Antonella: ‘A Stranger in the Family’—A Case Study of Eating Disorders Across Cultures

  • Open Access
  • First Online: 12 December 2020

Cite this chapter

You have full access to this open access chapter

case study for anorexia

  • Vincenzo Di Nicola 6 , 7  

7652 Accesses

2 Citations

7 Altmetric

The story of Antonella illustrates the way in which cultural and other values impact on the presentation and treatment of eating disorders. Displaced from her European home culture to live in Canada, Antonella presents with an eating disorder and a fluctuating tableau of anxiety and mood symptoms linked to her lack of a sense of identity. These arose against a background of her adoption as a foundling child in Italy and her attachment problems with her adoptive family generating chronically unfixed and unstable identities, resulting in her cross-cultural marriage as both flight and refuge followed by intense conflicts. Her predicament is resolved only when after an extended period in cultural family therapy she establishes a deep cross-species identification by becoming a breeder of husky dogs. The wider implications of Antonella’s story for understanding the relationship between cultural values and mental health are briefly considered.

You have full access to this open access chapter,  Download chapter PDF

Similar content being viewed by others

case study for anorexia

Overlaps and Disjunctures: A Cultural Case Study of a British Indian Young Woman’s Experiences of Bulimia Nervosa

René girard and the mimetic nature of eating disorders, the rise of eating disorders in asia: a review.

  • Eating disorders
  • Anorexia multiforme
  • Cultural values
  • Uniqueness of the individual
  • Role of animals
  • Cross-species identification
  • Cultural family therapy

1 Introduction

Eating disorders are a potentially fruitful area of study for understanding the links between values—in particular cultural values—and mental distress and disorder. Eating disorders show widely different prevalence rates across cultures, and much attention has been given to theories linking these differences with variations in cultural values. In particular, the cultural value placed on ‘fashionable slimness’ in the industrialised world has for some time been identified with the greater prevalence of eating disorders among women in Western societies [ 1 ]. Consistently with this view, the growing prevalence of eating disorders in other parts of the world does seem to be correlated with increasing industrialisation [ 2 , 3 ]. In my review of cultural distribution and historical evolution of eating disorders , I was so struck by its protean nature and its variability of clinical presentations of anorexia nervosa that I renamed this predicament ‘anorexia multiforme’ [ 4 , 5 ].

The story of Antonella that follows illustrates the potential importance of contemporary theories linking cultural values with eating disorders though also some of their limitations.

2 Case Narrative: Antonella’s Story

Ottawa in the early 1990s. Antonella Trevisan, a 24-year-old woman, was referred to me by an Italian psychiatrist and family therapist, Dr. Claudio Angelo, who had treated her in Italy [ 6 ] . When Antonella came to Canada to live with a man she had met through her work, Dr. Angelo referred her to me. Antonella’s presenting problems concerned two areas of her life: her eating problems, which emerged after her emigration from Italy, and her relationship with her partner in Canada.

2.1 Antonella’s Predicament

My initial psychiatric consultation (conducted in Italian) revealed the complexities of Antonella’s life. This was reflected in the difficulty of making an accurate diagnosis. Her food-related problems had some features of eating disorders , such as restriction of intake, the resulting weight loss, and a history of weight gain and being teased for it. What was missing was the ‘psychological engine’ of an eating disorder: a drive for thinness or a morbid fear of fatness. Her problem was perhaps better understood as a food-related anxiety arising from a ‘globus’ sensation (lump in the throat) and a learned avoidance response that generalized from one specific situation to eating in any context.

Although it was clear that her weight gain in late adolescence and the teasing and insults from her mother had sensitized her, other factors had to be considered. Antonella showed an exquisite rejection sensitivity that both arose from and was a metaphor for the circumstances of her birth and adoption. Her migration to Canada also seemed to generate anxieties and uncertainties, and there were hints of conflicts with her partner. Was she also re-enacting another, earlier trauma? In the first journey of her life, she was given up by her birth mother (or taken away?) and left on the steps of a foundry. In the first year of her life, Antonella had shown failure to thrive and developmental delays. And she had, at best, an insecure attachment to her adoptive family, predisposing her to lifelong insecurities.

2.2 A Therapeutic Buffet

After my assessment, we faced a choice: whether to treat the eating problem concretely, in purely behavioral terms, or more metaphorically, with some form of psychotherapy. Given the stabilization of her eating pattern and her weight and the larger context of her predicament, we negotiated to do psychotherapy. There were several components to her therapy. Starting with a psychiatric consultation, three types of therapy were negotiated, with Antonella sampling a kind of ‘therapeutic buffet’ over a period of some 2 years: individual therapy for Antonella, couple therapy for Antonella and Rick, and brief family therapy with Antonella’s adoptive family visiting from Italy.

The individual work with Antonella was at first exploratory, getting to know the complex bicultural world of the Italian Alps, how she experienced the move to Canada, examining her choices to move here and live with Rick. Sessions were conducted in a mix of Italian and English. At first, the Italian language was like a ‘transitional object’ in her acculturation process; slowly, as she gained confidence in her daily life, English began to dominate her sessions. Under stress, however, she would revert to Italian. I could follow her progress just by noting the balance of Italian and English in each session. This does not imply any superiority of English or language preferences; rather, it acknowledges the social realities of culture making its demands felt even in private encounters. This is the territory of sociolinguistics [ 7 , 8 ] . Like Italian, these individual sessions were a secure home base to which Antonella returned during times of stress or between other attempts to find solutions.

After some months in Canada and the stabilization of her eating problems, Antonella became more invested in examining her relationship to Rick. They had met through work while she was still in Italy. After communicating on the telephone, she daringly took him up on an offer to visit. During her holiday in Canada, a romance developed. After her return to Italy, Antonella made the extraordinary decision to emigrate, giving up an excellent position in industry, leaving her family for a country she did not know well. Rick is 22 years her senior and was only recently separated from his first wife.

In therapy she not only expressed ambivalence about her situation with Rick but enacted it. She asked for couple sessions to discuss some difficulties in their relationship. Beyond collecting basic information, couple sessions were unproductive. While Rick was frank about his physical attraction to her and his desire to have children, Antonella talked about their relationship in an oddly detached way. She could not quite articulate her concerns. As we got closer to examining the problems of their relationship, Antonella abruptly announced that they were planning their wedding. The conjoint sessions were put on hold as they dealt with the wedding arrangements.

Her parents did not approve of the marriage and boycotted the wedding. Her paternal aunt, however, agreed to come to Canada for the wedding. Since I was regarded by Antonella as part of her extended family support system, she brought her aunt to meet me. It gave me another view of Antonella’s family. Her aunt was warm and supportive of Antonella, trying to smooth over the family differences. A few months later, at Christmas time, her parents and sister visited, and Antonella brought them to meet me. To understand these family meetings, however, it is necessary to know Antonella’s early history.

2.3 A Foundling Child

Antonella was a foundling child. Abandoned on the steps of a foundry in Turin as a newborn, she was the subject of an investigation into the private medical clinics of Turin. This revealed that the staff of the clinic where she was born was ‘paid off to hide the circumstances of my birth.’ As a result, her date of birth could only be presumed because the clinic staff destroyed her birth records. She was taken into care by the state and, as her origins could not be established, she was put up for adoption.

Antonella has always tried to fill in this void of information with meaning that she draws from her own body. She questions me closely: ‘Just look at me. Don’t you think I look like a Japanese?’ She feels that her skin tone is different from other Italians, that her facial features and eyes have an ‘Asian’ cast. With a few, limited facts, and some speculation, she has constructed a personal myth: that she is the daughter of an Italian mother from a wealthy family (hence her hidden birth in a private clinic) and a Japanese father (hence her ‘Asian’ features). It is oddly reassuring to her, but also perhaps a source of her alienation from her family.

At about 6 months of age, Antonella was adopted into a family in the Italian Alps, near the border with Austria. This is a bicultural region where both Italian and German are spoken and services are available in both languages (much like Ottawa, which is bilingually English and French). Her father, Aldo, who is Italian, is a retired FIAT factory worker. Annalise, her mother, who is a homemaker, had an Italian father and an Austrian mother. About her family she said, ‘I had a wonderful childhood compared to what came afterwards.’ Years after her adoption, her parents had a natural child, Oriana, who is 15.

She describes her mother as the disciplinarian at home. Her mother, she said, was ‘tough, German.’ When she visited her Austrian grandmother, no playing was allowed in that strict home. Her own mother allowed her ‘no friends in the house,’ but her father ‘was my pal when I was a kid.’ Although she had a good relationship with her father, he became ‘colder’ when she turned 13. Her parents’ relationship is remembered as cordial, but she later learned that they had many marital problems. Mother told her that she married to get away from home, but in fact she was in love with someone else. Overall, the feeling is of a rigid family organization. Her father is clearly presented by Antonella as warmer and more sociable. She experiences her mother as being ‘tough’. But she is crying all the time, feeling betrayed by everybody.

2.4 A Family Visit from the Italian Alps

When her family finally came to visit, Antonella brought them to see me. At first, the session had the quality of a student introducing out-of-town parents to her college teacher. They were pleased that I spoke Italian and knew Dr. Angelo, who they trusted. I soon found that the Trevisans were hungry to tell their story. Instead of a social exchange of pleasantries, this meeting turned into the first session of an impromptu course of brief family therapy.

Present were Antonella’s parents, Aldo and Annalise, and her sister, Oriana. Annalise led the conversation. Relegating Aldo to a support role. Oriana alternated between disdain and agitation, punctuated by bored indifference. Annalise had much to complain about: her own troubled childhood, her sense of betrayal and abandonment, heightened by Antonella’s departure from the family and from Italy. I was struck by the parallel themes of abandonment in mother and daughter. Mother clearly needed to tell this story, so I tried to set the stage for the family to hear her, what narrative therapists call ‘recruiting an audience’ [ 9 ] . I used Antonella, who I knew best, as a barometer of the progress of the session, and by that indicator, believed it had gone well.

When I saw them again some 10 days later, I was stunned by the turn of events. Oriana had assaulted her parents. The father had bandages over his face and the mother had covered her bruises with heavy make-up and dark glasses. Annalise was very upset about Oriana, who was defiant and aggressive at home. For her part, Oriana defended herself by saying she had been provoked and hit by her mother. Worried by this dangerous escalation, I tried to open some space for a healthy standoff and renegotiation.

Somehow, the concern had shifted away from Antonella to Oriana. Antonella was off the hook, but I waited for an opening to deal with this. I first tried to explore the cultural attitudes to adolescence in Italy by asking how the Italian and the German subcultures in their area understood teenagers differently. What were Oriana’s concerns? Had they seen this outburst coming? The whole family participated in a kind of sociological overview of Italian adolescence, with me as their grateful audience. The parents demonstrated keen insight and empathy. Concerned about Oriana’s experience of the session, I made a concerted effort to draw her into it. Eventually, the tone of the session lightened. Knowing they would return to Italy soon, I explored whether they had considered family work. Since they had met a few times with Dr. Angelo over Antonella’s eating problems, they were comfortable seeing Dr. Angelo as a family to find ways to understand Oriana and her concerns and for Oriana to explore other, nonviolent ways to be heard in the family. I agreed to meet them again before their departure and to communicate with Dr. Angelo about their wishes. On their way out, I wondered aloud about the apparent switch in their focus from Antonella to Oriana. The parents reassured me that they were ready to let Antonella live her own life now.

When they returned to say goodbye, we had a brief session. Oriana and Antonella were oddly buoyant and at ease. The parents were relieved. Antonella had offered the possibility of Oriana returning to spend the summer in Canada with her. I tried to connect this back to the previous session, wondering how much the two sisters supported each other. I was delighted, I said emphatically, by the family’s apparent approval of Antonella’s marriage to Rick. It was striking that, even from a distance of thousands of miles away, Antonella was still a part of the Trevisan family. And Rick was still not in the room.

3 Discussion

In this section, I will consider the impact of cultural and other values on Antonella and those around her and then look briefly at the wider implications of her story for our understanding not only of eating disorders but of mental distress and disorders in general.

3.1 Antonella: Life Before Man

The key to understanding Antonella’s attachments was her passion for her Siberian huskies. In the language of values-based practice , it was above all her huskies that mattered or were important to her. And it is not hard to see why. From the beginning of her relationship with Rick, she used her interest in dogs as a way for them to be more socially active as a couple, getting them out of the house to go to dog shows, for example. As her interests expanded, she wanted to buy bitches for breeding and to set up a kennel. Rick was only reluctantly supportive in this. Nonetheless, they ended up buying a home in the country where she could establish a kennel. Her haggling with Rick over the dogs was quite instrumental on her part, representing her own choices and interests and a test of the extent to which Rick would support her.

Yet the importance to Antonella of her huskies rests I believe on deeper cultural factors, both negative and positive. As to negative factors , these are evident in the fact that from the first days of her life, Antonella was rejected by her birth parents, literally abandoned and exposed, and later adopted by what she experienced as a non-nurturing family. Positive cultural factors , on the other hand, are evident in the way that having thrown her net wider afield, she looked initially to Canada, and to Rick, for nurturance and for identity. Then, finding herself only partly satisfied, she turned to the nonhuman world for the constancy of affection she could not find with people. Her huskies gave her pleasure, a task, and an identity. She spent many sessions discussing their progress, showing me pictures of her dogs and their awards. As it happened, my secretary at the time was also a dog lover who raised Samoyed dogs (related to huskies) and the two of them exchanged stories of dog lore.

As to positive factors , again, is there something, too, in the mythology of Canada that helps us understand Antonella? Does Canada still hold a place in the European imagination as a ‘New World’ for radical departures and identity makeovers? Or does Canada specifically represent the ‘malevolent North,’ as Margaret Atwood [ 10 ] calls it in her exploration of Canadian fiction? Huskies are a Northern animal, close to the wolf in their origins and habits. Bypassing the human world, Antonella finds her identity within a new world through its animals. If people have failed her, then she will leave not only her own tribe (Italy), but skip the identification with Canada’s Native peoples, responding to the ‘call of the wild’ to identify with a ‘life before man’ (to use another of Atwood’s evocative phrases, [ 11 ]), finding companionship and solace with her dogs.

3.2 Wider Implications of Antonella’s Story

Antonella may seem on first inspection something of an outlier to the human tribe. Orphaned from her culture of origin, she finds her place not in another country but by identification with another and altogether wilder species, her husky dogs. Yet, understood through the lens of values-based practice Antonella’s story has, I believe, wider significance at a number of levels.

First, Antonella’s story is significant for our understanding of the role of values – of what is important or matters to the individual concerned – in the presentation and treatment of eating disorders , and, by extension, of perhaps many other forms of mental distress and disorder. Specifically, her story provides at least one clear ‘proof of principle’ example supporting the role of cultural values.

As noted in my introduction, much attention has been given in the literature to the correlations between the uneven geographical distribution of eating disorders and cultural values. Correlations are of course no proof of causation. But in Antonella’s story at least the role of cultural values seems clearly evident. They were key to understanding her presenting problems. And this understanding in turn proved to be key to the cultural family therapy [ 12 ] through which these problems were, at least to the extent of her presenting eating disorder, resolved.

The cultural values involved, it is true, were not those of fashionable slimness so widely discussed in the literature. But this takes us to a second level at which Antonella’s story has wider significance. For it shows that to the extent that cultural values are important in eating disorders , their importance plays out at the level of individually unique persons. In this sense, social stresses and cultural values are played out in the body of the individual suffering with an eating disorder, making her body the ‘final frontier’ of psychiatric phenomenology [ 13 ]. Yes, there are no doubt valid cultural generalisations to be made about eating disorders and mental disorders of other kinds. And yes, these generalisations no doubt include generalisations about cultural values—about things that matter or are important to this or that group of people as a whole. Yet, this does not mean that we can ignore the values of the particular individual concerned. It has been truly said in values-based practice that as to their values, everyone is an ‘ n of 1’ [ 14 ]. Antonella, then, in the very idiosyncrasies of her story, reminds us of the idiosyncrasies of the stories of each and every one of us, whatever the culture or cultures to which we belong.

Antonella’s identification with animals , furthermore, to come to yet another level at which her story has wider significance, was a strongly positive factor in her recovery. As with other areas of mental health, it is with the negative impact of cultural values that the literature has been largely concerned: the pathogenetic influences of cultural values of slimness being a case in point in respect of eating disorders . Antonella’s story illustrates what has been clear for some time in the ‘recovery movement’, that positive values are often the very key to recovery. Not only that, but as Antonella’s passion for her husky dogs illustrates, the particular positive values concerned may, and importantly often are, individually unique.

Not, it is worth adding finally, that Antonella’s values were in this respect entirely unprecedented. Animals , after all, are widely valued, positively and negatively, and for many different reasons, in many cultures [ 11 ]. Their healing powers are indeed acknowledged. Just how far these powers depend on the kind of cross-species identification shown by Antonella, remains a matter for speculation. But, again, her story even in this respect is far from unique. Elsewhere, I have described the story of a white boy with what has become known as the ‘Grey Owl Syndrome’ , wishing to be native [ 12 , chapter 5 ]. Similarly, in Bear , Canadian novelist Marion Engel [ 15 ] portrays Lou, a woman who lives in the wilderness and befriends a bear. Lou seeks her identity from him: ‘Bear, make me comfortable in the world at last. Give me your skin’ [ 15 , p. 106]. After some time with the bear, the woman changes: ‘What had passed to her from him she did not know…. She felt not that she was at last human, but that she was at last clean’ [ 15 , p. 137]. It was perhaps to some similarly partial resolution that Antonella came.

4 Conclusions

Antonella’s story as set out above goes to the heart of the importance of cultural values in mental health. Her presenting eating disorder develops when, displaced from her culture of origin in Italy, and in effect rejected by her birth family, she finds healing only through cross-species identification with the wildness of husky dogs in her adoptive country of Canada. Although somewhat unusual in its specifics, her story illustrates the importance of cultural values at a number of levels in the presentation and management of eating and other forms of mental distress disorder.

And Antonella? I met her again in a gallery in Ottawa, rummaging through old prints. She was asking about prints of dogs; I was looking for old prints of Brazil where my father had made a second life. How was she, I asked? ‘Well …,’ she said hesitantly. Was that a healthy ‘well’ or the start of an explanation? ‘Me and Rick are splitting up,’ she said without ceremony, ‘but I still have the huskies.’ For each of us, the prints represented another world of connections.

Makino M, Tsuboi K, Denerson L. Prevalence of eating disorders: a comparison of Western and non-Western countries. MedGenMed. 2004;6(3):49. Published online 2004 Sep 27 at: .

PubMed   PubMed Central   Google Scholar  

Erskine HE, Whiteford HA, Pike KM. The global burden of eating disorders. Curr Opin Psychiatry. 2016;29(6):346–53.

Article   Google Scholar  

Selvini Palazzoli M. Anorexia nervosa: a syndrome of the affluent society. Transcult Psychiatr Res Rev. 1985;22( 3 ):199–205.

Google Scholar  

Di Nicola VF. Overview: anorexia multiforme: self-starvation in historical and cultural context. I: self-starvation as a historical chameleon. Transcult Psychiatr Res Rev. 1990;27(3):165–96.

Di Nicola VF. Overview: anorexia multiforme: self-starvation in historical and cultural context. II: anorexia nervosa as a culture-reactive syndrome. Transcult Psychiatr Res Rev. 1990;27(4):245–86.

Andolfi M, Angelo C, de Nichilo M. The myth of atlas: families and the therapeutic story. Edited & translated by Di Nicola VF. New York: Brunner-Routledge; 1989.

Douglas M. Humans speak. Ch 11. In: Implicit meanings: essays in anthropology. London: Routledge & Kegan Paul; 1975. p. 173–80.

Crystal D. The Cambridge encyclopedia of language. Cambridge: Cambridge University Press; 1987.

Parry A, Doan RE. Story re-visions: narrative therapy in the postmodern world. New York: Guilford Press; 1995.

Atwood M. Strange things: the malevolent north in Canadian literature. Oxford: Oxford University Press; 1995.

Atwood M. Life before man: a novel. New York: Anchor Books; 1998.

Di Nicola VF. A stranger in the family: culture, families, and therapy. New York: W.W. Norton & Co.; 1997.

Nasser M, Di Nicola V. Changing bodies, changing cultures: an intercultural dialogue on the body as the final frontier. Ch 9. In: Nasser M, Katzman MA, Gordon RA, editors. Eating disorders and cultures in transition. East Sussex: Brunner-Routledge; 2001. p. 171–93.

Fulford KWM, Peile E, Carroll H. A smoking enigma: getting and not getting the knowledge. Ch 6. In: Fulford KWM, Peile E, Carroll H, editors. Essential values-based practice: clinical stories linking science with people. Cambridge: Cambridge University Press; 2012. p. 65–82.

Chapter   Google Scholar  

Engel M. Bear: a novel. Toronto: Emblem (Penguin Random House Books); 2009.

Download references


The story of Antonella was first published in reference [ 12 ] (pp. 214–220) and presented at the Advanced Studies Seminar of the Collaborating Centre for Values-based Practice in Health and Social Care at St Catherine’s College, Oxford in October 2019. The names and other details of the case have been altered to maintain confidentiality. Parts of the discussion are adapted from that publication and the Oxford seminar. I am grateful to the publishers for permission to reproduce these materials here and to Professor Fulford and the members of the Advanced Studies Seminar for their stimulating exchanges. The subheading to the discussion of Antonella’s story (‘Life before Man’) was inspired by Margaret Atwood’s novel, Life Before Man [ 11 ].

Author information

Authors and affiliations.

Canadian Association of Social Psychiatry (CASP), World Association of Social Psychiatry (WASP), Department of Psychiatry and Addictions, University of Montreal, Montreal, QC, Canada

Vincenzo Di Nicola

Department of Psychiatry and Behavioral Sciences, The George Washington University, Washington, DC, USA

You can also search for this author in PubMed   Google Scholar

Corresponding author

Correspondence to Vincenzo Di Nicola .

Editor information

Editors and affiliations.

Medical University Plovdiv, Plovdiv, Bulgaria

Drozdstoy Stoyanov

St Catherine’s College, University of Oxford, Oxford, UK

Bill Fulford

Department of Psychological, Health & Territorial Sciences, “G. D’Annunzio” University, Chieti Scalo, Italy

Giovanni Stanghellini

Centre for Ethics and Philosophy of Health Sciences, University of Pretoria, Pretoria, South Africa

Werdie Van Staden

Department of Psychiatry, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China

Michael TH Wong

Guide to Further Sources

For a more extended treatment of the role of culture in eating disorders and family therapy see:

Di Nicola VF (1990a) Overview: Anorexia multiforme: Self-starvation in historical and cultural context. I: Self-starvation as a historical chameleon. Transcultural Psychiatric Research Review, 27(3): 165–196.

Di Nicola VF (1990b) Overview: Anorexia multiforme: Self-starvation in historical and cultural context. II: Anorexia nervosa as a culture-reactive syndrome. Transcultural Psychiatric Research Review, 27(4): 245–286.

Di Nicola, V (1997) A Stranger in the Family: Culture, Families, and Therapy . New York & London: W.W. Norton & Co.

Nasser M and Di Nicola, V. (2001) Changing bodies, changing cultures: An intercultural dialogue on the body as the final frontier. In: Nasser M, Katzman M A, and Gordon R A, eds. Eating Disorders and Cultures in Transition . East Sussex, UK: Brunner-Routledge, pp. 171–193.

Rights and permissions

Open Access This chapter is licensed under the terms of the Creative Commons Attribution 4.0 International License ( ), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license and indicate if changes were made.

The images or other third party material in this chapter are included in the chapter's Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the chapter's Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.

Reprints and permissions

Copyright information

© 2021 The Author(s)

About this chapter

Di Nicola, V. (2021). Antonella: ‘A Stranger in the Family’—A Case Study of Eating Disorders Across Cultures. In: Stoyanov, D., Fulford, B., Stanghellini, G., Van Staden, W., Wong, M.T. (eds) International Perspectives in Values-Based Mental Health Practice. Springer, Cham.

Download citation


Published : 12 December 2020

Publisher Name : Springer, Cham

Print ISBN : 978-3-030-47851-3

Online ISBN : 978-3-030-47852-0

eBook Packages : Medicine Medicine (R0)

Share this chapter

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

  • Publish with us

Policies and ethics

  • Find a journal
  • Track your research

Search by category

Popular searches.

Blue text reading "Priory" with a red "0"

Eating disorder case study

case study for anorexia

Discover another eating disorder recovery story

"eating disorders tend to hide and they don't want to be seen, and if somebody else can see it ... it's a lot harder to hide".

case study for anorexia

Contact us to make an enquiry or for more information

  • Case report
  • Open access
  • Published: 05 June 2020

Case report: cognitive performance in an extreme case of anorexia nervosa with a body mass index of 7.7

  • Simone Daugaard Hemmingsen   ORCID: 1 , 2 , 3 , 4 , 5 ,
  • Mia Beck Lichtenstein   ORCID: 6 , 7 ,
  • Alia Arif Hussain   ORCID: 8 , 9 ,
  • Jan Magnus Sjögren   ORCID: 8 , 9 &
  • René Klinkby Støving   ORCID: 1 , 2 , 3 , 4 , 5  

BMC Psychiatry volume  20 , Article number:  284 ( 2020 ) Cite this article

4042 Accesses

6 Citations

1 Altmetric

Metrics details

Studies show that adult patients with anorexia nervosa display cognitive impairments. These impairments may be caused by illness-related circumstances such as low weight. However, the question is whether there is a cognitive adaptation to enduring undernutrition in anorexia nervosa. To our knowledge, cognitive performance has not been assessed previously in a patient with anorexia nervosa with a body mass index as low as 7.7 kg/m2.

Case presentation

We present the cognitive profile of a 35-year-old woman with severe and enduring anorexia nervosa who was diagnosed at the age of 10 years. She was assessed with a broad neuropsychological test battery three times during a year. Her body mass index was 8.4, 9.3, and 7.7 kg/m 2 , respectively. Her general memory performance was above the normal range and she performed well on verbal and design fluency tasks. Her working memory and processing speed were within the normal range. However, her results on cognitive flexibility tasks (set-shifting) were below the normal range.


The case study suggests that it is possible to perform normally cognitively despite extreme and chronic malnutrition though set-shifting ability may be affected. This opens for discussion whether patients with anorexia nervosa can maintain neuropsychological performance in spite of extreme underweight and starvation.

Trial registration, NCT02502617 . Registered 20 July 2015.

Peer Review reports

A growing amount of evidence indicate that anorexia nervosa (AN) is associated with impaired or inefficient neuropsychological performance in relation to healthy control subjects, regarding attention [ 1 , 2 ], memory [ 1 , 2 , 3 , 4 ], processing speed [ 4 ], and especially the executive functions [ 5 ] central coherence [ 6 ], decision-making [ 6 , 7 ], and cognitive flexibility [ 8 , 9 ]. It has been debated whether this is related to state (due to factors such as malnutrition) or trait (a premorbid trait or endophenotype of the disorder [ 10 ]). Some studies have found that patients who recovered from AN have impaired cognitive performance compared to healthy control subjects [ 11 , 12 ], supporting the trait theory of the disorder. However, longitudinal studies have found that executive functions can be normalized following weight stabilization in patients with AN [ 13 , 14 ], supporting the state theory.

Research on cognitive performance before and after re-nutrition in adult patients with extreme and chronic AN is sparse. Some studies have examined cognitive performance in patients with AN with a mean body mass index (BMI) below 15 kg/m2 (e.g. [ 10 ]), corresponding to extreme AN severity according to the Diagnostic and Statistical Manual of Mental Disorders 5 (DSM-5) [ 15 ]. However, it is unclear if patients with AN with BMI below 10 kg/m2 will display the same cognitive profile.

It has been suggested that malnutrition might affect cognitive performance since the classic Minnesota Semi-Starvation Experiment [ 16 ], where cognitive functions were studied in 36 healthy military objectors with normal weight before and after semistarvation with 25% weight-loss over a 24-week period. The men reported decline in concentration. However, the standardized tests that were administered did not confirm measurable alterations. Newer research on healthy subjects, although somewhat inconclusive, indicates affected psychomotor speed and executive functions following short-term semi-starvation [ 17 ].

However, other factors than malnutrition or weight-loss have been suggested to affect cognitive performance in patients with AN, such as long illness duration [ 18 ] and age [ 18 ]. This could explain a difference in results for children/adolescents and adults with AN mentioned in the literature [ 19 , 20 ], which cannot be explained by the trait theory.

The current case report was part of an ongoing longitudinal research project investigating the effect of re-nutrition on cognitive performance in patients with severe AN. The aim of the case study was to present the neuropsychological performance of a patient with chronic AN and extremely low BMI in order to discuss whether extremely low weight and long duration of illness are associated with cognitive impairment and if cognitive adaptation takes place. No study to our knowledge has previously reported on the cognitive profile of a patient with AN with a BMI as low as 7.7 kg/m2.

We want to introduce the idea of cognitive adaptation to severe malnutrition as a supplement to the discussion on cognitive impairment in AN. However, this idea should not be confused with Taylor’s Theory of Cognitive Adaptation [ 21 ]. The presented idea of cognitive adaptation is the idea that cognitive functions can adapt to persisting low weight in AN, i.e. cognitive performance can remain normal or regain normality in severe and enduring AN. The adaptation does not exclude specific cognitive impairment.

The current case report investigates the cognitive profile of a 35-year-old Caucasian woman with extremely severe and enduring AN who was diagnosed at the age of 10 years. The patient’s weight loss is accomplished through fasting. According to the DSM-5 [ 15 ], the patient’s symptoms are in accordance with the restricting type and the severity of AN for the patient is categorized as extreme. The patient has had low body weight since the onset of the disease 25 years ago. Consequently, she is still prepubescent.

The patient’s extreme malnutrition, the medical complications, and the refeeding treatment has previously been described in a case report [ 22 ]. Since the previous report [ 22 ], she has survived another 5 years, living in her own residence with several stabilizing hospitalizations. Her nadir BMI, defined as the lowest registered BMI, has decreased further to 7.2 kg/m2. To our knowledge, this is the lowest BMI reported in AN in the literature. During her long and severe illness course, she has participated in psychotherapy for years. However, during the past few years, she has refused to participate in psychotherapy, while she has continued the harm-reducing treatment in the nutrition department. No cognitive profile has been assessed before the current report.

She has continuously been provided supplementation with vitamins and minerals. At the present admission, she weighed 20.2 kg, including edema corresponding to at least 2 kg, and her height was 1.55 m, corresponding to a BMI of 8.41 kg/m 2 . After life-saving and stabilizing fluid and electrolyte correction, and refeeding according to guidelines [ 23 ] during 2 weeks of hospitalization, we tested her with a neuropsychological test battery (2 weeks after admission: T 0 ). After an additional 2 months of hospitalization, she could not be motivated to continue the treatment any longer. Due to years of history with rapid relapse after prolonged forced treatment, she was allowed to be discharged to outpatient follow-up. She was re-tested in the outpatient clinic 6 days following dropout from inpatient treatment and approximately 3 months after admission, (re-test: T 1 ) with a weight of 22.4 kg (BMI: 9.3 kg/m 2 ), and again at 12 months from T 0 , during a re-hospitalization, 7 days after admission (follow-up: T 2 ), with BMI 7.7 kg/m 2 . Thus, T 0 and T 2 were done at the hospital after initial stabilizing glycemic, fluid- and electrolyte correction, whereas T 1 was done in an outpatient setting, where she was in a clinically stable condition, but without the initial stabilizing treatment.

The psychopathological profile of the patient

The patient scored 21 on the Beck Depression Inventory II (BDI-II [ 24 ];) indicating moderate depression at 2 weeks after admission (T 0 ). Her scores on the Eating Disorder Inventory 3 (EDI-3 [ 25 ];) at T 0 are presented in Table 1 below. Compared to the Danish validation of EDI-3 for patients with AN ( [ 26 ]; Table 1 ), her low scores on the Drive for Thinness, the Interoceptive Deficits, the Perfectionism, and the Asceticism subscales are of interest.

Qualitative observations

During the first 2 weeks after admission, the patient was unable to participate in the neuropsychological assessment due to fatigue. Two weeks after admission, when the baseline assessment took place (T 0 ), the patient was lying down during the assessment and was noticeably tired. This was neither the case at retest (T 1 ) nor at follow-up (T 2 ) where the patient was sitting at a table. Her alertness and energy level at follow-up (T 2 ) were notable in light of her low BMI. The patient was calm during all three assessments (divided into six sessions) and expressed that the tests were fun. The aim of the study was explained to the patient before the first administration. However, only information written in the test manuals was given during each assessment.

The following validated neuropsychological tests were selected in cooperation with an experienced neuropsychologist to examine a wide range of cognitive functions: the Wechsler Memory Scale III (WMS-III) [ 27 ]; the d2-R Test of Attention – Revised [ 28 , 29 ]; the Processing Speed Index (PSI) of the Wechsler Adult Intelligence Scale IV (WAIS-IV) [ 30 ]; the Delis-Kaplan Executive Function System (D-KEFS) [ 31 ], Verbal Fluency Test, Design Fluency Test and Trail Making Test; and the Wisconsin Card Sorting Test Revised and Expanded (WCST) [ 32 ] (only administered at T 0 ). Information on each test variable, including internal consistency and test-retest reliability, are presented in Table  2 . The test battery can be administered in approximately 2 h. For all three administrations, the test battery was divided into two sessions (1 h per session) 1 day apart.

Neuropsychological findings

Table  3 gives an overview of the timeline of the patient’s raw scores and scaled scores on the test battery. Table  4 presents the patient’s norm scores and percentiles on the WMS-III, the WAIS-IV PSI, and the d2-R. Table  5 presents the patient’s WCST scores at 2 weeks after admission (T 0 ). Information on scoring are presented below each of the tables.

Memory performance on WMS-III

The patient’s scores on WMS-III indicate average to very superior auditory, visual, immediate and general memory performance (108 to 142; Mean: 100), and low average to average working memory (Table 4 ). The technical manual for WMS-III reports adequate test – retest reliability for all indexes in the age group 16–54 years, except for the Auditory Recognition Delayed Index ( [ 33 ]; Table 2 ). Estimated standard error of difference (S Diff ) scores were calculated based on Iverson and Grant ( [ 34 ]; Table 2 ). Differences between the three assessments are outlined here. Her scores on the Auditory Delayed Index decreased more than S diff : 6.70 from 132 (very superior) at 2 weeks after admission (T 0 ) to 108 (average) at re-test (T 1 ) and increased again to 132 (very superior) at follow-up (T 2 ). Her scores on the Visual Immediate Index increased slightly more than S diff : 6.70 from 118 (high average) at re-test (T 1 ) to 127 (superior) at follow-up (T 2 ). Her scores on the Visual Delayed Index decreased more than S diff : 7.65 from 125 (superior) at re-test (T 1 ) to 109 (average) at follow-up (T 2 ). Her scores on the Immediate Memory Index increased more than S diff : 3.17 from 134 (very superior) at re-test (T 1 ) to 142 (very superior) at follow-up (T 2 ). Her scores on the Working Memory Index decreased more than S diff : 8.22 from 102 (average) at 2 weeks after admission (T 0 ) to 88 (low average) at re-test (T 1 ). The scores on the rest of the indexes did not change more than the estimated S diff scores between time points.

Cognitive flexibility on D-KEFS and WCST

Overall, she performed above average on the Verbal Fluency Test (Table 3 ) at all three test times compared to the normative population for age, except for her performance at re-test (T 1 ) on the switching condition, which was decreased more than S diff : 2.42 to average, and the high number of repetition errors (7; below average) at re-test (T 1 ) and (3; average) at follow-up (T 2 ).

She performed average to above average on the Design Fluency Test at all three test sessions (Table 3 ). However, the switching condition score was lower [ 6 ] at follow-up (T 2 ) compared to 8 at 2 weeks after admission (T 0 ) and re-test (T 1 ), though still average.

During follow-up (T 2 ) on the Trail Making Test (Table 3 ), her performance on the Number-Letter Sequencing test, measuring cognitive flexibility, was below average (111 s), in spite of being average at 2 weeks after admission (T 0 ; 90 s) and re-test (T 1 ; 79 s). The numbers condition was very low at T 0 (55 s; below average), improving somewhat at re-test (T 1 ; 46 s; below average) and follow-up (T 3 ; 41 s; below average). We have no explanation for this result. On the other conditions, her performance was average at all three test times on the Trail Making Test.

Her scores on the WCST (Table 5 ) 2 weeks after admission (T 0 ) place her in the mild to moderately-to-severely range of impairment on cognitive flexibility according to this task. She completed one out of six categories (< 1st percentile). She made 52 perseverative responses (< 1st percentile; standard score 55; moderately-to-severely impaired range). She committed 50 errors (8th percentile; standard score 79: mildly impaired range), of which 36 were perseverative errors (1st percentile; standard score 55: moderately impaired range).

WAIS-IV processing speed

The scores on the Processing Speed Index (Table 4 ) were average compared to the normative population for age at all three test times. There were no relevant differences between time points. She scored 93 at admission (T 0 ) and re-test (T 1 ) and 98 at follow-up (T 2 ).

d2-R test of attention

At 2 weeks after admission (T 0 ) and re-test (T 1 ), she had a small number of processed targets (426 and 420), 18th to 21st percentile (Tables 3 and 4 ), her concentration performance was 175 and 176 corresponding to the 42nd percentile and she committed three and no errors respectively (> 90th percentile). At follow-up (T 2 ), her concentration performance was above the mean (185; 54th percentile) but not increased more than S diff : 24.89. The total processed targets score was still low (451; 34th percentile), and she committed few errors (four; 90th percentile).

Discussion and conclusions

The patient exhibited average to very superior performance on verbal fluency, design fluency, processing speed, and memory. However, her working memory performance was low average. Her attention and concentration performance were below average to average, and her performance on cognitive flexibility tasks were average to moderately-to-severely impaired.

The present case report demonstrates surprisingly good cognitive performance in a patient with severe and enduring AN with extremely low BMI varying between 7.7 and 9.3 during the study period of 1 year. However, some of her executive functions seem to be impaired. This is in line with previous research on patients with AN [ 5 , 8 ]. The present results suggest that her working memory was normal (low average) in line with previous studies [ 35 , 36 ]. However, her working memory performance was lower compared to the rest of her memory performance, which was average to very superior. The results from the D-KEFS indicate average to above-average performance with perhaps somewhat weaker cognitive flexibility (below average to average). On the other hand, the results from the WCST indicate impairment in cognitive flexibility. The overall differences in performance between the three assessments were minimal. This indicates that the minor differences in BMI between the test assessments did not significantly affect her cognitive performance, as expected.

Impaired cognitive flexibility

It could be that impaired cognitive flexibility existed prior to the illness as a premorbid trait as suggested previously [ 10 ], or that the malnutrition has affected the patient’s cognitive flexibility. Since we are missing data on her premorbid level, we cannot draw any firm conclusions.

Impaired cognitive flexibility has previously been reported in patients with AN with higher BMI [ 37 ], indicating that impairments in cognitive flexibility do not necessarily relate to undernutrition. In patients with AN who had recovered from the illness, cognitive flexibility was in the normal range in this study. However, other studies found that individuals who recovered from AN exhibited more or less impaired executive functioning [ 10 ]. Longitudinal research on the relationship between different BMI states and cognitive performance is highly needed.

Impaired cognitive flexibility may also play a role in the perpetuation of AN. Impaired cognitive flexibility has been suggested as a maintenance factor [ 38 ] and a factor related to lack of illness insight characteristic of patients with restrictive AN [ 39 ]. Lack of illness insight could be related to treatment resistance [ 40 ]. The patient’s low scores on EDI-3 subscales also reflect a discrepancy between illness severity and self-reported symptoms. This discrepancy or ambivalence is part of the nature of the disorder reflected in the low motivation for recovery and high number of dropouts from treatment alongside an expressed desire to change [ 41 ].

Cognitive adaptation in anorexia nervosa

Survival of long-term starvation is only possible due to extensive adaptive endocrine and metabolic alterations [ 42 ]. How these alterations affect cognitive functions still remains to be clarified. Well-designed longitudinal studies on severely underweight patients with a long illness duration are lacking. However, the present case report suggests that essential preservation of some cognitive functions occurs even in extreme chronic semi-starvation.

The mechanisms allowing for such preservation remains a subject of speculation. Links can be made to research on neuroplasticity and functional reorganization of cognitive functions after brain injury since patients with AN have white matter alterations [ 43 ]. Research shows that brain maturation processes of especially the prefrontal cortex continue until people are approximately 25 years old [ 44 ]. Nutritional status seems to impact this brain maturation [ 44 ]. Executive functions associated with the prefrontal cortex could therefore be affected by undernutrition during development of prefrontal connections in the brain in adolescence and young adulthood. Thus, impairment on executive functions may not arise until adulthood in patients with AN. This is in line with research that found no cognitive flexibility impairment in children and adolescents with AN but impairments in adults with AN [ 19 , 20 ]. The literature indicates that other cognitive functions associated with the prefrontal cortex, such as memory, are also impaired in adults with AN [ 3 ]. However, overall, this literature is not as explicit as the literature showing cognitive flexibility impairment in adults with AN. The ambiguity in the literature indicates differences between cognitive functions related to the prefrontal cortex in patients with AN. It might be that some prefrontal connections potentially being affected during low weight in adolescence could be reorganized or “compensated for” with time as is possible with reorganization or apparent functional recovery after brain injury [ 45 ]. In that case, cognitive performance could be regained after impairment has occurred. Some dimensions of cognitive flexibility might, however, be more difficult to compensate for. This could explain specific cognitive flexibility impairment in patients recovered from AN [ 10 ] and explain that the patient in the present case report performed normal and superior on some functions associated with prefrontal connections (memory and verbal fluency) but poorer on cognitive flexibility. We therefore suggest that reorganization of some cognitive functions can occur in spite of persisting low weight in patients with AN. In line with the possibility of cognitive reorganization in AN, Cognitive Remediation Therapy seems to improve executive functioning in patients with AN [ 46 ]. The suggested theory of cognitive adaptation may therefore not be specific to persisting low weight in AN. However, fast, substantial weight-loss could affect cognitive performance differently than persisting low weight. Therefore, studies on starving healthy subjects, including the Minnesota Semi-Starvation Experiment [ 16 ], could show different results than studies on patients with severe and enduring AN. Likewise, studies on patients with short illness duration might find different results than studies of patients with enduring AN. It is also unclear if patients developing AN in adulthood will display the same cognitive impairments. In line with these reflections, a case report of a 27-year-old Japanese woman in a coma, with BMI of 8.5 kg/m 2 at admission, describes a patient with AN where the outcome of severe malnutrition was persistent neurologic sequelae [ 47 ]. The woman developed AN at the age of 21 years where the patient in the present case report was diagnosed at the age of 10 years. The difference in age of onset, duration of illness, and/or manner of weight-loss (fast, substantial weight-loss compared to persisting low weight) may have resulted in different outcomes for the women. It is, however, also a possibility that the patient in the present case report might have an extreme phenotype which enables her to perform well in spite of her being extremely underweight.

We cannot say how high the patient’s scores on the neuropsychological test battery might be if she had not been as malnourished. We assume the patient would perform better on cognitive flexibility tasks, that her processing speed and working memory would be higher, and that she would be able to concentrate better had she not been malnourished. This is somewhat supported by previous research. Although the literature suggests impaired cognitive performance in patients with AN, the reported impairments were limited compared to healthy subjects [ 8 , 48 ]. Furthermore, it may be that severely underweight patients with AN have a higher verbal IQ [ 49 ], which does not, however, exclude the possibility of specific cognitive impairments [ 50 ]. This could explain the patient’s high memory performance (and probably global IQ) alongside specific impairment in cognitive flexibility on the WCST. This case may therefore not differ from other patients with severe AN regarding cognitive performance. It may be that the superior performance related to some cognitive functions is a trait of severely underweight patients with AN and/or that a cognitive adaptation to enduring AN increases performance to the premorbid level. In this case, (regained) superior performance of some cognitive functions (i.e. memory and verbal IQ) can exist alongside cognitive impairment in others (i.e. cognitive flexibility). This may change our view of the cognitive profile and its development in patients with severe and enduring AN.

Regardless, the fact that we were able to test the patient in the present case, raises a discussion as to whether she and others with extremely low weight may be responsive to psychotherapy as well. In the present case, the patient underwent psychotherapy for several years albeit without any impact on her weight. More research focusing on the validation of neuropsychological tests including investigation of the practice effect in this patient population is needed.

The individual scores on neuropsychological tests should always be interpreted with care. Factors other than persisting low weight may affect neuropsychological performance (e.g. dehydration, stress, depression, and anxiety). In the present case, the patient did express depressive symptoms corresponding to moderate depression, which might have influenced results on impairment in cognitive flexibility. Furthermore, the patient might experience other issues related to cognitive performance in daily life, which cannot be discovered in a neuropsychological assessment context.

Obviously, conclusions can never be drawn from one case. However, since the neuropsychological testing included a broad range of tests and was repeated three times during a year, the present case report is valid as a basis for reflecting on the affected individual’s cognitive performance at this stage. The present case report demonstrates that cognitive functions may be largely preserved under extreme chronic malnutrition or that cognitive functioning may be regained (reorganized) in spite of extreme chronic malnutrition. More research on patients with AN with extremely low BMI (< 10) is needed to determine whether cognitive performance is affected by starvation and malnutrition.

Availability of data and materials

All data analyzed during this study are included in this published article in tables or text. Raw data in a fully anonymized version is available from the corresponding author on reasonable request.


  • Anorexia nervosa

Intelligence quotient

Body mass index

The Beck Depression Inventory II

The Eating Disorder Inventory 3

The Wechsler Memory Scale III

The Wechsler Adult Intelligence Scale IV

The Processing Speed Index

The Delis-Kaplan Executive Function System

The Wisconsin Card Sorting Test Revised and Expanded

Seed JA, Dixon RA, McCluskey SE, Young AH. Basal activity of the hypothalamic-pituitary-adrenal axis and cognitive function in anorexia nervosa. Eur Arch Psychiatry Clin Neurosci. 2000;250(1):11–5.

Article   CAS   PubMed   Google Scholar  

Seed JA, McCue PM, Wesnes KA, Dahabra S, Young AH. Basal activity of the HPA axis and cognitive function in anorexia nervosa. Int J Neuropsychopharmacol. 2002;5(1):17–25.

Biezonski D, Cha J, Steinglass J, Posner J. Evidence for Thalamocortical circuit abnormalities and associated cognitive dysfunctions in underweight individuals with anorexia nervosa. Neuropsychopharmacology. 2016;41(6):1560–8.

Article   PubMed   Google Scholar  

Kjaersdam Telleus G, Jepsen JR, Bentz M, Christiansen E, Jensen SO, Fagerlund B, et al. Cognitive profile of children and adolescents with anorexia nervosa. Eur Eat Disord Rev. 2015;23(1):34–42.

Roberts ME, Tchanturia K, Stahl D, Southgate L, Treasure J. A systematic review and meta-analysis of set-shifting ability in eating disorders. Psychol Med. 2007;37(8):1075–84.

Abbate-Daga G, Buzzichelli S, Marzola E, Aloi M, Amianto F, Fassino S. Does depression matter in neuropsychological performances in anorexia nervosa? A descriptive review. Int J Eat Disord. 2015;48(6):736–45.

Bodell LP, Keel PK, Brumm MC, Akubuiro A, Caballero J, Tranel D, et al. Longitudinal examination of decision-making performance in anorexia nervosa: before and after weight restoration. J Psychiatr Res. 2014;56:150–7.

Article   PubMed   PubMed Central   Google Scholar  

Hirst RB, Beard CL, Colby KA, Quittner Z, Mills BM, Lavender JM. Anorexia nervosa and bulimia nervosa: a meta-analysis of executive functioning. Neurosci Biobehav Rev. 2017;83:678–90.

Tchanturia K, Davies H, Roberts M, Harrison A, Nakazato M, Schmidt U, et al. Poor cognitive flexibility in eating disorders: examining the evidence using the Wisconsin card sorting task. PLoS One. 2012;7(1):e28331.

Article   CAS   PubMed   PubMed Central   Google Scholar  

Tchanturia K, Morris RG, Anderluh MB, Collier DA, Nikolaou V, Treasure J. Set shifting in anorexia nervosa: an examination before and after weight gain, in full recovery and relationship to childhood and adult OCPD traits. J Psychiatr Res. 2004;38(5):545–52.

Danner UN, Sanders N, Smeets PA, van Meer F, Adan RA, Hoek HW, et al. Neuropsychological weaknesses in anorexia nervosa: set-shifting, central coherence, and decision making in currently ill and recovered women. Int J Eat Disord. 2012;45(5):685–94.

Wu M, Brockmeyer T, Hartmann M, Skunde M, Herzog W, Friederich H-C. Reward-related decision making in eating and weight disorders: a systematic review and meta-analysis of the evidence from neuropsychological studies. Neurosci Biobehav Rev. 2016;61:177–96.

Lozano-Serra E, Andres-Perpina S, Lazaro-Garcia L, Castro-Fornieles J. Adolescent anorexia nervosa: cognitive performance after weight recovery. J Psychosom Res. 2014;76(1):6–11.

Firk C, Mainz V, Schulte-Ruether M, Fink G, Herpertz-Dahlmann B, Konrad K. Implicit sequence learning in juvenile anorexia nervosa: neural mechanisms and the impact of starvation. J Child Psychol Psychiatry. 2015;56(11):1168–76.

American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th ed. Washington: Author; 2013.

Book   Google Scholar  

Keys A, Brozek J, Henschel A, Mickelsen O, Taylor HL. The biology of human starvation (2 volumes). Minnesota: University of Minnesota Press; 1950.

Benau EM, Orloff NC, Janke EA, Serpell L, Timko CA. A systematic review of the effects of experimental fasting on cognition. Appetite. 2014;77:52–61.

Buhren K, Mainz V, Herpertz-Dahlmann B, Schafer K, Kahraman-Lanzerath B, Lente C, et al. Cognitive flexibility in juvenile anorexia nervosa patients before and after weight recovery. J Neural Transm (Vienna). 2012;119(9):1047–57.

Article   Google Scholar  

Telleus GK, Fagerlund B, Jepsen JR, Bentz M, Christiansen E, Valentin JB, et al. Are weight status and cognition associated? An examination of cognitive development in children and adolescents with anorexia nervosa 1 year after first hospitalisation. Eur Eat Disord Rev. 2016;24(5):366–76.

Lang K, Stahl D, Espie J, Treasure J, Tchanturia K. Set shifting in children and adolescents with anorexia nervosa: an exploratory systematic review and meta-analysis. Int J Eat Disord. 2014;47(4):394–9.

Taylor SE. Adjustment to threatening events: a theory of cognitive adaptation. Am Psychol. 1983;38(11):1161–73.

Frolich J, Palm CV, Stoving RK. To the limit of extreme malnutrition. Nutrition. 2016;32(1):146–8.

Robinson P, Jones WR. MARSIPAN: management of really sick patients with anorexia nervosa. BJPsych Advances. 2018;24(1):20–32.

Beck AT, Steer RA, Brown GK. Manual for the Beck depression inventory-II. San Antonio: Psychological Corporation; 1996.

Google Scholar  

Garner DM. Eating disorder Inventory-3. Professional manual. Lutz: Psychological Assessment Resources, Inc.; 2004.

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 Psychopathol Behav Assess. 2011;33(1):101–10.

Wechsler D. WAIS-III WMS-III technical manual. San Antonio: The Psychological Corporation; 2002.

Brickenkamp R, Schmidt-Atzert L, Liepmann D. The d2 test of attention – revised. A test of attention and concentration. Oxford: Hogrefe; 2016.

Brickenkamp R. d2-testen – en vurdering af opmærksomhed of koncentration. Dansk vejledning. Hogrefe Psykologisk Forlag: Frederiksberg; 2006.

Wechsler D. Wechsler adult intelligence scale—fourth edition. Technical and interpretive manual. Pearson: San Antonio; 2008.

Delis DC, Kaplan E, Kramer JH. Delis-Kaplan executive function system - technical manual. Pearson: San Antonio; 2001.

Heaton RK, Chelune GJ, Talley JL, Kay GG, Curtiss G. Wisconsin Card Sorting Test Manual Revised and Expanded. 2nd edition ed. Lutz: Psychological Assessment Resources, Inc.; 1993.

Tulsky D, Zhu J, Ledbetter M, editors. WAIS-III WMS-III technical manual (Wechsler Adult Intelligence Scale & Wechsler Memory Scale) paperback updated. USA: The Psychological Corporation; 2002.

Iverson GL. Interpreting change on the WAIS-III/WMS-III in clinical samples. Arch Clin Neuropsychol. 2001;16(2):183–91.

Bradley SJ, Taylor MJ, Rovet JF, Goldberg E, Hood J, Wachsmuth R, et al. Assessment of brain function in adolescent anorexia nervosa before and after weight gain. J Clin Exp Neuropsychol. 1997;19(1):20–33.

Lauer CJ, Gorzewski B, Gerlinghoff M, Backmund H, Zihl J. Neuropsychological assessments before and after treatment in patients with anorexia nervosa and bulimia nervosa. J Psychiatr Res. 1999;33:129–38.

Tenconi E, Santonastaso P, Degortes D, Bosello R, Titton F, Mapelli D, et al. Set-shifting abilities, central coherence, and handedness in anorexia nervosa patients, their unaffected siblings and healthy controls: exploring putative endophenotypes. World J Biol Psychiatry. 2010;11(6):813–23.

Steinglass JE, Walsh BT, Stern Y. Set shifting deficit in anorexia nervosa. J Int Neuropsychol Soc. 2006;12(3):431–5.

Konstantakopoulos G, Tchanturia K, Surguladze SA, David AS. Insight in eating disorders: clinical and cognitive correlates. Psychol Med. 2011;41(9):1951–61.

Abbate-Daga G, Amianto F, Delsedime N, De-Bacco C, Fassino S. Resistance to treatment and change in anorexia nervosa: a clinical overview. BMC Psychiatry. 2013;13(1):294.

Guarda AS. Treatment of anorexia nervosa: insights and obstacles. Physiol Behav. 2008;94(1):113–20.

Stoving RK. Mechanisms In Endocrinology: Anorexia nervosa and endocrinology: a clinical update. Eur J Endocrinol. 2019;180(1):R9–r27.

Barona M, Brown M, Clark C, Frangou S, White T, Micali N. White matter alterations in anorexia nervosa: evidence from a voxel-based meta-analysis. Neurosci Biobehav Rev. 2019;100:285–95.

Arain M, Haque M, Johal L, Mathur P, Nel W, Rais A, et al. Maturation of the adolescent brain. Neuropsychiatr Dis Treat. 2013;9:449–61.

PubMed   PubMed Central   Google Scholar  

Mogensen J. Reorganization of the injured brain: implications for studies of the neural substrate of cognition. Front Psychol. 2011;2:7.

Tchanturia K, Lounes N, Holttum S. Cognitive remediation in anorexia nervosa and related conditions: a systematic review. Eur Eat Disord Rev. 2014;22(6):454–62.

Bando N, Watanabe K, Tomotake M, Taniguchi T, Ohmori T. Central pontine myelinolysis associated with a hypoglycemic coma in anorexia nervosa. Gen Hosp Psychiatry. 2005;27(5):372–4.

Dobson KS, Dozois DJ. Attentional biases in eating disorders: a meta-analytic review of Stroop performance. Clin Psychol Rev. 2004;23(8):1001–22.

Schilder CMT, van Elburg AA, Snellen WM, Sternheim LC, Hoek HW, Danner UN. Intellectual functioning of adolescent and adult patients with eating disorders. Int J Eat Disord. 2017;50(5):481–9.

Lena SM, Fiocco AJ, Leyenaar JK. The role of cognitive deficits in the development of eating disorders. Neuropsychol Rev. 2004;14(2):99–113.

Download references


We would like to thank Professor Jesper Mogensen at the Unit for Cognitive Neuroscience, University of Copenhagen, Denmark, for his inputs regarding neurocognitive reorganization and the possibility of extending his model to the research field of anorexia nervosa.

The study was supported by government funding: The Psychiatric Research Fund of Southern Denmark (grants for material and PhD salary) and the University of Southern Denmark (faculty scholarship). Furthermore, the study was supported with grants for material by private funds: the Jascha Foundation and the Beckett Foundation. The funding sources had no role in the design, execution, interpretation, analysis, or publication of the study.

Author information

Authors and affiliations.

Centre for Eating Disorder, Odense University Hospital, Odense, Denmark

Simone Daugaard Hemmingsen & René Klinkby Støving

Research Unit for Medical Endocrinology, Odense University Hospital, Odense, Denmark

Department of Clinical Research, University of Southern Denmark, Odense, Denmark

Open Patient data Explorative Network (OPEN), Odense, Denmark

The Research Unit, Child and Adolescent Psychiatry, Mental Health Services in the Region of Southern Denmark, Odense, Denmark

Centre for Telepsychiatry, Mental Health Services in the Region of Southern Denmark, Odense, Denmark

Mia Beck Lichtenstein

Department of Psychology, University of Southern Denmark, Odense, Denmark

Eating Disorder Unit, Mental Health Centre Ballerup, Mental Health Services in the Capital Region of Denmark, Copenhagen, Denmark

Alia Arif Hussain & Jan Magnus Sjögren

Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark

You can also search for this author in PubMed   Google Scholar


SDH and RKS completed the data collection. RKS was the initiator of the project. SDH, RKS, and MBL all took part in the design of the study. SDH, RKS, MBL, JMS and AAH were all contributors in writing the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Simone Daugaard Hemmingsen .

Ethics declarations

Ethics approval and consent to participate.

The research project has been approved by the Regional Scientific Ethical Committee for the Region of Southern Denmark and was carried out in accordance with the 1964 Helsinki declaration and its later amendments. The authors state that the patient has given written and informed consent for participation in the study.

Consent for publication

The authors state that the patient has given written and informed consent for publication of the case report.

Competing interests

The authors declare that there are no conflicts of interest. None of the authors have received financial support or benefits from commercial sources for this study.

Additional information

Publisher’s note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit . The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article.

Hemmingsen, S.D., Lichtenstein, M.B., Hussain, A.A. et al. Case report: cognitive performance in an extreme case of anorexia nervosa with a body mass index of 7.7. BMC Psychiatry 20 , 284 (2020).

Download citation

Received : 13 February 2020

Accepted : 28 May 2020

Published : 05 June 2020


Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

  • Cognitive performance
  • Neuropsychology
  • Undernutrition

BMC Psychiatry

ISSN: 1471-244X

case study for anorexia

“It’s Never About the Food” – an Anorexia Case Study

Dr. Sheri Jacobson

By: Debby ☂

In a 2015 report commissioned by the UK charity Beating Eating Disorders (B-EAT), it was estimated that over 725,000 Brits suffer from an eating disorder . Of that number, around 10% are thought to suffer from anorexia nervosa.

Laura* is one of the lucky ones who found support for her struggles with anorexia and recovered. Now happily married and a mother herself, she shares her story in hopes that parents and loved ones of anorexics can understand and help.

*name changed to protect privacy

Safety and control – an anorexia case study

It started when my grandma died when I was thirteen. We’d always been really close and I had spent many happy weekends and holidays with her. I couldn’t understand why she had to be taken from me, and in hindsight I think it sparked depression as from that moment things started to spiral out of control.

It’s funny I’d use the word control, as if there is one thing I understand now is that anorexia isn’t about food at all, but about control. Control and safety.

The world didn’t seem so safe without my Gran, and somehow I must have blamed myself, as what was growing was definitely self-hatred.

anorexia nervosa case study

By: Steve Bozak

At the time I was a little chubby, and the kids at school would tease me for my chubby cheeks and clothes that were too tight. Even family members commented on the ‘puppy fat’ I was carrying and one well-meaning aunt suggested to my mum I was put on a diet, which didn’t help.

The reality was I had friends, puberty was creeping up, I was bright and liked school. Sure, I was carrying a little extra weight, but it wasn’t anything serious and would have gone in time.

Am I stressed or depressed online quiz

But in my mind back then, I wasn’t pretty enough, I wasn’t tall enough, I was flat chested, I had spots, my hair was brown not blond, I didn’t fit in the popular clique.

And then I just summarised all that into being because I was fat. The only thing that could make me not a failure and geek was if I was thin. Really thin. I admired girls where I could see their bones. I wanted that, to see my hip bones jut out, my collarbone visible.

eating disorder case study

By: Gareth Williams

The changes were small – at first. We had a canteen that was packed with chips, beans and burgers but I started opting for the jacket potato, leaving half, and then just picking. Everyone was so busy talking about boys and pop groups they didn’t care what I was eating and no one ever commented.

Rather than hate cross-country I began to love it, as I knew that the pain in my chest equaled fat coming off my body.

By the time I turned 14 all I thought about was losing weight. I was young, there was no internet, no support forums or chat rooms, how was I to know there was anything wrong? I had never even heard the word anorexia.

But then a teacher at school took me aside to have a chat. She had seen me going from being a bubbly little thing with a smiley face and healthy appetite to a tiny, fragile girl who was always in cardigans and jumpers with blue fingers. I brushed it off out of utter embarrassment, said it was family genes and a fast metabolism, but headed straight to the library to look it up.

Anorexia was described in the encyclopaedia as a serious mental illness and sufferers would do anything to lose weight and maintain that loss. I didn’t think I was mental at all, I just wanted to be thin. I didn’t ever overeat , purge or vomit and I didn’t use laxatives.

So I put anorexia to the back of my mind and carried on with my quest.

Writing this I feel sad that only that teacher did anything. I can’t help but think, how did nobody else notice? Why did nobody else talk to me? The child inside of me doesn’t understand, even though as an adult and now mother myself I do see that my parents did know there was something wrong but just didn’t know what to do about it. It was the 1980s, people weren’t talking about eating disorders as much back then.

And like all good anorexics, I was secretive. I would lie that I had eaten and I was fine. Hide food and throw it in the bin on the way to school. I never went out with friends if food was involved – I pretended I was busy, or wasn’t allowed out.

Even at six-and-a-half stone I still thought I was fat and knew that if I wanted to hit the jackpot and see my bones sticking out then I would have to keep going.

My stomach hurt all the time, I was dizzy whenever I stood up, and my periods were nonexistent. Then there was the cold – I was always so chilly that sometimes my teeth chattered. And the fatigue. Nobody ever talks about how exhausting anorexia is. You just have no energy at all .

At fifteen I hit my goal and reached six stone. I wore tiny skirts. I felt so proud of my little legs sticking out. And it seemed to be working. Boys noticed me, and the cool girls did want to be my friend.

As a child I thought my newfound popularity was because I was thin, but now I can see that maybe it was because I sadly felt better about myself and thought I was more interesting thin. The other kids probably just bought into my confidence, not knowing that they were encouraging my illness.

Six stone must have looked very scary. My mother did, in the end, march me to the doctors. Did it matter by then? Not at all. I thought I looked great and they were jealous. I told them I would start to eat, and I’m afraid they believed me and that was that.

eating disorder case study

We sat in her room, wrapped in blankets and holding hot water bottles in the middle of a hot August, discussing how many apples and rice cakes we were keeping it to a day, and what size kids clothes we now fit into.

And then, at my summer job at a local cafe, I fainted. Right in front of customers and other staff. It was mortifying. And somehow, lying on the floor and looking up at their shocked and concerned faces, I woke up a little. I knew I’d taken it too far.

I started to notice the bad side of starving myself. The fur that had grown on my face, the way my hip bones dug into my mattress making it hard for me to sleep. I wasn’t proud of the problems it was causing at home and I hated having to lie all the time.

I went back to the GP, by myself this time, and we talked. He was kind, and he understood, but he showed me some tough love. These are the facts, he said. If you don’t stop you might never have kids, you could have a heart attack, your hair could fall out, your bones could crumble away and ultimately you might die.

I walked out of there shocked, a bit angry at him for laying in to me, but ultimately, with the decision taken that I wanted to get better. I was about to start sixth form. I knew that I needed to grow up and be responsible.

I won’t lie. Recovery was hard. Even eating a tuna sandwich was traumatic and it took over an hour the first time. I was convinced that everything I ate was going to make me fat.

More than anything, looking at food on my plate that I knew I had to eat, I felt vulnerable. Not eating had in a weird way been my way of feeling safe.

I started being open about my struggles, which meant my friends and family could finally support me and there was no more hiding.

I kept seeing the GP who then got me further help that I needed. I think what worked about eating disorder counselling was to have someone who wasn’t angry or scared that I was struggling, and didn’t force advice on me, but just listened.

When asked for advice for handling a loved one who is anorexic, that is the best tip I can offer – listen. Be there for them.

I think changing schools was lucky timing as my new friends were brilliant, and it let me create a new life for myself.

Because really, recovering from anorexia isn’t about the food, either. It’s about deciding to live, and for me that meant doing things that made me want to live. Laughing with my friends, for starters.

Being able to go out for dinner with my friends on my 17th birthday was a massive achievement and with thirty of us sat around the table it dawned on me that you didn’t need to be skeletal to be liked. You needed to be you. You needed to be comfortable in your own skin.

You needed to be happy. Not in a big, perfect, showy way. Just in a way that works for you.

Even now in my forties there are times when I think I am not attractive enough , not smart enough, not popular enough, not successful enough. But I catch the voice now, and rather than listen to it, I tell it, no. I am good enough. And now, when I see my sons smile at me and hear my husband tell me he loves me, I know it was all worth it and appreciate my healthy life so much.

Have you struggled with anorexia? Want to share your experience? Do so below.

find affordable online therapists

Your email address will not be published. Required fields are marked *

Currently you have JavaScript disabled. In order to post comments, please make sure JavaScript and Cookies are enabled, and reload the page. Click here for instructions on how to enable JavaScript in your browser.

Open Popup Form

Desktop - CTA Journalist


Dr. Sheri Jacobson


If you are a journalist writing about this subject, do get in touch - we may be able to comment or provide a pull quote from a professional therapist.

Yes, I am a journalist Click here to confirm you are a journalist

Related Posts

  • Methodology
  • Open access
  • Published: 20 September 2023

Co-producing principles to guide health research: an illustrative case study from an eating disorder research clinic

  • Cat Papastavrou Brooks   ORCID: 1 , 2 ,
  • Eshika Kafle 2 ,
  • Natali Butt 2 ,
  • Dave Chawner 2 , 3 ,
  • Anna Day 2 ,
  • Chloë Elsby-Pearson   ORCID: 2 ,
  • Emily Elson 2 ,
  • John Hammond 2 ,
  • Penny Herbert 2 ,
  • Catherine L. Jenkins 2 ,
  • Zach Johnson 2 ,
  • Sarah Helen Keith-Roach 2 ,
  • Eirini Papasileka 2 , 4 ,
  • Stella Reeves 2 , 5 ,
  • Natasha Stewart 2 ,
  • Nicola Gilbert 2 , 6 &
  • Helen Startup 2  

Research Involvement and Engagement volume  9 , Article number:  84 ( 2023 ) Cite this article

1699 Accesses

2 Citations

10 Altmetric

Metrics details

There is significant value in co-produced health research, however power-imbalances within research teams can pose a barrier to people with lived experience of an illness determining the direction of research in that area. This is especially true in eating disorder research, where the inclusion of co-production approaches lags other research areas. Appealing to principles or values can serve to ground collaborative working. Despite this, there has not been any prior attempt to co-produce principles to guide the work of a research group and serve as a basis for developing future projects.

The aim of this piece of work was to co-produce a set of principles to guide the conduct of research within our lived experience led research clinic, and to offer an illustrative case for the value of this as a novel co-production methodology. A lived experience panel were recruited to our eating disorder research group. Through an iterative series of workshops with the members of our research clinic (composed of a lived experience panel, clinicians, and researchers) we developed a set of principles which we agreed were important in ensuring both the direction of our research, and the way in which we wanted to work together.

Six key principles were developed using this process. They were that research should aim to be: 1) real world—offering a clear and concrete benefit to people with eating disorders, 2) tailored—suitable for marginalised groups and people with atypical diagnoses, 3) hopeful—ensuring that hope for recovery was centred in treatment, 4) experiential—privileging the ‘voice’ of people with eating disorders, 5) broad—encompassing non-standard therapeutic treatments and 6) democratic—co-produced by people with lived experience of eating disorders.


We reflect on some of the positives as well as limitations of the process, highlighting the importance of adequate funding for longer-term co-production approaches to be taken, and issues around ensuring representation of minority groups. We hope that other health research groups will see the value in co-producing principles to guide research in their own fields, and will adapt, develop, and refine this novel methodology.

Plain English summary

It important that when researchers are trying to understand illnesses they do this together with people who have experienced them. This can be difficult, because researchers often take over—even if everyone is meant to be working as a team. We are a group of people trying to understand eating disorders and help people who have them get better. In our group there are some people that have experienced an eating disorder, health workers and researchers.

We thought it might be helpful if we could start by working out what things were most important to us as a group, and then try to stick by them. We talked a lot together to come up with a list of principles.

The six principles we thought were the most important were that research should make a difference to people’s lives, see people as individuals, be hopeful, make sure that people have a voice, look at things that aren’t traditional therapies, and always work together as equals.

There are some issues with what we did; we found it hard to get a good mix of people in our group, and we were lucky in having enough money to pay people to do what we wanted to do, which is not always true. Despite this, we still hope that other teams might look at what we have done, and see if they could build on it, or change it, so it would work for them.

Peer Review reports

Co-production approaches

Co-production has been defined as the delivery of “public services in an equal and reciprocal relationship between professionals, people using services, their families and their neighbours” [ 21 ], placing a strong emphasis on the importance of citizens’ power and worth [ 26 ]. The initial emergence of co-production within health services stemmed from a critique of the limited power patients had to shape the service they received, and the failure of services to acknowledge and respond to patients’ often negative experiences [ 32 ]. Despite the argued importance of co-production in terms of its substantive, instrumental, normative and political value [ 94 ] there have been significant criticisms of what is typically described as ‘co-production’ in health services. This includes the claim that co-production rarely involves a transfer of power to patients [ 136 ], instead involving a co-option of people’s lived experience to be used for agendas which are foreign to them and their interests [ 102 ]. Genuine co-production is often impossible due to the reality of the power imbalances present in the psychiatric system [ 97 ], and—by masking and de-politicising these imbalances—it can serve to exacerbate them [ 124 ].

Within health research, co-production approaches come with their own associated set of difficulties [ 79 ]. Relationships within research often mirror those between patient and clinician and there can be a division between researchers who are seen as active, knowing and rational in contrast to the passive, known and irrational objects of health research—patients [ 66 ]. Although evidence-based practice is often reified as a values-neutral methodology [ 14 ], it involves the privileging a specific scientific or rationalistic voice, excluding ways of knowing which do not conform to this and often constituting a form of injustice against epistemically marginalized groups [ 30 , 37 ]. This critique is foundational to the emerging field of mad studies, which seeks not to just include mad people within mental health research by forcing them to assimilate within traditional methodological frameworks but demands instead substantial changes to the way we conceive of and conduct research [ 44 , 63 ]. Thus the aims of mad studies include both “showing that there is method in our madness; and on the other side, preserving madness in our method” [ 63 ].

In addition to these theoretical issues, co-producing research with patients can often have significant psychological and emotional costs for them, partially as a result of increased interpersonal conflict which often occurs [ 94 ]. Collaborating with patients on mental health research has been conceptualised as occurring on one of three distinct levels: consultation, collaboration, and user-controlled,Rose and Kalathil [ 105 ] argue that consultation is superficial and lacks value, and that collaboration only requires power imbalances to be hidden as opposed to abolished, meaning it inevitably collapses into consultation. On this model, methodologies like participatory action research—which centre around collaboration between researchers and participants [ 54 ] though do not challenge either the conceptual distinction or the power-relations between them typically fall under the category of collaboration. Only user-controlled research can preserve patients’ autonomy and ability to affect the research process without the risk of co-option [ 105 ].

Co-producing eating disorder research

Eating disorders (EDs) are a classification of disorders which involve feeding and eating disturbances which cause significant clinical distress [ 76 ]. An estimated 725,000 people in the UK are affected by EDs, at an estimated cost of 3.9–4.6 billion pounds annually to the NHS [ 15 ]. Anorexia Nervosa (AN) and Bulimia Nervosa (BN) are two eating disorders with high mortality rates, compared to the general population [ 11 , 128 ] with AN leading to the highest mortality rates compared to all other psychiatric illnesses [ 11 ].

Despite this, the strength of evidence for eating disorder treatments is modest [ 23 , 58 ] with no gold standard psychological interventions available for adult presentations of AN [ 83 ] or BN [ 96 ]. Systematic reviews of randomised control trials (RCTs) in eating disorders have found the evidence for psychological therapies for eating disorders inconclusive [ 24 , 58 ]. Therapies for eating disorders have a minimal evidence base, consisting of a very small number of studies [ 113 ], with and high impact factor journals publish significantly fewer papers on eating disorders than other psychiatric conditions [ 113 ]. This may be due, in part, to a deficit in funding for eating disorder research in comparison to the burden of illness [ 38 , 83 ], mirroring a lack of funding for clinical services [ 6 ].

However, another reason for the lack of effective evidence-based treatments for people with eating disorders could be comparative failings of integrating lived-experience perspectives into research in this area. Aspects of co-production have been incorporated into case-studies [ 4 , 5 , 19 ], the development of novel pathways such as FREED [ 7 ], within service delivery [ 75 ] and in research priority setting [ 9 , 92 ]. Feminist approaches within an eating disorder context have also been significant in challenging the politics and validity of diagnoses and power-imbalances within treatment, through drawing on women’s embodied and socially situated lived experience of having an eating disorder [ 72 ]. However, co-production within eating disorder research is not as established as service-user /survivor led research in other areas [ 44 , 104 ], where research teams and projects are either headed by or predominantly composed of lived-experience researchers.

Principles for co-production

A barrier to co-production in health research more generally, and eating disorder research specifically, might be that people with lived experience of an illness are often brought in to work on a specific research project, the parameters, aims and methodology of which have been set prior to their involvement. This contrasts with longer term work conducted by research teams including people with lived experience as key members—who might have the capacity to work together over a longer time-period to decide the direction they want their research to go in, and co-produce projects from the ground-up. Developing projects according to research principles has been found to be helpful in enabling this kind of longer-term collaboration, particularly around ideas of sharing power and building trust [ 31 ]. Many historically significant groups of mental patients advocating for their rights and to change mental health services have manifestos structured around shared values they collectively organize on the basis of CAPO [ 28 ], Mental Patients Union [ 81 ], MPU [ 82 ]. Within mental health services, there has been work carried on co-producing principles to guide the development and evaluation of peer worker roles [ 50 ], for best practice in school mental health [ 133 ] and within health research to develop principles for community-based research [ 107 ]. However, to our knowledge, there has not been an attempt to develop principles to form the basis for co-producing research between people with lived experience of a particular mental health issue and researchers, who though they might happen to have lived experience of what they are researching, are not employed in that capacity. Principles may help to guide the research process, facilitate collaborative working, and form the shared basis from which to derive research priorities. We believe that doing so could be an important way of preventing the collapse of collaboration into consultation [ 105 ].

The SPIRED research clinic

SPIRED (Sussex Partnership Innovation and Research in Eating Disorders) research clinic was founded in January 2021 and is composed of people with lived experience of eating disorders, researchers and clinicians working in the Sussex Eating Disorders Services within Sussex Partnership NHS Foundation Trust (SPFT). These identities are not mutually exclusive; many SPIRED clinic members will fall under two or more of these categories, and we aspire to be a team where clinicians and researchers are able to share their own experiences of mental health issues, regardless of their formal role [ 70 ].

To ensure those with lived experience had oversight in the research activities of the clinic, a lived experience panel was recruited in collaboration with SPFT’s Patient and Public Involvement (PPI) team [ 115 ]. The PPI team oversees the development of lived experience advisory panels (LEAPs) to ensure that those with lived experience can provide insight into the research conducted within SPFT. An advert was circulated on social media, within SPFT and with partner organisations to recruit individuals with diverse experiences of eating disorders and eating disorder treatment and was also circulated to patients within the trust eating disorder service who were at point of discharge. Sixteen individuals were recruited to the lived experience panel, and consequently SPIRED. The criteria for recruitment were that they had to identify as having experienced an eating disorder, regardless of whether that had been formally diagnosed. They were not required to reveal any information about their eating disorder. Since the eating disorder service SPIRED is connected to is for adults, all SPIRED lived experience panel members are over eighteen. Although these individuals were specifically recruited for a lived experience role, some of them also had clinical experience within the NHS, as well as research expertise. A co-production approach is followed in research conducted by SPIRED [ 32 ], echoing the rhetoric 'no decision about me without me' [ 41 ]. Within SPIRED, those with lived experience of EDs contribute to developing ideas, overseeing projects and conducting research.

To co-produce a set of principles to guide research, within an eating disorder research clinic composed of people with lived experience of an eating disorder, clinicians, and other researchers.

To provide an illustrative case for our approach as a novel co-production methodology, by demonstrating how co-producing developing principles can lead to a clear and defined research agenda.

Development of principles

Prior to the first SPIRED team meeting, the lived experience panel and SPIRED team members were invited to complete a questionnaire. The questionnaire was developed by the SPIRED clinic research assistant, a Service User and Carer Involvement Coordinator from the SPFT PPI team, and a member of the lived experience panel.

The questionnaire consisted of four open ended questions, and asked members to share whatever they felt comfortable sharing: their experience of eating disorders and eating disorder services, their view of what lived experience involvement in research meant, what they wanted to contribute to SPIRED aside from their lived experience of an eating disorder, and what they felt should be the key priorities for eating disorder research.

Responses were loosely summarised by theme and presented at the first SPIRED clinic meeting (facilitated over an online platform), where seventeen members were present, including eleven members of the lived experience panel. Small group discussions were held in break-out rooms to develop key principles, followed by feedback and a discussion with the whole group. Extensive notes were taken of all these discussions.

These notes formed the starting point of a smaller working group, with three lived experience panel members and two other SPIRED clinic members. A consensus-based decision making methodology [ 56 ] was used to derive core principles from the discussions of the wider SPIRED group. All the key principles derived from the initial meeting were discussed individually, with each working group member holding veto-power for any decision around a particular principle (whether that was to include or to exclude it). This then halted the decision, and the principle was then re-discussed and modified until consensus could be reached [ 56 ]. Following agreement about which principles to include, this consensus-based process was used for decision-making around which of the principles could be synthesized.

A group facilitator chaired the meeting and made notes on ongoing discussions to enable further reflection. The lead author then wrote up the main sections of this paper, which were then circulated to all SPIRED clinic members for comments and feedback, following which extensive changes were made to this paper.


Everyone who has contributed to this paper at any stage has been invited to co-author (including the lived experience panel). Although we felt it was vital to highlight the extent of the contribution of the lived experience panel in the co-production of these principles, we did not want to force any individual to identify themselves as someone with lived experience of an eating disorder. Therefore, all authors are listed solely as SPIRED clinic members.

The SPIRED clinic consists of individuals with a range of experiences of different eating disorders, eating disorder services, clinicians, and researchers. We aimed to ensure representation from neurodivergent people, LGBTIA people, men, and people of colour (POC), all of which are often marginalised within eating disorder treatment. However, we recognise that POC are particularly underrepresented on our lived experience panel, which may have impacted on the principles that our research team chose to prioritise.

The SPFT Research Governance department confirmed that ethical approval was not necessary for this project, as there were no participants.

Because of the increased sensitivity of sharing personal information about mental health, co-authors who were lived experience panel members also signed a consent form to be anonymously quoted in this paper.

As a result of the process outlined above, the following six principles were determined to be fundamental in guiding our research. We believe in eating disorder research which is: real world, tailored, hopeful, experiential, broad and democratic (see Fig.  1 ).

figure 1

Overview of SPIRED principles

We have chosen in this section to integrate the ‘results’ of our decision-making with existing literature, as this best reflects both our aims in doing this work and the process through which the principles came about. Traditional qualitative research results focus solely on ‘participant data’, viewing people experiences, viewpoints, and theorizing as data-points to be analysed by a researcher, and then contextualized within the discussion section of a paper. However, our lived experience panel (along with other clinic members) are not participants, but researchers, and drew on both their own individual experiences but also their understanding and critical assessment of the research literature during this process. This demonstrates the capacity of lived-experience led research to create new forms of knowing outside traditional research binaries, such as those between researcher and researched [ 63 ]. Because our discussions as a group, both in the meetings, and over email, involved sharing and reflecting on research findings, this structure has been mirrored in our write-up. The point of this work was to create a set of principles that would be foundational for our work together and could be shared with others. Although this paper describes the process by which we developed these principles, we consider the below results section not the output of a novel co-production process, but also an argument for change [ 16 ].

Given the paucity of research on efficacy and acceptability of ED treatments, there is an urgent need for research which is ‘real world’ and makes an immediate, practical impact on the lives of people with eating disorders. Within SPIRED, this could include developing and evaluating novel interventions for eating disorders [ 93 ], evaluating, improving and developing ED service provision [ 109 ] or engaging with policymaking to ensure it is evidence-based.

Current research does not seem to consistently meet the needs of those with EDs. Although recent research has established connections between the presence of an ED and brain structure and functioning [ 42 , 117 ], translating findings on neurofeedback and biofeedback into effective treatment has proven difficult, with current therapeutic options proving too invasive and costly [ 126 ].

Due to the high mortality rate of EDs and current lack of evidence-based treatment, we call for urgent prioritisation of funding for well-targeted research that can be translated into concrete and immediate changes in service provision [ 55 ].

Where evidence-based treatments do exist, researchers have often been slow to adapt them effectively for marginalised groups [ 2 ]. We believe that eating disorder treatments and services should adopt an intersectional approach [ 25 ], recognising that people have differing identities, such as race, class, gender and sexuality, which interact and result in differing experiences of oppression [ 36 ]. Consequently, ED research should offer evidence-based ways of tailoring existing interventions to include minority groups and acknowledge the systemic factors which may create inequalities in accessing ED treatment [ 17 ].

Within ED research, particular groups have been excluded from treatment development, and treatment and service provision, so are often missing in the dialogue within eating disorder research. These include: people with other comorbid mental health issues [ 10 , 17 , 69 , 137 ], autistic spectrum conditions [ 3 , 22 , 40 , 62 , 118 , 121 ], people with binge-eating disorder, EDNOS/OSFED or ARFID [ 11 , 13 , 106 ], men [ 103 , 112 , 120 , 134 , 138 , 140 ], racially minoritized groups [ 1 , 20 , 52 , 53 , 77 , 114 , 119 , 139 ] and LGBTIA people [ 8 , 27 , 51 , 80 , 85 , 95 , 98 ].

Whilst acknowledging the issues within current ED research is important, it is vital to hold an optimistic and forward-thinking stance on treatment for EDs. Individuals with eating disorders often experience high levels of hopelessness [ 116 ], and as a result interventions which target “hope” and forward looking thinking have been found to be effective in facilitating recovery [ 64 , 116 ]. Empathy and the provision of hope have been repeatedly found to be the most important features in health professionals working with patients with eating disorders [ 43 , 46 , 65 , 135 ].

Evidence suggests that peer support can provide the support and connection necessary to increase people’s sense of hope for recovery, as a key mechanism of change [ 29 , 48 , 86 , 101 , 110 ].

Interventions which harness peer support have included online discussion forums [ 67 , 86 ], formal mentoring programmes [ 57 , 99 , 100 ] and clinicians use of their own personal recovery in the treatment of eating disorders [ 34 , 131 ].


Eating disorder research often focuses on quantitative outcomes such as BMI to evaluate interventions [ 12 , 24 ]. However solely focusing on BMI as an indicator of recovery is not recommended by NICE guidelines [ 90 ]. This narrow focus on BMI can cause iatrogenic harm to patients [ 88 ], and marginalise patients with diagnoses aside from AN [ 130 ].

The importance placed on measuring people with eating disorders bodies, over listening to their experience, can be understood utilizing the philosophical concept of epistemic injustice; whereby patients’ knowledge about their own condition is disregarded, and they are reduced to passive ‘objects’ to be measured, instead of active and knowing subjects [ 37 ].

A significant part of recovery from eating disorders can involve developing a “recovery” voice separate from the illness [ 18 ], with effective therapeutic interventions utilising creative ways of developing this [ 59 , 60 ]. The current focus on BMI as an indicator of recovery does not take patients own knowledge and understanding of their illness into account and overlooks the subjective experiences of those with EDs receiving treatment.

We feel there is a need for an increase in qualitative research which explores the perspectives of ED sufferers and aims to understand their experiences. This may be key for developing more effective interventions in this area [ 35 ].

Although traditional therapies for EDs can form an important part of ED recovery, they do not address all the factors which have the capacity to have a positive impact of the lives of those with EDs. It is well established in the literature that carers play an important role in recovery [ 108 , 123 ], as well as peers [ 57 ]. Despite acknowledgment that carers might struggle in these roles [ 33 ], research exploring which factors impact carer wellbeing, and what support they might benefit from, is still a comparatively new field [ 122 ].

There is an emerging evidence base on the impact of holistic therapies on EDs, including art therapy [ 47 , 61 ], dance [ 71 ] and comedy [ 78 ]. This is consistent with an understanding that ED recovery involves rebuilding a life outside the ED [ 135 ] beyond simply managing the illness [ 39 , 74 , 111 ].

We believe that it is important to broaden out the research focus from the development and evaluation of therapies, to consider provision of support to all parts of the ‘system’ (family members, carers, peers, clinicians) as well as focusing on the development of novel and creative interventions.

Despite the importance of involving patients and carers in eating disorder research and service provision there is often limited ‘co-production in this area’ [ 87 ], with inclusion of lived-experience perspectives “scarce to date” [ 84 ].

It is our belief that many of the current issues we have highlighted in eating disorder research are the result of not including the perspectives and expertise of people who have experience of eating disorders. Co-production in eating disorder research is particularly important in determining how to define and evaluate recovery in eating disorders (moving away from narrow outcomes like BMI) [ 68 , 125 ] and towards a richer understanding of the recovery process [ 135 ].

We advocate an approach to research that involves service-users/survivors and clinicians working in partnership with other researchers, in all aspects of eating disorder research. This could include setting research priorities, designing research projects, conducting all aspects of research, and disseminating research and engaging the public.

We wanted to trial a ‘principles-first’ approach in developing research projects within our eating disorder research clinic (SPIRED), as we hoped that it would give us a direction and mandate for our work stemming from all members of the clinic. Through a series of workshops, we co-produced a set of principles to guide the direction and process of our work together, agreeing that the eating disorder research we conducted would be real world, tailored, hopeful, experiential, broad, and democratic.

In this section we first offer some reflections on the process from clinic members, highlighting strengths and weaknesses of the approach we took, before setting these in the context of the broader literature.


Members of the SPIRED research clinic wrote reflections on their experience of co-producing principles to guide our research and collaborating on this paper. We present these in their individuality and diversity, instead of coming to a single reflexive position (as authors) on the strengths and limitations of the process we took.

There was consensus that any division between members of the lived experience panel and other researchers and clinicians was not only artificial (as members had a multiplicity of roles and identities in their lives), but also undermined the democratic way we aimed to work together. People are identified here by whether they are a professional member or a lived experience panel member within the SPIRED clinic, however we wanted to emphasize that they will have other identities and areas of expertise. We identified people in this way as we thought it was important to acknowledge the power imbalances that exist between lived experience panel members, and those employed by the trust in a more permanent capacity.

“[Contrasting lived experience perspectives with clinicians and researchers] creates an artificial binary where our ED defines us—instead of recognising multiple identities. I fit into each of these 'categories’, but the research process runs the risk of reinforcing power differentials and that we ARE the ED. An ED can silence our sense of self and other aspects of identity—the research process shouldn't replay this.” -Lived Experience Panel Member
"I was looking forward to contributing as someone with Lived Experience, because I work as a research student in my day job, so I wear two hats and have seen first-hand the value in incorporating Lived Experience perspectives.” -Lived Experience Panel Member
“As a clinician and researcher who has also had experiences of being on the other side of service provision, I was acutely aware of the ‘us and them’ divisions that play out in both clinical and research settings, and how these divisions can make it harder for people to open up and express fully their views about any care they might or might not have received. We are then missing important information around how to develop interventions and improve care delivery.” -Professional Member

One of the most significant things about the process for many SPIRED members was that the initial meeting was one of the first times they were able to be open about, integrate and use their multiple identities. This meeting was felt by many as cathartic, hopeful and powerful, as well as providing a solid foundation for collaboration.

“As a mental health professional, who was sharing my experiences of being a service user for the first time in front of other professionals, I felt scared and shy at first. Everyone was supportive and reassuring, and I never felt “less than” for sharing my lived experience.” -Lived Experience Panel Member
“I was keen that the LEAP was a place that welcomed all perspectives and we put a lot of thought into the initial meetings to create a psychologically safe arena for people to know they could be open and honest. An example of this was me sharing that I had not had good experiences of service use, to help others feel that all perspectives were welcome and to counter the us and them divide.” -Professional Member
“There was such a really open atmosphere in that first meeting—I shared things about my mental illness for the first time in a work context. I think this was such a respectful and trusting basis for the later consensus-based decision-making work we did together in developing the principles.” -Professional Member

Part of why the process of co-producing principles was felt to be successful, was because everyone shared similar motivations for wanting to be part of the SPIRED research clinic. These included a motivation to improve eating disorder treatment, alongside a commitment to genuine co-production, as opposed to lived experience involvement just having a ‘rubber-stamping’ function.

“Having been denied help because of a “normal BMI”, deteriorating and then being on a waiting list for months I felt the need to do something- just anything to take this disappointment and anger towards services and turn it into something a bit positive.” -Lived Experience Panel Member
“I think my main motivations for helping out are guilt, being bluntly honest. I had amazing treatment—the best. Not everyone is so lucky. So, I want to pay that forward and try in any meagre way to give back.” -Lived Experience Panel Member
“I really wanted to work at SPIRED because the people who set it up were so clear about how much they valued co-production as core to the way they worked.” -Professional Member
“I was happy that everyone seemed to be on the same page and have a shared passion for improving lives for people with eating disorders.” -Lived Experience Panel Member

All the co-authors of this paper except two, were present for the initial meeting and subsequent discussions. However even those who joined the process later, felt aligned with what had already been done.

“I have been struck by the paucity of research focused on ED interventions, particularly the lack of research which is co-produced with those with lived experience. Despite not being involved in the discussions in which SPIRED principles emerged, I believe the research priorities outlined by SPIRED are incredibly important and reflective of my own values.” -Professional Member
“As I was reading through, I couldn’t believe how aligned they were with my own personal views on co-production and the importance of lived experience perspectives in research […]. This is such a hopeful piece of work.” -Professional Member

Those responsible for facilitating the initial meeting, and supporting the lived experience panel going forward, were keen to reduce the burden on them from engaging in this work.

“I was also aware that speaking about your own difficult experiences can be exhausting, triggering and recovery is not neat; people can relapse and struggle. I didn’t want there to be only a couple of people who were relied on excessively for contributions, so there was an idea that people could dip in and out depending on capacity and interest.” -Professional Member

However, despite the shared wish to make lived experience work core to the SPIRED clinic, structural inequalities between the clinic members were a significant barrier to democratic working. Clinicians and researchers were employed on a substantive basis, whereas the lived experience panel were employed on a casualized basis, occasionally doing work—but with limited funding. This meant that often they were not able to lead on aspects of the research.

“Although I do have lived experience of mental illness (including disordered eating) I’m not one of the Lived Experience Panel members for SPIRED, and it should have been one or many of them that wrote up this paper—which they would have been much better placed to do than me. However sadly we didn’t have a permanently employed lived experience researcher, or enough in our PPI budget to pay for this work to be done on a casualised basis.” -Professional Member

Some people felt that this led to differences between how lived experience panel members and other SPIRED clinic members were treated, though others didn’t share this view.

“[There was a] 'distance' between the researchers and those assigned a 'lived experience' identity in having limited communications from the project.” -Lived Experience Panel Member
"Every communication I had from the PPI team felt like they were talking to an equal member of the team. Same for the paper- I didn’t feel like my thoughts and comments counted less because I was a LEAP member and not a researcher." -Lived Experience Panel Member

In general, people felt pride in what we’d achieved together and positive about the personal benefits of creating this paper.

“I remember feeling very proud of having contributed on that piece of collective work.” -Lived Experience Panel Member
“Lived Experience contributors don't often have a "career pathway" or professional development opportunities, so helping to shape an academic paper—and this was before I had published anything in my own field, as a student—was a really valuable experience.” -Lived Experience Panel Member

Our work in context

We set-up our lived experience led research clinic due to a belief that ED research was not currently adequately meeting the needs of the population it aimed to serve.

It is our view current issues in ED research are partially due to the distinct absence of the voices of those with lived experience of EDs and a lack of co-production in ED research.

We wanted to address the absence or superficiality of co-production in ED research by co-producing a set of principles which would be a mandate for our work together and ensure that it was grounded in what we cared about as a team. Although it initially seemed unlikely that a consensus-based decision-making methodology [ 56 ] would be successful, given the range of people with different backgrounds and experiences and priorities in our initial clinical meeting, this has not been our experience. Even the initial questionnaires that were completed by all clinic members — prior to meeting —s howed significant overlap in which principles people wanted to prioritize, and discussions further solidified these shared understandings and commitment. There was debate at all stages of the process of developing the principles, from initial workshops through to comments on drafts of the paper. These issues were resolved through discussion (during meetings as well as via email),this resolution tended to occur by describing the principles in a nuanced way that incorporated critical feedback from clinic members. All members enthusiastically agreed with the way the principles were framed in the final draft of this paper.

We were fortunate as a research clinic in having funding allocated to us for about 60 h of PPI time annually, as well as a dedicated PPI co-ordinator for our clinic, and a broader PPI team within our NHS trust who were able to advise on issues. This enabled us to take a longer-term strategy for PPI, as opposed to only having funding tied to specific research projects — where the aims and the method of the project had already been determined. Even though UK funders often include a requirement for PPI to have occurred at the project development stage [ 91 ], meaning that research institutions often have funding available for this specific purpose, it is rarer that PPI funding is allocated to a research team to spend in any way they think appropriate. However, this was essential to the kind of approach we were able to take. Additional funding would have allowed us time and research capacity to use a wider variety of methodological approaches to co-produce principles,we would love to see the work outlined in this paper built on and added to by other researchers trialling different and more systematic approaches for doing so. We believe that it is important to have more substantive lived-experience positions in research, something that we would like to see in our research clinic.

We recruited our PPI panel from social media, as well as patients who were at the point of discharge. As outlined above, POC are not adequately represented on our lived experience advisory panel, something that is a significant issue with many cases of co-production and PPI within research [ 49 ]. Developing ongoing collaborations with organisations focused on health research specific to POC, as well as putting systems in place to enhance recruitment of POC to senior positions within research teams [ 45 ] are both strategies that could improve these issues. However, neither of these constitutes a ‘quick fix’, and we were keen to work to address the underlying issue causing under-presentation of POC on our LEAP, as opposed to just advertising specifically for more POC which we felt was tokenistic.

We wanted to ensure that the research funding that we applied for corresponded to our research agenda — which was derived directly from our principles. However, in trying to develop competitive funding applications which fell under the ‘broad’ principle (i.e., developing and evaluating non-standard therapeutic treatments, including peer-support) it became clear that fewer health research funding sources would consider these kinds of treatments, as opposed to more traditional therapies. It appears that currently, ED research priorities can be guided by funders [ 38 ], rather than those with lived experience of EDs, who can provide valuable insight into where research efforts need to be urgently directed.

Priorities and principles and developed as a result of co-production approaches such as that one taken in this paper are often critical in approach and conflict with existing recommendations for eating disorder treatments [ 89 ], as approaches which seek to elevate the voices of service users have found in other areas [ 129 ]. However, we feel that this conflict has arisen because of the historic marginalization of lived experience voices within mental health research, and the lack of power people with lived experience still have in collaborating on research projects [ 73 ]. Given the evidence that research priorities determined by ED service-users produce better interventions and outcomes [ 132 ], and the ineffectiveness of current ED treatments [ 58 ], we believe it time for a new approach—led by those with lived-experience of eating disorders.

To our knowledge, we are the first health research group to have co-produced principles as the basis for our work together—putting us more in line with grassroots campaigning organisations [ 81 , 82 ]. However, these historic organizations rarely outline the process by which they produce their manifestos, which makes it hard to replicated and develop their methodology. There are several limitations to this piece of work, however we hope that other researchers will both build upon and refine the approach outlined in this paper and develop new methodologies for enhancing co-production within health research through the creation of principles to guide their collaborative work. More broadly, we wanted to provide an illustrative case for the value and generative potential of co-producing principles to guide health research and enable long-term collaboration between people with lived experience of an illness, and other researchers [ 127 ].

Following the development of SPIRED principles they were included in an All-Party parliamentary group report on eating disorders led by BEAT [ 16 ], as an example of how "a relatively small investment can make a big impact in building local research capacity and supporting the application of research findings into clinical practice."

Availability of data and materials

Not applicable.


  • Anorexia nervosa
  • Bulimia nervosa

Eating disorder

Patient and public involvement (in research)

Sussex Partnership NHS Foundation Trust

Abood DA, Chandler SB. Race and the role of weight, weight change, and body dissatisfaction in eating disorders. Am J Health Behav. 1997;21(1):21–5.

Google Scholar  

Acle A, Cook BJ, Siegfried N, Beasley T. Cultural considerations in the treatment of eating disorders among racial/ethnic minorities: a systematic review. J Cross Cult Psychol. 2021;52(5):468–88.

Article   Google Scholar  

Adamson J, Kinnaird E, Glennon D, Oakley M, Tchanturia K. Carers’ views on autism and eating disorders comorbidity: qualitative study. BJPsych Open. 2020. .

Article   PubMed   PubMed Central   Google Scholar  

Adlam J. Shared work and existential engagement in the therapeutic milieu. (2016)

Adlam J. ‘Project Antigone’: a psychosocial exploration of the dynamics of food refusal and force feeding (2014). Doi:

Allen KL, Mountford VA, Elwyn R, Flynn M, Fursland A, Obeid N, Partida G, Richards K, Schmidt U, Serpell L, Silverstein S, Wade T. A framework for conceptualising early intervention for eating disorders. Eur Eat Disord Rev. 2023;31(2):320–34. .

Article   PubMed   Google Scholar  

Allen KL, Mountford V, Brown A, Richards K, Grant N, Austin A, Glennon D, Schmidt U. First episode rapid early intervention for eating disorders (FREED): from research to routine clinical practice. Early Interv Psychiatry. 2020;14(5):625–30. .

Amianto F. Homosexuality and anorexia nervosa: an explorative study on personality traits. Acta Psychopathol. 2016. .

Aouad P, Hambleton A, Marks P, Maloney D, Calvert S, Caldwell B, McLean SA, Shelton B, Cowan K, Feneley J, Pepin G, Paxton S, Williams M, Meddick T, Squire S, Hickie I, Kay Lambkin F, Touyz S, Maguire S. Setting the top 10 eating disorder research and translation priorities for Australia. Aust N Z J Psychiatry. 2022. .

Araujo DMR, da Santos GF, Nardi AE. Binge eating disorder and depression: a systematic review. World J Biol Psychiatry. 2010;11(2–2):199–207. .

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 Psychiatry. 2011;68(7):724–31. .

Atwood ME, Friedman A. A systematic review of enhanced cognitive behavioral therapy (CBT-E) for eating disorders. Int J Eat Disord. 2020;53(3):311–30. .

Bailey AP, Parker AG, Colautti LA, Hart LM, Liu P, Hetrick SE. Mapping the evidence for the prevention and treatment of eating disorders in young people. J Eat Disord. 2014;2(1):5. .

Beale J. Scientism and scientific imperialism. Int J Philos Stud. 2019;27(1):73–102. .

BEAT. Types of Eating Disorder—Beat (2020).

BEAT. All-Party Parliamentary Group (APPG) on Eating Disorders (2021). Beat.

Becker AE, Eddy KT, Perloe A. Clarifying criteria for cognitive signs and symptoms for eating disorders in DSM-V. Int J Eat Disord. 2009;42(7):611–9. .

Bell NJ. Rhythm and semiotic structures of long-term ambivalence in the dialogical self: eating disorder and recovery voices. J Constr Psychol. 2013;26(4):280–92. .

Blackburn J, Minogue V. Developing an eating disorder pathway: a case study. J Ment Health Train Educ Pract. 2014;9(4):244–60. .

Bodell LP, Wildes JE, Cheng Y, Goldschmidt AB, Keenan K, Hipwell AE, Stepp SD. Associations between race and eating disorder symptom trajectories in black and white girls. J Abnorm Child Psychol. 2018;46(3):625–38. .

Boyle D, Harris M. The challenge of co-production. Lond New Econ Found. 2009;56:18.

Brede J, Babb C, Jones C, Elliott M, Zanker C, Tchanturia K, Serpell L, Fox J, Mandy W. “For me, the anorexia is Just a symptom, and the cause is the autism”: investigating restrictive eating disorders in autistic women. J Autism Dev Disord. 2020;50(12):4280–96. .

Brownley KA, Berkman ND, Sedway JA, Lohr KN, Bulik CM. Binge eating disorder treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007;40(4):337–48. .

Bulik CM, Berkman ND, Brownley KA, Sedway JA, Lohr KN. Anorexia nervosa treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007;40(4):310–20. .

Burke NL, Schaefer LM, Hazzard VM, Rodgers RF. Where identities converge: the importance of intersectionality in eating disorders research. Int J Eat Disord. 2020;53(10):1605–9.

Cahn ES. No more throw-away people: the co-production imperative. Edgar Cahn (2000)

Calzo JP, Austin SB, Micali N. Sexual orientation disparities in eating disorder symptoms among adolescent boys and girls in the UK. Eur Child Adolesc Psychiatry. 2018;27(11):1483–90. .

CAPO. Introduction, manifesto, demands (n.d.).

Cardi V, Ambwani S, Crosby R, Macdonald P, Todd G, Park J, Moss S, Schmidt U, Treasure J. Self-help and recovery guide for eating disorders (SHARED): study protocol for a randomized controlled trial. Trials. 2015;16(1):165. .

Carel H, Kidd IJ. Epistemic injustice in medicine and healthcare. In: Kidd IJ, Medina J, Pohlhaus G Jr, editors. The Routledge handbook of epistemic injustice. Routledge; 2017. p. 336–46.

Christopher S, Saha R, Lachapelle P, Jennings D, Colclough Y, Cooper C, Cummins C, Eggers MJ, FourStar K, Harris K, Kuntz SW, LaFromboise V, LaVeaux D, McDonald T, Bird JR, Rink E, Webster L. Applying indigenous community-based participatory research principles to partnership development in health disparities research. Fam Commun Health. 2011;34(3):246–55. .

Clark M. Co-production in mental health care. Ment Health Rev J. 2015;20(4):213–9. .

Coomber K, King RM. Coping strategies and social support as predictors and mediators of eating disorder carer burden and psychological distress. Soc Psychiatry Psychiatr Epidemiol. 2012;47(5):789–96. .

Costin C. Been there, done that: clinicians’ use of personal recovery in the treatment of eating disorders. Eat Disord. 2002;10(4):293–303.

Craig P, Dieppe P, Macintyre S, Michie S, Nazareth I, Petticrew M. Developing and evaluating complex interventions: The new medical research council guidance. Int J Nurs Stud. 2013;50(5):587–92.

Crenshaw K. Demarginalizing the intersection of race and sex: a Black feminist critique of antidiscrimination doctrine, feminist theory, and antiracist politics [1989]. In: Bartlett K, editor. Feminist legal theory. Routledge; 2018. p. 57–80.

Crichton P, Carel H, Kidd IJ. Epistemic injustice in psychiatry. BJPsych Bull. 2017;41(2):65–70.

Davies H. Eating disorders bear the brunt of the paucity in mental health research funding. The Psych PhD Pathway. 2020. .

Dawson L, Rhodes P, Touyz S. “Doing the impossible”: the process of recovery from chronic anorexia nervosa. Qual Health Res. 2014;24(4):494–505. .

Dell’Osso L, Carpita B, Gesi C, Cremone IM, Corsi M, Massimetti E, Muti D, Calderani E, Castellini G, Luciano M, Ricca V, Carmassi C, Maj M. Subthreshold autism spectrum disorder in patients with eating disorders. Compr Psychiatry. 2018;81:66–72. .

Department of Health. Liberating the NHS: No decision about me, without me. 2012.

Donnelly B, Touyz S, Hay P, Burton A, Russell J, Caterson I. Neuroimaging in bulimia nervosa and binge eating disorder: a systematic review. J Eat Disord. 2018;6(1):3. .

Evans EJ, Hay PJ, Mond J, Paxton SJ, Quirk F, Rodgers B, Jhajj AK, Sawoniewska MA. Barriers to help-seeking in young women with eating disorders: a qualitative exploration in a longitudinal community survey. Eat Disord. 2011;19(3):270–85. .

Faulkner A. Survivor research and mad studies: the role and value of experiential knowledge in mental health research. Disabil Soc. 2017;32(4):500–20. .

Faulkner A, Thompson R. Uncovering the emotional labour of involvement and co-production in mental health research. Disabil Soc. 2021. .

Fogarty S, Ramjan LM. Factors impacting treatment and recovery in anorexia nervosa: qualitative findings from an online questionnaire. J Eat Disord. 2016;4(1):18. .

Frisch MJ, Franko DL, Herzog DB. Arts-based therapies in the treatment of eating disorders. Eat Disord. 2006;14(2):131–42.

Gallagher MW, Long LJ, Richardson A, D’Souza J, Boswell JF, Farchione TJ, Barlow DH. Examining hope as a transdiagnostic mechanism of change across anxiety disorders and CBT treatment protocols. Behav Ther. 2020;51(1):190–202.

Gibbins KJ, Lo JO. What matters to whom: patient and public involvement in research. Clin Obstet Gynecol. 2022;65(2):268–76.

Gillard S, Foster R, Gibson S, Goldsmith L, Marks J, White S. Describing a principles-based approach to developing and evaluating peer worker roles as peer support moves into mainstream mental health services. Ment Health Soc Incl. 2017;21(3):133–43. .

Goldhammer HB, Maston ED, Keuroghlian AS. Addressing eating disorders and body dissatisfaction in sexual and gender minority youth. Am J Prev Med. 2019;56(2):318–22. .

Gordon KH, Brattole MM, Wingate LR, Joiner TE. The impact of client race on clinician detection of eating disorders. Behav Ther. 2006;37(4):319–25. .

Gordon KH, Perez M, Joiner TE. The impact of racial stereotypes on eating disorder recognition. Int J Eat Disord. 2002;32(2):219–24. .

Grattidge L, Purton T, Auckland S, Lees D, Mond J. Participatory action research in suicide prevention program evaluation: opportunities and challenges from the National Suicide Prevention Trial, Tasmania. Aust N Z J Public Health. 2021;45(4):311–4. .

Great Britain & Parliamentary and Health Service Ombudsman. Ignoring the alarms: how NHS eating disorder services are failing patients. 2017.

Guinaudie C, Mireault C, Tan J, Pelling Y, Jalali S, Malla A, Iyer SN. Shared decision making in a youth mental health service design and research project: insights from the pan-canadian access open minds network. Patient Patient-Center Outcomes Res. 2020;13(6):653–66. .

Hanly F, Torrens-Witherow B, Warren N, Castle D, Phillipou A, Beveridge J, Jenkins Z, Newton R, Brennan L. Peer mentoring for individuals with an eating disorder: a qualitative evaluation of a pilot program. J Eat Disord. 2020;8(1):29. .

Hay P. A systematic review of evidence for psychological treatments in eating disorders: 2005–2012. Int J Eat Disord. 2013;46(5):462–9. .

Hilliard RE. The use of cognitive-behavioral music therapy in the treatment of women with eating disorders. Music Ther Perspect. 2001;19(2):109–13. .

Hodge L, Simpson S. Speaking the unspeakable: artistic expression in eating disorder research and schema therapy. Arts Psychother. 2016;50:1–8. .

Holmqvist G, Persson CL. Is there evidence for the use of art therapy in treatment of psychosomatic disorders, eating disorders and crisis? A comparative study of two different systems for evaluation. Scand J Psychol. 2012;53(1):47–53.

Huke V, Turk J, Saeidi S, Kent A, Morgan JF. Autism spectrum disorders in eating disorder populations: a systematic review. Eur Eat Disord Rev. 2013;21(5):345–51. .

Ingram RA. Doing mad studies: making (non)sense together. Intersect Glob J Soc Work Anal Res Polity Pract. 2016;5(3):11–7.

Irving LM, Cannon R. Chapter 14 - starving for hope: goals, agency, and pathways in the development and treatment of eating disorders. In: Snyder CR, editor. Handbook of hope. Cambridge: Academic Press; 2000. p. 261–283. .

Chapter   Google Scholar  

Jewell T, Blessitt E, Stewart C, Simic M, Eisler I. Family therapy for child and adolescent eating disorders: a critical review. Fam Process. 2016;55(3):577–94. .

Karnieli-Miller O, Strier R, Pessach L. Power relations in qualitative research. Qual Health Res. 2009;19(2):279–89.

Kendal S, Kirk S, Elvey R, Catchpole R, Pryjmachuk S. How a moderated online discussion forum facilitates support for young people with eating disorders. Health Expect. 2017;20(1):98–111. .

Kenny TE, Lewis SP. reconceptualizing recovery: integrating lived experience perspectives into traditional eating disorder recovery frameworks. Psychiatr Serv. 2021. .

Keski-Rahkonen A, Mustelin L. Epidemiology of eating disorders in Europe: prevalence, incidence, comorbidity, course, consequences, and risk factors. Curr Opin Psychiatry. 2016;29(6):340–5. .

King AJ, Brophy LM, Fortune TL, Byrne L. factors affecting mental health professionals’ sharing of their lived experience in the workplace: a scoping review. Psychiatr Serv. 2020;71(10):1047–64. .

Krantz AM. Growing into her body: dance/movement therapy for women with eating disorders. Am J Dance Ther. 1999;21(2):81–103.

LaMarre A, Levine MP, Holmes S, Malson H. An open invitation to productive conversations about feminism and the spectrum of eating disorders (part 1): basic principles of feminist approaches. J Eat Disord. 2022. .

Lambert N, Carr S. ‘Outside the original remit’: co-production in UK mental health research, lessons from the field. Int J Ment Health Nurs. 2018;27(4):1273–81.

Lamoureux M, Bottorff J. “Becoming the real me”: recovering from anorexia nervosa. Health Care Women Int. 2005;26(2):170–88. .

Lewis HK, Foye U. From prevention to peer support: a systematic review exploring the involvement of lived-experience in eating disorder interventions. Ment Health Rev J. 2021.

Lindvall Dahlgren C, Wisting L, Rø Ø. Feeding and eating disorders in the DSM-5 era: a systematic review of prevalence rates in non-clinical male and female samples. J Eat Disord. 2017;5(1):56. .

Lynch SL. Eating disorders in African American women: Incorporating race into considerations of etiology and treatment [Psy.D., Widener University, Institute for Graduate Clinical Psychology]. 2003. .

MacRury I. Humour as ‘social dreaming’: stand-up comedy as therapeutic performance. Psychoanal Cult Soc. 2012;17(2):185–203. .

Madden M, Speed E. Beware zombies and unicorns: toward critical patient and public involvement in health research in a neoliberal context. Front Sociol. 2017. .

McClain Z, Peebles R. Body image and eating disorders among lesbian, gay, bisexual, and transgender youth. Pediatr Clin. 2016;63(6):1079–90.

Mental Patients Union. Declaration of Intent. 1973. .

MPU. The Need for a Mental Patients’ Union. Some Proposals. 1976.

Murray SB, Pila E, Griffiths S, Le Grange D. When illness severity and research dollars do not align: are we overlooking eating disorders? World Psychiatry. 2017;16(3):321. .

Musić S, Elwyn R, Fountas G, Gnatt I, Jenkins ZM, Malcolm A, Miles S, Neill E, Simpson T, Yolland CO, Phillipou A. Valuing the voice of lived experience of eating disorders in the research process: benefits and considerations. Aust N Z J Psychiatry. 2021. .

Nagata JM, Ganson KT, Austin SB. Emerging trends in eating disorders among sexual and gender minorities. Curr Opin Psychiatry. 2020;33(6):562–7. .

Naslund JA, Aschbrenner KA, Marsch LA, Bartels SJ. The future of mental health care: peer-to-peer support and social media. Epidemiol Psychiatr Sci. 2016;25(2):113–22. .

Article   CAS   PubMed   PubMed Central   Google Scholar  

Newton T. Consumer involvement in the appraisal of treatments for people with eating disorders: a neglected area of research? Eur Eat Disord Rev. 2001;9(5):301–8. .

NHS England. Adult eating disorders: community, inpatient and intensive day patient care: guidance for commissioners and providers, 28 (2019).

NICE. Eating disorders: Recognition and treatment (2017a).

NICE. Overview | Eating disorders: recognition and treatment | Guidance | NICE. (2017b). NICE. .

NIHR. A brief guide to public involvement in funding applications. 2020. .

Obeid N, McVey G, Seale E, Preskow W, Norris ML. Cocreating research priorities for anorexia nervosa: the Canadian eating disorder priority setting partnership. Int J Eat Disord. 2020;53(5):662–72. .

Oldershaw A, Lavender T, Basra R, Startup H. SPEAKS study: study protocol of a multisite feasibility trial of the Specialist Psychotherapy with Emotion for Anorexia in Kent and Sussex (SPEAKS) intervention for outpatients with anorexia nervosa or otherwise specified feeding and eating disorders, anorexia nervosa type. BMJ Open. 2022;12(2):e050350.

Oliver K, Kothari A, Mays N. The dark side of coproduction: do the costs outweigh the benefits for health research? Health Res Policy Syst. 2019;17(1):1–10.

Parker LL, Harriger JA. Eating disorders and disordered eating behaviors in the LGBT population: a review of the literature. J Eat Disord. 2020;8(1):51. .

Peat CM, Berkman ND, Lohr KN, Brownley KA, Bann CM, Cullen K, Quattlebaum MJ, Bulik CM. Comparative effectiveness of treatments for binge-eating disorder: systematic review and network meta-analysis. Eur Eat Disord Rev. 2017;25(5):317–28. .

Pilgrim D. Co-production and involuntary psychiatric settings. Ment Health Rev J. 2018;23(4):269–79. .

Protos K. Restricting the gendered body: understanding the trans-masculine adolescent with anorexia. Clin Soc Work J. 2020. .

Purcell J, Lister S, McCormack J, Caswell J, Logie K, Wade S, Stringer M. Reaching out for hope—a peer support program. J Eat Disord. 2014;2(1):O63. .

Article   PubMed Central   Google Scholar  

Ramjan LM, Fogarty S, Nicholls D, Hay P. Instilling hope for a brighter future: a mixed-method mentoring support programme for individuals with and recovered from anorexia nervosa. J Clin Nurs. 2018;27(5–6):e845–57. .

Ranzenhofer LM, Wilhelmy M, Hochschild A, Sanzone K, Walsh BT, Attia E. Peer mentorship as an adjunct intervention for the treatment of eating disorders: a pilot randomized trial. Int J Eat Disord. 2020;53(5):767–79. .

recoveryinthebin, A. A simple guide to co-production. Recovery in the Bin. 2018. .

Robinson KJ, Mountford VA, Sperlinger DJ. Being men with eating disorders: perspectives of male eating disorder service-users. J Health Psychol. 2013;18(2):176–86. .

Rose D. Service user/survivor-led research in mental health: epistemological possibilities. Disabil Soc. 2017;32(6):773–89. .

Rose D, Kalathil J. Power, privilege and knowledge: the untenable promise of co-production in mental “health.” Front Sociol. 2019;4:57.

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 Psychiatry. 2021;8(4):320–8. .

Schulz AJ, Israel BA, Selig SM, Bayer IS. Development and implementation of principles for community-based research in public health. In:Research strategies for community practice. Routledge; 1998.

Sepulveda AR, Lopez C, Todd G, Whitaker W, Treasure J. An examination of the impact of “the Maudsley eating disorder collaborative care skills workshops” on the well being of carers: a pilot study. Soc Psychiatry Psychiatr Epidemiol. 2008;43(7):584–91. .

Shaw H, Robertson S, Ranceva N. What was the impact of a global pandemic (COVID-19) lockdown period on experiences within an eating disorder service? A service evaluation of the views of patients, parents/carers and staff. J Eat Disord. 2021;9(1):14. .

Smale K, Pitt J. Eating disorder mentor program. J Eat Disord. 2013;1(1):O11. .

Smethurst L, Kuss D. ‘Learning to live your life again’: an interpretative phenomenological analysis of weblogs documenting the inside experience of recovering from anorexia nervosa. J Health Psychol. 2018;23(10):1287–98. .

Soban C. What about the boys?: addressing issues of masculinity within male anorexia nervosa in a feminist therapeutic environment. Int J Men’s Health. 2006;5(3):251–67.

Solmi F, Bould H, Lloyd EC, Lewis G. The shrouded visibility of eating disorders research. Lancet Psychiatry. 2021;8(2):91–2. .

Sonneville KR, Lipson SK. Disparities in eating disorder diagnosis and treatment according to weight status, race/ethnicity, socioeconomic background, and sex among college students. Int J Eat Disord. 2018;51(6):518–26. .

Article   CAS   PubMed   Google Scholar  

SPFT. Get Involved in Research. Sussex Partnership NHS Foundation Trust. 2023c.

Stavarski DH, Alexander RK, Ortiz SN, Wasser T. Exploring nurses’ and patients’ perceptions of hope and hope-engendering nurse interventions in an eating disorder facility: a descriptive cross-sectional study. J Psychiatr Ment Health Nurs. 2019;26(1–2):29–38. .

Steward T, Menchon JM, Jiménez-Murcia S, Soriano-Mas C, Fernandez-Aranda F. Neural network alterations across eating disorders: a narrative review of fMRI studies. Curr Neuropharmacol. 2018;16(8):1150–63. .

Stewart CS, McEwen FS, Konstantellou A, Eisler I, Simic M. Impact of ASD traits on treatment outcomes of eating disorders in girls. Eur Eat Disord Rev. 2017;25(2):123–8. .

Striegel-Moore RH, Wilfley DE, Pike KM, Dohm F-A, Fairburn CG. Recurrent binge eating in black American women. Arch Fam Med. 2000;9(1):83.

Thapliyal P, Mitchison D, Hay P. Insights into the experiences of treatment for an eating disorder in men: a qualitative study of autobiographies. Behav Sci. 2017. .

Treasure J. Coherence and other autistic spectrum traits and eating disorders: building from mechanism to treatment. The Birgit Olsson lecture. Nord J Psychiatry. 2013;67(1):38–42. .

Treasure J, Nazar BP. Interventions for the carers of patients with eating disorders. Curr Psychiatry Rep. 2016;18(2):16. .

Treasure J, Todd G. Interpersonal maintaining factors in eating disorder: skill sharing interventions for carers. In: Latzer Y, Stein D, editors. Bio-psycho-social contributions to understanding eating disorders. Berlin: Springer International Publishing; 2016. p. 125–37. .

Turnhout E, Metze T, Wyborn C, Klenk N, Louder E. The politics of co-production: participation, power, and transformation. Curr Opin Environ Sustainabil. 2020;42:15–21. .

Turton P, Demetriou A, Boland W, Gillard S, Kavuma M, Mezey G, Mountford V, Turner K, White S, Zadeh E, Wright C. One size fits all: or horses for courses? recovery-based care in specialist mental health services. Soc Psychiatry Psychiatr Epidemiol. 2011;46(2):127–36. .

Val Laillet D, Aarts E, Weber B, Ferrari M, QuaresimaStoeckel VLE, Alonso-Alonso M, Audette M, Malbert CH, Stice E. Neuroimaging and neuromodulation approaches to study eating behavior and prevent and treat eating disorders and obesity. NeuroImage Clin. 2015;8:1–31. .

van Furth EF, van der Meer A, Cowan K. Top 10 research priorities for eating disorders. Lancet Psychiatry. 2016;3(8):706–7. .

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

Verschuere B, Brandsen T, Pestoff V. Co-production: the state of the art in research and the future agenda. VOLUNTAS Int J Volunt Nonprofit Organ. 2012;23(4):1083–101. .

Virgo H, NCMH, Stewart C. Dump The Scales Campaign. NCMH. 2019. .

de Vos JA, Netten C, Noordenbos G. Recovered eating disorder therapists using their experiential knowledge in therapy: a qualitative examination of the therapists’ and the patients’ view. Eat Disord. 2016;24(3):207–23. .

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 Disord Rev. 2021;29(3):346–54.

Weist MD, Sander MA, Walrath C, Link B, Nabors L, Adelsheim S, Moore E, Jennings J, Carrillo K. Developing principles for best practice in expanded school mental health. J Youth Adolesc. 2005;34(1):7–13. .

Weltzin TE, Weisensel N, Franczyk D, Burnett K, Klitz C, Bean P. Eating disorders in men: update. J Men’s Health Gend. 2005;2(2):186–93. .

Wetzler S, Hackmann C, Peryer G, Clayman K, Friedman D, Saffran K, Silver J, Swarbrick M, Magill E, van Furth EF, Pike KM. 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. .

Williams O, Robert G, Martin G, Hanna E, O’Hara J. Is Co-production just really good PPI? Making sense of patient and public involvement and co-production networks. Decent Health Care Netw Reshap Org Deliv Healthc. 2020;2:13–237. .

Woodside BD, Staab R. Management of psychiatric comorbidity in anorexia nervosa and bulimia nervosa. CNS Drugs. 2006;20(8):655–63. .

Wooldridge T, Lytle PP. An overview of anorexia nervosa in males. Eat Disord. 2012;20(5):368–78. .

Yanovski SZ. Eating disorders, race, and mythology. Arch Fam Med. 2000;9(1):88. .

Zhang C. What can we learn from the history of male anorexia nervosa? J Eat Disord. 2014;2(1):138. .

Download references


Verity Millar-Sarahs edited a final draft of this paper, improving the clarity and quality of expression significantly. We are also grateful to the four anonymous reviewers for their thoughtful, comprehensive, and generous comments on this paper which have strengthened and shaped it substantially.

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Author information

Authors and affiliations.

Population Health Sciences, Bristol Medical School, University of Bristol, Canynge Hall, 39 Whatley Road, Bristol, BS8 2PS, UK

Cat Papastavrou Brooks

SPIRED Clinic, Research and Development Department, Sussex Partnership NHS Foundation Trust, Sussex Education Centre, Nevill Avenue, Hove, BN3 7HZ, UK

Cat Papastavrou Brooks, Eshika Kafle, Natali Butt, Dave Chawner, Anna Day, Chloë Elsby-Pearson, Emily Elson, John Hammond, Penny Herbert, Catherine L. Jenkins, Zach Johnson, Sarah Helen Keith-Roach, Eirini Papasileka, Stella Reeves, Natasha Stewart, Nicola Gilbert & Helen Startup

Comedy for Coping, Aesthetics Research Centre, University of Kent, Room 2.16, Jarman Building, Canterbury, Kent, CT2 7UG, UK

Dave Chawner

Department of Psychology, City, University of London, Northampton Square, London, EC1V 0HB, UK

Eirini Papasileka

School of Human and Behavioural Sciences, Bangor University, Bangor, LL57 2DG, UK

Stella Reeves

Maudsley Learning, ORTUS Conferencing and Events Venue, 82-96 Grove Lane, London, SE5 8SN, UK

Nicola Gilbert

You can also search for this author in PubMed   Google Scholar


CPB led on writing up this paper, with significant contributions to write-up by EK. CPB, NG, HS and JH designed the methodology of the paper. All authors significantly contributed to the development of the ideas in this paper (as outlined in the ‘process’ section), gave substantive comments on drafts of this paper, and agreed a final draft of this paper.

Corresponding author

Correspondence to Cat Papastavrou Brooks .

Ethics declarations

Ethical approval and consent to participate.

The SPFT Research Governance department confirmed that ethical approval was not necessary for this project, as there were no participants. Because of the increased sensitivity of sharing personal information about mental health, co-authors who were lived experience panel members also signed a consent form to be anonymously quoted in this paper.

Consent for publication

Competing interests.

The authors declare that they have no competing interests.

Additional information

Publisher's note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit . The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article.

Papastavrou Brooks, C., Kafle, E., Butt, N. et al. Co-producing principles to guide health research: an illustrative case study from an eating disorder research clinic. Res Involv Engagem 9 , 84 (2023).

Download citation

Received : 21 February 2023

Accepted : 26 June 2023

Published : 20 September 2023


Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

  • Co-production
  • Lived experience
  • Eating disorders
  • Research priority setting
  • Service-user led research

Research Involvement and Engagement

ISSN: 2056-7529

case study for anorexia

  • Introduction
  • Conclusions
  • Article Information

IKF indicates impaired kidney function.

SI conversion factor: To convert creatinine to mmol/L, multiply by 88.42.

BMI indicates body mass index (calculated as weight in kilograms divided by height in meters squared); eGFR, estimated glomerular filtration rate.

See More About

Sign up for emails based on your interests, select your interests.

Customize your JAMA Network experience by selecting one or more topics from the list below.

  • Academic Medicine
  • Acid Base, Electrolytes, Fluids
  • Allergy and Clinical Immunology
  • American Indian or Alaska Natives
  • Anesthesiology
  • Anticoagulation
  • Art and Images in Psychiatry
  • Artificial Intelligence
  • Assisted Reproduction
  • Bleeding and Transfusion
  • Caring for the Critically Ill Patient
  • Challenges in Clinical Electrocardiography
  • Climate and Health
  • Climate Change
  • Clinical Challenge
  • Clinical Decision Support
  • Clinical Implications of Basic Neuroscience
  • Clinical Pharmacy and Pharmacology
  • Complementary and Alternative Medicine
  • Consensus Statements
  • Coronavirus (COVID-19)
  • Critical Care Medicine
  • Cultural Competency
  • Dental Medicine
  • Dermatology
  • Diabetes and Endocrinology
  • Diagnostic Test Interpretation
  • Drug Development
  • Electronic Health Records
  • Emergency Medicine
  • End of Life, Hospice, Palliative Care
  • Environmental Health
  • Equity, Diversity, and Inclusion
  • Facial Plastic Surgery
  • Gastroenterology and Hepatology
  • Genetics and Genomics
  • Genomics and Precision Health
  • Global Health
  • Guide to Statistics and Methods
  • Hair Disorders
  • Health Care Delivery Models
  • Health Care Economics, Insurance, Payment
  • Health Care Quality
  • Health Care Reform
  • Health Care Safety
  • Health Care Workforce
  • Health Disparities
  • Health Inequities
  • Health Policy
  • Health Systems Science
  • History of Medicine
  • Hypertension
  • Images in Neurology
  • Implementation Science
  • Infectious Diseases
  • Innovations in Health Care Delivery
  • JAMA Infographic
  • Law and Medicine
  • Leading Change
  • Less is More
  • LGBTQIA Medicine
  • Lifestyle Behaviors
  • Medical Coding
  • Medical Devices and Equipment
  • Medical Education
  • Medical Education and Training
  • Medical Journals and Publishing
  • Mobile Health and Telemedicine
  • Narrative Medicine
  • Neuroscience and Psychiatry
  • Notable Notes
  • Nutrition, Obesity, Exercise
  • Obstetrics and Gynecology
  • Occupational Health
  • Ophthalmology
  • Orthopedics
  • Otolaryngology
  • Pain Medicine
  • Palliative Care
  • Pathology and Laboratory Medicine
  • Patient Care
  • Patient Information
  • Performance Improvement
  • Performance Measures
  • Perioperative Care and Consultation
  • Pharmacoeconomics
  • Pharmacoepidemiology
  • Pharmacogenetics
  • Pharmacy and Clinical Pharmacology
  • Physical Medicine and Rehabilitation
  • Physical Therapy
  • Physician Leadership
  • Population Health
  • Primary Care
  • Professional Well-being
  • Professionalism
  • Psychiatry and Behavioral Health
  • Public Health
  • Pulmonary Medicine
  • Regulatory Agencies
  • Reproductive Health
  • Research, Methods, Statistics
  • Resuscitation
  • Rheumatology
  • Risk Management
  • Scientific Discovery and the Future of Medicine
  • Shared Decision Making and Communication
  • Sleep Medicine
  • Sports Medicine
  • Stem Cell Transplantation
  • Substance Use and Addiction Medicine
  • Surgical Innovation
  • Surgical Pearls
  • Teachable Moment
  • Technology and Finance
  • The Art of JAMA
  • The Arts and Medicine
  • The Rational Clinical Examination
  • Tobacco and e-Cigarettes
  • Translational Medicine
  • Trauma and Injury
  • Treatment Adherence
  • Ultrasonography
  • Users' Guide to the Medical Literature
  • Vaccination
  • Venous Thromboembolism
  • Veterans Health
  • Women's Health
  • Workflow and Process
  • Wound Care, Infection, Healing

Get the latest research based on your areas of interest.

Others also liked.

  • Download PDF
  • X Facebook More LinkedIn

Gurevich E , Steiling S , Landau D. Incidence of Impaired Kidney Function Among Adolescent Patients Hospitalized With Anorexia Nervosa. JAMA Netw Open. 2021;4(11):e2134908. doi:10.1001/jamanetworkopen.2021.34908

Manage citations:

© 2024

  • Permissions

Incidence of Impaired Kidney Function Among Adolescent Patients Hospitalized With Anorexia Nervosa

  • 1 Department of Nephrology, Schneider Children's Medical Center of Israel, Petach Tikva, Israel
  • 2 Department of Dietary Services, Schneider Children's Medical Center of Israel, Petach Tikva, Israel
  • 3 Sackler School of Medicine, Tel Aviv University

Question   What is the incidence of impaired kidney function in adolescents with anorexia nervosa, and how does it correlate with body mass index and physiologic parameters of anorexia nervosa severity?

Findings   In this case-control study of 395 adolescent patients with recent diagnosis of anorexia nervosa, impaired kidney function was found in 36.8%. Minimal heart rate and free triiodothyronine levels showed correlation with eGFR but not with admission body mass index.

Meaning   Results of this case-control study suggest that impaired kidney function may be a better parameter of anorexia nervosa severity than body mass index.

Importance   Anorexia nervosa (AN) is a common psychiatric disorder associated with electrolyte imbalances and impaired kidney function, but their incidence and association with disease severity are unknown.

Objective   To analyze kidney function in patients with AN and its association with body mass index (BMI) and physiologic parameters of disease severity.

Design, Setting, and Participants   Single-center retrospective case-control study of recently hospitalized patients with a diagnosis of AN according to International Classification of Diseases, Ninth Revision . All patients were aged 9 to 18 years and hospitalized in the general pediatric ward between 2010 and 2019. BMI and estimated glomerular filtration rate (eGFR) were compared with age- and sex-matched controls hospitalized with other diagnoses.

Main Outcomes and Measures   Impaired kidney function was defined as eGFR less than 90 mL/min/1.73 m 2 . Association between eGFR, BMI, minimal heart rate, and free triiodothyronine (T3) levels were determined using logistic regression.

Results   A total of 395 patients were included in the study group (81.6% were female; mean [SD] age, 14.6 [2.2] years; median BMI percentile, 12.3 [IQR, 0.9-42.0]). Impaired kidney function was found in 36.8% (146 of 395). Mean (SD) eGFR decreased during hospitalization in the group with kidney function impairment (admission: 83 [10.9] mL/min/1.73 m 2 ; nadir: 79.1 [8.5] mL/min/1.73 m 2 ; latest: 97.7 [15.7] mL/min/1.73 m 2 ; P  < .001). Mean (SD) serum creatinine (SCr) to BMI ratio was higher in both anorexia groups compared with controls in impaired kidney function (4.9% [1.0%]), non–impaired kidney function (3.55% [0.84%]); and control groups (2.8 [1.1%]) ( P  < .001). There was no difference in admission BMI between anorexia groups with and without kidney function impairment. Mean (SD) free T 3 levels (3.5 [0.2] pmol/L vs 4.08 [1.2] pmol/L; P  < .001) and mean (SD) minimal heart rate (44 [11] beats per min vs 56 [16] beats per min; P  < .001) were lower and hospital stay was longer (median, 13 [IQR, 6-21] days vs 8 [IQR, 4-19] days; P  = .03) in the impaired kidney function group. The highest correlation was found between minimal heart rate and minimal eGFR ( R  = 0.53; P  < .001).

Conclusions and Relevance   Impaired kidney function in patients with AN is common and transiently worsens during hospitalization. SCr values probably underestimate the degree of kidney function impairment in AN. Results of this study found that patients with impaired kidney function had worse anorexia severity parameters unrelated to admission BMI. Therefore, kidney function impairment may be a better marker of anorexia severity.

Anorexia nervosa (AN) is a common psychiatric disorder that disproportionately affects adolescents and young adults and is associated with high rates of morbidity and mortality. Its complications are associated with the combination of food restriction, weight loss, psychological stress, and the endocrinological and metabolic adaptations to this condition. The reduction of energy intake in patients with AN induces metabolic changes leading to different complications, 1 including: bradycardia, impaired thyroid function, amenorrhea, and in some cases specific nutritional deficiencies. Kidney-related complications such as electrolyte disturbances, nephrocalcinosis and alterations in water metabolism are common. Acute and chronic kidney disease (CKD) are also described in patients with AN. 2 Chronic hypokalemia, volume depletion, hypophosphatemia with rhabdomyolysis, and nephrolithiasis are potentially important factors in the development of CKD in patients with AN. 3 - 5 However, the exact pathophysiologic mechanism of kidney function impairment is not well characterized and the main body of evidence for these phenomena is from studies performed more than 30 years ago.

Previous case series 6 , 7 of patients with long-standing AN and severe and irreversible kidney disease have been reported. Kidney histologic findings revealed hypertrophy of the juxtaglomerular apparatus, advanced glomerular collapse, and interstitial fibrosis, consistent with ischemic kidney injury. 6 In another AN cohort, 7 end-stage kidney disease was reported in 5.2% of the patients. However, these studies provide data on adults with long-standing (>20 years) AN. The incidence of impaired kidney function (IKF) at the time of AN diagnosis has not yet been determined. We hypothesized that IKF may be an important indicator of AN physiologic severity. The aim of the study was to determine IKF prevalence and its association with disease severity in a cohort of pediatric patients with recent diagnosis of AN.

The Rabin-Schneider Institutional Review Board approved the study protocol. We performed a single-center retrospective study of data from all patients aged 9 to 18 years hospitalized in general pediatric wards at Schneider Children's Medical Center in Israel with a recent diagnosis of AN between 2010 and 2019. The ethics committee granted a waiver of informed consent. Hospital medical records were screened for patients with first-time hospitalization with a diagnosis of a norexia nervosa , e ating disorder , e ating disorder, unspecified , l oss of weight or b radycardia (n = 538). For the latter 2 diagnoses, medical records were investigated, and data from patients with other diagnoses, such as inflammatory bowel disease, cancer, or cardiac conductance abnormalities, were excluded.

Anorexia nervosa was diagnosed according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) 8 (before 2013) and Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition) (after 2013). 9 The diagnosis was based on clinical interviews, patient observation, parental information, and medical evaluations by child psychiatrist or psychologist. Patients with AN are usually referred to a general pediatric ward in the Schneider Children's Medical Center when first diagnosed, for the purpose of acute medical stabilization for a serious decrease in weight or finding of severe bradycardia despite maximally intensive community-based care. Cases with AN hospitalized for other medical conditions were not included in the study group.

The computerized medical record review included the estimated glomerular filtration rate (eGFR), calculated by serum creatinine (SCr) and height using the modified Schwartz equation, 10 and its correlation to body mass index (BMI) and physiologic parameters of AN severity (free triiodothyronine [T3], nadir nocturnal heart rate, and length of hospitalization). Assuming that eGFR calculation may underestimate the degree of GFR decrease (because of a discrepancy between the preserved height and decreased muscle mass in patients with AN) we also calculated the SCr/BMI ratio. For comparison of normal SCr and SCr/BMI ratio, a randomly selected group of age- and sex-matched patients with normal age- and sex-adjusted SCr values, hospitalized during the same period with other diagnoses (excluding patients hospitalized in oncology and intensive care units) served as controls. The SCr was determined using the enzymatic assay. Missing data on height (n = 103) were approximated, based on the 50th percentile for age and sex, as height should not be depressed in short-term calorically restricted patients in this age range.

Data were analyzed using BMDP software. 11 Pearson χ 2 test or Fisher exact test (2-tailed) were used for analysis of between-group differences in discrete variables, and the analysis of variance was used for continuous variables. Pearson correlations were applied to assess for correlations between variables. Using those variables found to be significant ( P  < .10) on univariate analysis, we applied a stepwise logistic regression to determine those variables significantly associated with eGFR. We used analysis of variance with repeated measures to describe changes in SCr during hospitalization. A P value ≤.05 was considered statistically significant. The study followed the Strengthening the Reporting of Observational Studies in Epidemiology ( STROBE ) reporting guideline for case-control studies.

A total of 395 individuals were included in the study group and 495 were included in the control group. Mean (SD) age at hospitalization was 14.6 (2.2) years in the study group and 13.6 (2.6) years in the control group; 80.2% of the patients (397 of 495) were girls in the control group and 81.6% (298 of 395) were girls in the group with AN ( Table 1 ). Median BMI percentile on admission was 12.3 (IQR, 0.9-42.0) in the study group vs 49.0 (IQR, 17.0-85.0) in the control group ( P  < .001).

Median length of hospitalization in AN group was 10 (IQR, 5-20) days, mean (SD) blood pressure (BP) on admission was 102.6 (11.0)/62.7 (9.6) mm Hg and mean (SD) heart rate (HR) on admission was 89 (11) beats per min. Mean (SD) minimal HR was 51.6 (15.8) beats per min. FT 3 levels were slightly decreased (mean [SD], 3.83 [1.14] pmol/L; normal: 3.1-6.8 pmol/L), with 28% of patients with an FT3 value below normal. Mean (SD) SCr was in the normal range in the entire study group, but was higher in comparison with controls (0.68 [0.15] mg/dL vs 0.54 [0.14] mg/dL: P  < .001), similar to minimal eGFR (99.8 [22] mL/min/1.73 m 2 vs 124 [26.5] mL/min/1.73 m 2 ; P  < .001). The mean (SD) SCr significantly increased during hospitalization and then decreased to a lower than admission value in the AN group (admission: 0.66 [0.15] mg/dL, maximal: 0.68 [0.15] mg/dL; discharge: 0.6 [0.13] mg/dL; P  < .001 by repeated measures analysis of variance) ( Figure 1 ). The SCr/BMI ratio was higher in the AN group compared with controls (4.0% [1.2%] vs 2.8% [1.0%], P  < .001). Stepwise logistic regression comparing AN cases with controls revealed that SCr/BMI (OR, 3.63; 95% CI, 2.85-4.62; P  < .001), age (OR, 1.11; 95% CI, 1.04-1.20; P  < .001), sex (OR, 1.63; 95% CI, 1.05-2.52; P  = .04), and minimum eGFR (OR, 0.99; 95% CI, 0.98-1.00; P  = .06) had higher ORs than SCr or eGFR or admission BMI. These parameters yielded a receiver operating characteristics area under the curve of 0.84. Electrolyte abnormalities during hospitalization included hypophosphatemia (<2.5 mg/dL): 5 of 376 (1.3%), hypomagnesemia (<1.7 mg/dL): 1 of 281 (0.35%), hyponatremia (<135 meq/L): 11 of 378 (2.9%), hypokalemia (<3.5 meq/L): 13 of 389 (3.3%) available tests.

For further analysis of kidney function and its association with AN severity, we divided this study cohort into 2 groups according to the minimal eGFR above or below 90 mL/min/1.73 m 2 . The latter (IKF) was found in 36.8% (146 of 395) of patients. The SCr changed substantially during hospitalization (initially increased, then decreased) in both IKF and non IKF groups. However, the mean values were higher in the IKF group (mean [SD] admission 0.79 [0.13] mg/dL, peak 0.83 [0.12] mg/dL, and latest values 0.68 [0.12] mg/dL; P  < .001) ( Figure 1 ).

Comparison between IKF and non-IKF groups is presented in Table 2 . There was no difference in admission median BMI percentile between the groups (13.1 [IQR, 0.5-45] vs 11.7 [IQR, 2.3-35.1]; P  = .41). A significant difference between IKF and non-IKF groups was found in maximal SCr during hospitalization (mean [SD] 0.83 [0.12] mg/dL vs 0.59 [0.09] mg/dL; P  < .001). Accordingly, there was a significant difference in mean (SD) minimal eGFR (79.1 [8.5] mL/min/1.73 m 2 vs 112 [18.5] mL/min/1.73 m 2 ; P  = .001) and SCr/BMI (4.9% [1.0%] vs 3.55% [0.84%]; P  < .001) between IKF and non IKF groups. Mean (SD) eGFR decreased during hospitalization in the group with IKF for admission (83 [10.9] mL/min/1.73 m 2 ) as well as latest (97.7 [15.7] mL/min/1.73 m 2 ; P  < .001). Mean (SD) SCr, eGFR, and SCr/BMI values were not only significantly different between the whole AN group vs controls ( Table 1 ), but also between the non-IKF group vs controls (SCr: 0.59 [0.09] mg/dL vs 0.54 [0.14] mg/dL; P  < .001; SCr/BMI: 3.6% [0.8%] vs 2.8% [1.1%]; P  < .001; minimal eGFR: 112 [18.5] mL/min/1.73 m 2 vs 124 [26.5] mL/min/1.73 m 2 ; P  < .001).

The FT 3 levels, available for fewer patients in the AN group (n = 187), were lower in the IKF Vs non IKF group (mean [SD] 3.5 [0.2] pmol/L vs 4.08 [1.2] pmol/L; P  = .001). A similar difference was seen for minimal mean (SD) HR (44 [11] beats per min vs 56 [16] beats per min; P  < .001). Length of hospitalization was longer in the IKF group (median 13 [IQR, 6-21] days vs 8 [IQR, 4-19] days; P  = .03).

We used stepwise logistic regression analysis for the cases group (n = 383), using eGFR above or below 89.9 mL per minute as a cut-off value. We found that SCr/BMI (odds ratio [OR], 8.16 [95% CI, 5.24-12.17]; P  < .001), minimal HR (OR, 0.96 [95% CI, 0.93-0.98]; P  < .001), and diastolic and systolic blood pressure on admission independently estimated low vs normal eGFR, yielding an AUC of 0.89.

Using Pearson correlation, we found the strongest correlation between minimal HR and minimal eGFR (n = 392; R  = 0.527; P  < .001), higher than correlations between minimal HR and SCr/BMI (n = 392; R  = −0.399; P  < .001). The FT3 levels also showed a significant correlation with minimal eGFR (n = 83; R  = 0.34; P  < .001) similar to SCr/BMI (n = 393; R  = −0.41; P  < .001). No correlation between minimal HR and BMI ( R  = 0.02; P  = .06) or between HR and BMI percentile on admission ( R  = 0.08; P  = .10) was seen ( Figure 2 ). There was a mild inverse correlation between length of hospitalization to admission BMI percentile (n = 395; R  = −0.17; P  < .001).

We describe a large cohort of pediatric patients hospitalized with recent AN diagnosis in one medical center over a period of 10 years. In this cohort, IKF was found in 37% of patients. SCr remained unchanged during hospitalization in the non-IKF group, but increased in the IKF group. Since proper hydration could be assured during hospitalization, this finding suggests the presence of a unique yet undefined mechanism other than dehydration.

To our knowledge, this is the largest cohort of patients with AN with IKF. Previous data exist in cohorts of 14 females 6 and 45 patients with different types of AN. 12 Another series reported on long term follow up of 84 patients with AN: 5.2% of them developed end-stage kidney disease and underwent kidney replacement therapy. 7 As we chose only patients with AN who needed hospitalization, a possible selection bias could exist. Therefore, caution should be used when extrapolating our results to the general AN population.

The GFR calculation usually relies on SCr measurements. As SCr production depends on muscle mass, its level is lower in individuals with reduced muscle mass. Dietary animal protein consumption may also affect serum creatinine concentration. 13 Patients with AN often have both reduced muscle mass and low dietary animal protein consumption. Therefore, their SCr values are supposed to be lower, compared to individuals with normal muscle mass on a normal diet. In patients with AN, height is supposed to be less affected than weight. Therefore, apparently normal SCr values can lead to overestimation of their renal function, which is based in children on height as the representative surrogate marker of muscle mass. In this AN cohort, mean SCr was in the normal range but higher than in controls. To overcome the potential overestimation of GFR, we describe here data on SCr/BMI ratio as an additional parameter to assess kidney function in such patients. A significant difference in SCr/BMI was found between the whole AN group and controls ( Table 1 ). As may be expected, this difference was more prominent in the IKF group vs controls. However, even in the non-IKF group, with a normal estimated GFR, SCr/BMI was significantly higher compared to controls, hinting for higher SCr values relative to muscle mass in the whole AN group. Thus, normal SCr values in patients with AN may not reflect appropriately kidney function. As serum cystatin C levels reflect eGFR without any dependency on muscle mass, 14 it could serve as an attractive alternative for this group of patients. This test is not routinely available in Israel. Another alternative way to assess GFR based only on SCr would be the use of the Cockroft Gault formula, which was originally described for adults, but later suggested for adolescents. However, Filler et al 15 found that the Cockroft Gault formula showed the worst agreement with measured GFR in children aged 1 to 18 years, and therefore is not recommended for use in children.

The exact mechanism of kidney function impairment in AN is not well understood. Nutrition plays a substantial role in renal function. 16 While GFR increases with animal protein intake, it decreases in a state of protein-energy malnutrition, as well as sodium and acid excretion and urinary concentrating ability. 17 Healthy patients fed a calorie-deficient diet demonstrate a reduction in creatinine clearance. 18 Also, healthy patients with decreased protein intake demonstrated a fall in GFR and effective renal plasma flow (RPF), that reversed to normal by protein repletion. 19 Children with calorie-protein malnutrition demonstrated significant reductions in GFR, RPF and filtration fraction. 20 Reports on chronic tubulo-interstitial nephropathy in AN attributed it to chronic hypokalemia, acute kidney injury induced by rhabdomyolysis and glomerulosclerosis. 21 - 23 Histopathologic changes in patients with long-standing AN associated with decreased eGFR and hypokalemia have been reported. 24 In this cohort, there was no difference in admission BMI between IKF and non-IKF groups, but as mentioned, we describe these patients at the time of AN initial diagnosis in contrast to longer follow up periods described in the literature.

Cardiovascular and endocrinological complications are common in AN, including impaired thyroid function. Total and free triiodothyronine levels are low, as an adaptive mechanism for conserving energy for vital functions, and normalize during weight gain. 25 Bradycardia and hypotension are cardiovascular responses to starvation due to the profound parasympathetic predominance of low body weights or significant weight loss. 26 In a retrospective study 27 of children and teenagers with AN, low GFR was linked to low BMI and bradycardia. Dehydration was not solely responsible for renal impairment. 27 In this cohort, bradycardia and low FT3 levels were more prominent in the IKF compared to non-IKF group. The strongest correlation was seen between minimal HR and minimal eGFR, higher than correlations between minimal HR vs SCr/BMI. FT3 levels showed a similar correlation with minimal eGFR and SCr/BMI. The length of hospitalization was longer in IKF group than in non-IKF group also indicating IKF as reflecting a more severe AN condition.

Correlation between degree of bradycardia and IKF shown in this cohort may be partly explained by hemodynamic changes due to increased parasympathetic activity and low cardiac outflow. In our study, no correlations between minimal HR and BMI, or between FT3 and BMI were seen. Median BMI percentile in this cohort was low but 40% of the AN cohort had a BMI percentile value above 40, reflecting the increased incidence of atypical AN, in which significant weight loss within the normal range occurs. 28 In addition, binging/purging subtype of AN may be more commonly associated with reduced kidney function. 5 As this study was retrospective, we could not obtain data on either weight loss rate or the subtype of eating disorder.

Given the retrospective nature of this study, there was not sufficient information to fully characterize IKF associated conditions, including urine analysis, electrolyte abnormalities and kidney imaging. In addition, we had to approximate height data in part of the cases group. Serum cystatin C levels were not available. We could not obtain data on weight loss rate.

In this study, IKF in patients with AN is common and worsens during hospitalization. SCr values may underestimate the degree of IKF. Patients with IKF had lower minimal HR and FT3 and longer hospitalization, without differences in admission BMI. Therefore, IKF may be a better marker of AN severity.

Accepted for Publication: August 22, 2021.

Published: November 22, 2021. doi:10.1001/jamanetworkopen.2021.34908

Open Access: This is an open access article distributed under the terms of the CC-BY License . © 2021 Gurevich E et al. JAMA Network Open .

Corresponding Author: Daniel Landau, MD, Department of Nephrology, Schneider Children's Medical Center of Israel, 14 Kaplan St, Petach Tikva 4920235, Israel ( [email protected] ).

Author Contributions : Drs Gurevich and Landau had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Gurevich, Landau.

Acquisition, analysis, or interpretation of data: All authors.

Drafting of the manuscript: Gurevich.

Critical revision of the manuscript for important intellectual content: All authors.

Supervision: Landau.

Conflict of Interest Disclosures: None reported.

Additional Contributions: We thank Pearl Lilos, PhD (formerly with Tel Aviv University)for her assistance in the statistical analyses. No compensation was received.

  • Register for email alerts with links to free full-text articles
  • Access PDFs of free articles
  • Manage your interests
  • Save searches and receive search alerts
  • Open access
  • Published: 10 May 2024

Screening for eating disorders in adolescents with chronic pain: the Eating Attitudes Test–16–Chronic Pain

  • Leslie Sim 1 ,
  • Amy Fahrenkamp 2 ,
  • Jennifer R. Geske 3 ,
  • Jocelyn Lebow 1 , 4 ,
  • Hope Thilges 5 ,
  • Carol B. Peterson 6 ,
  • Abigail Matthews 1 &
  • Cynthia Harbeck-Weber 1  

Journal of Eating Disorders volume  12 , Article number:  56 ( 2024 ) Cite this article

176 Accesses

Metrics details

Few measures have been validated to screen for eating disorders (ED) in youth with chronic pain. We conducted confirmatory (CFA) of two established factor structures of the Eating Attitudes Test-26 (EAT-26) in a sample of youth with chronic pain attending an intensive interdisciplinary pain treatment (IIPT) program and examined the validity of the best-fitting model in predicting ED diagnoses in this sample.

Participants were 880 adolescents ( M age = 16.1, SD  = 2.1) consecutively admitted into an IIPT program who completed the EAT-26 upon admission. CFA was conducted and in the case of inadequate fit, EFA was planned to identify alternative models. Factors of the best-fitting model were included in a logistic regression analysis to predict ED diagnoses.

The TLIs (0.70; 0.90), RMSEAs (0.09; 0.07) and CFIs (0.73; 0.92) suggested poor fit of one model and adequate of the second model. Goodness of fit indices from EFA (TLI:0.85, RMSEA:0.06) did not outperform the fit of the second CFA. As such, the second model was retained with the exception of one factor. The items loaded onto a 16-item, five factor model: Fear of Getting Fat , Social Pressure to Gain Weight, Eating-Related Control, Eating-Related Guilt and Food Preoccupation . Based on chart review, 19.1% of the participants were diagnosed with an eating disorder. Logistic regression analyses indicated the new 16-item measure and Fear of Getting Fat , significantly predicted an ED diagnosis that did not include avoidant restrictive food intake disorder (ARFID) and Social Pressure to Gain Weight significantly predicted a diagnosis of ARFID.


An alternative 16-item, 5-factor structure of the EAT-26 should be considered in screening for EDs with youth with chronic pain.

Pain English Summary

Youth with chronic pain are at risk for eating disorders, yet there are few validated measures to screen for these conditions in this population. The Eating Attitudes Test (EAT-26) is a widely used measure of eating disorders that has been evaluated on eating disorder and community samples. This study examined whether the EAT-26 and its widely used subscales are appropriate for use with adolescents with chronic pain. Results from confirmatory factor analyses indicate that a modification of a previous 6 factor model of the measure is relevant to the eating pathology of adolescents with chronic pain. This 16-item measure with 5 subscales ( Fear of Getting Fat , Social Pressure to Gain Weight, Eating-Related Control, Eating-Related Guilt , and Food Preoccupation) better fits this population. The shorter measure, EAT-16-Chronic Pain , and new scales were associated with eating disorder diagnoses in the sample of youth with chronic pain, suggesting their validity for use with this population.

Many adolescents with chronic pain (pain lasting longer than 3–6 months) identify eating as a central area of concern [ 1 , 2 , 3 , 4 , 5 ]. Adolescents with chronic pain commonly restrict their dietary intake in response to pain, nausea, poor appetite, disrupted sleep-wake cycles, medication side effects and elimination diets [ 3 , 5 , 6 , 7 , 8 ]. Although dietary alterations may achieve a temporary reduction in physical symptoms, if these behaviors persist, such dietary restriction may increase the risk for the development of an eating disorder [ 1 , 3 , 7 , 9 ].

In fact, research highlights that a subset of adolescents with pain-related restrictive eating go on to develop drive for thinness, fear of weight gain, and purposeful efforts to control weight and shape [ 5 ]. This shift in motivation for restrictive eating from efforts to manage pain to controlling weight and shape may develop from starvation-related changes to the brain, fasting-related reduction in anxiety, as well as social reinforcement for weight loss [ 9 , 10 , 11 ]. In addition to risk for the development of eating disorders involving weight or shape concerns, youth with chronic pain are also at risk for avoidant restrictive food intake disorder (ARFID). Similar to ARFID, adolescents with chronic pain frequently restrict their diet in the context of aversive gastrointestinal symptoms, sensory sensitivities, and/or low appetite, dietary restriction that poses consequences to their health and social functioning [ 12 ].

In spite of findings indicating a higher prevalence of eating disorders across various chronic pain conditions including migraine headache, functional gastrointestinal disorders, fibromyalgia, and chronic facial pain [ 13 , 14 , 15 , 16 , 17 , 18 ], research on the overlap between eating disorders and chronic pain has been limited. One of the few studies to examine this relationship found adolescents with chronic pain and comorbid eating disorders take longer to be identified and referred for eating disorder treatment than a matched sample of adolescents without chronic pain [ 5 ]. This delay may stem in part from the lack of appropriate measures to screen for eating disorders. The absence of eating disorder screening measures for this population also limits our understanding of how to best prevent and treat eating disorders in these youth [ 19 , 20 ].

The Eating Attitudes Test − 26 21 is one of the most widely used instruments to screen for disordered eating attitudes and behaviors [ 22 ]. It has been examined in a range of populations including adults and adolescents with eating disorders, athletes, community samples, as well as has been examined across many cultures [ 22 ]. However, it has not been evaluated in adolescents with chronic pain or those with ARFID. Given data on adolescent norms [ 23 ], as well as the short administration time and straightforward scoring, this measure has potential for screening for eating disorders in a chronic pain population.

The original factor structure of the EAT-26, initially derived from an all-female sample and later replicated with adolescent school-aged girls, includes Dieting (i.e., food avoidance and drive for thinness), Bulimia (i.e., cognitions about food and binge-eating/purging items), and Oral Control (i.e., social pressures to gain weight and self-control over eating) [ 24 ]. However, factor analytic studies with adolescents have largely failed to replicate Garner et al.’s 3 factor solution, particularly among non-clinical samples [ 24 , 25 , 26 , 27 , 28 ]. In mixed gender, community samples, an alternative factor structure has been identified and replicated for the EAT-26 [ 27 , 28 ]. Given that at least one third of youth with chronic pain identify as male, this model may have more relevance to screening for eating disorders in youth with chronic pain [ 29 ].

Given the need for eating disorder screening in patients with chronic pain, the primary goal of the study was to conduct a confirmatory factor analysis on two established models in a sample of adolescents attending an intensive, interdisciplinary pain treatment (IIPT) program. These models include Garner’s original factor structure of the EAT-26 and an alternative 6-factor model (i.e., Fear of Getting Fat, Social Pressure to Gain Weight, Vomiting-Purging Behavior, Eating Related Control, Food Preoccupation, Eating Related Guilt) identified by Maiano’s (2016) [ 27 ] factor analysis and replicated by McEnery (2016) [ 28 ]. Given the mixed gender sample of youth who attend the IIPT, we hypothesized that the Maiano model would yield a better fit for the data.

In the case of less than adequate fit, we planned to conduct exploratory factor analysis to identify an alternative model that better fit the data. A final aim of this study was to examine whether the factors of the best-fitting model predict eating disorder diagnoses based on chart review. In the process of the chart review, we examined the prevalence of adolescents who scored above clinical cutoffs on the EAT-26, as well as of those who received an eating disorder diagnosis. We hypothesized that the prevalence of eating disorders, as well as ARFID would be higher than the general population.

Materials and methods


Participants were 880 adolescents (mean age = 16.1, SD  = 2.1; 72.4% female) consecutively enrolled in a pediatric IIPT program at a tertiary medical center in the Midwestern United States between 2013 and 2018. This IIPT program serves patients from across the United States with high impact non-cancer chronic pain and comorbid conditions. Participants identified as predominantly White ( n  = 794; 90.2%) and resided in the United States, the Virgin Islands, and Canada. At the time of their participation, the majority were in high school (74.7%). See Table  1 for detailed demographic characteristics of participants.

Eating attitudes test-26 (EAT-26)

The Eating Attitudes Test – 26 (EAT-26; Garner et al., 1982) [ 21 ] is a 26-item, self-report measure used to assess disordered eating attitudes and behavior. Items are rated on a six-point scale from “never” to “always.” Scores on each item are recoded such that a score of 0 is assigned to the first 3 scores in the least symptomatic direction and the 3 scores in the symptomatic direction are weighted 1,2,3, respectively. The recoded items are summed with a clinical screening cutoff of 20 or higher indicating significant concern for a potential eating disorder. The EAT demonstrates good sensitivity and specificity for identifying eating disorders in community and clinical samples [ 22 ].

As part of standard IIPT admission procedures, participants in both samples completed the EAT-26 along with other intake questionnaires at the time of their admission. The IIPT is a 3-week, intensive program for adolescents and young adults struggling with chronic pain that takes place from 8am to 4pm each weekday. Participants engage in cognitive-behavior therapy, occupational therapy, physical therapy, recreation therapy and biofeedback in a group setting and receive individual and family interventions, as well as psychiatric and medical services. During the program, patients showing risk for psychiatric symptoms are referred for evaluation and brief interventions with a board-certified child and adolescent psychologist or psychology post-doctoral fellow under the supervision of a board-certified psychologist. In the current sample, most patients had an individual meeting with a psychologist, with 22.7% participating in a focused evaluation for an eating disorder.

Three independent coders extracted data from the adolescents’ electronic medical records from visits at Mayo Clinic beginning with participants’ initial visit to Mayo Clinicthrough all subsequent medical record documents including medical and psychiatric inpatient and outpatient visits. Coders included a doctoral level clinical psychologist, a postdoctoral clinical psychology fellow, and a bachelor’s level research assistant who underwent training by the study co-PIs (LAS and AF) to systematically review records for evidence of DSM-5 feeding and eating disorders criteria.

Coders extracted data from the nursing admission note which included systematically collected information regarding eating disorder history, dietary intake, eating behavior and weight, as well as the notes from the patients’ episode of care while they were in the program on: (1) primary pain diagnoses (diagnosed by a board-certified pediatric pain physician), (2) body mass index (BMI) percentile (adjusted for age and biological sex) at admission, (3) eating disorder history, and (4) formal eating disorder diagnoses in the medical record associated with eating disorder assessment. To confirm the eating disorder diagnoses listed in the medical record, coders extracted chart information related to DSM-5 diagnostic criteria for eating disorders including anorexia nervosa (AN), bulimia nervosa (BN), binge-eating disorder (BED), other specified feeding and eating disorder (OSFED) and avoidant restrictive food intake disorder (ARFID), and only included the chart diagnosis if it was consistent with diagnostic criteria. 20% of the records were extracted by an independent rater (LS) who reached 94.7% agreement (Kappa = 0.84). Disagreements were resolved by consensus. Adolescents’ primary pain diagnosis was determined by the first listed pain diagnosis diagnosed by a board-certified pain physician associated with the program. The Mayo Clinic Institutional Review Board approved study procedures for this study. Only records from patients and/or parents/guardians who had provided research authorization were included.

Data analyses

Participant characteristics, eating disorder diagnoses, and scores on the EAT-26 were summarized with mean and standard deviation or N and percent (See Table  1 ). To examine the fit of Garner’s original 3-factor model [ 21 ] and Maiano’s 6-factor model [ 27 ] in our sample of youth with chronic pain, confirmatory factor analysis was conducted. To determine whether the models provided an acceptable fit to the data, model fit statistics, factor loadings, and modification indices were examined using the following criteria: (1) the Tucker-Lewis index (TLI) with values ideally 0.90 or greater, suggesting the model improves 90% relative to the null model; (2) The Root Mean Square Error Approximation (RMSEA) with values closer to 0 representing a better fit; (3) The Comparative Fit index (CFI) which is similar to the TLI with values ideally > 0.9; and the standardized root mean square residual (SRMR), defined as the difference between the residuals of the covariance matrix and the hypothesized models. The SRMR considers when items vary in range with optimal values < 0.08.

Exploratory factor analysis was conducted to examine whether a new factor structure better fit our sample using square multiple correlations as prior communality estimates with oblique rotation of the factors. The number of factors was ascertained using scree plots, proportion of common variance explained by the factors, parallel analysis, and interpretability of factors. Variables were considered to load on a factor if the factor loading was ≥ 0.40.

Finally, three BMI percentile-adjusted multivariable logistic regression models were conducted to examine the scores for all five factors of the best fitting model as predictors of: 1) a diagnosis of any eating disorder (i.e., AN, BN, BED, OSFED, ARFID; 2), a diagnosis of an eating disorder that does not include ARFID (i.e., AN, BN, BED, or OSFED); 3) or an ARFID diagnosis. Finally, multivariable models were run for each outcome with all factors included in the model, adjusted for BMI percentile. C-statistics measure binary models’ performance, with values greater than 0.7 indicating a good model fit and values greater than or equal to 0.8 indicating an excellent model fit. Data analyses were conducted using R (version 4.0.3) using the Psych and Lavaan package.

Confirmatory factor analysis of Garner’s original 3-factor model [ 21 ] with our sample of adolescents and young adults with chronic pain yielded a TLI (0.70), RMSEA (0.093, 90% CI: 0.090–0.096), and CFI (0.73) suggesting poor fit. Maiano’s 6-factor model [ 27 ] would not converge, due to too few subjects endorsing vomiting after eating for item 9. The reduced 5-factor model yielded a TLI (0.9), RMSEA (0.072, 90% CI: 0.066–0.78), and CFI (0.92) suggesting an improved fit; however, we hypothesized this could be further improved.

As such, exploratory common factor analysis was conducted to determine the most meaningful factor structure of the EAT-26 with our sample using square multiple correlations as prior communality estimates with oblique rotation of the factors. A new four-factor structure did not improve the fit with a TLI of 0.85 and RMSEA of 0.065 (90% CI: 0.061–0.069) in an EFA.

As shown in Fig.  1 , Maiano’s 5-factor structure gives clearly interpretable factors previously documented as Fear of Getting Fat , (e.g., “I am preoccupied with a desire to be thinner,” “I am terrified of being overweight”), Social Pressure to Gain Weight (e.g., “I feel that others would prefer if I ate more,” “I feel that others pressure me to eat,”), Eating-Related Control (e.g., “I avoid foods with sugar,” “I eat diet foods”), Food Preoccupation (e.g., “I feel that food controls my life”) and Eating-Related Guilt (e.g.,"I feel extremely guilty after eating") . Cronbach’s Standardized alpha was 0.85 overall and ≥ 0.74 for each factor demonstrating good or better reliability. The hierarchical Omegas (ω h ) similarly demonstrated sufficient (ω h  = 0.66 for Eating-Related Control; 0.67 for Eating-Related Guilt) and excellent reliability (ω h  = 0.88 for Fear of Getting Fat; ωh = 0.78 for Social Pressure to Gain Weight and Food Preoccupation).

figure 1

Factor structure of the Eating Attitudes Test− 16 - Chronic Pain

Based on chart review, 19.1% of the sample of youth with chronic pain attending an intensive, interdisciplinary pain treatment program were diagnosed with an eating disorder. Of this sample, 7.1% received an eating disorder diagnosis other than ARFID (e.g., AN, BN, BED, OSFED) and 12.1% were diagnosed with ARFID.

In examining BMI percentile-adjusted logistic regression models with the five factor scores as predictors, the factor, Social Pressure to Gain Weight , significantly predicted higher odds of an ARFID diagnosis (OR = 1.5, p  < .01) and any eating disorder (OR = 1.4, p  < .05). The factor, Fear of Gaining Weight , was negatively associated with any eating disorder diagnosis (OR = 0.5, p  < .05). The factor, Eating-Related Guilt , significantly predicted receiving an non-ARFID eating disorder diagnosis (OR = 4.5, p  < .05) and any eating disorder diagnosis (OR = 3.3, p < .05) . Food Preoccupation and Eating-Related Control did not predict any of our eating disorder related outcomes. These models showed good predictive (diagnostic) accuracy with C-statistics ranging from 0.77 to 0.80. See Table  2 for BMI percentile-adjusted logistic regression models for each of the four factors.

BMI percentile-adjusted logistic regression models with the 16-item model as a predictor of eating disorder diagnoses and evaluation are presented in Table  3 . Higher EAT-16 total scores were significantly associated with increased risk of all eating disorder diagnoses categories with the exception of ARFID ( p  = .17). These models showed good predictive (diagnostic) accuracy with C-statistics ranging from 0.75 to 0.77.

Based on the need for a reliable and valid screening measure for this population, we conducted a factor analysis of the EAT-26 in a sample of adolescents with chronic pain attending an IIPT program. Results suggest that youth with chronic pain demonstrate variant eating pathology that is not adequately captured in Garner’s original 3-factor solution for the EAT-26. This is consistent with prior research that similarly failed to replicate Garner’s original factor structure in a general population of mixed-gender adolescents [ 27 , 28 ]. However, our confirmatory and exploratory factor analysis also did not replicate a 6-factor solution of the EAT-26 from Maiano’s et al., that was identified using mixed gender adolescent samples [ 27 , 28 ]. Instead, our best-fit factor analysis was a version of Maiano et al.’s confirmatory factor analysis that loaded onto five of their six unique factors. The sixth factor lacked the endorsement of vomiting indicated in items 9 and 26, and therefore was incalculable. The lack of improved exploratory factor analysis may be related to our sample of youth with chronic pain with a unique gender distribution compared to the Maino and McEnery samples EAT-26 (72% vs. 50–60% female, respectively) [ 27 , 28 ].

Findings of confirmatory factor analysis suggest a new scale which we titled, EAT-16-Chronic Pain. This model is a slight modification to the Maiano structure using a 16-item model with five unique factors (Fear of Getting Fat , Eating-Related Guilt, Eating-Related Control, Social Pressure to Gain Weight , Food Preoccupation) which is a better fit for young patients with chronic pain. Supporting the convergent and discriminant validity of the unitary construct to evaluate non-ARFID eating disorders in these youth, higher EAT-16 -Chronic Pain total scores were significantly associated with increased risk of all eating disorder diagnoses categories with the exception of ARFID ( p  = .17).

Similarly, the factor Fear of Getting Fat was associated with an eating disorder diagnosis not including ARFID (i.e., AN, BN, BED, OSFED) but not an ARFID diagnosis. However, adolescents’ score on the factor, Social Pressure to Gain Weight, did significantly predict an ARFID diagnosis. Because adolescents with ARFID may perceive food avoidance as adaptive to minimize aversive experiences, they may not view their eating as problematic but may instead recognize others’ concerns about their dietary intake and weight. Since many adolescents with chronic pain eliminate specific foods from their diet that they believe exacerbate pain, it was surprising that the third factor, Eating-Related Control , did not predict an ARFID diagnosis. It is possible that the particular type of control over eating that this scale captures is more closely tied to achieving weight loss rather than symptom reduction.

Clinical and research implications

Our finding that a high proportion (19.1%) of adolescents attending an IIPT for treatment of high-impact, non-malignant chronic pain qualified for an eating disorder diagnosis highlights the importance of screening for eating disorders in this population. As a screening for non-ARFID related eating disorders (i.e., AN, BN, BED, OSFED), an alternative 16-item measure along with Factor 1, Fear of Getting Fat , showed convergent and discriminant validity, as they predicted all eating disorders except for ARFID. Factor 2, Social Pressure to Gain Weight , a scale comprising items that highlights the perception of others’ concerns about the patients’ eating and weight, was the only factor associated with an ARFID diagnosis. Given that Social Pressure to Gain Weight was associated with ARFID, in addition to the use of ARFID-specific assessment measures, inquiry into patients’ perceptions of eating and weight related concerns from others may represent a fruitful avenue to screen for ARFID-related eating pathology in this population. Clinically, the findings of this study have implications for brief assessment using an abbreviated 16-item version of the measure which may be useful in busy medical settings when evaluating these youth.

Our chart review of a large sample of youth with chronic pain identified that 19.1% of this sample met criteria for any eating disorder, with 7.1% meeting the criteria for a non-ARFID eating disorder (i.e., AN, BN, BED, OSFED) and 12.2% meeting criteria for ARFID. The study also found that 16.1% of the sample scored above clinical cutoffs on the EAT-26. The fact that fewer patients scored above clinical cutoffs on the screening measure than received eating disorder diagnoses is consistent with the large proportion of patients with ARFID in this sample which is not adequately measured by the EAT-16-Chronic Pain.

The prevalence of eating disorders identified in this sample of adolescents with chronic pain is considerably higher than that in the general population of adolescents (19.1 vs. 6.1%) [ 30 ]. Given that comorbid eating disorders involving active restrictive eating and/or purging behaviors can significantly interfere with program participation, participants with known eating disorders at the time of the pre-program evaluation are not deemed eligible for the progam until they receive successful treatment. As such, the prevalence of eating disorders identified in this sample may represent an underestimate of eating disorders in youth with chronic pain in the general population. Notably, the number of patients diagnosed with ARFID was also substantially higher than prevalence estimates from a large chart review study of pediatric gastroenterology patients (1.5%) [ 31 ], a finding which may be related to the severity of a patient population who requires intensive interdisciplinary pain treatment. Given that ARFID was the most common eating disorder in this sample and our findings validate that the EAT-26 is not a valid measure to screen for ARFID, it is important that ARFID specific screening measures such as the Nine Item ARFID Screen [ 32 ] be incorporated into the assessment of youth with chronic pain.

The findings of this study need to be considered within the context of several limitations. First, given the lack of socioeconomic and ethnic/racial diversity in this sample, it is unclear whether these results would generalize beyond a population of white, middle-class adolescents. Another clear limitation is that participants did not have their eating disorder confirmed with a structured clinical interview and only a subset of patients had an eating disorder evaluation. As such, it is possible this is an underestimate of eating disorders in this sample. However, all of the evaluations were conducted or supervised by a board-certified child and adolescent psychologist with a specialty in eating disorders, and referrals for eating disorder evaluations were based on parent and self-report of eating concerns, food logs, reviews of patient growth charts and behavioral observations over a three-week period, making it less likely that eating concerns were missed. Given that larger sample sizes are critical in factor analysis and add to the credibility of the results, a major strength of this study is the large mixed gender sample of adolescents with high impact chronic pain.

In summary, factor analysis of the EAT-26 with adolescent patients with chronic pain yielded a five factor solution with scales highlighting fear of weight gain, concerns from others related to eating and weight, eating-related guilt, dietary restriction, and food preoccupation. The results suggest that the identified factor structure of the EAT-16-Chronic Pain is useful for identifying eating disorders other than ARFID in patients with high impact chronic pain and a new factor, Social Pressure to Gain Weight may assist in recognition of ARFID in conjunction with ARFID specific screening measures. Given that disordered eating seems to be a pertinent, yet often neglected area of inquiry in medical work up for chronic pain, this measure has potential to enhance the diagnosis and treatment of these adolescent patients.

Data availability

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Benjamin J, Sim L, Owens MT, Schwichtenberg A, Harrison T, Harbeck-Weber C. Postural Orthostatic Tachycardia Syndrome and Disordered Eating: clarifying the overlap. J Dev Behav Pediatr. 2021;1(4):291–8. .

Article   Google Scholar  

Demirci K, Demirci S, Akpinar A, Demirdaş A, Atay İM. Evaluation of eating attitude in patients with migraine. Noro Psikiyatr Ars 2015;52(4):367–70. .

Harris S, Gilbert M, Beasant L, Linney C, Broughton J, Crawley E. A qualitative investigation of eating difficulties in adolescents with chronic fatigue syndrome/myalgic encephalomyelitis. Clin Child Psychol Psychiatry. 2017;22(1):128–39. .

Oetjen L, Johannsen A, Bean J et al. The goals and outcomes of adolescent and young adults with POTS attending an intensive Interdisciplinary Treatment Program. Occup Ther Health Care. 2022:1–15. .

Sim LA, Lebow J, Weiss K, Harrison T, Bruce B. Eating disorders in adolescents with Chronic Pain. J Pediatr Health Care. 2017;31(1):67–74. .

Lebow J, Chuy JA, Cedermark K, Cook K, Sim LA. The development or exacerbation of eating disorder symptoms after topiramate initiation. Pediatr. 2015;135(5):e1312–6. .

Quick VM, Byrd-Bredbenner C, Neumark-Sztainer D. Chronic illness and disordered eating: a discussion of the literature. Adv Nutr. 2013;1(3):277–86. .

Reed-Knight B, Squires M, Chitkara DK, van Tilburg MA. Adolescents with irritable bowel syndrome report increased eating-associated symptoms, changes in dietary composition, and altered eating behaviors: a pilot comparison study to healthy adolescents. Neurogastroenterol Motil. 2016;28(12):1915–20. .

Keys A, Brožek J, Henschel A, Mickelsen O, Taylor HL. The biology of human starvation. (2 vols). The biology of human starvation (2 vols). Univ. of Minnesota; 1950:xxxii, 1385-xxxii, 1385.

Kaye WH, Barbarich NC, Putnam K, et al. Anxiolytic effects of acute tryptophan depletion in anorexia nervosa. Int J Eat Disord. 2003;33(3):257–67. . discussion 268 – 70.

Kaye WH, Wierenga CE, Bailer UF, Simmons AN, Bischoff-Grethe A. Nothing tastes as good as skinny feels: the neurobiology of anorexia nervosa. Trends Neurosci. 2013;36(2):110–20. .

Sim L, Harbeck Weber C, Harrison T, Peterson C. Central Sensitization in Chronic Pain and Eating disorders: a potential Shared Pathogenesis. J Clin Psychol Med Settings. 2021;28(1):40–52. .

D’Andrea G, Ostuzzi R, Francesconi F, et al. Migraine prevalence in eating disorders and pathophysiological correlations. Neurol Sci. 2009;30(Suppl 1):S55–9. .

Goldberg MB, Katzman DK, Woodside DB, Baker GI. Do eating disorders and chronic facial pain coexist? A preliminary study. J Can Dent Assoc. 2006;72(1):51.

Google Scholar  

Johansson AK, Johansson A, Unell L, Norring C, Carlsson GE. Eating disorders and signs and symptoms of temporomandibular disorders: a matched case-control study. Swed Dent J. 2010;34(3):139–47.

PubMed   Google Scholar  

Murray HB, Bailey AP, Keshishian AC, et al. Prevalence and Characteristics of Avoidant/Restrictive Food Intake Disorder in adult neurogastroenterology patients. Clin Gastroenterol Hepatol. 2020;18(9):1995–e20021. .

Sleurs D, Tebeka S, Scognamiglio C, Dubertret C, Le Strat Y. Comorbidities of self-reported fibromyalgia in United States adults: a cross-sectional study from the National Epidemiological Survey on Alcohol and related conditions (NESARC-III). Eur J Pain. 2020;24(8):1471–83. .

Stein K, Warne N, Heron J, Zucker N, Bould H. Do children with recurrent abdominal pain grow up to become adolescents who control their weight by fasting? Results from a UK population-based cohort. Int J Eat Disord. 2021;54(6):915–24. .

de Lauzon-Guillain B, Oliveira A, Charles MA, et al. A review of methods to assess parental feeding practices and preschool children’s eating behavior: the need for further development of tools. J Acad Nutr Diet. 2012;112(10):1578–602. .

Dovey TM, Aldridge VK, Martin CI, Wilken M, Meyer C. Screening Avoidant/Restrictive Food Intake Disorder (ARFID) in children: Outcomes from utilitarian versus specialist psychometrics. Eating Behaviors. 2016/12/01/ 2016;23:162–167. .

Garner DM, Olmsted MP, Bohr Y, Garfinkel PE. The eating attitudes test: psychometric features and clinical correlates. Psychol Med. 1982;12(4):871–8. .

Garfinkel PE, Newman A. The eating attitudes test: twenty-five years later. Eat Weight Disord. 2001;6(1):1–24. .

Rosen JC, Silberg NT, Gross J. Eating attitudes Test and Eating disorders Inventory: norms for adolescent girls and boys. J Consult Clin Psychol. 1988;56(2):305–8. .

Wells JE, Coope PA, Gabb DC, Pears RK. The factor structure of the Eating attitudes Test with adolescent schoolgirls. Psychol Med. 1985;15(1):141–6. .

Choudry IY, Mumford DB. A pilot study of eating disorders in Mirpur (Pakistan) using an Urdu version of the eating attitudes test. Int J Eat Disord. 1992;11:243–51.

Lee S, Lee AM. Disordered eating in three communities of China: a comparative study of female high school students in hong kong, Shenzhen, and rural Hunan. Int J Eat Disord. 2000;27(3):317–27.;2-2 .

Maïano C, Morin AJ, Lanfranchi MC, Therme P. The Eating attitudes Test-26 revisited using exploratory structural equation modeling. J Abnorm Child Psychol. 2013;41(5):775–88. .

McEnery F, Fitzgerald A, McNicholas F, Dooley B. Fit for purpose, Psychometric Assessment of the Eating attitudes Test-26 in an Irish adolescent sample. Eat Behav. 2016;23:52–7. .

King S, Chambers CT, Huguet A, et al. The epidemiology of chronic pain in children and adolescents revisited: a systematic review. Pain. 2011;152(12):2729–38. . 2011/12/01.

Article   PubMed   Google Scholar  

Swanson SA, Crow SJ, Le Grange D, Swendsen J, Merikangas KR. Prevalence and correlates of eating disorders in adolescents. Results from the national comorbidity survey replication adolescent supplement. Arch Gen Psychiatry. 2011;68(7):714–23. .

Eddy KT, Thomas JJ, Hastings E, et al. Prevalence of DSM-5 avoidant/restrictive food intake disorder in a pediatric gastroenterology healthcare network. Int J Eat Disord. 2015;48(5):464–70. .

Zickgraf HF, Ellis JM. Initial validation of the Nine Item Avoidant/Restrictive Food Intake disorder screen (NIAS): a measure of three restrictive eating patterns. Appetite. 2018;123:32–42. . 2018/04/01.

Download references


We greatly appreciate the work of our interdisciplinary pediatric pain rehabilitation team, as we collaborate together to provide evidence-based treatment for adolescents and families. We extend that appreciation to the adolescents and families who participate in our program after their unique journeys of pain and suffering.

No funding was received for this study.

Author information

Authors and affiliations.

Department of Psychiatry and Psychology, Mayo Clinic College of Medicine and Science, 200 First Street SW, Rochester, MN, 55905, USA

Leslie Sim, Jocelyn Lebow, Abigail Matthews & Cynthia Harbeck-Weber

Pain, Palliative Care, and Integrative Medicine Department, Children’s Hospitals and Clinics of Minnesota, Minneapolis, MN, USA

Amy Fahrenkamp

Department of Quantitative Health Sciences, Mayo Clinic College of Medicine and Science, Rochester, MN, USA

Jennifer R. Geske

Department of Pediatric and Adolescent Medicine, Mayo Clinic College of Medicine and Science, Rochester, MN, USA

Jocelyn Lebow

Department of Psychology, University of Nebraska-Lincoln, Lincoln, NE, USA

Hope Thilges

Department of Psychiatry and Behavioral Sciences, University of Minnesota Medical School, Minneapolis, MN, USA

Carol B. Peterson

You can also search for this author in PubMed   Google Scholar


Author Contributions: LS, AF, CH and JL conceptualized the study. They also supervised data collection and contributed to the drafting and editing of the entire manuscript. AM contributed to drafting and critical evaluation of the manuscript. CP provided expertise on psychometrics and contributed to the drafting and editing of the manuscript. JG conceptualized the data analyses strategy and analyzed the data. She contributed to the drafting of the methods and result section, and contributed to the editing of the manuscript. HT extracted medical chart data and edited the manuscript. AF and LS also contributed to data extraction. All authors reviewed and approved the final draft of this manuscript.

Corresponding author

Correspondence to Leslie Sim .

Ethics declarations

Ethics approval.

This study was approved by the Mayo Clinic Institutional Review Board. Only records from patients whose parents/guardians had provided research authorization were included.

Consent for publication

All authors provide consent for publication.

Competing interests

The authors have no conflicts to declare.

Additional information

Publisher’s note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit . The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article.

Sim, L., Fahrenkamp, A., Geske, J.R. et al. Screening for eating disorders in adolescents with chronic pain: the Eating Attitudes Test–16–Chronic Pain. J Eat Disord 12 , 56 (2024).

Download citation

Received : 05 January 2024

Accepted : 01 May 2024

Published : 10 May 2024


Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

  • Eating disorders
  • Chronic pain
  • Adolescents
  • Factor analysis

Journal of Eating Disorders

ISSN: 2050-2974

case study for anorexia

U.S. flag

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

  • Publications
  • Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

  • Advanced Search
  • Journal List
  • HHS Author Manuscripts

Logo of nihpa

Clinical Case Discussion: Binge Eating Disorder, Obesity and Tobacco Smoking

Marney a. white.

1 Department of Psychiatry, Yale University School of Medicine

Carlos M. Grilo

2 Department of Psychology, Yale University School of Medicine

Stephanie S. O'Malley

Marc n. potenza.

3 Child Study Center, Yale University School of Medicine

This clinical case involves an obese woman requesting treatment for her binge eating and obesity. The information is presented to expert clinicians who provide their thoughts regarding the case, assessment, treatment formulation, and associated clinical and research issues.

Case Description

A 48-year old African American woman presented for treatment for binge eating and weight loss. She presented for treatment following a recent routine physical examination during which her primary care physician noted concerns about her increasing weight. The physician recommended that she try to lose weight but did not provide any specific or further guidance. In light of her previous “failed” experiences with commercial weight loss programs, she decided to seek treatment at a university-based program. At initial evaluation, she was 64 inches tall and weighed 230 pounds yielding a body mass index (BMI) of 39.5, which reflects obesity. She had moderately elevated blood pressure and high cholesterol but was otherwise in good health. The patient completed college and a master's degree in education and had been employed as a special education teacher in the same job for 11 years. She lived with her husband of 24 years, and one of her two adult children. She reported that her relationships with her husband and family were good, that her job was enjoyable and rewarding, and that she had a good circle of close relationships.

Weight and dieting history

The patient reported an onset of overweight during adulthood. She reported having been involved in sports throughout childhood, and although she viewed herself as ‘big-boned’, she did not have body image concerns nor did she recall feeling dissatisfied with her weight or shape when younger. She denied any significant dieting behaviors until age 29. She reported maintaining a weight of approximately 150 pounds (BMI = 25.7) until age 28, at which age she became pregnant with her second child. She reported that she never fully lost the ‘baby weight’ and subsequently began to gradually gain weight throughout her 30s despite numerous dieting efforts. She reported a rapid weight gain of approximately 25 pounds in the past 6 months.

Binge eating

The patient reported an onset of “eating binges” at approximately age 16. The binge eating began soon after she began babysitting for neighborhood children. She estimated that she would engage in binge eating approximately 1-2 times per month which occurred during times that she babysat at night and had access to assorted snack foods. During those times she would ‘load up on junk food’ that the family had provided. She recalled that she would eat chips, cookies, and brownies “non-stop,” and that these eating episodes often lasted throughout the evening. She recalled feeling a loss of control during these episodes and stated that she would continue to eat despite not feeling physically hungry and that she would not stop until feeling physically ill. She reported that she was very embarrassed and secretive about these eating behaviors. She also recalled feeling embarrassed when worried that it was likely that the missing food was apparent to the family for whom she was babysitting. She denied any history of extreme inappropriate weight control or purging behaviors such as self-inducing vomiting or misusing laxatives.

The patient reported infrequent and sporadic binge eating throughout her late teens and early 20s, estimating a frequency of once per month which tended to correspond with social functions. During her 30s, however, the frequency of her binge eating increased considerably and became more regular except during periods of dieting efforts. The patient reported that she had enrolled in commercial weight loss programs approximately five different times, and had, in addition, tried to follow multiple self-help diets. She reported that when she was following a weight loss plan, she could successfully lose approximately 10 pounds, but that she would ‘hit a wall’ and discontinue after about one month of dieting. She reported that in-between diets, her binge eating would resume at a frequency of 2 to 3 times per week, and persist at that level until the next dieting attempt. The patient reported that she had not engaged any formal dieting in the past 18 months, although she frequently skipped meals in an effort to reduce her weight.

Recent course

The patient noted an increase in binge eating frequency approximately six months ago, corresponding with her mother's hospitalization and rapid physical decline. The patient was the primary caregiver for her mother, and noted that the months preceding her mother's death were extremely stressful. She reported that her binge eating increased in frequency to 3 to 4 times per week during her mother's illness, and increased to 6 to 7 times per week following her mother's death.

The patient described her typical binge episode as starting with an evening meal and extending for several hours. Her daily pattern of eating was to skip breakfast, and to consume a standard school cafeteria lunch at 11:30 a.m. She would then not eat again until preparing the evening meal, at which point she would ‘graze’ while cooking. The patient reported that most nights she would eat a ‘normal’ meal with her family, consisting of 5-6 ounces of meat, 2 or 3 types of vegetables, and bread. However, she would then eat the ‘leftovers’ while cleaning up after the meal, such that overall she would have consumed the equivalent of two full meals. She would then eat various foods throughout the rest of the evening until bedtime. During these episodes, she would alternate between salty and sweet snacks. One example binge episode, occurring approximately 30 minutes after the evening meal and spanning the two hours before bedtime, included: a roll of Ritz crackers with 6 ounces of cheese, 2 doughnuts, 4 handfuls of Chex mix, and ½ of a large (12 oz.) Cadbury candy bar.

Smoking History and Cessation

The patient reported that she had recently quit smoking ‘cold turkey’ and had successfully maintained abstinence for four months. She reported quitting smoking following the death of her mother because she died of cancer. She quit smoking without any professional help and without the use of any nicotine replacements or medications to assist with the smoking cessation.

In terms of her smoking history, the patient reported that she began smoking at age 18, that she had successfully quit smoking upon becoming pregnant at age 24, but resumed when she returned to work 11 years ago. She reported a daily smoking frequency of 15 to 20 cigarettes per day. She reported no serious efforts to stop smoking during the past 11 years prior to this recent period of complete abstinence. The patient reported that since quitting smoking, she has experienced more frequent and intense urges to binge eat, and that in the few weeks prior to intake the urges to smoke had increased in frequency and intensity. She reported urges to smoke primarily in the evenings.

Diagnostic Instrument

In addition to a standard intake history, the patient was administered the Eating Disorder Examination (EDE; Fairburn and Cooper, 1993 ). The EDE is a semi-structured investigator-based interview that evaluates current eating behaviors and eating disorder psychopathology. The EDE focuses on the previous 28 days, except for diagnostic items – such as binge eating behaviors - which are assessed for the duration stipulations for each ED. More specifically, the EDE assesses the frequency of different forms of overeating, including objective bulimic episodes (binge eating defined as unusually large amounts of food with a subjective sense of loss of control) and various inappropriate weight control methods (e.g., purging, laxative abuse, etc). The EDE contains four scales reflecting different aspects of ED psychopathology (dietary restraint, eating concerns, weight concern, and shape concern). The EDE is considered the best-established method for assessing and tracking over time the behavioral and cognitive features of EDs and has psychometric support specifically with BED ( Grilo, Masheb, Lozano-Blanco, & Barry, 2004 ; Grilo, Masheb, & Wilson, 2001 ). The interview was administered before treatment and at treatment conclusion to evaluate treatment gains.

The patient was treated with 12 weekly individual sessions of cognitive behavioral therapy (CBT) for binge eating. Expert opinion ( Wilson, Grilo, & Vitousek, 2007 ) and quantitative meta-analytic reviews ( NICE, 2004 ) conclude CBT is the best-established and treatment-of-choice for BED. CBT, a focal and structured treatment, consists of three overlapping phases conducted in a collaborative and interactive method with patients. The first phase focused on educating the patient about the nature of binge eating. Standard behavioral strategies such as self-monitoring and record keeping were used to help the patient identify better her disordered eating patterns while working towards the central goal of normalizing and achieving a structured regular pattern of eating (i.e., not skipping meals). The second phase integrated cognitive procedures to help the patient identify and challenge maladaptive cognitions regarding her eating, possible triggers for dyscontrol, and associated eating/shape concerns. The final phase focuses on consolidating and maintaining the changes and relapse prevention issues.

During the overview of treatment and the ‘meal pattern prescription,’ the patient became tearful, stating that she is not organized enough to follow a meal pattern consisting of three meals and three snacks. She expressed a fear that eating more frequent meals would result in more weight gain, and stated that she was fearful of failing at another weight loss effort. The patient was encouraged to follow the meal and snack pattern as an ‘experiment’ for the first week of treatment. When the patient's fears were alleviated (i.e., disproved owing to weight maintenance during the first week of treatment), she moved through the treatment steps without difficulty. Although she initially voiced concern about the self-monitoring she eventually regarded it as one of the most essential tools that she gained during the treatment.

Overall, at treatment completion the patient's binge eating had remitted fully. She reported no objective bulimic episodes in the last 4 weeks of treatment. Her weight remained relatively stable, with a post-treatment weight loss of five pounds (final weight = 225; BMI = 38.6). Although the patient was pleased to have stopped binge eating, she reported continued distress over her weight and a persisting desire to lose weight.

Carlos M. Grilo, Ph.D.

This clinical case involves a combination of a behavioral (BED) and a physical medical problem (obesity) that often co-occur. This case is also notable for a positive lifetime history of a pharmacological addiction (nicotine) despite not being “active” at the time of presentation for treatment for the eating/weight concerns might nonetheless have important implications. In several respects, this case is fairly typical of BED in obese persons and serves to illustrate a number of important issues facing clinicians and researchers.

Background: Diagnosis, Distribution, and Clinical Features of BED

BED is a specific example of eating disorder not-otherwise-specified (EDNOS) and was included as a “research category” with provisional research diagnostic criteria in Appendix B of the DSM-IV ( American Psychiatric Association, 1994 ). BED is defined primarily by recurrent episodes of binge eating without the regular use of inappropriate compensatory weight control methods (such as purging) that characterize bulimia nervosa (BN). Binge eating is defined as eating unusually large amounts of food while experiencing a subjective sense of loss of control. The research criteria require marked distress about the binge eating and that the binge eating occurs on at least two days per week over the past six months. Unlike the two “formal” eating disorders (anorexia nervosa and bulimia nervosa), the DSM-IV does not include a cognitive criterion pertaining to disturbed body image (i.e., overvaluation of shape or weight) for the diagnosis of BED although such disturbances are present in many patients with BED ( Grilo, Hrabosky, White, Allison, Stunkard, & Masheb, 2008 ). Research has supported the distinctiveness of BED from both other eating disorders (BN) and from obesity without co-existing binge eating (Grilo, Crosby et al., in press; Grilo, Masheb, & White, in press ). A recent critical review of the literature concluded that there exists sufficient empirical evidence to support the inclusion of BED as a distinct and formal ED diagnosis in the DSM-V ( Striegel-Moore & Franko, 2008 ).

Recent epidemiological research has reported a prevalence rate for BED of roughly 3.5% in adult women, which is greater than anorexia nervosa and bulimia nervosa combined ( Hudson, Hiripi, Pope, & Kessler, 2007 ). The distribution of BED is much broader and more diverse than that of the other eating disorders. BED is evenly distributed throughout adulthood and is common in both men and women as well as across ethnic and racial groups ( Hudson et al., 2007 ; Grilo, Lozano, & Masheb, 2005 ). BED is strongly associated with obesity (which is not a required criterion) ( Hudson et al., 2007 ) and therefore with substantially increased morbidity associated with excess weight (e.g., diabetes, metabolic problems). The excess weight in patients with BED is attributable to a combination of binge eating in the absence of weight compensatory behaviors in addition to a general lack of dietary “restraint” that is salient and characteristic of the other eating disorders ( Grilo, 2010 ). Patients with BED who seek treatment are typically older than patients with other eating disorders despite the fact that many report a longstanding duration of the binge eating often dating back to adolescence ( Reas & Grilo, 2007 ). Moreover, unlike the case for the other eating disorders, which most frequently begin following intensive dieting attempts, nearly half of patients with BED report that the onset of their binge eating preceded their first diet ( Reas & Grilo, 2007 ). Regardless of the exact longitudinal sequence, the binge eating and the associated weight gain over time motivate multiple diet attempts over time many of which are not successful ( Reas & Grilo, 2007 ; Roehrig, Masheb, White, & Grilo, 2009 ).

Observations About the Specific Case

I will offer a number of observations regarding this specific case that are illustrative regarding selected issues of relevance to clinicians and researchers. This case is typical in a number of important respects yet it differs in several important ways that I will note with a view of characterizing the heterogeneity of this behavioral disorder. Evolving research has identified a number of treatments that have efficacy for a majority of such patients although two major challenges remain. First, many patients with BED do not get accurately identified, and few receive empirically-supported treatments ( Wilson, Grilo, & Vitousek, 2007 ).


Although obese patients with BED have elevated psychiatric and medical problems and greater health care utilization patterns relative to their obese peers who do not binge eat, they infrequently seek specialized psychological or psychiatric care for their binge eating. Obese persons who binge eat, along with many generalist health care providers, frequently see the binge eating problem as merely reflecting their obesity and need for better diet and weight loss. In this case, the patient and her physician discussed the need for weight loss, although her binge eating problem was not specifically addressed. Despite not being able to provide the patient with specific guidance, this interaction nonetheless represents an important first step. Many health care providers are uncomfortable in raising or discussing excess weight issues with their patients. This is likely due to a many reasons including, for example, negative biases or views about obesity, personal discomfort, perceived lack of expertise, and concerns about “harming” the therapeutic relationship ( Puhl & Heuer, 2009 ). The patient-physician interaction in this case seemed positive enough to support and motivate the patient to seek more specialized care. It is critically important for generalist health care providers to be receptive and open when discussing their patients' excess weight and potential treatment avenues.

Clinical Presenting Picture

This patient presented with co-occurring obesity and BED. Although she had moderately elevated blood pressure and high cholesterol, she had not yet developed metabolic syndrome although she was clearly at risk to do so along with other medical problems. Thus, her proactive treatment-seeking is certainly a very positive step. This is noteworthy because some research has suggested that black women who are obese and who binge eat are less likely to seek treatment than their white peers until both problems are substantially worse ( Grilo, Lozano, & Masheb, 2005 ; Pike, Dohm, Striegel-Moore, Wilfley, Fairburn, 2001 ). Her primary concern was her increasingly weight gain that started in her 30s despite numerous dieting attempts. More recently, her weight gain had increased markedly and this seemed related, in part, to her increased binge eating behaviors. Based on her clinical history, she did not seem to suffer from body image dissatisfaction or from body image disturbance that are characteristic of eating disorders. The EDE interview provides specific quantification of different aspects of body image disturbance and would yield detailed information regarding behavioral, affective, and cognitive aspects of body image to inform both treatment interventions and to assess changes over time ( Grilo et al., 2001 ). Although the absence of such body image problems in this specific patient signals a less disturbed variant of BED ( Grilo et al., 2008 ) with a positive prognosis ( Masheb & Grilo, 2008a ), treating the obese patient with BED will still remain challenging relative to treating obesity only ( Grilo et al., 2008 ). She did not appear to have significant psychosocial problems either independent or associated with the obesity and BED. Her psychosocial functioning seemed rather positive and this is not uncharacteristic of many patients with BED. Conversely, since it is not uncommon for many patients to have associated psychosocial problems, clinicians should routinely assess for any on-going difficulties as context for formulating and implementing treatment. Importantly, the patient did report a specific life stressor (her mother's death) which seemed associated with an intensification of her binge eating.

Psychiatrically, no additional lifetime or current problems were reported, although no formal structured diagnostic interview was administered. Patients with BED have elevated lifetime rates of psychiatric disorders, including most notably mood, anxiety, and substance use disorders ( Grilo, White, & Masheb, 2009 ), although roughly 25% have never experienced another psychiatric problem. For comprehensive treatment formulation and planning, the presence of other psychiatric disorders should be carefully ascertained. However, it is noteworthy that psychiatric co-morbidity has not emerged as a significant predictor or moderator of outcomes for BED treatments that have empirical support ( Masheb & Grilo, 2008b ; see Wilson et al., 2007 ).

The positive smoking history is especially noteworthy in this patient. Unfortunately, the significance of smoking in this patient group is still poorly understood and is often overlooked by clinicians and researchers alike. This case suggests some potentially important associations among smoking, eating, and weight domains. First, preliminary research suggests that smoking histories are not uncommon in patients with BED and, if present, signal increased risk for psychiatric problems, most notably anxiety disorders ( White & Grilo, 2006 ). Although this patient was not determined to have anxiety disorder co-morbidity, both binge eating and smoking may serve to regulate affect. The exacerbation of the patient's binge eating immediately following her mother's death and her smoking quit attempt can perhaps be conceptualized in this way (i.e., increased binge eating to cope with increased negative affect). Second, preliminary research also suggests that BED patients with smoking histories are characterized by heightened levels of maladaptive and rigid eating and dieting behaviors as well as heightened food “cravings” that must be addressed along with the binge eating ( White & Grilo, 2007 ). Third, weight gain following smoking cessation is common and may be especially problematic for obese patients with BED. A recent study found that obese patients with BED reported gaining significantly more weight following a smoking quit attempt than their non-binge-eating obese peers ( White, Masheb, & Grilo, in press ). This patient's rapid recent weight gain following her most recent smoking quit attempt is consistent with this finding and represents an important clinical challenge because it potentially represents a challenge to continued abstinence.

This patient's eating behavior and patterns are fairly representative of patients with BED. First, binge eating occurs most frequently during evenings, although many patients report having episodes at varying times throughout the day. The large amount consisting of mixed foods often based on availability and ease is typical. Also typical in this patient group is that the binge eating often follows eating behaviors or episodes that are occurring without a sense loss of control. Unlike bulimia nervosa where the binge eating episodes are very clear episodes following excessive restraint, patients with BED are characterized by a more chaotic and amorphous eating pattern. This patient attempts some dietary restraint (skipping breakfast, not eating for long period following lunch) but her eating is fairly continuous throughout the evening. Rather than eating a clear meal (dinner), she appears to eat continuously and during part of this time also experiences a sense of loss of control. Thus, these patients require assistance in several complex tasks including: normalizing and scheduling their eating (i.e., not skipping meals), lessening certain maladaptive restraint behaviors (i.e., not going long periods without eating), increasing certain adaptive restraint behaviors (i.e., not overeating during meals, not grazing or nibbling at odd times), in addition to eliminating the binge eating episodes (Allison, Grilo, Masheb, & Stunkard, 2006; Masheb & Grilo, 2006 ).

Treatment Options

Critical meta-analytic ( NICE, 2004 ) and qualitative reviews ( Wilson et al., 2007 ) of the treatment literature have concluded that cognitive behavioral therapy is the treatment of choice for BED. Studies of CBT for BED consistently report remission rates of 50% or greater along with broad improvements in associated psychological and psychosocial functioning, although weight loss tends to be minimal ( Wilson et al., 2007 ). Different research groups have documented that CBT is superior to other active treatments, including behavioral weight loss therapy ( Grilo & Masheb, 2005 ; Wilson et al., in press ) and pharmacotherapy with fluoxetine ( Grilo et al., 2005 ; Ricca et al., 2001 ), and that the benefits of CBT for BED are well-maintained through 24-months (Wilfley, Wilson, & Agras, 2008) following treatment. There is also some empirical support for two alternative psychotherapies (interpersonal psychotherapy and dialectical behavior therapy) which also produce substantial reductions in binge eating but, like CBT, fail to reduce weight ( Wilson et al., 2007 ). Finally, there is also empirical support for behavioral weight control therapy (structured manualized treatment delivered by professionals but not necessarily for the widely-available commercial programs or self-help diets) for reducing binge eating although findings regarding weight losses are also surprisingly mixed ( Grilo & Masheb, 2005 ; Wilson et al., 2007 ). Lastly, a critical meta-analysis of pharmacotherapy treatment research concluded that certain medications have a clinically significant advantage over placebo for producing short-term remission from binge eating and for reducing weight, although the weight losses tend to be quite modest and of uncertain clinical significance ( Reas & Grilo, 2008 ). The meta-analysis highlighted the potential efficacy of an anti-obesity agent (sibutramine) and anti-epileptic medications (particularly topiramate) but suggested more limited utility of SSRIs given their smaller effects on binge eating and essentially no effect on weight. Unlike the psychosocial treatments, the longer-term effects of these medications are unknown. The few available data from blinded ( Grilo, Masheb, & Wilson, 2005 ) and open-label ( Ricca et al., 2001 ) trials directly comparing the effectiveness of pharmacotherapy and psychological treatments indicate that CBT is significantly superior to SSRIs. In terms of combining approaches, most studies have found that adding pharmacotherapy to psychological approaches has generally not enhanced outcomes ( Reas & Grilo, 2008 ). Noteworthy exceptions are studies that reported adding orlistat ( Grilo, Masheb, & Salant, 2005 ) or topiramate ( Claudino et al., 2007 ) to CBT significantly enhanced the weight losses.

Treatment Course

Thus, it is fortunate that this patient sought treatment at a university-based program where she was offered an empirically-supported treatment. This patient's response to CBT was fairly typical in that she experienced an early and rapid response to the treatment ( Grilo, Masheb, & Wilson, 2006 ; Masheb & Grilo, 2007 ), stopped binge eating entirely by the end of treatment, but unfortunately did not lose weight. Many obese patients with BED fail to lose clinically meaningful amounts of weight despite the substantial reductions in binge eating achieved via CBT, which is not unlike the case for other psychological ( Wilson et al., 2007 ) and pharmacological treatments ( Reas & Grilo, 2008 ). Although the patient failed to lose significant weight (only five pounds), the CBT and presumably the cessation of binge eating were associated with a stabilization of weight. The patient entered treatment following a period of rapid and marked weight gain so the weight stabilization does represent a potentially important first step. Unfortunately, the failure to produce weight loss does leave this patient at risk for developing medical problems and given her frustration and distress about the weight may put her at heightened risk for relapse in both the binge eating and the smoking domains.

Future Directions

Finding ways to produce or enhance weight loss in obese patients with BED represents a major research priority ( Grilo, 2010 ). Interestingly, research has found that combining treatments, for example combining pharmacotherapy, has generally not enhanced outcomes ( Reas & Grilo, 2008 ). Possible notable exceptions have included findings from controlled trials suggesting that adding orlistat ( Grilo, Masheb, & Salant, 2005 ) or topiramate ( Claudino et al., 2007 ) may enhance weight losses achieved with CBT for BED. It has been suggested that greater attention to non-normative eating behaviors and patterns ( Masheb & Grilo, 2006 ) in addition to the CBT focus on normalization of eating meals and reducing binge eating may facilitate greater weight loss. Future treatment studies should include analyses of mediators of outcomes in order to guide the process of improving further our existing treatments ( Wilson et al., 2007 ).

Stephanie S. O'Malley, Ph.D.

This case history highlights the important interface between smoking and binge eating behavior and suggests how treatment of binge eating may have beneficial effects on maintenance of smoking abstinence.

Co-occurring Conditions and Complicating Factors

While smokers tend to be leaner compared to nonsmokers, a significant proportion of obese individuals smoke, placing them at increased risk of attendant health consequences such as diabetes and cardiovascular disease. Smoking related health consequences, experienced by the smoker or another family member, often motivate a smoker to quit as was the case for this patient. However, women compared to men are less likely to remain abstinent from smoking despite a motivating “health shock” for a variety of reasons, including concerns about weight gain. Smoking cessation can result in weight gain at one year of about 11 pounds on average, due to decreased energy expenditure, increased appetite and greater food intake. The degree of weight gain, however, is variable. Binge eating appears to be an important risk factor. In a retrospective study of overweight individuals who had quit smoking, those with significant binge eating problems gained substantially more weight in the year following smoking cessation (24.6 pounds) compared to those without binge eating (11 pounds) ( White, Masheb & Grilo, in press ).

Consistent with this report, this patient recently experienced rapid weight gain that initially began during the stressful period of her mother's illness and coincided with a four-month period of smoking abstinence. Her weight gain of 25 pounds over the recent six months, four of which followed smoking cessation, suggests that without intervention her binge eating is a major risk factor for continued weight gain.

Her maladaptive eating may also place her at risk of smoking relapse. Indeed, she reports that her urges to smoke had increased in recent weeks and were more intense in the evenings. Her pattern of depriving herself of food during the day and then binge eating in the evening could undermine maintenance of smoking abstinence in several ways. Food deprivation can increase the reinforcing effects of drugs, including nicotine, making any lapses to smoking more likely to promote continued smoking. Her efforts to resist eating may also tax her self-control resources and undermine her ability to resist smoking. The evening binge eating episodes she reports follow restricted eating during the day and may result in abstinence violation effects in which she experiences demoralizing recriminations over her loss of control. The resulting increase in negative affect and decreased self-efficacy could promote smoking urges and place her at risk of resorting to smoking to cope with negative affect, a common risk factor for smoking relapse. Finally, the expectation that smoking can limit binge eating is another risk factor for smoking relapse.

Treatment Considerations

Given this conceptualization, the treatment plan for her binge eating may help her also remain abstinent from smoking. The “meal prescription” of regular meals and several small snacks should prevent periods of food deprivation that could increase smoking urges, and diminished frequency of binge eating should increase feelings of self-efficacy and remove the compensatory need for smoking to limit binge eating. The remission of her binge eating and the resulting stabilization of her weight may remove the motivation to resume smoking in an effort to manage her weight.

Cognitive behavioral therapy for eating disorders, including binge eating, also addresses the development of alternative coping skills for handling negative affective states and other triggers of maladaptive eating patterns. Given that many smokers use smoking to cope with negative affective states, teaching her alternative coping skills for handling negative affect is likely to have benefits that generalize and help her maintain abstinence from smoking. The therapist could make this connection explicit by examining the circumstances that elicit the urge to smoke, noting any parallels with the circumstances that provoke binge eating as a coping strategy and emphasizing that the new coping skills learned as alternatives to maladaptive eating could serve as alternatives to smoking as a coping response. Evidence for coping skills therapy targeted to one maladaptive behavior generalizing to another behavior is evident in a study of cognitive behavioral therapy for alcoholism, in which improvements in eating disturbances occurred in addition to reductions in alcohol intake ( O'Malley et al., 2007 ). Learning new coping skills and introducing a regular pattern of eating during the day could ultimately minimize stress, a major precipitant of binge eating and smoking.

In the smoking literature, a recent meta-analysis concluded that smoking interventions that incorporate a weight control component result in short-term (< 3 months) improvements in smoking abstinence and reduced weight gain compared to smoking cessation interventions alone ( Spring et al., 2009 ). In one study, for example, a cognitive behavioral intervention designed to reduce over-concern with weight gain improved smoking quit rates and reduce weight gain compared to standard care or a weight control intervention ( Perkins et al., 2001 ). Further development of CBT interventions for weight concerned smokers may be well served by incorporating additional elements of CBT for binge eating, such as meal patterning, especially for those with a history of binge eating or other eating disorder that may predispose for the development or worsening of eating problems during a quit attempt. Likewise, the clinician should consider smoking history in the management of obese patients who present for treatment of binge eating disorder. As a group, these individuals have higher overall psychiatric co-morbidity and more severe binge eating pathology than overweight individuals without a history of smoking and may require specialized care ( White & Grilo, 2006 , 2007 ).

Marc N. Potenza, M.D., Ph.D.

Diagnostic considerations.

The current case describes the treatment of an individual who has demonstrated seemingly excessive engagement in two domains – tobacco use and food consumption. In anticipation of DSM-V, there exist discussions about how best to define and categorize disorders seemingly addictive in nature, and whether excessive engagement in non-drug behaviors (e.g., pathological gambling) might be grouped together with substance use disorders as addictions ( Petry, 2006 ; Potenza, 2006 ). The current case raises questions about whether excessive eating behaviors manifesting in BED and/or obesity might similarly be considered within an addiction framework, and, if so, how such a conceptualization might influence studies into the etiology, prevention and treatment of “behavioral” and drug addictions ( Grant et al., 2006 ; Holden, 2001 ).

Historically, the term “addiction” has undergone multiple changes in usage. Derived from the Latin word meaning “bound to” or “enslaved by”, the term was originally used independent of drug use. However, several hundred years ago the term became linked to excessive patterns of alcohol use and more recently drug use such that by the time when DSM-III-R was being generated, expert consensus was that “addiction” referred to compulsive drug-taking ( O'Brien et al., 2006 ). More recently researchers have proposed core elements of addiction (continued engagement despite adverse consequences, a compulsive quality, an appetitive urge typically preceding engagement in the behavior, and diminished self-control over the behavior) ( Potenza, 2006 ; Shaffer, 1999 ). If these features are seen as the defining qualities of addiction, then conditions like BED and obesity might be considered as addictions ( Volkow and O'Brien, 2007 ; Volkow and Wise, 2005 ).

Mechanisms and Treatment

Obesity, like addictions, appears to have multiple environmental and biological factors contributing to the disorder ( Gearhardt, Corbin, & Brownell, 2009 ; Gold et al., 2009 ). For example, food availability and advertising may increase the societal rates of obesity ( Brownell, 2004 ), and individual difference factors (e.g., specific genetic allelic variants) may predispose people to greater risks for obesity ( Paracchini et al., 2005 ; van Deneen et al., 2009 ). Arguably, a historical focus on the biological mechanisms underlying obesity has involved metabolism and imbalanced energy homeostasis (i.e., “energy in” and “energy out”) ( Abizaid et al., 2006 ). However, the application of motivational behavioral models to food consumption, like those that have been applied to drug use ( Chambers et al., 2003 ; Everitt and Robbins, 2005 ), may lead to identification of novel factors involved in the pathophysiology of obesity and BED ( Volkow and Wise, 2005 ; Hoebel et al.., 2009 ). Given that neurocircuity implicated in drug abuse appears similarly implicated in obesity (e.g., relatively diminished dopamine D2-like receptor availability in the striatum ( Wang et al., 2004 ; Wang et al., 2009 )), additional research is warranted to understand more completely the biological similarities and differences between drug addictions and obesity. The more complete and precise identification of these similarities and differences could help advance prevention and treatment strategies across disorders. Such a strategy has proven fruitful for pathological gambling, where proposed mechanisms underlying pathological gambling and substance addictions led to the hypothesis that opioid antagonists such as naltrexone, approved for the treatments of alcohol dependence and opioid dependence, would be efficacious in the treatment of pathological gambling ( Brewer et al., 2008 ; Grant et al., 2008 ; Tamminga and Nestler, 2006 ). Analogously, glutamatergic agents (e.g, N-acetyl cysteine) have demonstrated initial promise with respect to weight loss, tobacco smoking, pathological gambling and cocaine dependence ( Souza et al., 2008 ; Knackstadt et al., 2009; Grant et al., 2007 ; LaRowe et al., 2006 ), and further research is needed to further evaluate their efficacies and tolerabilities, particularly amongst dually diagnoses populations.

Specific aspects of the case also warrant mention as they relate to the relationship between disorders, like drug dependence, typically have been conceptualized as addictions and others, like obesity and BED, that typically have not. For example, it is noteworthy that the patient reports having recently quit smoking prior to entering treatment, as well as having had several periods of time of time when she was smoking regularly and others when she had quit for prolonged durations. This pattern raises questions about the natural history of smoking and eating behaviors, both individually and in conjunction. Addictions have historically been considered chronic relapsing conditions, a conceptualization based in considerable part on clinical samples. Epidemiological data suggest that both “behavioral” and drug addictions might follow less pernicious natural histories than originally thought, with many individuals recovering without formal interventions ( Slutske, 2006 ; Tamminga et al., 2006 ). Nonetheless, many individuals do require formal interventions, often on multiple occasions. Furthermore, how one behavioral domain might influence the other is incompletely understood. The phenomenon of “switching addictions”, as is suggested in other domains (e.g., alcoholism and problem gambling ( Potenza et al., 2005 )), may be reflected here in increased food cravings, food consumption and weight gain following smoking cessation, with multiple possible contributing mechanisms related to motivation, metabolic changes, stress reduction, or coping with uncomfortable or dysphoric states, as Dr. O'Malley indicates.

Life stressors appear to play an important role in the patient's clinical course, both with respect to smoking and eating. As such, therapies like CBT that include instruction in healthy coping strategies might be particularly relevant for the patient. From a biological perspective, the neural mechanisms underlying stress responses overlap with those implicated in impulse control and addiction ( Kalivas and Duffy, 1989 ; Piazza and Le Moal, 1996 ). Consistently, identification of specific intermediary phenotypes or endophenotypes in the domains of stress responsiveness and impulsivity would appear to have important implications across a broad range of disorders, including obesity, BED and nicotine dependence ( Blanco et al., 2009 ). As Dr. Grilo notes, combinations of pharmacological and behavioral therapies might be most helpful for BED, and consideration of pharmacological agents that target important intermediary phenotypes will represent important areas of future development.

Concluding Comments and Future Directions

The changes over time in the patient's smoking and eating behaviors highlight the importance of considering behaviors with addictive potential within a developmental framework, particularly as early problems have important implications for adult functioning ( Chambers et al., 2003 ). Early life interventions aimed at developing healthy eating, exercise, stress-coping skills, emotional regulation and general health behaviors at early ages, and particularly involving youth who might be considered high-risk, will be important in preventing the development of a broad range of addictive disorders including obesity ( Merlo et al., 2009 ). Public health interventions like those that appear effective in reducing youth smoking (e.g., increased taxation of cigarettes) warrant consideration for foods associated with obesity ( Brownell et al., 2009 ). It is likely that only through multiple interdisciplinary approaches will we be able to effectively target the public health concerns of obesity and drug addictions, ones that currently are estimated to cost US society hundreds of billions of dollars annually and impart significant personal and familial suffering ( Surgeon General, 2001 ; Uhl and Grow, 2004 ; Potenza and Taylor, 2009 ).


Acknowledgments and Disclosures: This work was supported by the NIH grants RL1 AA017539, UL1 DE19586, K23 KD071646, K24 DK070052, R01 DK49587, RC1 DA028279, P50 AA015632, NIH Roadmap for Medical Research/Common Fund, and the VA VISN1 MIRECC. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of any of the funding agencies. Dr. Potenza has received financial support or compensation for the following: Dr. Potenza consults for and is an advisor to Boehringer Ingelheim; has consulted for and has financial interests in Somaxon; has received research support from the National Institutes of Health, Veteran's Administration, Mohegan Sun Casino, the National Center for Responsible Gaming and its affiliated Institute for Research on Gambling Disorders, and Forest Laboratories, Ortho-McNeil, Oy-Control/Biotie and Glaxo-SmithKline pharmaceuticals; has participated in surveys, mailings or telephone consultations related to drug addiction, impulse control disorders or other health topics; has consulted for law offices and the federal public defender's office in issues related to impulse control disorders; provides clinical care in the Connecticut Department of Mental Health and Addiction Services Problem Gambling Services Program; has performed grant reviews for the National Institutes of Health and other agencies; has given academic lectures in grand rounds, CME events and other clinical or scientific venues; and has generated books or book chapters for publishers of mental health texts. Dr. Grilo has received research support from the National Institutes of Health, medical research foundations (Donaghue Foundation, American Heart Association, Borderline Personality Research Foundation), has delivered lectures and papers at scientific conferences, and has generated books and chapters for academic book publishers. Dr. O'Malley is a member of the ACNP workgroup, the Alcohol Clinical Trial Initiative, sponsored by Eli Lilly, Janssen, Schering Plough, Lundbeck, Glaxo-Smith Kline and Alkermes; a partner in Applied Behavioral Research; a Scientific Panel member, Butler Center for Research at Hazelden. Dr. O'Malley participates in studies in which Nabi Biopharmaceuticals and Sanofi Aventis donated medications, has given academic lectures at professional societies and has received grant support form the National Institutes of Health.

All authors report no conflicts of interest with the current manuscript.

  • Abizaid A, Gao Q, Horvath TL. Thoughts for food: brain mechanisms and peripheral energy balance. Neuron. 2006; 51 :691–702. [ PubMed ] [ Google Scholar ]
  • Allison KC, Grilo CM, Masheb RM, Stunkard AJ. Binge eating disorder and night eating syndrome: a comparative study of disordered eating. Journal of Consulting and Clinical Psychology. 2005; 73 :1107–1115. [ PubMed ] [ Google Scholar ]
  • American Psychiatric Association. Diagnostic and statistical manual of mental disorders. Fourth. Washington, DC: American Psychiatric Association; 1994. [ Google Scholar ]
  • Blanco C, Potenza MN, Kim SW, Ibanez A, Zaninelli R, Saiz-Ruiz J, Grant JE. A pilot study of impulsivity and compulsivity in pathological gambling. Psychiatric Research. 2009; 167 :161–168. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Brewer JA, Grant JE, Potenza MN. The treatment of pathologic gambling. Addictive Disorders and Their Treatment. 2008; 7 :1–14. [ Google Scholar ]
  • Brownell KD. Fast food and obesity in children. Pediatrics. 2004; 113 :132. [ PubMed ] [ Google Scholar ]
  • Brownell KD, Farley T, Willett WC, Popkin BM, Chaloupka FJ, Thompson JW, Ludwig DS. The public health and economic benefits of taxing sugar-sweetened beverages. New England Journal of Medicine. 2009; 361 :1599–1605. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Chambers RA, Taylor JR, Potenza MN. Developmental neurocircuitry of motivation in adolescence: A critical period of addiction vulnerability. American Journal of Psychiatry. 2003; 160 :1041–1052. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Claudino AM, de Oliveira IR, Appolinario JC, Cordas TA, Duchesne M, Sichieri R, Bacaltchuk J. Double-blind, randomized, placebo-controlled trial of topiramate plus cognitive-behavior therapy in binge eating disorder. Journal of Clinical Psychiatry. 2007; 68 :1324–1332. [ PubMed ] [ Google Scholar ]
  • Everitt B, Robbins TW. Neural systems of reinforcement for drug addiction: from actions to habits to compulsion. Nature Neuroscience. 2005; 8 :1481–1489. [ PubMed ] [ Google Scholar ]
  • Fairburn CG, Cooper Z. The Eating Disorder Examination. In: Fairburn CG, Wilson GT, editors. Binge eating: nature, assessment, and treatment. 12th. New York: Guilford Press; 1993. pp. 317–360. [ Google Scholar ]
  • Gearhardt AN, Corbin WR, Brownell KD. Food Addiction: An Examination of the Diagnostic Criteria for Dependence. Journal of Addiction Medicine. 2009; 3 :1–7. [ PubMed ] [ Google Scholar ]
  • Gold MS, Graham NA, Cocores JA, Nixon SJ. Food addiction? Journal of Addiction Medicine. 2009; 3 :42–45. [ PubMed ] [ Google Scholar ]
  • Grant JE, Kim SW, Hollander E, Potenza MN. Predicting Response to Opiate Antagonists and Placebo in the Treatment of Pathological Gambling. Psychopharmacology. 2008; 200 :521–527. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Grant JE, Brewer JA, Potenza MN. Neurobiology of substance and behavioral addictions. CNS Spectrums. 2006; 11 :924–930. [ PubMed ] [ Google Scholar ]
  • Grant JE, Kim SW, Odlaug BL. N-Acetyl cysteine, a glutamate-modulating agent, in the treatment of pathological gambling: a pilot study. Biological Psychiatry. 2007; 62 :652–657. [ PubMed ] [ Google Scholar ]
  • Grilo CM. What treatment research is needed for eating disorder not otherwise specified and binge eating disorder? In: Grilo CG, Mitchell JE, editors. The treatment of eating disorders: a clinical handbook. New York: Guilford Press; 2010. pp. 554–568. [ Google Scholar ]
  • Grilo CM, Crosby RD, Masheb RM, White MA, Peterson CB, Wonderlich SA, Engel SG, Crow SJ, Mitchell JE. Overvaluation of shape and weight in binge eating disorder, bulimia nervosa, and subthreshold bulimia nervosa. Behaviour Research and Therapy [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Grilo CM, Hrabosky JI, White MA, Allison KC, Stunkard AJ, Masheb RM. Overvaluation of shape and weight in binge eating disorder and overweight controls: refinement of a diagnostic construct. Journal of Abnormal Psychology. 2008; 117 :414–419. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Grilo CM, Lozano C, Masheb RM. Ethnicity and sampling bias in binge eating disorder: black women who seek treatment have different characteristics than those who do not. International Journal of Eating Disorders. 2005; 38 :257–262. [ PubMed ] [ Google Scholar ]
  • Grilo CM, Masheb RM, Lozano-Blanco C, Barry DT. Reliability of the Eating Disorder Examination in patients with binge eating disorder. International Journal of Eating Disorders. 2004; 35 :80–85. [ PubMed ] [ Google Scholar ]
  • Grilo CM, Masheb RM, Wilson GT. A comparison of different methods for assessing the features of eating disorders in patients with binge eating disorder. Journal of Consulting and Clinical Psychology. 2001; 69 :317–322. [ PubMed ] [ Google Scholar ]
  • Grilo CM, Masheb RM. A randomized controlled comparison of guided self-help cognitive behavioral therapy and behavioral weight loss for binge eating disorder. Behaviour Research and Therapy. 2005; 43 :1509–1525. [ PubMed ] [ Google Scholar ]
  • Grilo CM, Masheb RM, Salant SL. Cognitive behavioral therapy guided self-help and orlistat for the treatment of binge eating disorder: a randomized, double-blind, placebo-controlled trial. Biological Psychiatry. 2005; 57 :1193–1201. [ PubMed ] [ Google Scholar ]
  • Grilo CM, Masheb RM, White MA. Significance of overvaluation of shape/weight in binge eating disorder: comparative study with overweight and bulimia nervosa. Obesity in press. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Grilo CM, Masheb RM, Wilson GT. Efficacy of cognitive behavioral therapy and fluoxetine for the treatment of binge eating disorder: a randomized double-blind placebo-controlled comparison. Biological Psychiatry. 2005; 57 :301–309. [ PubMed ] [ Google Scholar ]
  • Grilo CM, Masheb RM, Wilson GT. Rapid response to treatment for binge eating disorder. Journal of Consulting and Clinical Psychology. 2006; 74 :602–613. [ PubMed ] [ Google Scholar ]
  • Grilo CM, White MA, Masheb RM. DSM-IV psychiatric disorder comorbidity and its correlates in binge eating disorder. International journal of Eating disorders. 2009; 42 :228–234. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Hoebel BG, Avena NM, Bocarsly ME, Rada P. Natural addiction: a behavioral and circuit model based on sugar addiction in rats. Journal of Addiction Medicine. 2009; 3 :33–41. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Holden C. ‘Behavioral’ addictions: Do they exist? Science. 2001; 294 :980–982. [ PubMed ] [ Google Scholar ]
  • Hudson JI, Hiripi E, Pope HG, Kessler RC. The prevalence and correlates of eating disorders in the NCS Replication. Biological Psychiatry. 2007; 61 :348–358. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Kalivas PW, Duffy P. Similar effects of daily cocaine and stress on mesocorticolimbic dopamine neurotransmission in the rat. Biological Psychiatry. 1989; 25 :913–928. [ PubMed ] [ Google Scholar ]
  • Knackstedt LA, LaRowe S, Mardikian P, Malcolm R, Upadhyaya H, Hedden S, et al. The role of cystine-glutamate exchange in nicotine dependence in rats and humans. Biological Psychiatry. 2009; 65 :841–845. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • LaRowe SD, Mardikian P, Malcolm R, Myrick H, Kalivas P, McFarland K, et al. Safety and tolerability of N-acetylcysteine in cocaine-dependent individuals. American Journal of Addictions. 2006; 15 :105–110. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Masheb RM, Grilo CM. Eating patterns and breakfast consumption in obese patients with binge eating disorder. Behaviour Research and Therapy. 2006; 44 :1545–1553. [ PubMed ] [ Google Scholar ]
  • Masheb RM, Grilo CM. Rapid response predicts treatment outcomes in binge eating disorder: implications for stepped care. Journal of Consulting and Clinical Psychology. 2007; 75 :639–644. [ PubMed ] [ Google Scholar ]
  • Masheb RM, Grilo CM. Prognostic significance of two sub-categorization methods for the treatment of binge eating disorder: negative affect and overvaluation predict, but do not moderate, specific outcomes. Behaviour Research and Therapy. 2008a; 46 :428–437. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Masheb RM, Grilo CM. Examination of predictors and moderators for self-help treatments of binge eating disorder. Journal of Consulting and Clinical Psychology. 2008b; 76 :900–904. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Merlo LJ, Klingman C, Malasanos TH, Silverstein JH. Exploration of food addiction in pediatric patients: a preliminary investigation. Journal of Addiction Medicine. 2009; 3 :26–32. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • O'Brien CP, Volkow N, Li TK. What's in a word? Addiction versus dependence in DSM-V. American Journal of Psychiatry. 2006; 163 :764–765. [ PubMed ] [ Google Scholar ]
  • O'Malley SS, Sinha R, Grilo CM, Capone C, Farren CK, McKee SA, Rounsaville BJ, Wu R. Naltrexone and cognitive behavioral coping skills therapy for the treatment of alcohol drinking and eating disorder features in alcohol dependent women: A randomized, double-blind, placebo controlled trial. Alcoholism: Clinical and Experimental Research. 2007; 31 :625–634. [ PubMed ] [ Google Scholar ]
  • Pike KM, Dohm FA, Striegel-Moore RH, Wilfley DE, Fairburn CG. A comparison of black and white women with binge eating disorder. Am J Psychiatry. 2001; 158 (9):1455–60. [ 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 (Clinical Guideline No 9) London: Author; 2004. available at . [ PubMed ] [ Google Scholar ]
  • Paracchini V, Pedotti P, Taioli E. Genetics of leptin and obesity: a HuGE review. American Journal of Epidemiology. 2005; 162 :101–114. [ PubMed ] [ Google Scholar ]
  • Perkins KA, Marcus MD, Levine MD, D'Amico D, Miller A, Broge M, Ashcom J, Shiffman S. Cognitive-behavioral therapy to reduce weight concerns improves smoking cessation outcome in weight-concerned women. Journal of Consulting and Clinical Psychology. 2001; 69 :604–13. [ PubMed ] [ Google Scholar ]
  • Petry NM. Should the scope of addictive behaviors be broadened to include pathological gambling? Addiction. 2006; 101 (s1):152–160. [ PubMed ] [ Google Scholar ]
  • Piazza PV, Le Moal M. Pathophysiological basis of vulnerability to drug abuse: Role of an interaction between stress, glucocorticoids, and dopaminergic neurons. Annual Review of Pharmacology and Toxicology. 1996; 36 :359–378. [ PubMed ] [ Google Scholar ]
  • Potenza MN, Steinberg MA, Wu R. Characteristics of Gambling Helpline Callers with Self-Reported Gambling and Alcohol Use Problems. Journal of Gambling Studies. 2005; 21 :233–254. [ PubMed ] [ Google Scholar ]
  • Potenza MN. Should addictive disorders include non-substance-related conditions? Addiction. 2006; 101 (s1):142–151. [ PubMed ] [ Google Scholar ]
  • Potenza MN, Taylor JR. Found in Translation: Understanding Impulsivity and Related Constructs Through Integrative Preclinical and Clinical Research. Biological Psychiatry. 2009; 66 :714–716. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Puhl RM, Heuer CA. The stigma of obesity: a review and update. Obesity. 2009; 17 :941–964. [ PubMed ] [ Google Scholar ]
  • Reas DL, Grilo CM. Timing and sequence of the onset of overweight, dieting, and binge eating in overweight patients with binge eating disorder. International Journal of Eating Disorders. 2007; 40 :165–170. [ PubMed ] [ Google Scholar ]
  • Reas DL, Grilo CM. Review and meta-analysis of pharmacotherapy for binge eating disorder. Obesity. 2008; 16 :2024–2038. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Ricca V, Mannucci E, Mezzani B, Moretti S, Di Bernardo M, Bertelli M, Rotella CM, Faravelli C. Fluoxetine and fluvoxamine combined with individual cognitive-behavioral therapy in binge eating disorder: a one-year follow-up study. Psychotherapy and Psychosomatics. 2001; 70 :298–306. [ PubMed ] [ Google Scholar ]
  • Roehrig M, Masheb RM, White MA, Grilo CM. Dieting frequency in obese patients with binge eating disorder: behavioral and metabolic correlates. Obesity. 2009; 17 :689–697. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Shaffer HJ. Strange bedfellows: a critical view of pathological gambling and addiction. Addiction. 1999; 94 :1445–1448. [ PubMed ] [ Google Scholar ]
  • Slutske WS. Natural recovery and treatment-seeking in pathological gambling: results of two national surveys. American Journal of Psychiatry. 2006; 163 :297–302. [ PubMed ] [ Google Scholar ]
  • Souza GA, Ebaid GE, Seiva FRF, Rocha KHR, Galhardi CM, Mani F, et al. N-acetylcysteine an Allium plant compound improves high-sucrose diet-induced obesity and related effects. eCAM. 2008 :1–7. [November 11, 2008]; doi: 10.193/ecam/neun070. [ PMC free article ] [ PubMed ] [ CrossRef ] [ Google Scholar ]
  • Spring B, Howe D, Berendsen M, McFadden G, Hitchcock K Rademaker, Hitchcock K, Rademaker AW, Hitsman B. Behavioral intervention to promote smoking cessation and prevent weight gain: a systematic review and meta-analysis. Addiction. 2009; 104 :1472–1486. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Striegel-Moore RH, Frank DL. Should binge eating disorder be included in the DSM-V? A critical review of the state of the evidence. Annual Review of Clinical Psychology. 2008; 4 :305–324. [ PubMed ] [ Google Scholar ]
  • Surgeon General. The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity. United States Department of Health and Human Services. 2001. [11/22/06]. .
  • Tamminga CA, Nestler EJ. Pathological gambling: Focusing on the addiction, not the activity. American Journal of Psychiatry. 2006; 163 :180–181. [ PubMed ] [ Google Scholar ]
  • Uhl GR, Grow RW. The burden of complex genetics in brain disorders. Archives of General Psychiatry. 2004; 61 :223–229. [ PubMed ] [ Google Scholar ]
  • van Deneen KM, Gold MS, Liu Y. Food addiction and cues in Prader-Willi syndrome. Journal of Addiction Medicine. 2009; 3 :19–26. [ PubMed ] [ Google Scholar ]
  • Volkow ND, O'Brien CP. Issues for DSM-V: Should obesity be included as a brain disorder? American Journal of Psychiatry. 2007; 164 :708–710. [ PubMed ] [ Google Scholar ]
  • Volkow ND, Wise RA. How can drug addiction help us understand obesity? Nature Neuroscience. 2005; 8 :555–560. [ PubMed ] [ Google Scholar ]
  • Wang GJ, Volkow ND, Thanos P, Fowler J. Similarity between obseity and drug addiction as assessed by neurofunctional imaging: A concept review. Eating Disorders, Overeating, and Pathological Attachment to Food. 2004; 23 (3):39–53. [ PubMed ] [ Google Scholar ]
  • Wang GJ, Volkow ND, Thanos PK, Fowler JS. Imaging of brain dopamine pathways: implications for understanding obesity. Journal of Addiction Medicine. 2009; 3 :8–18. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • White MA, Grilo CM. Psychiatric comorbidity in binge eating disorder as a function of smoking history. Journal of Clinical Psychiatry. 2006; 67 :594–599. [ PubMed ] [ Google Scholar ]
  • White MA, Grilo CM. Symptom severity in obese women with binge eating disorder as a function of smoking history. International Journal of Eating Disorders. 2007; 40 :77–81. [ PubMed ] [ Google Scholar ]
  • White MA, Masheb RM, Grilo CM. Self-reported weight gain following smoking cessation: a function of binge eating behaviour. International Journal of Eating Disorders in press. [ PMC free article ] [ PubMed ] [ Google Scholar ]
  • Wilson GT, Wilfley DE, Bryson S, Agras WS. A multi-site randomized controlled trial of interpersonal psychotherapy, behavioral weight loss, and guided self-help in the treatment of overweight individuals with binge eating disorder. Archives of General Psychiatry in press. [ Google Scholar ]
  • Wilson GT, Grilo CM, Vitousek K. Psychological treatments for eating disorders. American Psychologist. 2007; 62 :199–216. [ PubMed ] [ Google Scholar ]


  1. (PDF) A Case Study of Anorexia Nervosa and Obsessive Personality

    case study for anorexia

  2. Anorexia Case Study

    case study for anorexia

  3. case study of anorexia nervosa

    case study for anorexia

  4. Case Study Anorexia-1-1.docx

    case study for anorexia

  5. Anorexia Case Study.docx

    case study for anorexia

  6. PPT

    case study for anorexia


  1. Chronic case of anorexia in buffalo l pashuon Mein Bhookh ka ilaaj । Dr umar Khan

  2. Medical Interprofessional Case Study: Anorexia Health System Issues

  3. The Real Story Behind the Record-Breaking Anorexia Case (Valeria Levitin, Part 2)

  4. Case Study On MANIA||NCP on Mania||Mania#psychiatris

  5. Detecting Mental Disorders in Social Media Through Emotional Patterns case of Anorexia,Depression



  1. An Adolescent with Anorexia Nervosa

    Anorexia nervosa is a chronic eating disorder which primarily affects adolescent girls and young women. 1 The prevalence of anorexia nervosa varies between 0.1-1%. 1 Although the prevalence is low, the morbidity is high and the mortality varies between 0.1-25%. 2 Relapse is common and chances of recovery are less than 50% in 10 years while 25% ...

  2. Case 18-2017

    The medical complications of eating disorders are well established in the medical literature. 4,5 This patient was ketotic and dehydrated and essentially refused to eat, and thus she met the ...

  3. Terminal anorexia nervosa: three cases and proposed clinical

    Most individuals with eating disorders will either recover, settle into an unrecovered but self-defined acceptable quality of life, or continue to cycle from crisis to relative stability over time. ... and who are hampered and limited by the paucity of literature on end-of-life care for those with anorexia nervosa. Three case studies elucidate ...

  4. Case Report on Anorexia Nervosa

    Abstract. Anorexia nervosa is an eating disorder characterized by excessive restriction on food intake and irrational fear of gaining weight, often accompanied by a distorted body self-perception. It is clinically diagnosed more frequently in females, with type and severity varying with each case. The current report is a case of a 25-year-old ...

  5. Severe-Enduring Anorexia Nervosa (SE-AN): a case series

    Anorexia Nervosa (AN) poses significant therapeutic challenges, especially in cases meeting the criteria for Severe and Enduring Anorexia Nervosa (SE-AN). This subset of AN is associated with severe medical complications, frequent use of services, and the highest mortality rate among psychiatric disorders. In the present case series, 14 patients were selected from those currently or previously ...

  6. A case report of anorexia nervosa in a 23‐year‐old Ethiopian woman

    There are limited community-based studies worldwide and all available published reports agree on the rare incidence of anorexia nervosa. 2 Most of the existing epidemiological studies on anorexia were conducted in Western countries. 7 In Africa including Ethiopia studies assessing anorexia nervosa are scarce. 7, 14 This case reflects a 23-year ...

  7. Antonella: 'A Stranger in the Family'—A Case Study of Eating Disorders

    Eating disorders are a potentially fruitful area of study for understanding the links between values—in particular cultural values—and mental distress and disorder. Eating disorders show widely different prevalence rates across cultures, and much attention has been given to theories linking these differences with variations in cultural values.

  8. An eating disorder case study

    Eating disorder case study. Call us. Treatment enquiries. 0330 056 6041. General enquiries. 0800 138 8680. Enquire. Emma's* parents, Mr and Mrs James*, were worried about their 16 year old; for over a year she had been on a diet that didn't seem to stop. They didn't understand why she was on a diet because she had never been overweight ...

  9. Maria (binge eating disorder)

    Case Study Details. Maria is a 38-year-old divorced woman who works in a higher level administrative position for a large federal agency. She is well-established in her career and has several close friends with whom she enjoys spending time. She comes to you following years of unsuccessful attempts to get appropriate treatment for her binge eating.

  10. Case report: cognitive performance in an extreme case of anorexia

    The case study suggests that it is possible to perform normally cognitively despite extreme and chronic malnutrition though set-shifting ability may be affected. This opens for discussion whether patients with anorexia nervosa can maintain neuropsychological performance in spite of extreme underweight and starvation. ...

  11. The Treatment Experience of Anorexia Nervosa in Adolescents from

    1. Introduction. Anorexia nervosa (AN) is a serious illness characterized by self-induced underweight, body image distortion and fear of weight gain [1,2,3,4].AN is one of the most common chronic diseases in teenage girls, ranking third after obesity and asthma, and continues to rise in that population [].Its treatment is long and complex, involving a multidisciplinary team [6,7].

  12. Anorexia nervosa in adolescents: An overview : Nursing2023

    Metrics. Abstract. In Brief. Anorexia nervosa (AN) is an eating disorder that is difficult to treat, and relapse is common. This article addresses management strategies and nursing interventions for adolescents diagnosed with AN. Figure. DX, 16, WAS ADMITTED with anorexia nervosa (AN) after unsuccessful outpatient treatment.

  13. What keeps Maya from eating? A case study of disordered eating from

    For example, Chandra et al. (1995) described three case studies of anorexia in India, but only one of them fulfilled the biomedical criteria for anorexia nervosa, which include refusal to maintain one's body weight at or above the minimally normal weight for specific age and height; intense fear of gaining body weight or becoming fat; and ...

  14. PDF Clinical Case Studies A Case Study of Anorexia © The Author(s) 2011

    A Case Study of Anorexia Nervosa and Obsessive Personality Disorder Using Third-Generation Behavioral Therapies Francisco Martín-Murcia1, Adolfo J. Cangas Díaz1, and Luisa Pardo Gonzalez1 Abstract This article presents a case study of anorexia nervosa and obsessive personality disorder as a

  15. Exploring the experience of being viewed as "not sick enough": a

    Despite common misconceptions, an individual may be seriously ill with a restrictive eating disorder without an outwardly recognizable physical sign of the illness. The aim of this qualitative study was to investigate the perspectives of individuals who have previously battled a restrictive eating disorder who were considered "not sick enough" by others (e.g., peers, families, healthcare ...

  16. A Case Study of Anorexia Nervosa

    A Case Study of Anorexia Nervosa. Lucy Howarth, Corresponding Author. Southampton University Medical School Southampton General Hospital, Tremona Road Southampton, U.K. Southampton University Medical School Southampton General Hospital, Tremona Road Southampton, U.K.Search for more papers by this author.

  17. "It's Never About the Food"

    By: Debby. In a 2015 report commissioned by the UK charity Beating Eating Disorders (B-EAT), it was estimated that over 725,000 Brits suffer from an eating disorder. Of that number, around 10% are thought to suffer from anorexia nervosa. Laura* is one of the lucky ones who found support for her struggles with anorexia and recovered.

  18. Anorexia nervosa: A case study.

    Presents the case of a single 19-yr-old female anorexic who was admitted to a mental health center inpatient unit weighing 64 lb, approximately 54 lb underweight, with liver, kidney, and pancreas damage. Treatment consisted of utilizing a hierarchy of reinforcements in the form of privileges mutually agreed upon between patient and therapist, psychodynamic and supportive psychotherapy, and ...

  19. Incidence, prevalence and mortality of anorexia nervosa and bulimia

    Incidence is the number of new cases of a disorder in a population over a specified period of time (usually 1 year). The incidence rate of eating disorders is commonly expressed per 100 000 persons per year (100 000 person-years). The study of newly developed cases of an eating disorder provides clues to unravel its etiology . It is noteworthy ...

  20. (PDF) Case study

    Case study - Young girl with persistent depressive disorder, obsessive compulsive disorder and anorexia ... eating disorders, such as anorexia nervosa, especially those with the re stricting type ...

  21. Co-producing principles to guide health research: an illustrative case

    Background There is significant value in co-produced health research, however power-imbalances within research teams can pose a barrier to people with lived experience of an illness determining the direction of research in that area. This is especially true in eating disorder research, where the inclusion of co-production approaches lags other research areas. Appealing to principles or values ...

  22. Case Report: Kwashiorkor: an unexpected complication to anorexia

    We present the case of a woman aged 48 years, diagnosed with anorexia nervosa (AN) at the age of 12. She was admitted to a highly specialised eating disorder facility with distended abdomen, muscular atrophy, ulcerative dermatitis, electrolyte derangements and low serum albumin. Her weight was 53.1 kg, corresponding to a body mass index (BMI ...

  23. Incidence of Impaired Kidney Function Among Adolescent Patients

    Key Points. Question What is the incidence of impaired kidney function in adolescents with anorexia nervosa, and how does it correlate with body mass index and physiologic parameters of anorexia nervosa severity?. Findings In this case-control study of 395 adolescent patients with recent diagnosis of anorexia nervosa, impaired kidney function was found in 36.8%.

  24. Screening for eating disorders in adolescents with chronic pain: the

    Background Few measures have been validated to screen for eating disorders (ED) in youth with chronic pain. We conducted confirmatory (CFA) of two established factor structures of the Eating Attitudes Test-26 (EAT-26) in a sample of youth with chronic pain attending an intensive interdisciplinary pain treatment (IIPT) program and examined the validity of the best-fitting model in predicting ED ...

  25. Clinical Case Discussion: Binge Eating Disorder, Obesity and Tobacco

    Moreover, unlike the case for the other eating disorders, ... Significance of overvaluation of shape/weight in binge eating disorder: comparative study with overweight and bulimia nervosa. Obesity in press. [PMC free article] [Google Scholar] Grilo CM, Masheb RM, Wilson GT. Efficacy of cognitive behavioral therapy and fluoxetine for the ...