often contributes to case formulation, decisions made at the conclusion of assessment, and subsequent treatment planning. Yet assessment of this is far from straight forward. Motivation may be symptom-specific: there may be high engagement in strategies to control physical side effects, but minimal engagement in behaviours directed towards weight gain. Engaging in conversations that highlight this variability at the beginning of a therapeutic interaction is likely to build alliance. As noted by [ 18 ], assessing what makes people want to recover, and what recovery represents to them, is important, and this is something highly valued by patients themselves.

Of note, there is controversy regarding the ability of clinicians to accurately assess motivation, and whether this predicts anything about the likelihood of engagement or even treatment outcome. Waller [ 19 ] provides a compelling overview of the complexities involved, including clinician overreliance on verbal expressions of change. Interestingly, similar critical analyses are now being extended to motivational enhancement techniques, noting that in regard to AN, the evidence is mixed at best [ 20 ]. Rieger et al. [ 21 ] specifically suggests motivation is not only required to alter the behavioural aspects of the illness (namely how much weight are patients are prepared to gain each week until they reach a healthy weight, and how motivated they feel to be at a normal weight) but also feeling of self-efficacy about achieving this. Some patients will state that they are very motivated to be at a normal weight and would be prepared to gain up to a kilo a week to do so, but when asked how confident they are that they can actually do this, the answer is quite different.

Clinicians as barriers

People presenting for assessment are often fearful of being judged or criticised. These fears are not unfounded as it has been repeatedly demonstrated that attitudes of health professionals, including mental health specialists towards EDs, are not always positive [ 22 ], and are no more empathic than those of non-professionals [ 23 ]. Negative professional attitudes may arise through lack of training or experience [ 24 ], inadequate resources and work pressure, and genuinely held stereotypes about AN being a personal choice. These factors can contribute to AN being seen as a disorder with relatively low prestige by health care professionals [ 25 ]. Training and support strategies may go some way to counter these effects. As clinical experience decreases the likelihood of negative reactions, services significantly benefit from retaining highly skilled staff.

Early drop-out

Failure to engage, or drop out once treatment begins has a negative association with prognosis [ 26 , 27 ] and increases the likelihood of intensive treatment utilisation in later stages of illness [ 28 ]. Specialist services have lower treatment drop out and allow greater continuity of care with the same service, yet studies suggest that amongst those with EDs who actually attend assessment, approximately one-in-five drop out before treatment can start [ 29 ]. Reliable predictors (clinical or otherwise) of drop-out from services are scarce [ 17 , 26 , 30 ], meaning that future assessment interviews should be seen as an opportunity to explore the factors involved from the patient’s perspective. Hudson et al. [ 31 ] found life-time treatment for AN to be 33.8%, and thus much lower than other DSM-IV eating disorders (BN 43.2%; BED 43.6). Reducing drop-out before and after assessment is an obvious means to increase treatment take-up.

Diagnostic issues at assessment

AN is a syndrome involving considerable symptom variability between and within cases over time. Cross-over between AN subtypes is common, suggesting that those with AN-Restricting Type and AN-Binge-Eating/Purging Type may be phases of the same condition rather than distinct groups [ 32 ]. Diagnostic weight cut-offs are debated [ 9 ] and the severity of psychological versus physical symptomatology may not always highly correlate, albeit these will be highly intertwined at extremely low weights due to the behavioural, psychological, and cognitive effects of starvation [ 33 ]. The following sections discuss key issues regarding diagnostic variability.

Revised diagnostic criteria

The American Psychiatric Association diagnostic criteria (DSM-5) [ 34 ] have recently been reviewed. Hebebrand et al. [ 9 ] comprehensively discusses the rationale behind revised criteria, highlighting the reframing of psychological symptoms so that some pejorative attitudes are removed and other criteria are redefined to reflect the evidence. For example, eliminating the term ‘refusal’ (to maintain body weight), and replacing this with more objective terms describing food restriction. The removal of the diagnostic criteria of amenorrhea in post-menarcheal females is well overdue given the mounting evidence that this is of questionable utility. Similar changes are proposed for ICD-11 [ 35 ]. Clinicians involved in the assessment of AN should become familiar with current and future diagnostic debates in order to reduce the risk of adopting a rigid or outdated approach to formulating core psychopathology of AN and the expressions of this.

Effect of symptoms

Some features of AN can be difficult to assess meaningfully in that they decrease in ‘severity’ as illness severity increases. For example, fear of fatness can decrease as the individual’s weight drops and they are no longer confronted with fat on their own body. Similarly, drive for thinness and body image dissatisfaction can also decrease as weight decreases. To generalist clinicians, this could result in a failure to diagnose individuals with potentially severe AN, as they appear to lack either one or both of the essential symptoms. Other clinicians may misconstrue this as ‘denial’ and engage in confrontational discussions with patients, which may be unhelpful.

At very low weights, the effects of starvation will always distort the expression of distress, and patients in general are not necessarily aware of why they behave in certain ways or why they may pursue certain goals. It may be useful to assess certain symptoms from the perspective of what it would be like not to have them. For example, assessing body dissatisfaction/drive for thinness not from the standpoint of how the person with AN feels about their body at its current weight, but rather how they would feel about their body, and how intense their drive to lose weight would be if they imagined their weight being within a normal weight range, holds some utility [ 36 ].

Culture and ethnicity

AN may present differently in people with a non-Western background (see Soh et al. [ 37 ] for a review), and there are significant body composition differences across ethnicities. For example, Asian women show higher levels of body fat for the same BMI than their Western peers [ 38 ]. There is more mixed evidence that cultural issues influence psychological symptom variability. While a commonly cited difference is that fear of fatness is less evident in patients from a non-Western background, many studies do not show this [ 39 ]. Likewise, levels of body image disturbance amongst clinical groups from different cultures have been found to be largely identical despite genuine cultural differences in body image concern in those who do not have an ED [ 40 ]. Studies that have historically highlighted symptom variability across cultures have commonly examined ethnic minorities residing in Western countries: when an ethnic group is studied in their country of origin, many of the proposed differences in clinical presentation cannot be found. Likewise, struggles with psychological control reported in AN appear universal, but importantly it is deviation from the cultural norm (whatever the culture) that seems to distinguish women with EDs from their peer group [ 41 ]. In short, rather than ethnicity explaining any noted symptom variations, the pertinent assessment issues may relate to understanding the current cultural norms and their dissonance with the culture of their ethnic background.

Although representing around one in ten people with AN [ 42 ], males with this condition are much less likely to be recognised. Amongst those who do present for assessment, medical complications are more likely apparent than with their female counterparts [ 43 ]. There are mixed views about whether males present for assessment much earlier (see Carlat et al. [ 44 ]) or later (see Siegel et al. [ 43 ]) than their female counterparts. Psychological symptoms are largely identical, although there is some limited evidence that males may have less severe scores on diagnostic tools and symptom rating scales [ 45 ] and are more likely present with particular weight control strategies (for example, excessive exercise [ 46 ]) and dissatisfaction with muscle size and shape. Too few studies have been conducted to examine whether the natural course of the illness differs by gender. Some studies report a more benign outcome in men at one year (e.g. Strober et al. [ 47 ]), while a recent long term follow-up study found no gender differences in 10-year survival rates [ 48 ]. Causal models particularly relevant to males are still largely speculative, although sexual orientation issues feature prominently in males [ 49 ]. However it may be that gay men may be more willing to seek help for psychological problems. At this stage therefore, the assessment of males presenting with AN largely should follow the same assessment considerations as females.

Assessment screening and severity tools

Screening tools.

A large number of standardised self-report and interview-based measures are available to clinicians. There is longstanding debate about the superiority of interviews as opposed to self-report measures (whether paper and pencil or computerised), and ultimately the selection of any measure will depend on the purpose and context of assessment, along with constraints on time, availability of training and clinical factors. These issues are now discussed.

Self-report questionnaires are easy and quick to administer, although they differ in their utility. Shorter measures such as the Eating Attitudes Test (EAT-12; EAT-26) [ 50 ] and SCOFF [ 10 ] are useful in primary care situations where an ED may be suspected (NICE Guidelines; Allen et al., 2011), and identifying the need for second screening steps is a focus. However these are less useful in specialist settings where the more relevant task is to gather systematic information about severity and the extent of psychopathology. Here, longer self-report measures (for example, Eating Disorder Inventory (EDI-3) [ 51 ], Eating Disorder Examination Questionnaire (EDE-Q) [ 52 ], and Yale-Brown-Cornell Eating Disorders Scale (YBC-EDS, [ 53 ]) tend to assess two factors - a combination of risk factors and psychological disturbances associated with AN [ 54 ]. Detailed information about psychological symptoms can be elicited from these, which in turn adds to any clinical formulations. As standardised measures, they can be useful in assessing symptom change.

Semi-structured or structured clinical interviews such as the Structured Clinical Interview for DSM-IV Axis I Disorders Clinical Version (SCID-CV) [ 55 ], and Eating Disorder Examination (EDE) [ 56 ] are often referred to as “ gold standards ” (APA, 2006, p.46). These are more time-consuming, involve training and are more likely suitable for research purposes rather than clinical settings, although they do possess the advantage of being validated to render an ED diagnosis.

Irrespective of the measure used, scores are affected by a number of clinical, demographic and psychometric issues. Denial may occur in interviews due to embarrassment and reluctance to disclose, whereas the risk with self-report measures is that patients may inaccurately estimate the seriousness of core symptoms [ 57 , 58 ], or simply disagree that symptoms are problematic [ 59 ]. In very severe cases, administration of psychometric tests (AN-related or otherwise) is clearly inappropriate. Wider psychometric limitations arise from differences in international norms and few national clinical norms [ 54 ], and the utility of measures differ between adults and adolescents [ 60 ]. Furthermore, different formats of the same measure (e.g. EDE and EDE-Q) have only modest agreement ratings, with rates of agreement being dependent on the type of symptom being assessed [ 58 ]. In terms of AN, no measure reliably distinguishes between AN and EDNOS-AN [ 61 ].

A positive diagnosis can be made in most cases without the need for a battery of psychometric tests. The more useful place of standardised psychometric tools is to screen, assess symptom change and research. In the end, standardised psychometric tools cannot replace the advantages of a thorough clinical interview. As noted by Nordbø et al. [ 62 ], “ an assessment tool should never be regarded as a substitute for treating the patients individually or replace the need for an individual exploration in each single patient ” (page 660). This is further discussed in the final section of this paper.

What constitutes severity?

The use of the concept of illness severity is common in ED settings, and there are solid grounds for this. For example, severity markers can help aid treatment decisions, potentially aid prognosis, and promote more uniform international understandings about clinical presentations [ 63 ]. However, empirically supported definitions of severity are largely lacking. Clinicians commonly default to one or more symptom markers or treatment intensity markers such as BMI [ 64 ] or multiple severity indices based on different symptoms (not all of which are AN symptoms [ 65 ]), hospitalisation [ 66 ] or length of illness [ 67 ]. In an attempt to address problems with all of the above strategies, a more recent approach has been the development of empirically derived tools to stage AN severity [ 36 , 68 ]. Early indicators suggest that such measures involve multiple symptom dimensions, and neatly capture both clinical reality and patient subjective reality [ 36 ]. One of these instruments [ 67 ], the CASIAN, largely assess the behavioural features of the ED so as to minimise the factors of denial and the often perverse reduction in psychological distress discussed above, as the illness progresses (i.e. drive for thinness and body dissatisfaction can decrease with severity). Longitudinal data is still needed to determine how staging instruments could usefully aid assessment, treatment pathway decisions and the prediction of prognosis.

Family involvement and family assessment

Where possible, it is highly desirable to have carers or family involved in the assessment process given they provide much of the on-going care and share the extensive burden of the disorder. For younger patients still living at home, family members may need to be directly involved as treatment agents [ 69 ] as long as they are appropriately supported and advised, noting that family members can become entangled with behaviours that maintain the disorder [ 70 ]. For adolescents, the assessment phase may more directly involve assessment of family functioning. The inevitable distress about having a family member with AN may need addressing in its own right and assessment of family functioning is core where family therapy treatment models are to be employed. There is no clearly superior way to assess family functioning: approaches are likely to reflect the model of family therapy employed and there are several variants of this. Family therapy models have been met with enthusiasm although a recent Cochrane Collaboration review suggests a need to temper this enthusiasm due to a range of methodological shortcomings in the small number of published treatment trials [ 71 ]. Such moderation should equally apply to assessment processes meaning that rigid approaches to assess families should be avoided.

Co-morbidity

Given psychiatric co-morbidity is common in people with AN, consideration of these associated problems should be routine. Those presenting for assessment may have higher rates of co-morbidity than AN community samples due to the additional burden and distress of these comorbid conditions. Indeed, these conditions may be the precipitant for presentation rather than AN itself. If psychiatric co-morbidity is recognised, conclusions about the actual presence of a primary anxiety (or mood disorder) is often best delayed until the symptom contribution of AN can be clarified, especially in the case of severe AN. Co-morbidity may impact on treatment engagement, in both directions, with co-morbidity prompting assessment or in other circumstances reducing engagement. The following sections discuss common forms of co-morbidity and implications for assessment.

Mood disorders

While major depression features prominently, depressive symptoms may also result from severe malnutrition, which almost certainly elevate these rates. Generally, however, there is robust evidence for elevated rates of major depression in all AN populations, irrespective of whether these are clinic or community samples. Godart et al. [ 72 ] found life-time prevalence rates ranging from 9.5% - 71.3%, with the variability in findings likely due to methodological differences across studies. The overall lifetime prevalence for eating disorders patients is estimated at 40%. There is debate about the most common sequencing of these comorbidities with some suggesting that the mood disorder more often precedes the ED (Cooper et al., 2002) and others highlighting past problems of over-diagnosing depression when instead symptoms may be secondary to malnutrition [ 57 ]. The consensus is that the relationship is complex. Scores on depression screening measures can be significantly elevated by an ED [ 73 ] resulting in a need to set higher cut-off scores in order to be meaningful. Vigilance for mood symptoms should also be ongoing given that improvements in AN can be experienced as depressogenic, with some sufferers construing the relinquishing of symptoms as a sign of losing control or giving in (to treatment) [ 74 ].

Bipolar disorder co-morbidity in AN is rare [ 75 ]. Affective disorders along this spectrum are more likely to be associated with forms of disordered eating involving bingeing or over-eating. How EDs and bipolar disorders overlap requires further study.

Assessment of self-harm and suicide risk

A recent meta-analysis observed a decreased risk of completed suicide in AN [ 76 ] over recent decades, with a standardised mortality ratio (SMR) of 31. This SMR still represents an elevated risk when compared with other EDs and the general population. The extent to which AN directly contributes to this risk as opposed to the combined effects of AN and co-morbidity to this risk is still debated [ 77 ].

Information gathering about risk comprises a two stepped approach. First, standard suicide self-harm risk assessment considerations apply. Thus, just with non-ED populations, the presence of depression increases the risk of suicidal behaviours and completed suicide and a sizeable proportion of these people will have had contact with their GP in the week or months before death. Other risk factors include a history of mental disorder, more severe psychopathology overall, Axis 2 psychopathology, history of self-harm/suicide attempts, and substance misuse (see Hawton et al. [ 78 ]). It follows that assessment of these standard risk factors should always occur when engaging with a person presenting with AN.

Second, the presence of particular AN symptoms or a history of AN may produce additional risks. These include the presence of binge-purge patterns [ 79 ], markers of chronicity including illness duration and very low weight [ 80 ], and high anxiety in AN-R [ 79 ]. Rates of completed suicides in people with AN are debated [ 2 ], with one study reporting suicide as the second most frequent cause of death in a retrospective study of those treated in an ED service [ 81 ]. The most consistent finding is approximately 20% of deaths in AN are attributable to suicide [ 82 ]. It is self-evident that assessment of suicidal ideation and behaviours is important, especially in those presenting with co-morbidity.

Unusual forms of self-harm have been reported that are directly linked with efforts to maintain AN. For example, ingesting large quantities of salt [ 83 ], scratching [ 84 ] and blood-letting [ 85 ]. How these phenomena fall under the umbrella of wider deliberate self-harm (DSH) phenomena is unclear as DSH has multiple intended functions [ 86 ]. If present, such behaviours are unlikely to come to light in outpatient assessment settings. Although the conscientious clinician will assess for them, these may only be revealed following close monitoring, as occurs in inpatient settings.

Anxiety disorders

There is extensive overlap between anxiety and AN symptoms, with AN exacerbating concurrent anxiety disorders in addition to extensive anxiety symptoms forming part of the AN syndrome [ 87 ]. This makes assessment of anxiety a necessary component of any formulation, irrespective of any suspected Axis 1 anxiety disorder. This is because common anxiety treatment techniques inevitably will be part of treatment. Assessment questions include the extent of pre-morbid anxiety, the presence of genuine co-morbidity and the degree to which anxiety symptoms are actually part of AN. These issues are addressed in turn.

Reported lifetime prevalence rates of anxiety disorders vary considerably ranging from 23%-75% (see Swinbourne and Touyz [ 88 ] for a review). Generally the anxiety disorder is more likely to precede the onset of AN rather than the other way around [ 89 ], although this may depend on the anxiety disorder in question [ 90 ]. Of the anxiety disorders, obsessive-compulsive disorder (OCD) is the most researched condition [ 91 ], although social phobia, other phobic states and Generalised Anxiety Disorder (GAD) and anxiety-based problems such as clinical perfectionism [ 92 ] have all received attention.

Teasing out the functional relationship between wider anxiety phenomena and/or the presence of a primary anxiety disorder can be challenging, and even after weight-restoration anxiety symptoms tend to persist [ 93 ]. Detailed functional analysis of behavioural and cognitive rituals, the scope of intrusive thoughts, the scope of avoidance, and any other symptoms of fear may help clarify how these features are directly part of AN or more correctly attributed to another primary anxiety disorder. Importantly, anxiety symptoms may not be reported due to the success of avoidance or engaging in subtle “safety behaviours” that keep symptoms at bay. In such cases, anxiety symptoms may only emerge once there are treatment demands for change. As a result, the absence of anxiety symptoms on initial assessment should not be taken as evidence of the absence of anxiety.

Obsessions and compulsions particularly increase with starvation, and sometimes to an intensity that is comparable to people with OCD. Conclusions about the presence of a primary anxiety disorder should wait until the effects of starvation have abated.

Substance abuse and dependence

Reported rates of substance abuse in AN vary widely and are significantly associated with AN subtype (binge/purge), with rates as high as 35% in those who cross over to Bulimia Nervosa (BN) after weight restoration [ 94 ]. In general, the presence of any bulimic symptomatology significantly increases the likelihood of co-morbidity involving a variety of substances, both illicit and legal [ 95 , 96 ]. The sequencing of co-morbid alcohol problems and AN shows no distinctive pattern [ 97 ]. However the concurrent presence of alcohol misuse and AN should prompt enquiry into wider psychopathology given the increased odds of this in this subpopulation [ 98 ] and the known increased mortality [ 2 ].

Other substance abuse and dependence problems include the use of diet pills, laxatives, diuretics and other illicit stimulants for appetite suppression and increased metabolic effects [ 99 ]. Opioid and sedative use is also significantly elevated. In short, the assessment of substance misuse should cast a wide net, seeking information about illicit and over-the-counter drugs, including common substances containing high levels of caffeine. The assessment should also include patient understandings about how these substances maintain AN symptoms (for example, warding off normal signals of hunger) or manage other psychological symptoms or distress.

Nutritional, weight, and eating behaviour assessment

Obtaining a weight and nutritional history is a critical component of assessment, although this can be far from straight-forward. Being asked to be weighed is one of the most anxiety-provoking demands for someone with AN, even when many know their weight due to excessive self-monitoring. In the situation of outright refusal to be weighed, this can be a temporary impasse if the anxiety about this is explored. Clinicians who allow the continued avoidance of assessing weight may find themselves inadvertently colluding with the disorder.

Body mass index (BMI) is the most common metric used, with extreme levels (BMI ≤ 13) consistently showing a risk of a poorer outcome and elevated medical risks [ 81 , 100 ]. Centile charts are recommended for patients who are younger than 18 years of age [ 101 ]. Percentage of body fat is another useful indicator of risk as this also has been associated with outcome [ 102 ].

Apart from ascertaining current weight, there are several aspects of weight history that are clinically important. These include obtaining information about highest and lowest-ever weight (BMI), means of weight control, and if amenorrhea is present, weight at which menses were lost or in the case of primary amenorrhea consideration of the effect of delayed puberty. A history of a very low BMI at any point in the illness trajectory is a risk factor for premature death [ 2 ]. BMI alone is problematic in younger populations for whom BMI-for-age is argued as more appropriate [ 103 ]. Patient perception of their ‘ideal’ weight, and how they determined this, can provide useful clinical information about maintaining factors, and how AN is serving to manage psychological difficulties. Commonly, a particular weight may be fixated upon with an expectation that achieving this will bring a sense of well-being and success. Inevitably such rewards are not forthcoming often resulting in a decision to work towards a lower weight - as if the original goal was miscalculated.

A food and fluid diary may help assess aspects of nutritional pathology, or at least start the discussion about nutritional intake. Shame, embarrassment, and anxiety about increasing nutritional intake, are amongst the factors that affect the accuracy of food diaries and other forms of self-recording. Additional enquiry should be made about avoided foods, behaviours and rituals around eating, evidence of self-imposed caloric limits, and the full repertoire of compensatory behaviours.

Medical assessment

The main causes of increased mortality in AN are those directly related to the disease [ 82 ]. Fortunately advances in assessment and careful treatment of AN-related medical abnormalities have helped reduce the rates of mortality [ 104 ] compared with earlier practices. Multiple organ systems should be reviewed at assessment and abnormal medical findings can provide compelling objective evidence to ambivalent attendees who may contest the need for treatment. The types of medical complications presenting are influenced by age, clinical history, and weight history. The extent of medical and physical investigations undertaken will depend on these factors although there is some consensus on commonly recommended laboratory investigations. These include a full blood count, urea and electrolytes, biochemistry including calcium, magnesium, and phosphate, and glucose and liver functioning [ 105 ]. Assessment and monitoring for phosphate depletion is particularly important. Hypophosphatemia is well known to be associated with catastrophic consequences in the context of refeeding particularly for the severely underweight person.

Of concern, complications that are not reversible can occur in those who have yet to develop a chronic problem, and these include altered linear growth, osteoporosis, and structural or functional brain changes [ 106 ]. It is important to recognise that patients may initially appear asymptomatic due to slow adaptation to starvation over time. More detailed medical assessments may be indicated for those presenting with severe AN, as it is a mistake to consider mild AN as a benign condition. Even those with mild AN may experience prolonged periods of debilitating symptoms [ 11 ].

A full medical history and physical examination is essential to highlight immediate medical problems such as hypotension, hypothermia, bradycardia, skin conditions, and intercellular changes such as dehydration. Enquiry should extend to other gastrointestinal problems such as diarrhoea, constipation and abdominal cramping. A small number of patients may have had extensive previous medical work-up in an attempt to locate a medical condition that could explain symptoms that are more correctly caused by AN. Likewise, although rare, other non-psychiatric causes of significant weight loss (for example, medical conditions resulting in mal-absorbing consequences) should be considered early in the assessment process.

A medical review should include considering the presence of other conditions that may have serious consequences while occurring in the context of AN (e.g. diabetes) or other causes of weight loss unrelated to AN (e.g. primary gastrointestinal disorders), along with a review of medications that may compromise or contribute to medical risks occurring (for example, medications that prolong QT intervals). Since cardiac abnormalities have been estimated to occur in up to 86% of patients [ 107 ], and cardiovascular causes are a major cause of death [ 108 ], cardiac investigations (ECG) should check for a range of cardiomyopathies, of which there are many [ 109 ]. Studies suggest that is unclear when QT prolongation first occurs in the natural history of AN and when the period of greatest risk of cardiac abnormalities may occur [ 107 ]. Endocrine screens are useful, particularly checking thyroid functions and other hormonal disturbances.

Other checks may need to include bone density scans assessing for osteoporosis and spontaneous or low impact fractures, particularly if pain is a presenting complaint. When symptoms of self-induced vomiting are present, the risk of dental complications is high even after a relatively short history of vomiting [ 110 ] and dental reviews are recommended. Common gastrointestinal disturbances include gastric pain, prolonged gastric emptying and constipation [ 108 ], all of which can perpetuate the desire to continue restricting.

The presence of medical complications may or may not lead to hospital admission. As noted earlier, significant contextual factors, availability and regional treatment philosophies influence admission decisions [ 111 ] both within and between countries. When acute medical presentations occur, particular care is needed to avoid the refeeding syndrome and other treatment-related complications. Medical symptoms may be alarming and prompt consideration of urgent steps, but cautious use of otherwise considered routine interventions (for example, intravenous fluids) is required in order to avoid catastrophic consequences [ 112 ]. A small number of patients will require an explicit medical admission.

Compulsory assessments

On occasions, preliminary assessments occur under duress after formal steps have been taken to initiate the assessment. Engagement of a reluctant patient who may require persuasion, formal or otherwise, to accept urgent investigations or treatment requires skill and tact. The legal options and legislative pathways for compulsory assessment vary across countries, but the principles are relatively universal and well discussed in the literature [ 113 , 114 ]. Legal coercion is required relatively infrequently [ 115 ]. Importantly, patient perceptions of coercion, with or without the use of formal compulsion, occur along a continuum [ 116 ] with many later describing formal treatment orders as helpful. Much can be done to mitigate distress when a compassionate and trusting approach is taken [ 117 ]. Decision-making must consider patient capacity to make decisions, the urgency of presenting symptoms and the outcomes where compulsory steps have been previously utilised to detain the patient.

Synthesis and formulation of assessment information

A comprehensive assessment interview is likely to take several hours, and where clinically indicated, may require several appointments. Once sufficient and necessary information has been gathered, the next step is to synthesise this with other findings from other standard assessment steps such as history taking and mental status examination.

A case formulation approach is recommended to develop “ a more complete picture of the patient than can be associated with a diagnosis ” [[ 118 ], page 1] incorporating all presenting issues, past treatment outcomes and patient perspectives. It involves assimilating information from multiple sources and using clinical judgement to weigh up both converging and conflicting data. A case formulation approach is also conducive to building a therapeutic alliance which is vital in psychotherapeutic treatments both generally and specifically in regarding to AN [ 119 ].

The formulation may include tentative hypotheses about predisposing, precipitating and maintaining factors. Families commonly ask about causal factors fearing that assessment findings will implicate them in some way. Pressed for answers from distressed families (and patients themselves), clinicians may be tempted to be drawn on predisposing factors. However causes of AN are far from understood. Tentative hypotheses are best, and better framed as general risk factors in the interim. Given the typically prolonged time between onset and assessment combined with difficulties establishing age of onset, articulating more immediate precipitating factors is equally fraught. It will be more possible to draw conclusions about maintaining factors due to the extensive knowledge about reinforcement schedules and behavioural traps in the lived experience of AN.

In a large multidisciplinary team, varying perspectives and formulations may emerge and this can be clinically useful. However such differences should never divert from the importance of all team members uniting behind any arising triage or treatment plan. The end result of the case formulation should be a set of working hypotheses articulated into a coordinated care plan followed by all team members. This care plan should be both detailed and broad covering immediate treatment needs and priorities for further investigation.

This overview in limited in its ability to fully discuss all relevant factors in assessment; a decision was made to include issues that would be pertinent to a wide audience. Likewise, the scope of this overview precludes discussion of the steps instigating treatment following from assessment, although it follows that management of acute physical and psychiatric problems naturally take priority.

Experienced clinicians know that the process of assessment is an on-going one, encompassing a need to repeat and monitor medical investigations and revise psychological formulations as more information comes to light, symptoms worsen or improve and priorities shift. A preliminary assessment should never attempt to reach firm opinions about cause although formulations relating to factors maintaining the disorder may be more apparent.

In conclusion, assessments require a systematic, rigorous, and empathic approach that strikes an important balance between carefully listening to patient needs and dilemmas, while remaining firm and focused about the need for treatment. Even difficult assessment interviews conducted under duress should leave the patient with a sense of dignity and that they have been heard. The assessment interaction should be seen as an important therapeutic interaction to begin building a therapeutic alliance, balancing both an atmosphere of acceptance [ 120 ] yet firmness without being over-confident or paternalistic. The most important assessment tool is the clinician and the knowledge and stance they take into the interpersonal interaction. An assessment will always be a deeply complex interpersonal interaction requiring a careful clinical interview, and one based on a sound understanding of the symptoms and issues faced by the patient.

On-going efforts are required to address substantive knowledge gaps and to encourage the uptake of evidenced-based approaches where such evidence is assessed as strong. As noted recently, “ the bond that tethers our patient to our treatment is a fragile one ” [[ 121 ], page 178]. At times this could be rephrased to say that the bond that tethers assessing clinicians to the evidence is equally fragile. There is a universal problem transferring research evidence into clinical practice, and this overview aims to reduce that ‘leakage’ [ 122 ] between research and practice.

While not above criticism themselves, a number of practice guidelines are available that outline in some detail the required and desired assessment investigations, and at least draw clinicians’ attention to the quality and limitations of evidence. These include the Australasian [ 123 ] (currently undergoing review), North American [ 124 ], and the British [ 101 ] guidelines. The latter of these (and the most recently published) appeared just under a decade ago, but a recent review of the literature indicates that these guidelines are as relevant today as they were in 2004, ( http://www.nice.org.uk/nicemedia/live/10932/55781/55781.pdf , downloaded 17 Sept 2012).

Competing interests

Both authors declare that they have no competing interest.

Authors’ contributions

LS carried out the literature review and drafted the early version. SM revised initial manuscript drafts and critically commented on the intellectual content. Both authors read and approved the final manuscript.

Contributor Information

Lois J Surgenor, Email: [email protected].

Sarah Maguire, Email: [email protected].

• Harris EC, Barraclough B. Excess mortality of mental disorder. Br J Psychiatry. 1998;1:11–53. doi: 10.1192/bjp.173.1.11. [ DOI ] [ PubMed ] [ Google Scholar ]
• Button EJ, Chadalavada B, Palmer RL. Mortality and predictors of death in a cohort of patients presenting to an eating disorders service. Int J Eat Disord. 2010;1:387–392. doi: 10.1002/eat.20715. [ DOI ] [ PubMed ] [ Google Scholar ]
• Butterfly Foundation. Paying the Price: The economic and social impact of eating disorders. Butterfly Foundation: Melbourne; 2012. Available from: http://www.thebutterflyfoundation.org.au . [ Google Scholar ]
• Dooley-Hash S, Lipson SK, Walton MA, Cunningham RM. Increased emergency department use by adolescents and young adults with eating disorders. Int J Eat Disord. 2012;1:883–890. doi: 10.1002/eat.22026. [ DOI ] [ PubMed ] [ Google Scholar ]
• Simon J, Schmidt U, Pilling S. The health service use and cost of eating disorders. Psychol Med. 2005;1:1543–1551. doi: 10.1017/S0033291705004708. [ DOI ] [ PubMed ] [ Google Scholar ]
• House J, Schmidt U, Craig M, Landau S, Simic M, Nicholls D, Hugo P, Berelowitz M, Eisler I. Comparison of specialist and nonspecialist care pathways for adolescents with anorexia nervosa and related eating disorders. In J Eat Disord. 2012;1:949–956. doi: 10.1002/eat.22065. [ DOI ] [ PubMed ] [ Google Scholar ]
• Marks P, Beumont P, Birmingham CL. GPs managing patients with eating disorders. a tiered approach. Aust Fam Physician. 2003;1:509–514. [ PubMed ] [ Google Scholar ]
• Allen KL, Fursland A, Watson H, Byrne SM. Eating disorder diagnoses in general practice settings: comparison with structured clinical interview and self-report questionnaires. J Ment Health. 2011;1:270–280. doi: 10.3109/09638237.2011.562259. [ DOI ] [ PubMed ] [ Google Scholar ]
• Hebebrand J, Bulik CM. Critical appraisal of the provisional DSM-5 criteria for anorexia nervosa and an alternative proposal. Int J Eat Disord. 2011;1:665–678. doi: 10.1002/eat.20875. [ DOI ] [ PubMed ] [ Google Scholar ]
• Hill LS, Reid F, Morgan JF, Lacey JH. SCOFF, the development of an eating disorder screening questionnaire. Int J Eat Disord. 2010;1:344–351. doi: 10.1002/eat.20679. [ DOI ] [ PubMed ] [ Google Scholar ]
• Treasure J, Russell G. The case for early intervention in anorexia nervosa: theoretical exploration of maintaining factors. Br J Psychiatry. 2011;1:5–7. doi: 10.1192/bjp.bp.110.087585. [ DOI ] [ PubMed ] [ Google Scholar ]
• Von Holle A, Pinheiro AP, Thornton LM, Klump KL, Berrettini WH, Brandt H, Crawford S, Crow S, Fichter MM, Halmi KA, Johnson C, Kaplan AS, Keel P, La Via M, Mitchell J, Strober M, Woodside DB, Kaye WH, Bulik CM. Temporal patterns of recovery across eating disorder subtypes. Aust NZ J Psychiatry. 2008;1:108–117. doi: 10.1080/00048670701787610. [ DOI ] [ PubMed ] [ Google Scholar ]
• Hart LM, Granillo MT, Jorm AF, Paxton SJ. Unmet need for treatment in the eating disorders: a systematic review of eating disorder specific treatment seeking among community cases. Clin Psychol Rev. 2011;1:727–735. doi: 10.1016/j.cpr.2011.03.004. [ DOI ] [ PubMed ] [ Google Scholar ]
• Waller G, Schmidt U, Treasure J, Murray K, Aleyna J, Emanuelli F, Crockett J, Yeomans M. Problems across care pathways in specialist adult eating disorder services. Psychiatr Bull. 2009;1:26–29. doi: 10.1192/pb.bp.107.018325. [ DOI ] [ Google Scholar ]
• Tatham M, Stringer H, Perera S, Waller G. "Do you still want to be seen?": the pros and cons of active waiting list management. Int J Eat Disord. 2012;1:57–62. doi: 10.1002/eat.20920. [ DOI ] [ PubMed ] [ Google Scholar ]
• Carmen D, Shah S, Gilbert S, Russell F. Improving attendance at an eating disorder clinic by means of an "opt in" letter. Clin Psych Forum. 2007;1:22–25. [ Google Scholar ]
• Surgenor LJ, Plumridge EW, Horn J. 'Knowing one's self' anorexic: implications for therapeutic practice. Int J Eat Disord. 2003;1:22–32. doi: 10.1002/eat.10117. [ DOI ] [ PubMed ] [ Google Scholar ]
• Nordbo RH, Gulliksen KS, Espeset EM, Skarderud F, Geller J, Holte A. Expanding the concept of motivation to change: the content of patients' wish to recover from anorexia nervosa. Int J Eat Disord. 2008;1:635–642. doi: 10.1002/eat.20547. [ DOI ] [ PubMed ] [ Google Scholar ]
• Waller G. The myths of motivation: time for a fresh look at some received wisdom in the eating disorders? Int J Eat Disord. 2012;1:1–16. doi: 10.1002/eat.20900. [ DOI ] [ PubMed ] [ Google Scholar ]
• Knowles L, Anokhina A, Serpell L. Motivational interventions in the eating disorders: What is the evidence? Int J Eat Disord. 2012;1:97–107. doi: 10.1002/eat.22053. [ DOI ] [ PubMed ] [ Google Scholar ]
• Rieger E, Touyz SW, Beumont PJV. The anorexia nervosa stages of change questionnaire (ANSOCQ): Information regarding its psychometric properties. Int J Eat Disord. 2002;1:24–38. doi: 10.1002/eat.10056. [ DOI ] [ PubMed ] [ Google Scholar ]
• Morgan JF, Jones WR, Saeidi S. Knowledge and attitudes of psychiatrists towards eating disorders. Eur Eat Disord Rev. 2012;1:84–88. doi: 10.1002/erv.2155. [ DOI ] [ PubMed ] [ Google Scholar ]
• Stewart MC, Schiavo RS, Herzog DB, Franko DL. Stereotypes, prejudice and discrimination of women with anorexia nervosa. Eur Eat Disord Rev. 2008;1:311–318. doi: 10.1002/erv.849. [ DOI ] [ PubMed ] [ Google Scholar ]
• Reid M, Williams S, Burr J. Perspectives on eating disorders and service provision: A qualitative study of healthcare professionals. Eur Eat Disord Rev. 2010;1:390–398. doi: 10.1002/erv.976. [ DOI ] [ PubMed ] [ Google Scholar ]
• Album D, Westin S. Do diseases have a prestige hierarchy? A survey among physicians and medical students. Soc Sci Med. 2008;1:182–188. doi: 10.1016/j.socscimed.2007.07.003. [ DOI ] [ PubMed ] [ Google Scholar ]
• Sly R. What's in a name? Classifying 'the dropout' from treatment for anorexia nervosa. Eur Eat Disord Rev. 2009;1:405–407. doi: 10.1002/erv.964. [ DOI ] [ PubMed ] [ Google Scholar ]
• Strober M, Freeman R, Morrell W. The long-term course of severe anorexia nervosa in adolescents: survival analysis of recovery, relapse, and outcome predictors over 10–15 years in a prospective study. Int J Eat Disord. 1997;1:339–360. doi: 10.1002/(SICI)1098-108X(199712)22:4&#x0003c;339::AID-EAT1&#x0003e;3.0.CO;2-N. [ DOI ] [ PubMed ] [ Google Scholar ]
• Baran SA, Weltzin TE, Kaye WH. Low discharge weight and outcome in anorexia nervosa. Am J Psychiatry. 1995;1:1070–1072. doi: 10.1176/ajp.152.7.1070. [ DOI ] [ PubMed ] [ Google Scholar ]
• Watkins CE Jr. The supervision of psychotherapy supervisor trainees. Am J Psychother. 1994;1:417–431. doi: 10.1176/appi.psychotherapy.1994.48.3.417. [ DOI ] [ PubMed ] [ Google Scholar ]
• Wallier J, Vibert S, Berthoz S, Huas C, Hubert T, Godart N. Dropout from inpatient treatment for anorexia nervosa: critical review of the literature. Int J Eat Disord. 2009;1:636–647. doi: 10.1002/eat.20609. [ DOI ] [ PubMed ] [ Google Scholar ]
• Hudson JI, Hiripi E, Pope HG Jr, Kessler RC. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry. 2007;1:348–358. doi: 10.1016/j.biopsych.2006.03.040. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Eddy KT, Dorer DJ, Franko DL, Tahilani K, Thompson-Brenner H, Herzog DB. Diagnostic crossover in anorexia nervosa and bulimia nervosa: implications for DSM-V. Am J Psychiatry. 2008;1:245–250. doi: 10.1176/appi.ajp.2007.07060951. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Keys A, Brozek J, Henschel A, Mickelsen O, Taylor HL. The biology of human starvation. Minneapolis: University of Minnesota Press; 1950. [ Google Scholar ]
• American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-5) American Psychiatric Publishing: Washington, DC; 2013. [ Google Scholar ]
• Uher R, Rutter M. Classification of feeding and eating disorders: review of evidence and proposals for ICD-11. World Psychiatry. 2012;1:80–92. doi: 10.1016/j.wpsyc.2012.05.005. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Maguire S, Touyz S, Surgenor L, Crosby RD, Engel SG, Lacey H, Heywood-Everett S, Grange DL. The clinician administered staging instrument for anorexia nervosa: development and psychometric properties. Int J Eat Disord. 2012;1:390–399. doi: 10.1002/eat.20951. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Soh N, Touyz S, Surgenor LJ. Eating and body image disturbances across cultures. Eur Eat Disord Rev. 2006;1:54–65. doi: 10.1002/erv.678. [ DOI ] [ Google Scholar ]
• Wang J, Thornton JC, Russell M, Burastero S, Heymsfield S, Pierson RN Jr. Asians have lower body mass index (BMI) but higher percent body fat than do whites: comparisons of anthropometric measurements. Am J Clin Nutr. 1994;1:23–28. doi: 10.1093/ajcn/60.1.23. [ DOI ] [ PubMed ] [ Google Scholar ]
• Ung EK, Lee S, Kua EH. Anorexia nervosa and bulimia–a Singapore perspective. Singapore Med J. 1997;1:332–335. [ PubMed ] [ Google Scholar ]
• Soh NL, Touyz S, Dobbins T, Surgenor L, Clarke S, Kohn M, Lee EL, Leow V, Rieger E, Ung KE, Walter G. Body image disturbance in young North European and East Asian women with and without eating disorders in Australia and in Singapore. Eur Eat Disord Rev. 2008;1:287–296. doi: 10.1002/erv.836. [ DOI ] [ PubMed ] [ Google Scholar ]
• Soh N, Surgenor LJ, Touyz S, Walter G. Eating disorders across two cultures: does the expression of psychological control vary? Aust NZ J Psychiatry. 2007;1:351–358. doi: 10.1080/00048670701213278. [ DOI ] [ PubMed ] [ Google Scholar ]
• Rhys Jones W, Morgan JF. Eating disorders in men: a review of the literature. J Public Ment Health. 2010;1:23–31. doi: 10.5042/jpmh.2010.0326. [ DOI ] [ Google Scholar ]
• Siegel JH, Hardoff D, Golden NH, Shenker IR. Medical complications in male adolescents with anorexia nervosa. J Adolesc Health. 1995;1:448–453. doi: 10.1016/1054-139X(94)00003-W. [ DOI ] [ PubMed ] [ Google Scholar ]
• Carlat DJ, Camargo CA Jr, Herzog DB. Eating disorders in males: a report on 135 patients. Am J Psychiatry. 1997;1:1127–1132. doi: 10.1176/ajp.154.8.1127. [ DOI ] [ PubMed ] [ Google Scholar ]
• Nunez-Navarro A, Aguera Z, Krug I, Jimenez-Murcia S, Sanchez I, Araguz N, Gorwood P, Granero R, Penelo E, Karwautz A, Moragas L, Saldana S, Treasure J, Menchon JM, Fernandez-Aranda F. Do men with eating disorders differ from women in clinics, psychopathology and personality? Eur Eat Disord Rev. 2012;1:23–31. doi: 10.1002/erv.1146. [ DOI ] [ PubMed ] [ Google Scholar ]
• Marks LI. Deconstructing locus of control: Implications for practitioners. J Counsel Devel. 1998;1:251–260. doi: 10.1002/j.1556-6676.1998.tb02540.x. [ DOI ] [ Google Scholar ]
• Strober M, Freeman R, Lampert C, Diamond J, Teplinsky C, DeAntonio M. Are there gender differences in core symptoms, temperament, and short-term prospective outcome in anorexia nervosa? Int J Eat Disord. 2006;1:570–575. doi: 10.1002/eat.20293. [ DOI ] [ PubMed ] [ Google Scholar ]
• Gueguen J, Godart N, Chambry J, Brun-Eberentz A, Foulon C, Divac Phd SM, Guelfi JD, Rouillon F, Falissard B, Huas C. Severe anorexia nervosa in men: comparison with severe AN in women and analysis of mortality. Int J Eat Disord. 2012;1:537–545. doi: 10.1002/eat.20987. [ DOI ] [ PubMed ] [ Google Scholar ]
• Keel PK, Brown TA. The impact of relationships on the association between sexual orientation and disordered eating in men. Int J Eat Disord. 2012;1:792–799. doi: 10.1002/eat.22013. [ DOI ] [ PubMed ] [ Google Scholar ]
• Garner DM, Olmsted MP, Bohr Y, Garfinkel PE. The eating attitudes test: Psychometric features and clinical correlates. Psychol Med. 1982;1:871–878. doi: 10.1017/S0033291700049163. [ DOI ] [ PubMed ] [ Google Scholar ]
• Garner DM. Eating disorder inventory-3. Lutz, Florida: Psychological Assessment Resources, Inc.; 2004. [ Google Scholar ]
• Beglin S, Fairburn CG. In: Cognitive behaviour therapy and eating disorders. Fairburn CG, editor. New York: Guildford Press; 2008. Eating Disorder Examination Questionnaire (EDQ-Q 6.0) pp. 265–308. [ Google Scholar ]
• Sunday SR, Halmi KA, Einhorn A. The Yale-Brown-Cornell Eating Disorder Scale: a new scale to assess eating disorder symptomatology. Int J Eat Disord. 1995;1:237–245. doi: 10.1002/1098-108X(199511)18:3&#x0003c;237::AID-EAT2260180305&#x0003e;3.0.CO;2-1. [ DOI ] [ PubMed ] [ Google Scholar ]
• Clausen L, Rosenvinge JH, Friborg O, Rokkedal K. Validating the Eating Disorder Inventory-3 (EDI-3): A Comparison Between 561 Female Eating Disorders Patients and 878 Females from the General Population. J Psychopath Behav Assess. 2011;1:101–110. doi: 10.1007/s10862-010-9207-4. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• First MB, Spitzer RL, Gibbon M, Williams JBW. Structured Clinical Interview for DSM-IV Axis I Disorders, Clinical Version (SCID-CV) Washington, DC: American Psychiatric Press Inc.; 1996. [ Google Scholar ]
• Fairburn CG, Cooper Z. In: Binge Eating: Nature, Assessment and Treatment. Fairburn CG, Wilson GT, editor. New York: Guildford Press; 1993. The eating disorders examination; pp. 317–360. [ Google Scholar ]
• Mattar L, Huas C, Duclos J, Apfel A, Godart N. Relationship between malnutrition and depression or anxiety in Anorexia Nervosa: a critical review of the literature. J Affect Disord. 2011;1:311–318. doi: 10.1016/j.jad.2010.09.014. [ DOI ] [ PubMed ] [ Google Scholar ]
• Wolk SL, Loeb KL, Walsh BT. Assessment of patients with anorexia nervosa: interview versus self-report. Int J Eat Disord. 2005;1:92–99. doi: 10.1002/eat.20076. [ DOI ] [ PubMed ] [ Google Scholar ]
• Allen S, Dalton WT. Treatment of eating disorders in primary care: a systematic review. J Health Psychol. 2011;1:1165–1176. doi: 10.1177/1359105311402244. [ DOI ] [ PubMed ] [ Google Scholar ]
• Binford RB, Le Grange D, Jellar CC. Eating Disorders Examination versus Eating Disorders Examination-Questionnaire in adolescents with full and partial-syndrome bulimia nervosa and anorexia nervosa. Int J Eat Disord. 2005;1:44–49. doi: 10.1002/eat.20062. [ DOI ] [ PubMed ] [ Google Scholar ]
• Le Grange D, Crosby RD, Engel SG, Cao L, Ndungu A, Crow SJ, Peterson CB, Mitchell JE, Wonderlich SA. DSM-IV-defined anorexia nervosa versus subthreshold anorexia nervosa (EDNOS-AN) Eur Eat Disord Rev. 2013;1:1–7. doi: 10.1002/erv.2192. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Nordbo RH, Espeset EM, Gulliksen KS, Skarderud F, Geller J, Holte A. Reluctance to recover in anorexia nervosa. Eur Eat Disord Rev. 2012;1:60–67. doi: 10.1002/erv.1097. [ DOI ] [ PubMed ] [ Google Scholar ]
• Maguire S, Le Grange D, Surgenor LJ, Marks P, Lacey H, Touyz S. Staging anorexia nervosa: conceptualising illness severity. Early Intervent Psych. 2008;1:3–10. doi: 10.1111/j.1751-7893.2007.00049.x. [ DOI ] [ PubMed ] [ Google Scholar ]
• Touyz S, Thornton C, Rieger E, George L, Beumont P. The incorporation of the stage of change model in the day hospital treatment of patients with anorexia nervosa. Eur Child Adolesc Psychiatry. 2003;1(Suppl 1):I65–I71. doi: 10.1007/s00787-003-1109-5. [ DOI ] [ PubMed ] [ Google Scholar ]
• Loeb KL, Jones J, Roberto CA, Sonia Gugga S, Marcus SM, Attia E, Timothy Walsh B. Adolescent-adult discrepancies on the eating disorder examination: a function of developmental stage or severity of illness? Int J Eat Disord. 2011;1:567–572. doi: 10.1002/eat.20882. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Milos G, Spindler A, Schnyder U, Martz J, Hoek HW, Willi J. Incidence of severe anorexia nervosa in Switzerland: 40 years of development. Int J Eat Disord. 2004;1:250–258. doi: 10.1002/eat.10244. [ DOI ] [ PubMed ] [ Google Scholar ]
• Treasure J, Tchanturia K, Harrison A, Davies H, Roberts M, Oldershaw A, Stahl D, Morris R, Schmidt U. Cognitive flexibility and clinical severity in eating disorders. Plos One (Electronic Resource) 2001;1:e20462. doi: 10.1371/journal.pone.0020462. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Bauer S, Winn S, Schmidt U, Kordy H. Construction, scoring, and validation of the short evaluation of eating disorders (SEED) Eur Eat Disord Rev. 2005;1:191–200. doi: 10.1002/erv.637. [ DOI ] [ Google Scholar ]
• Treasure J, Sepulveda AR, MacDonald P, Whitaker W, Lopez C, Zabala M, Kyriacou O, Todd G. The assessment of the family of people with eating disorders. Eur Eat Disord Rev. 2008;1:247–255. doi: 10.1002/erv.859. [ DOI ] [ PubMed ] [ Google Scholar ]
• Schmidt U, Treasure J. Anorexia nervosa: valued and visible. A cognitive-interpersonal maintenance model and its implications for research and practice. Br J Clin Psychol. 2006;1:343–366. doi: 10.1348/014466505X53902. [ DOI ] [ PubMed ] [ Google Scholar ]
• Fisher CA, Hetrick SE, Rushford N. Family therapy for anorexia nervosa. Cochrane Database Syst Rev. 2010. Issue 4: Art. No: CD004780. [ DOI ] [ PubMed ]
• Godart NT, Perdereau F, Rein Z, Berthoz S, Wallier J, Jeammet P, Flament MF. Comorbidity studies of eating disorders and mood disorders. Critical review of the literature. J Affect Disord. 2007;1:37–49. doi: 10.1016/j.jad.2006.06.023. [ DOI ] [ PubMed ] [ Google Scholar ]
• Kennedy SH, Kaplan AS, Garfinkel PE, Rockert W, Toner B, Abbey SE. Depression in anorexia nervosa and bulimia nervosa: discriminating depressive symptoms and episodes. J Psychosom Res. 1994;1:773–782. doi: 10.1016/0022-3999(94)90030-2. [ DOI ] [ PubMed ] [ Google Scholar ]
• Mischoulon D, Eddy KT, Keshaviah A, Dinescu D, Ross SL, Kass AE, Franko DL, Herzog DB. Depression and Eating Disorders. J Affect Disord. 2011;1:470–477. doi: 10.1016/j.jad.2010.10.043. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• McElroy SL, Frye MA, Hellemann G, Altshuler L, Leverich GS, Suppes T, Keck PE, Nolen WA, Kupka R, Post RM. Prevalence and correlates of eating disorders in 875 patients with bipolar disorder. J Affect Disord. 2011;1:191–198. doi: 10.1016/j.jad.2010.06.037. [ DOI ] [ PubMed ] [ Google Scholar ]
• Preti A, Rocchi MB, Sisti D, Camboni MV, Miotto P. A comprehensive meta-analysis of the risk of suicide in eating disorders. Acta Psychiatr Scand. 2011;1:6–17. doi: 10.1111/j.1600-0447.2010.01641.x. [ DOI ] [ PubMed ] [ Google Scholar ]
• Bodell LP, Joiner TE, Keel PK. Comorbidity-independent risk for suicidality increases with bulimia nervosa but not with anorexia nervosa. J Psychiatr Res. 2013;1:617–621. doi: 10.1016/j.jpsychires.2013.01.005. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Hawton K, Casanas ICC, Haw C, Saunders K. Risk factors for suicide in individuals with depression: A systematic review. J Affect Disord. 2013;1:17–28. doi: 10.1016/j.jad.2013.01.004. [ DOI ] [ PubMed ] [ Google Scholar ]
• Forcano L, Alvarez E, Santamaria JJ, Jimenez-Murcia S, Granero R, Penelo E, Alonso P, Sanchez I, Menchon JM, Ulman F, Bulik CM, Fernandez-Aranda F. Suicide attempts in anorexia nervosa subtypes. Compr Psychiatry. 2011;1:352–358. doi: 10.1016/j.comppsych.2010.09.003. [ DOI ] [ PubMed ] [ Google Scholar ]
• Favaro A, Santonastaso P. Suicidality in eating disorders: clinical and psychological correlates. Acta Psychiatr Scand. 1997;1:508–514. doi: 10.1111/j.1600-0447.1997.tb10139.x. [ DOI ] [ PubMed ] [ Google Scholar ]
• Rosling AM, Sparen P, Norring C, von Knorring AL. Mortality of eating disorders: a follow-up study of treatment in a specialist unit 1974–2000. Int J Eat Disord. 2011;1:304–310. doi: 10.1002/eat.20827. [ DOI ] [ PubMed ] [ Google Scholar ]
• Papadopoulos FC, Ekbom A, Brandt L, Ekselius L. Excess mortality, causes of death and prognostic factors in anorexia nervosa. Br J Psychiatry. 2009;1:10–17. doi: 10.1192/bjp.bp.108.054742. [ DOI ] [ PubMed ] [ Google Scholar ]
• Morgan JF, Ahene P, Lacey JH. Salinophagia in anorexia nervosa: case reports. Int J Eat Disord. 2010;1:190–192. doi: 10.1002/eat.20673. [ DOI ] [ PubMed ] [ Google Scholar ]
• Morgan JF, Lacey JH. Scratching and fasting: a study of pruritus and anorexia nervosa. Br J Dermatol. 1999;1:453–456. doi: 10.1046/j.1365-2133.1999.02708.x. [ DOI ] [ PubMed ] [ Google Scholar ]
• Morgan JF, Lacey JH. Blood-letting in anorexia nervosa: a case study. Int J Eat Disord. 2000;1:483–485. doi: 10.1002/(SICI)1098-108X(200005)27:4&#x0003c;483::AID-EAT15&#x0003e;3.0.CO;2-Y. [ DOI ] [ PubMed ] [ Google Scholar ]
• Skegg K. Self-harm. Lancet. 2005;1:1471–1483. doi: 10.1016/S0140-6736(05)67600-3. [ DOI ] [ PubMed ] [ Google Scholar ]
• Steinglass JE, Sysko R, Glasofer D, Albano AM, Simpson HB, Walsh BT. Rationale for the application of exposure and response prevention to the treatment of anorexia nervosa. Int J Eat Disord. 2011;1:134–141. doi: 10.1002/eat.20784. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Swinbourne JM, Touyz SW. The co-morbidity of eating disorders and anxiety disorders: a review. Eur Eat Disord Rev. 2007;1:253–274. doi: 10.1002/erv.784. [ DOI ] [ PubMed ] [ Google Scholar ]
• Touyz S, Swinbourne J, Hunt C, Abbott M, Russell J, St Clare T. The comorbidity between eating disorders and anxiety disorders: prevalence in an eating disorder sample and anxiety disorder sample. Aust NZ J Psychiatry. 2012;1:118–131. doi: 10.1177/0004867411432071. [ DOI ] [ PubMed ] [ Google Scholar ]
• Pallister E, Waller G. Anxiety in the eating disorders: understanding the overlap. Clin Psychol Rev. 2008;1:366–386. doi: 10.1016/j.cpr.2007.07.001. [ DOI ] [ PubMed ] [ Google Scholar ]
• Godart NT, Flament MF, Perdereau F, Jeammet P. Comorbidity between eating disorders and anxiety disorders: a review. Int J Eat Disord. 2002;1:253–270. doi: 10.1002/eat.10096. [ DOI ] [ PubMed ] [ Google Scholar ]
• Fairburn CG, Cooper Z, Shafran R. Cognitive behaviour therapy for eating disorders: a "transdiagnostic" theory and treatment. Behav Res Ther. 2003;1:509–528. doi: 10.1016/S0005-7967(02)00088-8. [ DOI ] [ PubMed ] [ Google Scholar ]
• Yackobovitch-Gavan M, Golan M, Valevski A, Kreitler S, Bachar E, Lieblich A, Mitrani E, Weizman A, Stein D. An integrative quantitative model of factors influencing the course of anorexia nervosa over time. Int J Eat Disord. 2009;1:306–317. doi: 10.1002/eat.20624. [ DOI ] [ PubMed ] [ Google Scholar ]
• Krug I, Pinheiro AP, Bulik C, Jimenez-Murcia S, Granero R, Penelo E, Masuet C, Aguera Z, Fernandez-Aranda F. Lifetime substance abuse, family history of alcohol abuse/dependence and novelty seeking in eating disorders: comparison study of eating disorder subgroups. Psychiatry Clin Neurosci. 2009;1:82–87. doi: 10.1111/j.1440-1819.2008.01908.x. [ DOI ] [ PubMed ] [ Google Scholar ]
• Herzog DB, Franko DL, Dorer DJ, Keel PK, Jackson S, Manzo MP. Drug abuse in women with eating disorders. Int J Eat Disord. 2006;1:364–368. doi: 10.1002/eat.20257. [ DOI ] [ PubMed ] [ Google Scholar ]
• O'Brien KM, Vincent NK. Psychiatric comorbidity in anorexia and bulimia nervosa: nature, prevalence, and causal relationships. Clin Psychol Rev. 2003;1:57–74. doi: 10.1016/S0272-7358(02)00201-5. [ DOI ] [ PubMed ] [ Google Scholar ]
• Baker JH, Thornton LM, Strober M, Brandt H, Crawford S, Fichter MM, Halmi KA, Johnson C, Jones I, Kaplan AS, Klump KL, Mitchell JE, Treasure J, Woodside DB, Berrettini WH, Kaye WH, Bulik CM. Temporal sequence of comorbid alcohol use disorder and anorexia nervosa. Addict Behav. 2013;1:1704–1709. doi: 10.1016/j.addbeh.2012.10.005. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Bulik CM, Klump KL, Thornton L, Kaplan AS, Devlin B, Fichter MM, Halmi KA, Strober M, Woodside DB, Crow S, Mitchell JE, Rotondo A, Mauri M, Cassano GB, Keel PK, Berrettini WH, Kaye WH. Alcohol use disorder comorbidity in eating disorders: a multicenter study. J Clin Psychiatry. 2004;1:1000–1006. doi: 10.4088/JCP.v65n0718. [ DOI ] [ PubMed ] [ Google Scholar ]
• Root TL, Pisetsky EM, Thornton L, Lichtenstein P, Pedersen NL, Bulik CM. Patterns of co-morbidity of eating disorders and substance use in Swedish females. Psychol Med. 2010;1:105–115. doi: 10.1017/S0033291709005662. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Pinter O, Probst M, Vandereycken W, Pieters G, Goris M. The predictive value of body mass index for the weight evolution in anorexia nervosa. Eat Weight Disord. 2004;1:232–235. doi: 10.1007/BF03325073. [ DOI ] [ PubMed ] [ Google Scholar ]
• National Institute for Clinical Excellence. Eating disorders: Core interventions in the treatment and management of anorexia nervosa, bulimia nervosa, and related eating disorders. London: National Institute for Clinical Excellence; 2004. [ PubMed ] [ Google Scholar ]
• Bodell LP, Mayer LE. Percent body fat is a risk factor for relapse in anorexia nervosa: a replication study. Int J Eat Disord. 2011;1:118–123. doi: 10.1002/eat.20801. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Flegal KM, Wei R, Ogden C. Weight-for-stature compared with body mass index-for-age growth charts for the United States from the Centers for Disease Control and Prevention. Am J Clin Nutr. 2002;1:761–766. doi: 10.1093/ajcn/75.4.761. [ DOI ] [ PubMed ] [ Google Scholar ]
• Lindblad F, Lindberg L, Hjern A. Improved survival in adolescent patients with anorexia nervosa: a comparison of two Swedish national cohorts of female inpatients. Am J Psychiatry. 2006;1:1433–1435. doi: 10.1176/appi.ajp.163.8.1433. [ DOI ] [ PubMed ] [ Google Scholar ]
• Nicholls D, Hudson L, Mahomed F. Managing anorexia nervosa. Arch Dis Child. 2011;1:977–982. doi: 10.1136/adc.2009.177394. [ DOI ] [ PubMed ] [ Google Scholar ]
• Katzman DK. Medical complications in adolescents with anorexia nervosa: a review of the literature. Int J Eat Disord. 2005;1(Suppl):S52–S59. doi: 10.1002/eat.20118. discussion S87-9. [ DOI ] [ PubMed ] [ Google Scholar ]
• Lesinskiene S, Barkus A, Ranceva N, Dembinskas A. A meta-analysis of heart rate and QT interval alteration in anorexia nervosa. World J Biol Psychia. 2008;1:86–91. doi: 10.1080/15622970701230963. [ DOI ] [ PubMed ] [ Google Scholar ]
• Zipfel S, Sammet I, Rapps N, Herzog W, Herpertz S, Martens U. Gastrointestinal disturbances in eating disorders: clinical and neurobiological aspects. Auton Neurosci. 2006;1:99–106. doi: 10.1016/j.autneu.2006.07.023. [ DOI ] [ PubMed ] [ Google Scholar ]
• Casiero D, Frishman WH. Cardiovascular complications of eating disorders. Cardiol Rev. 2006;1:227–231. doi: 10.1097/01.crd.0000216745.96062.7c. [ DOI ] [ PubMed ] [ Google Scholar ]
• Montecchi PP, Custureri V, Polimeni A, Cordaro M, Costa L, Marinucci S, Montecchi F. Oral manifestations in a group of young patients with anorexia nervosa. Eat Weight Disord. 2003;1:164–167. doi: 10.1007/BF03325007. [ DOI ] [ PubMed ] [ Google Scholar ]
• Sylvester CJ, Forman SF. Clinical practice guidelines for treating restrictive eating disorder patients during medical hospitalization. Curr Opin Pediatr. 2008;1:390–397. doi: 10.1097/MOP.0b013e32830504ae. [ DOI ] [ PubMed ] [ Google Scholar ]
• Mascolo M, Trent S, Colwell C, Mehler PS. What the emergency department needs to know when caring for your patients with eating disorders. Int J Eat Disord. 2012;1:977–981. doi: 10.1002/eat.22035. Early view - Online Only. [ DOI ] [ PubMed ] [ Google Scholar ]
• Ayton A, Keen C, Lask B. Pros and cons of using the Mental Health Act for severe eating disorders in adolescents. Eur Eat Disord Rev. 2009;1:14–23. doi: 10.1002/erv.887. [ DOI ] [ PubMed ] [ Google Scholar ]
• Carney T, Tait D, Touyz S, Ingvarson M, Saunders D, Wakefield A. Managing anorexia nervosa: Clinical, legal, and social perspectives on involuntary treatment. New York: Nova; 2006. [ Google Scholar ]
• Carney T, Tait D, Touyz S. Coercion is coercion? Reflections on trends in the use of compulsion in treating anorexia nervosa. Australas Psychiatry. 2007;1:390–395. doi: 10.1080/10398560701458202. [ DOI ] [ PubMed ] [ Google Scholar ]
• Guarda AS, Pinto AM, Coughlin JW, Hussain S, Haug NA, Heinberg LJ. Perceived coercion and change in perceived need for admission in patients hospitalized for eating disorders. Am J Psychiatry. 2007;1:108–114. doi: 10.1176/appi.ajp.164.1.108. [ DOI ] [ PubMed ] [ Google Scholar ]
• Tan JO, Stewart A, Fitzpatrick R, Hope T. Attitudes of patients with anorexia nervosa to compulsory treatment and coercion. Int J Law Psychiatry. 2010;1:13–19. doi: 10.1016/j.ijlp.2009.10.003. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Gody A, Haynes SN. Clinical case formulation: Introduction to a special section. Eur J Psychol Assess. 2011;1:1–3. doi: 10.1027/1015-5759/a000055. [ DOI ] [ PubMed ] [ Google Scholar ]
• Swain-Campbell NR, Surgenor LJ, Snell DL. An analysis of consumer perspectives following contact with an eating-disorders service. Aust NZ J Psychiatry. 2001;1:99–103. doi: 10.1046/j.1440-1614.2001.00855.x. [ DOI ] [ PubMed ] [ Google Scholar ]
• Holte A, Gulliksen KS, Espeset EM, Nordbo RH, Skarderud F, Geller J. Preferred therapist characteristics in treatment of anorexia nervosa: The patient's perspective. Int J Eat Disord. 2012;1:932–941. doi: 10.1002/eat.22033. Early View. [ DOI ] [ PubMed ] [ Google Scholar ]
• Strober M, Johnson C. The need for complex ideas in anorexia nervosa: why biology, environment, and psyche all matter, why therapists make mistakes, and why clinical benchmarks are needed for managing weight correction. Int J Eat Disord. 2012;1:155–178. doi: 10.1002/eat.22005. [ DOI ] [ PubMed ] [ Google Scholar ]
• Mickan S, Burls A, Glasziou P. Patterns of 'leakage' in the utilisation of clinical guidelines: a systematic review. Postgrad Med J. 2011;1:670–679. doi: 10.1136/pgmj.2010.116012. [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Royal Australian and New Zealand College of Psychiatrists Clinical Practice Guidelines Team for Anorexia Nervosa. Australian and New Zealand clinical practice guidelines for the treatment of anorexia nervosa. Aust NZ J Psychiatry. 2004;1:659–670. [ Google Scholar ]
• American Psychiatric Association. Practice guidelines for the treatment of patients. Am J Psychiatry. 2000;1:1–39. [ PubMed ] [ Google Scholar ]
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