research books about anorexia

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The Oxford Handbook of Eating Disorders

W. Stewart Agras Department of Psychiatry and Behavioral Sciences Stanford University School of Medicine Stanford, CA

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The Oxford Handbook of Eating Disorders reviews current research and clinical developments through synthetic articles written by experts from various fields of study and clinical backgrounds. Epidemiologic studies suggest that eating disorders are not only common but have increased in prevalence in recent decades, and this book refines and updates the state of research. The book is divided into four sections: phenomenology and epidemiology of the eating disorders, approaches to understanding the disorders, assessment and comorbidities of the disorders, and prevention and treatment. The first section deals with classification and epidemiology of the disorders, considerations for revisions to the Diagnostic and Statistical Manual of Mental Disorders, and the somewhat neglected topic of eating disorders in childhood and early adolescence. The second section describes research basic to understanding the eating disorders and addresses biological factors, psychosocial risk factors, cultural factors, and the effects of behaviors such as dieting and eating and weight concerns in the genesis of the eating disorders. The third section describes assessment of the eating disorders, medical and psychological comorbidities, and medical management. The final section deals with various treatment modalities that have been found successful, including psychotherapeutic and psychopharmacologic approaches; an overview of evidence-based treatment for the eating disorders; and a consideration of what we know about cost-effectiveness of existing treatments.

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Journal of Eating Disorders

Call for papers: moving the needle on eating disorder treatment: precision psychiatry and personalized treatment advances.

Phillipa Hay , Editor-in-Chief

Western Sydney University, Australia

Professor Phillipa Hay is a leading mental health researcher, educator, and practicing Psychiatrist. Her research has been translational, guided policy and practice, and award winning, e.g., in 2015 she received the Lifetime Leadership Award from the ANZ Academy for Eating Disorders, and in 2020 she was awarded the Royal Australian and New Zealand College of Psychiatrists (RANZCP) Senior Research Award. She laid the foundations for mental health programs in two new medical schools James Cook and Western Sydney. She has a DPhil in Psychiatry from the University of Oxford and MD (Medicine) from University of Otago, is a Fellow of the RANZCP, and Fellow of the Academy for Eating Disorders (AED).

Stephen Touyz , Editor-in-Chief

University of Sydney, Australia

Stephen Touyz is an Emeritus Professor at the University of Sydney and Director of the Inside Out Institute, a joint partnership between the Sydney Local Health District and the University of Sydney. He is Editor in Chief of the Journal of Eating Disorders which he co-founded a decade ago. He is a past president of the Eating Disorders Research Society. He is a member of the Commonwealth Government of Australia’s Technical Advisory Group for Eating Disorders and a member of the steering committee of the National Eating Disorders Collaboration. He was presented with a leadership award in research by the Academy of Eating Disorders in 2012, the first ever Lifetime Achievement Award by the Australian and New Zealand Academy of Eating Disorders in 2014 and the Ian M Campbell Prize in Clinical Psychology from the Australian Psychological Society in 2014. He has edited/co-edited 6 books and published over 480 scholarly papers/book chapters.

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Anorexia nervosa and familial risk factors: a systematic review of the literature

• Open access
• Published: 25 August 2022
• Volume 42 , pages 25476–25484, ( 2023 )

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• Antonio Del Casale   ORCID: orcid.org/0000-0003-2427-6944 1 ,
• Barbara Adriani 2 ,
• Martina Nicole Modesti 2 ,
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Anorexia Nervosa (AN) is a psychological disorder involving body manipulation, self-inflicted hunger, and fear of gaining weight.We performed an overview of the existing literature in the field of AN, highlighting the main intrafamilial risk factors for anorexia. We searched the PubMed database by using keywords such as “anorexia” and “risk factors” and “family”. After appropriate selection, 16 scientific articles were identified. The main intrafamilial risk factors for AN identified include: increased family food intake, higher parental demands, emotional reactivity, sexual family taboos, low familial involvement, family discord, negative family history for Eating Disorders (ED), family history of psychiatric disorders, alcohol and drug abuse, having a sibling with AN, relational trauma. Some other risk factors identified relate to the mother: lack of maternal caresses, dysfunctional interaction during feeding (for IA), attachment insecurity, dependence. Further studies are needed, to identify better personalized intervention strategies for patients suffering from AN.

Highlights:

This systematic review aims at identifying the main intrafamilial risk factors for anorexia nervosa, including maternal ones.

Intrafamilial risk factors identified mostly regard family environment and relational issues, as well as family history of psychiatric diseases.

Family risk factors identified may interact with genetic, environmental, and personal risk factors.

These findings may help develop tailored diagnostic procedures and therapeutic interventions.

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Risk factors for eating disorders: findings from a rapid review.

Avoid common mistakes on your manuscript.

Introduction

Eating behavior encompasses all responses associated with the act of eating and is influenced by social conditions, individual perception, previous experiences, and nutritional status. Additional influencing factors include mass media and idealization of thinness. Anorexia nervosa (AN) is a psychological disorder concerning body manipulation, including fear of becoming fat and self-inflicted hunger. This disorder is interpreted as a response to the social context and a woman’s rejection of fat to deny mature sexuality (Gonçalves et al., 2013 ; Korb, 1994 ) and it was once supposed to have “hysterical” causes (Valente, 2016 ). The current definition of AN provided by the DSM-5 describes it as “a restriction of energy intake relative to requirements such as to lead to a significantly low body weight […]; intense fear of gaining weight or becoming fat, or persistence in behaviors that interfere with weight gain […]; alteration in the way weight or body shape are experienced […]” (Cuzzolaro, 2014 ). The lifetime prevalence of AN is estimated being of 1.4% (0.1–3.6%) in women and 0.2% (0-0.3%) in men (Galmiche et al., 2019 ). The lifetime prevalence rates of anorexia nervosa might be up to 4% among females and 0.3% among males (Van Eeden et al., 2021 ). AN finds its roots in biological, psychological, social, and familial risk factors.

More precisely, heritable risk factors for AN can be found in 48–74% of cases (Baker et al., 2017 ): for example, it has a higher prevalence in female relatives of individuals with AN (Bulik et al., 2019 ). The presence of genetic correlations between AN and metabolic and anthropometric traits may explain why people with AN achieve very low BMIs and may even maintain and relapse to low body weight despite clinical improvement (Bulik et al., 2019 ). On the other hand, psychological risk factors include excessive concerns about weight and figure, low self-esteem, and depression; while social risk factors are related to peer diet, peer criticism, and poor social support (Haynos et al., 2016 ). As far as family is concerned, it has been observed that anorexic girls’ families are often characterized by poor communication with one another, overprotection, conflicts, and hostility (Emanuelli et al., 2003 ; Horesh et al., 2015 ; Sim et al., 2009 ).

Overall, the puzzle of AN risk factors is still obscure and needs deeper investigations as far as some predisposing aspects are concerned, such as intrafamilial risk factors, which have been extensively analyzed but not properly clarified for clinical applications. Because of the multifactorial etiology of AN, intrafamilial risk factors identification can help to establish preventive interventions in at-risk individuals, and to provide tailored treatments from the earliest stages of the disorder. Our main hypothesis is that intrafamilial as well as maternal risk factors play an essential role in the development of the disease.

Therefore, the main objective of this work is to provide a scientific review of the existing literature about familial relational risk factors involved in the development of AN, with the aim of improving: prevention, establishment of an early diagnosis, and development of a tailored treatment.

Methodology

On February the 16th, 2022, a first research was conducted on PubMed with the title/abstract filter, using the terms “anorexia AND risk factors AND family” in the search bar. For eligibility, we included only randomized controlled studies and case-control studies focused on the issue, as well as case-control studies with at least 50 participants. We excluded reviews, single case studies, case reports, other types of articles and other studies that did not focus on the main topic. The system provided 76 articles, of which 24 were ignored for low relevance. Hence, 52 were assessed for eligibility, from which 26 articles were excluded for not respecting the inclusion criteria, and 12 were excluded for not analyzing the research subject specifically. To the remaining 14 articles, 2 were added from citation search.

In the PRISMA diagram below (Fig.  1 ), the articles identified for the review (76) are reported schematically: screened (76), assessed for eligibility (52) and included (16).

PRISMA diagram of the study

The main results of the studies analyzed are summarized in Table  1 .

Despite anorexia having been usually considered an expression of age-specific conflicts intensified by constrictive cultural ideas and certain kinds of familial constellations (Bemporad et al., 1988 ), having our review included studies from 1990 to 2021 and conducted across many countries (i.e. US, Japan, Poland, UK, etc.) we can hypothesize that such a condition just evolves with culture and time, still maintaining certain background issues that we are aiming to emphasize in order to recognize certain red flags.

Eating disorders mark deficits in the ability to be nourished and to symbolize embodied experience. Psychoanalytic theories suggest that mothers who are insufficiently developed leave the child either austerely avoiding intrusion or struggling to digest maternal provisions without becoming lost in them. (Charles, 2021 ). Infantile Anorexia (IA) has been defined as a child’s refusal of food for more than 1 month, between 6 months and 3 years of age; acute and/or chronic malnutrition; parental concern about the child’s eating; mother-child conflict, talk, and distraction during mealtime (Chatoor et al., 1998 ). Maternal risk factors for (IA) we have identified across the review can confirm this widely accepted theory, specifically lack of maternal caresses (Mangweth et al., 2005 ), dysfunctional interaction during feeding in IA (Ammaniti et al., 2010 ), and attachment insecurity (Chatoor et al., 2000 ). Regarding maternal history of psychiatric diseases, it has been noted that maternal depression has an influence on the development of conflicts during mother-child interaction in younger children, while maternal psychoticism predicts mother-child conflict during feeding in older children (Ammaniti et al., 2010 ). This means that depressed mothers engage in less positive interactions with their infants while breastfeeding, with difficulties in empathically recognizing their infant’s affective states at mealtimes (Ammaniti, Ambruzzi et al., 2004 ; Feldman et al., 2004 ).

In addition to the relational risk factors, maternal diet seems to play a role in the development of AN (Haynos et al., 2016 ). This mechanism seems to find its roots early during childhood, since the infant’s weight appears to be inversely related to the mother’s degree of concern about her body shape (Ammaniti, Lucarelli et al., 2004 ). The “modelling theory of AN” (Pike & Rodin, 1991 ) argues that adolescent girls begin the diet by mimicking their dieting mothers. It seems that family concerns about weight and appearance are directly linked to the development of low satisfaction with one’s body, and therefore directly or indirectly related to eating problems (Leung et al., 1996 ).

Maternal risk factors are synthesized in Table  2 .

Enlarging our highlight from the mother to the whole family nucleus, the onset and maintenance of AN seems to be closely related to familial risk factors, and knowing them is crucial to identify the best therapeutic approach in order to target the unhealthy family environment as well as the needs of the patient. In addition, being aware of the familiar background may help in strengthening the hypothesis of genetic correlates within Eating Disorders (ED). Intrafamilial risk factors for the development of ED seem to have a greater impact when they occur early in adolescence (Field et al., 2008 ), but most of them are chronic in time and one can suppose they can be found in a family at any time during the life of the patient.

The major intrafamilial risk factors identified in this review are summarized in the following Table  3 .

Increased food intake in the family (Hilbert et al., 2014 ) seems to play a role in the development of ED. This seems counterintuitive, but the discrepancy between one’s family food intake and peer and media influences on body ideals may contribute to triggering a subtle mechanism by which diet represents a way to affirm oneself in front of the family and reestablish social acceptance.

Perfectionism (Hilbert et al., 2014 ; Pike et al., 2008 , 2021 ) is widely recognized as a familiar risk factor across many studies, and it can be assimilated to higher parental demands (Pike et al., 2008 ). It surely contributes to creating a tense family environment in which the development of oneself is more difficult, therefore inhibiting progressive differentiation of self from other (Charles, 2021 ). Perfectionism itself will become a personal risk factor for the outcome and severity of disease (Longo, Aloi et al., 2021 ) in a way that could be mimicking the family environment.

In general, unhealthy family functioning is predictive of adolescence problems (Lyke & Matsen, 2013 ). General family malfunction is predictive for AD onset during adolescence, and the level of affective expression of the family seems to be relate to ED risk during adolescence (Felker & Stivers, 1994 ), but our review has highlighted that all those features of what could be described as a “toxic” family environment in the common sense play a role in the development of AN. Emotional reactivity (Lyke & Matsen, 2013 ), as well as family taboos regarding nudity and sexuality (Mangweth et al., 2005 ), low familial involvement (Haynos et al., 2016 ), negative affectivity (Pike et al., 2008 , 2021 ), and family discord (Pike et al., 2008 ) may lie in the background in the lives of a future AN patient, and should be recognized as environmental risk factors in order to develop a tailored psychotherapeutic intervention that may involve the family as well as the patient, since it seems clear that the quality of family functioning influences the development (McGrane & Carr, 2002 ) and maintenance of EDs (North et al., 1997 ; Strober et al., 1997 ; Wewetzer et al., 1996 ).

As far as the presence of other disorders in family members is concerned, our review established that a familiar history of almost any psychiatric disorder (Longo, Marzola et al., 2021 ; Pike et al., 2021 ), including depression (Lyon et al., 1997 ), affective disorders (Steinhausen et al., 2015 ), alcohol and drug abuse (Lyon et al., 1997 ) plays a role in the development of AN. Nevertheless, having a sibling with AN increases the risk of developing AN (Machado et al., 2014 ; Steinhausen et al., 2015 ). We can hypothesize that the role of genetics in this mechanism is crucial yet still obscure, and nevertheless, talking about the presence of these diseases in members of the family nucleus, having to cope and live with the difficulties of others’ conditions is what can predispose to AN. In addition, the opposite may happen as well: there is an increased risk for relatives of patients with AN and BN to develop subclinical forms of ED, major depressive disorder, obsessive-compulsive disorder, and anxiety disorders (Lilenfeld et al., 1998 ). What is curious to note is that, on the one hand, having a sibling with AN predisposes to the development of AN (Felker & Stivers, 1994 ; Machado et al., 2014 ; Steinhausen et al., 2015 ), probably because of shared intrafamilial risk factors, therefore underlining the importance of the aim of this review; but, on the other hand, negative family history for ED predicts poor outcome (Ackard et al., 2014 ), probably because of the familiar unpreparedness to cope with such a difficult condition and the discrepancy created between the healthy members and the patient, which remains alone and uncapable of sharing certain issues with the others, so close yet so far from them.

Another risk factor identified is having suffered a relational trauma (Longo, Marzola et al., 2021 ). In general, individuals who have suffered from traumatic events (physical violence, being threatened with a weapon, sexual violence, being a victim of robbery) more frequently develop maladaptive eating behaviors (Field et al., 2008 ). Some evidence also suggests an increase of severe life events in the year preceding the onset of AN (Råstam & Gillberg, 1991 ). Children of mothers who have experienced the loss of a vital member of their family (i.e. older child or partner) in the six months prior to pregnancy have a higher risk of ED than children and infants who have not been exposed to this risk factor (Su et al., 2015 ). Further confirming the possible role of relational trauma as a red flag not only in the development of AN, but also in determining the severity of the disease, patients with AN and comorbid Post Traumatic Stress Disorder (PTSD) show more severe concerns about body shape and weight (Field et al., 2008 ). Having suffered physical and sexual abuse during childhood appears to be related to the onset of psychiatric pathologies in general, and not specifically to the onset of EDs in the young adult (Bruch, 1977 ; McGrane & Carr, 2002 ; Smith et al., 1995 ): therefore, this risk factor needs further investigation to confirm its specific role in the development of AN.

Strength and limits

The strength of this work lies in the comparison between different studies regarding AN showing high level of evidence and providing a complete picture of the constellation of intrafamilial risk factors of anorexia nervosa. There main limit of this study is that few articles from those included are from the very last years, while many other studies were conducted and published earlier (1990–2014), underlining the need of further investigations.

Conclusions

The main intrafamilial risk factors for AN identified from this study are: increased food intake in the family, perfectionism, higher parental demands, emotional reactivity, family taboos regarding nudity and sexuality, low familial involvement, negative affectivity, family discord, dependence, negative family history for ED (as a predictor of poor outcome), family history of depression, positive family history for psychiatric disorders, affective disorders in family members, alcohol and drug abuse, having a sibling with AN, relational trauma. Some other risk factors identified may relate to the role of the mother during childhood especially, and are as follows: lack of maternal caresses, dysfunctional interaction during feeding (for IA), attachment insecurity, dependence, maternal diet.

Complex interactions occur between intrafamilial risk factors and other personal aspects and symptoms, including perfectionism, individual body image issues, social concerns, excessive preoccupation with weight control, stress and adjustment problems, lack of close friends, social prejudice.

In conclusion, further studies are needed to understand more clearly how intrafamilial risk factors for AN interact with other environmental, personal and genetic ones, in order to connect the dots that can lead to an improvement of diagnostic and therapeutic procedures, and to the development of tailored intervention strategies that may target multiple issues in the life of the patient, including intrafamilial mechanisms that may be identified precociously and addressed through familial therapy, for the sake of the whole family nucleus.

Data availability

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

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Del Casale, A., Adriani, B., Modesti, M.N. et al. Anorexia nervosa and familial risk factors: a systematic review of the literature. Curr Psychol 42 , 25476–25484 (2023). https://doi.org/10.1007/s12144-022-03563-4

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Anorexia nervosa is considered the most deadly psychological illness. Individuals with and recovered from anorexia nervosa experience numerous physical and mental health difficulties, and treatment outcomes remain unpromising. Anorexia nervosa is rare in the general population, but common among individuals with a first-degree relative with the disorder. In addition, the onset of anorexia nervosa is developmentally specific, which suggests a partly biological etiology. A better understanding of the biological and neurobiological etiology of anorexia nervosa is direly needed to inform new therapies and to identify individuals at risk for the disorder. This paper summarizes the research related to neurotransmitter abnormalities, aberrant brain activity, and genetic and epigenetic mechanisms that may contribute to the etiology of this deadly disorder.

• anorexia nervosa
• neurobiology
• neurotransmitters

Author Information

Ashley higgins *.

• Immaculata University, Malvern, PA, United States of America

*Address all correspondence to: [email protected]

1. Introduction

Anorexia nervosa (AN) is a serious psychological disorder characterized by low body weight, unhealthy weight loss methods, and an extreme focus on weight and body shape [ 1 ]. AN is associated with significant mortality risks due to medical complications, as well as the fact that one in five patients with AN die by suicide [ 2 , 3 ]. The physical sequelae of AN, which are caused by self-starvation, affect nearly every major organ system. For instance, the gastrointestinal complications of AN include dysphagia [ 4 ], delayed gastric emptying [ 5 ], and risk of gastric dilation or even perforation [ 6 ]. Hematological and musculoskeletal complications include osteoporosis, fracture risk [ 7 ], and low red and white blood cell counts [ 8 ]. The endocrine system is impacted via elevated cortisol and growth hormones, low serum thyroid levels, and hypoglycemia [ 5 , 9 ]. Dermatological complications include lanugo, acrocyanosis, and thinning hair [ 10 ]. Neurological complications, which will be discussed in depth throughout this chapter, are well-documented in terms of the effects of long-terms caloric restriction on brain volume and neural activity [ 11 ]. Finally, cardiac complications, which are most often linked to mortality in AN, include bradycardia [ 12 ], prolonged QTc interval [ 13 ], and left ventricular atrophy [ 14 ].

Current medication and psychotherapies have limited success in treating AN. The prognosis is especially poor if treatment begins more than 3 years after the onset of symptoms [ 15 ]. AN currently has no viable treatment options [ 16 ], as current medications and psychotherapies provide only minor to modest effects, with especially poor outcomes among women with entrenched AN [ 16 , 17 , 18 ]. It is estimated that only half of individuals with AN achieve full remission of symptoms, and even recovered patients typically maintain a low weight and experience chronic depressive symptoms [ 19 ]. Given the lack of viable treatment options for AN, leading eating disorders researchers are now recommending that future research focus on identification of risk factors and other preventive strategies [ 20 , 21 ].

Many of the identified risk factors for AN are biological or genetic in nature. AN is a rare disorder, with estimated lifetime prevalence ranging from 0.1 to 3.6%, and a point prevalence rate ranging from 0.1 to 1.2% in the general population [ 22 ]. Though the overall prevalence of AN is quite low, AN represents the third most common chronic illness with adolescent onset [ 23 ]. In addition, the risk of AN is elevated among individuals with a family history of AN. It is a well-documented finding that AN tends to run in families [ 24 , 25 ]. Some studies have found a 10-fold risk of AN among first-degree relatives of individuals with the disorder [ 26 , 27 , 28 ] or an overall heritability of 0.56 [ 25 ]. Furthermore, AN has a developmentally specific age of onset. Taken together, these findings suggest the presence of biological and/or genetic risk factors in the etiology of AN [ 29 ].

Individuals with AN often display a relentless pursuit of further weight loss and believe themselves to be overweight even when they are emaciated. In addition to pathological eating patterns, individuals with EDs also experience a host of unusual symptoms, such as “(1) extremes of behavioral inhibition and dysinhibition; (2) anxiety, depression, and obsessionality; and (3) puzzling symptoms such as body image distortion, perfectionism, and anhedonia” ([ 30 ], p. 38) as well as “intense body-focused anxiety, self-disgust, compulsive behavior and altered information processing—i.e. raised pain threshold, reduced sense of taste, anosognosia, inability to integrate thoughts and feelings, poor visuospatial memory, cognitive rigidity and weak central coherence” ([ 31 ], p. 580). Any biological mechanisms accounting for the inherent eating pathology of AN should also modulate these emotional and cognitive phenomena.

Identifying true risk factors for AN presents a complicated methodological problem. By definition, a risk factor must be present prior to the onset of illness, and identifying these factors prior to the symptom onset requires a prospective design [ 32 ]. However, given the low prevalence rate of AN, prospective studies are often too complicated to perform; thus, the research literature on AN risk factors is often limited to retrospective studies, with their inherent bias in retrospective recall [ 33 ].

Another methodological approach samples from individuals who have recovered from AN (RECAN). While recovery from AN is a long and ill-defined process, more than half of individuals with AN are able to completely or partly achieve remission [ 34 ]. Individuals RECAN are assumed to no longer be experiencing the sequelae of the starvation state. However, the use of individuals RECAN is limited as a methodological approach in that “scar” effects from a period of illness could be misidentified as premorbid risk factors [ 35 ]. In order to circumvent the possibility of “scar” effects, studies must identify endophenotypes that are present among individuals with active AN, individuals RECAN, and among unaffected family members [ 36 , 37 ]. Utilizing this approach, several potential endophenotypes have been identified, by eliminating any neurobiological findings that improve with refeeding and identifying abnormalities that are shared by individuals with AN and their unaffected family members [ 16 ].

Many of the neurobiological phenomena to be discussed in this paper are present premorbidly, exaggerated by malnutrition, and return to premorbid levels after recovery [ 38 ]. There are currently promising lines of research on dopaminergic [ 29 ], serotonergic [ 39 ], and noradrenergic pathways [ 31 ], as well as dysregulations in appetitive functioning [ 30 ], genetic and epigenetic contributions [ 40 , 41 ], contributions from gonadal hormones [ 42 ], and aberrations in brain activity [ 43 ].

2. Dopamine

Dopaminergic functioning modulates reward and affect, and an aberration in dopaminergic functioning has been implicated in obsessive or ritualistic behaviors, such as the food rituals observed in individuals with AN [ 29 ]. It seems intuitive that reward functioning is impaired in AN, as individuals with AN often present as abstemious, anhedonic, and temperate in a multitude of behaviors even in childhood, long before the onset of symptoms [ 44 ]. Dopamine is central in processing reward in both primary and secondary reinforcers, including food [ 45 , 46 , 47 ]. Several research studies have revealed altered striatal dopamine function in individuals with and RECAN [ 29 , 48 , 49 ]. Ingestion of highly palatable foods, such as high-sugar foods, may trigger dopamine release in individuals without AN; this release of dopamine in response to food is similar to the release of dopamine elicited by amphetamine use, which is often associated with feelings of euphoria [ 50 ]. However, among individuals RECAN, amphetamine use triggers the expected endogenous dopamine release, but this release of dopamine is experienced as highly unpleasant and anxiogenic [ 51 ]. If similar processes take effect during exposure to highly palatable food, which would be experienced as highly anxiogenic to individuals with AN, this could partially account for the persistence that individuals with AN display in their pursuit of self-starvation; if food is anxiogenic, self-starvation downregulates this anxiety. Whereas individuals without AN experience pleasure from foods, individuals with AN find it aversive. Thus, the reinforcing aspects of food are not experienced by individuals with active AN or individuals RECAN.

Reward processing in general appears to be altered in individuals with AN, even in situations that do not involve food- or weight-related cues. In fMRI research, individuals RECAN failed to differentiate between winning and losing money in a gambling task [ 52 ]. Therefore, individuals with AN may have a diminished ability to identify the positive or negative value of a stimulus. Individuals with AN fail to show appropriate appetitive motivational system activation to a variety of cues [ 49 ]. Thus, altered dopaminergic function reflects high conditioning of reward for disease-salient stimuli, but a failure to respond appropriately to other positive and negative cues [ 18 ].

Among individuals RECAN, dopamine metabolite concentrations in the cerebral spinal fluid remain depleted years after the disorder [ 53 ]. Perhaps to correct for this depletion, dopamine 2 and 3 (D 2 /D 3 ) receptor binding in the ventral striatum is elevated among individuals RECAN [ 44 ]. At this time there are no publications on dopamine aberrations in unaffected family members. However, animal models of anorexia strongly suggest a dopaminergic endophenotype, as administering dopamine antagonists in activity-based anorexia in rats facilitates increased food intake [ 54 ]. This hints at a dopaminergic role in promoting weight loss, which can be reversed with psychopharmacology that acts on the dopamine system.

3. Serotonin

Additionally, serotonergic (5-HT) dysfunction may be a biological marker for AN. Serotonin has seemed a likely candidate for some time, given this neurotransmitter’s active influence in modulating mood and appetite [ 29 ]. A recent meta-analysis has concluded that being a carrier of the S allele of the 5-HTTLPR polymorphism of the serotonin transporter gene is predictive of eating disorders, particularly anorexia [ 55 ]. The gene coding of the serotonin transporter (5-HTT) works in the presynaptic neuron to terminate serotonin activity in the synapse and recycle serotonin back into the presynaptic neuron. 5-HTT is coded by a gene on chromosome 17, and the 5-HTTLPR polymorphism of this gene has the greatest impact on behavior. The S allele is a short variant of this 5-HTTLPR polymorphism, which decreases the availability of 5-HTT and results in dysphoria.

In terms of appetite, any treatment that increases intrasynaptic 5-HT or activates 5-HT receptors will reduce appetite and food consumption, while any treatment that reduces transmission or blocks receptors will promote weight gain [ 56 ]. Caloric restriction has an enormous impact on the available serotonin in the brain [ 29 ]. Tryptophan is one of 20 essential amino acids and can be absorbed only through caloric intake, especially carbohydrate intake [ 57 ]. Tryptophan, through a series of chemical processes, becomes serotonin. A restricted diet limits the amount of tryptophan (and, therefore, the amount of serotonin) that is available to the brain [ 58 ]. In addition, a restricted diet decreases the rate of synthesis in serotonin receptors and the density of serotonin transporters, which results in oversensitivity to serotonin in postsynaptic receptors [ 59 ]. Not surprisingly, individuals in the acutely ill state have lowered concentrations of the 5-HT metabolite 5-HIAA in the cerebral spinal fluid [ 56 ]. However, elevated levels of 5-HIAA were likely present premorbidly. Individuals with AN premorbidly report high levels of anxiety, dysphoria, and obsessionality, which are associated with high levels of 5-HT in the synapse [ 42 ]. Dieting actually serves to regulate the 5-HT in the synapse. This reduction of serotonin, in the short term, results in anxiolytic effects for people who restrict calories [ 29 ]. These anxiolytic effects could explain why individuals with AN cling so desperately to their restrictive behaviors: these behaviors are inadvertently medicating underlying anxiety.

The serotonin system includes at least 14 different receptors. The 5-HT 1A and 5-HT 2A receptors appear most influential in the pathogenesis of AN. The 5-HT 1A autoreceptor serves to decrease 5-HT transmission [ 56 ]. Individuals with AN have 50–70% more binding at these receptors, and retain 20–40% more binding after recovery. In addition, the 5-HT 1A receptor may play a role in the efficacy of selective serotonin reuptake inhibitors (SSRIs), which are potently effective at treating depression and anxiety [ 60 , 61 ]. While starvation decreases 5-HT across the brain, the overactive 5-HT 1A receptor continues to inhibit 5-HT transmission. The combination of these forces is so powerful that SSRIs exert minimal impact in increasing intrasynaptic 5-HT, which fails to provide symptom relief for individuals with AN [ 56 ]. In AN, SSRIs fail to desensitize 5-HT 1A receptors, which inhibits presynaptic 5-HT.

Newer imaging technologies, such as PET imaging with selective neurotransmitter radioligands, allow for viewing in vivo neurotransmitter activity in the brain. Postsynaptic 5-HT 2A receptors have been studied in this way. The 5-HT 2A receptor has been afforded special attention because activity at this receptor is influential in two of the central, yet most perplexing, symptoms of AN: poor problem-solving abilities and distorted body image [ 62 , 63 ]. 5-HT 2A receptor binding is reduced in several brain areas, especially in the cingulate and temporal regions. The cingulate-temporal dysfunction could be related to inefficient problem-solving behaviors among individuals with AN, who struggle with incorporating affective and social stimuli into tasks [ 64 ]. Individuals with AN do not seem to learn from mistakes, but stubbornly and obsessively use the same strategies, despite poor results. This could indicate dysfunction in executive functioning and planning. In terms of distorted body image, which is characterological for individuals with AN, 5-HT 2A disturbances in the left parietal region of the brain are thought to be responsible [ 62 ]. Lesions in the right parietal region have been associated with neglect, which could be theoretically related to body image distortion, especially if this information is coded in the parietal regions of each hemisphere [ 56 ]. The activity at 5-HT 2A receptors remains dysregulated even after a year of maintaining normal weight, regular menstruation, and no binge/purging/restricting. Prolonged dysregulation at these receptors may partially account for the inefficacy of SSRIs in treating AN, regardless of the phase of the disorder [ 17 , 18 ].

Additionally, serotonergic dysfunction is common to other psychiatric concerns, especially those that are likely to be comorbid with AN, such as major depression [ 65 ] and anxiety disorders [ 66 ]. While abnormalities in serotonergic functioning are common to all of these disorders, different patterns of serotonergic functioning emerge on a molecular level [ 67 ]. While 5-HT 1A receptor binding is often decreased in individuals with or recovered from depression [ 68 , 69 ] and panic disorder [ 70 ], 5-HT 1A receptor binding is increased in individuals with AN [ 29 ]. This could indicate that serotonergic dysfunction is a common vulnerability for a variety of disorders, with disorder-specific patterns at the neuronal level. This also accounts for higher rates of psychiatric concerns among family members of individuals with AN.

Given etiological research on the separate roles of dopamine and serotonin, it is not surprising that the most recent research suggests that interactions between serotonin and dopamine activity truly elicit and maintain the eating pathology of AN [ 56 ]. This interaction is not well understood, but could hold promise for future pharmacological interventions for AN.

4. Norepinephrine

Based on previous research on dopaminergic and serotonergic dysfunction in individuals with active AN, individuals RECAN, and unaffected family members, it is safe to conclude that neurotransmitter activity is aberrant both during the premorbid, active, and recovery periods of AN. Dopaminergic and serotonergic pathways could account for some, though not all, of the core symptoms of AN [ 29 , 42 ]. While these pathways (particularly the serotonergic pathway) partly account for rigidity and perfectionism among individuals with AN, individuals with AN display a variety of perplexing symptoms that seem unrelated to both the starvation state itself or serotonin dysfunction alone; individuals with AN report difficulty with pain perceptual, alexithymia, reduced sense of taste, as well as numerous other perplexing symptoms [ 31 ]. Aberrant activity in the noradrenergic pathway could better account for this vast range of deficits.

Norepinephrine is a neurotransmitter which serves multiple functions in the body and brain, including regulation of sympathetic arousal/anxiety and cerebral blood flow [ 71 ]. Norepinephrine levels are elevated premorbidly in AN [ 72 ], but appear to be decreased in plasma and cerebrospinal fluid during active AN ad RECAN [ 72 , 73 , 74 ]. Premorbidly high levels of norepinephrine lead to high sympathetic arousal and anxiety [ 31 ]. Among individuals with AN, this anxiety is often focused on food- and weight-related issues, though the inherently high trait levels of perfectionism and neuroticism can manifest in other achievement domains such as schoolwork or sports [ 75 ]. Since this anxiety is linked an abundance of norepinephrine, dieting in the early stages of AN counteracts this by depleting the brain of the precursors to norepinephrine that are normally ingested through food [ 31 ]. Dieting is then maintained through negative reinforcement, leading to a reduction in body weight and entrenchment of AN symptoms. Furthermore, aberrant activity in the noradrenergic system has been linked to irregular patterns of activation in the insula, which will be discussed in the next section.

5. Brain volume, blood flow, and neural activity

Various neuroimaging studies show substantial structural abnormalities in the brain among individuals with active AN [ 30 , 76 , 77 ]. However, significant questions remain as to:

whether such anomalies reflect regionally specific disturbances that might help explain disorder-defining psychopathology or merely generic, global consequences of malnutrition. Similarly, it remains unclear whether structural alterations in AN constitute premorbid traits or persisting “scars,” as might be the case if they would still be evident following weight restoration ([ 76 ], p. 214) .

Decreased volumes of white and gray brain matter have been documented throughout the brain during the acute phases of illness [ 77 , 78 ]. More specifically, gray matter atrophy has been noted in the cerebellum, hypothalamus, caudate nucleus and frontal, parietal and temporal areas [ 77 , 79 , 80 ], as well as in the cingulate cortex [ 81 ] and the precuneus [ 82 ]. The rate of gray matter atrophy is not uniform across the brain during active AN; atrophy in the hypothalamus may appear early in AN, whereas atrophy in the cerebellum is a late consequence of AN among patients with longer durations of illness [ 77 ].

However, these gray and white matter findings appear to be specific to the acute phase of illness and caused by malnutrition and cerebral dehydration [ 77 ]. A meta-analysis revealed that gray matter is reduced by 5.6% during the acute phases of AN, whereas white matter is reduced by 3.8% [ 83 ]. A few months of treatment and results in approximately 50% of gray matter regain and nearly all of the white matter being regained. A few years following remission of AN, gray matter and white matter depletions are no longer statistically significant. It is possible that hormone levels impact how much gray matter is recovered, as high levels of cortisol at the time of hospitalization are negatively correlated with gray matter restoration following weight gain [ 84 ]. All told, the decreased volume of white and gray matter in individuals with AN normalizes with proper nutrition [ 38 , 85 ]. Thus, these gray and white matter findings are not likely to be a contributing factor to the neurobiological etiology of AN.

In contrast, abnormal patterns of blood flow to the brain and brain activity persist after recovery. For instance, individuals who have recovered from AN often have hypoperfusion in the frontal, parietal, temporal and occipital areas of the brain [ 86 ]. In addition, overactivation of the frontal and anterior cingulate cortex (ACC) and insula following exposure to pictures of food or the taste of food is present both during active AN and after recovery [ 87 , 88 ]. Hyperactivity in these regions could be an endophenotype for AN and be related to more global difficulties with appetitive mechanisms.

The complex eating pathology inherent in AN may indicate atypical functioning in appetitive mechanisms. Despite the unique and stereotypic presentation of altered eating patterns in the eating disorder diagnoses, it is still unknown whether individuals with AN have disordered appetitive functioning. The neural and limbic circuits are more likely candidates for deregulating appetitive functioning in AN than peripheral signs (such as hormonal imbalances or abnormalities in the gastrointestinal tract), because these neural and limbic circuits also regulate reward processing and emotionality, which are known to be disordered in AN [ 89 ]. Individuals with AN display an almost phobic avoidance of high-fat foods, which persists after recovery. Individuals who have recovered from AN fail to connect hunger cues with positive ratings of food [ 88 ]. Particularly promising research has focused specifically on the anterior insula, which is positioned in the primary gustatory cortex [ 90 ]. While this is still debated, researchers posit that the anterior insula codes a representation of food and its hedonic value, and projects to other parts of the brain [ 91 , 92 ]. The anterior insula resides next to the orbito-frontal cortex, which interprets information from the anterior insula and is responsible for flexible decision-making with ever-changing stimuli [ 93 ]. Put another way, the anterior insula represents the food and its hedonic value, while the orbito-frontal cortex weighs those representation against hunger and other variables. Critically, the orbito-frontal cortex is very sensitive to changes in serotonin, which could account for the inflexibility in eating pathology in individuals with AN [ 94 ]. Even though research in this area is still in its infancy, the aforementioned processing abnormalities in the anterior insula and orbito-frontal cortex shed some light as to how “AN individuals fail to become appropriately hungry when starved, and thus are able to become emaciated” ([ 30 ], p. 45).

Though disturbances related to the gustatory modulation of the anterior insula certainly appear to be a key part of a biological risk factor in AN, the anterior insula influences many processes unrelated to gustatory mechanisms [ 30 ]. Disturbances in the anterior insula could be related to a more general deficit in interoceptive awareness [ 95 , 96 ]. Altered activity in the insula “supports the idea that they might suffer from a fundamentally and physiologically altered sense of self” ([ 97 ], p. 111). Some of the more mysterious symptoms of AN, such as a denial of signs of malnutrition and lack of motivation to change pathological eating behaviors, could be linked to abnormal patterns of activity in the insula [ 98 ].

6. Genetics

There is clear and compelling evidence that having a first-degree relative with AN significantly elevates one’s risk for developing AN; in fact, relatives of individuals with AN are 11.3 times more likely to develop AN [ 27 ]. There is likely some genetic contribution to the etiology of AN. Current heritability estimates range between 50 and 80% [ 99 , 100 ], though specific genetic mechanisms have been difficult to identify. A noteworthy paradox was pointed out regarding the high heritability of AN and the likelihood of reduced reproductive fitness from prolonged periods of malnutrition [ 101 ]. Thus, one can conclude that genes that contribute to the etiology of AN must be rare and of recent origin. In addition, high rates of diagnostic crossover between eating disorder categories (see [ 102 ]) and high rates of comorbidity with mood and anxiety disorders (see [ 103 ]) also complicate the genetic etiology of AN, since any genetic predispositions for AN should be non-specific and shared with these other conditions.

One method of identifying genes relevant to the pathophysiology of AN is the candidate gene approach. The candidate gene approach is defined as an examination of genes that could be involved in a particular disease or syndrome because the function of those genes is related to the sequelae of the illness [ 104 ]. The candidate gene approach could be likened to finding “a needle in the haystack” of 27,000 human genes. Thus, it is not surprising that candidate gene studies for AN are controversial and many fail to replicate genetic association.

Family-based linkage analyses, or the process of detecting the location of disease genes on the chromosome, have identified three chromosomal regions of interest for AN; one resides on chromosome 13 (specifically, 13q13.3) and is related to drive-for-thinness, another resides on chromosome 2 (2p11.2) and is related to obsessionality, and a third on chromosome 1 (specifically, 1q1.3) which is related to both obsessionality and drive-for-thinness [ 105 ].

Genes related to dopamine transfer (DAT1) and dopamine receptors (DRD2) have been examined among patients with AN. Individuals with AN show elevated expression of DAT1 and reduced expression of DRD2 [ 106 ]; while the implications of these expression are not fully understood, a genetic contribution to the etiology of AN related to dopamine expression is consistent with previously mentioned research on altered reward processing in AN. Other genetic research has also identified an interaction of three genes that clear serotonin and norepinephrine from the synapse; these genes (a serotonin transporter gene, a norepinephrine transporter gene, and a monoamine oxidase A gene) appear to contribute to the risk of restricting AN [ 41 ]. While the presence of each gene variant alone is associated with a somewhat increased risk of restricting AN, the combination of all three gene variants leads to a risk that is up to eight times greater than the risk associated with one gene variant alone.

Finally, there are epigenetic factors to consider. Perhaps the most important epigenetic mechanism to consider is the role of estradiol in triggering genetic risk for AN, which is discussed below. All told, the genetic and epigenetic contributions to AN remain largely unknown. Genetic studies are limited by previously mentioned methodological issues, such as the low prevalence of AN and the near impossibility of recruiting individuals with AN during the premorbid period for genetic research. However, progress in identifying genes or patterns of gene expression could lead to pharmacological advances that are direly needed for this population given the poor response to common psychotropics such as selective serotonin reuptake inhibitors, tricyclic antidepressants, and antipsychotics [ 17 , 18 ].

7. Pubertal hormones

The vast majority of individuals with AN are biologically female and begin experiencing symptoms of AN during the pubertal and pre-pubertal periods of development [ 1 ]. These findings suggest that gonadal hormones specific to females may play a role in the epigenesis of AN. It is possible that genetic factors may be more impactful for females than males with regards to drive for thinness and body dissatisfaction [ 107 ] as well as for concerns about body shape and weight [ 108 ]. In addition to gender differences in genetic factors, genetic risk for eating disorders appears to be moderated by age, as there is almost no genetic effect (5% or less on disordered eating among preadolescent female twins, but by late adolescence there is evidence of substantial genetic effects [ 109 ]. Upon closer examination, the genetic effect appears to be due to pubertal status and not age, as 11-year-old twins who had begun puberty showed a higher magnitude of genetic effects compared to same-age twins who had not begun puberty [ 110 ]. Pubertal hormones, such as estradiol, which steadily increases during puberty among females, may trigger the genetic risk for disordered eating, as high levels of estradiol are associated with magnitude of genetic effects in a manner independent of age and physical signs of puberty development, such as body hair or breast development [ 111 ].

In addition to triggering the genetic risk for AN, low estradiol levels are associated with a number of negative effects during the active phases of AN. Not surprisingly, malnourished individuals show a variety of hormonal imbalances, most of which return to baseline after recovery [ 42 ]. Pubertal hormones appear to follow this same pattern of alteration during active illness but return to baseline upon weight regain. In a typically developing adolescent, an increase in pubertal hormones aids in brain maturation, most notably in the limbic system [ 112 , 113 ]. These hormone levels are altered among individuals diagnosed with AN, who may experience amenorrhea due to low body weight and/or body fat [ 114 ]. When individuals achieve weight regain and recommence with menstruation, cognitive functioning improves, suggesting that increasing levels of estradiol during weight regain may assist with neural recovery [ 115 ].

8. Conclusions and future directions

The etiology of AN is multifaceted, with contributions from genetic factors, biological factors, family dynamics, personality characteristics, and sociocultural influences. The development of this disorder and its maintenance remain poorly understood despite a significant increase in rigorous scientific study into risk factors and shared vulnerabilities with other eating disorders and psychological disorders.

In recent years, the neurobiological etiology of AN has been examined through a wide variety of imaging studies, genetic studies, and hormonal/biological studies (see [ 97 ]). A number of key findings are summarized in this paper. Across these studies, it is clear that the brains of individuals with AN show evidence of altered reward processing and appetitive mechanisms, which are linked to a number of dopaminergic findings (perhaps, most importantly, how the brains of individuals with AN process cues of palatable foods as highly anxiogenic and aversive [ 50 , 51 ]. Serotonergic functioning has been long-thought to account for behavioral rigidity and trait obsessionality in AN [ 56 ], and recent genetic research has identified a number of potential serotonergic genetic candidates or interactions of genetic candidates that represent significant risk factors for AN [ 44 , 74 , 104 , 107 ]. Finally, altered noradrenergic functioning and aberrant activity in the insula represent a unique but comprehensive view of the global difficulties individuals with AN have with emotions, insight, and interoceptive awareness [ 31 , 71 ]. These findings, taken together, can illuminate future pathways for pharmacotherapies that will be more effective for individuals with AN. Other brain-based findings discussed in this paper, such as gray and white matter atrophy, are unlikely to represent true risk factors, because the vast majority improve with proper nutrition.

In conclusion, the neurobiological etiology of AN in-and-of-itself is complex and complicated by factors such as the low prevalence rate of AN [ 1 ], lack of prospective research [ 32 ], and the at-times catastrophic impact of malnutrition on the brain and body [ 38 ]. AN continues to be considered the most deadly psychological illness, and individuals RECAN may face a lifetime of physical and emotional challenges [ 1 ]. Given the ego-syntonic nature of this disorder and that current treatment outcomes are suboptimal for this population, a better understanding of the biological vulnerabilities of this illness and the development of new therapies are direly needed.

Conflict of interest

There are no conflicts of interest to report.

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Oxford University Press's Academic Insights for the Thinking World

Six books to help us understand eating disorders

If Your Adolescent Has An Eating Disorder, Second Edition

• By Abigail Luke
• July 16 th 2020

Some  70 million people worldwide  have an eating disorder and, with the prevalence of disordered eating on the rise,  it’s clear that this presents a significant public health issue. Despite this, many myths and misconceptions abound that are significant barriers to both treatment and public understanding of eating disorders. Anyone can develop an eating disorder, regardless of age, gender, or cultural background.

We’ve put together a list of books that provide practical information to dispel misconceptions, as well as guidance for people affected by eating disorders and their loved ones.

2.  Eating Disorders: What Everyone Needs to Know   by B. Timothy Walsh, Evelyn Attia, and Deborah R. Glasofer Practical yet authoritative, this book defines eating disorders, explains what we know about them based on the latest science, and describes how treatment works. The book dispels common myths about eating disorders, such as the notion that they occur only amongst the affluent, that they affect only girls and women, or that they simply result from environmental factors such as the fashion industry and society’s obsession with thinness. This book is essential reading for those seeking authoritative and current information about these often-misunderstood illnesses.

4.  Exposure Therapy for Eating Disorders  by Carolyn Black Becker, Nicholas R. Farrell, and Glenn Waller This book is designed to augment existing eating disorder treatment manuals by providing clinicians with practical advice for maximizing the effectiveness of exposure, regardless of clinical background or evidence-based treatment used. Suitable for use with a range of diagnoses, this easy-to-use guide describes the most up to date empirical research on exposure for eating disorders. The book also provides strategies for overcoming obstacles, including institutional resistance to implementation of exposure therapy.

6.  Eating Disorders: The Facts by Suzanne Abraham Sympathetically and clearly written, this guide considers why eating disorders occur, and then looks at each in turn, describing the eating behaviours, diagnosis, and treatments available. Case histories and patient perspectives provide insights into the mind of the eating disorder sufferer, making it easier for patients and their families to relate to the topics discussed. The book   provides an authoritative resource on eating disorders that will prove valuable for sufferers and their families.

These titles highlight some of the most pressing issues in the field of eating disorder research. Greater awareness among stakeholders – including healthcare workers, researchers, policymakers, and the general public – can address ongoing challenges and inform future directions.

Featured Image Credit:  Image  by jannoon028 via Freepik

Abigail Luke is a marketing executive at Oxford University Press

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2020 Breakthrough Research in Anorexia Nervosa: Drs. Cynthia Bulik and Walter Kaye

Anorexia Nervosa (AN) is a puzzle for many reasons. What is it, and what can we do to treat it are commonly asked questions by students and health professionals alike? While we do not have a blood or other test to make a diagnosis, the combination of signs and symptoms are classic and are virtually identical to those seen centuries ago.

AN was the same in 1689 as it was in 1873 as it was in 1983 when Karen Carpenter died of this disease [1]. It is the same today. AN appears to be a biopsychosocial determined disease with important genetic and neurobiological roots.

Anorexia Nervosa occurred as part of religious fasting dating from the Hellenistic era. Mary, Queen of Scots, among others, appears to have suffered from AN. The English physician Richard Morton described AN in 1689, but the medical profession did not consider it seriously until the late 19th century.

In 1873, Queen Victoria’s physicians, Sir William Gull, published the classic, seminal paper which established the term anorexia nervosa. He described cases and treatments. In the same year, French physician Ernest-Charles Lasègue similarly published details of several cases in a paper entitled De l’Anorexie Hystérique.

In an addendum to his Anorexia Nervosa paper, Sir William Gull provides the following comment on Lasègue’s work: “It is understandable that Dr. Lasègue and I have the same sickness in mind, though the forms of our illustrations are different.

Dr. Lasègue does not refer to my address at Oxford, and it is most likely he knew nothing of it. There is, therefore, the more value in his paper, as our observations have been made independently. We have both chosen the same expression to characterize the malady.

In the address at Oxford, I used the term Apepsia hysterica, but before seeing Dr. Lasègue’s paper, it had equally occurred to me that Anorexia would be more correct ” [2]. Still, awareness of AN limited to MDs until the latter part of the 20th century, when German-American psychoanalyst Hilde Bruch published her famous work “The Golden Cage: the Enigma of Anorexia Nervosa” in 1978.

Anorexia Nervosa

The National Eating Disorders Association (NEDA) estimates that between 0.3 and 0.4 percent of all young women and 0.1 percent of young men suffer from AN on this or any day. They estimate that approximately 1 percent of women and 0.3 percent of men reported Anorexia during their lifetimes.

AN is a major cause of death among adolescents and young adults. Young people between the ages of 15 and 24 with AN are estimated to be at ten times greater risk of dying compared to same-aged peers. Although the disorder also affects males, the overwhelming predominance of women is undeniable.

Bulik has led many of the recent efforts. Bulik and her collaborators have a long history of reporting new data, which is really significant progress in AN genetic research. Most recently, with her collaborators, in Nature Genetics [3].

Quick Summary-Review of AN

Mitchell & Peterson’s 2020 review in the New England Journal of Medicine [4] reminds us that AN is often fatal. About 10% of those patients with Anorexia Nervosa will die of the disease. Medical complications, suicide, and co-occurring substance use disorders (SUD) are all too commonly reported.

• Anorexia nervosa is a severe, sometimes fatal, psychiatric disorder characterized by starvation and malnutrition
• Weight preoccupation, overvaluation, and dissatisfaction are related to eating disorders, but no one body image construct can capture clinical risk in eating disorders.
• Preoccupation is the best-studied, most consistent concurrent and longitudinal predictor
• Coexisting psychiatric conditions often accompany Anorexia Nervosa
• AN is a disease that is usually progressive, difficult to treat with episodes where there is no response to treatment, frequent medical complications, and a substantial risk of death.
• Anorexia nervosa has two subtypes, but can progress from one sub-type to another: binge eating, purging, or both, and food restricting only
• AN patients are often hospitalized, which can be life-saving as they have severe starvation, dehydration hypotension, electrolyte abnormalities, arrhythmias or severe bradycardia, suicide risk. Just having a body-mass index (the weight in kilograms divided by the square of the height in meters) of 15 or less is a significant concern.
• Several psychotherapeutic approaches are commonly used in treatment by psychologists and psychiatrists
• Psychotropic medications are generally ineffective in promoting weight gain, reducing depressive symptoms, or preventing relapse in patients with anorexia nervosa.
• While current treatment is psychological and not personalized or informed by genes or improved by medications, about half of adolescents recover, and another 30% significantly improve

Scientific Progress: 2020

New insights will eventually lead to new treatments . Medications, psychedelic medicine, and deep brain stimulation may offer hope and help us to understand which diseases are the most like Anorexia Nervosa, major depression, OCD, or SUDs.

Scientific progress seen in the rest of psychiatry is finding its way to Anorexia Nervosa. The more researchers look into this disease, the more it appears to have important genetic and neurobiological causes. The circuitry of the brain’s reward system behaves differently in unaffected volunteers than in people with Anorexia and those who have recovered.

We have studied eating, eating sugar, and compared food and sugar rewards to those naturally occurring species survival reinforcement [5]. Hunger drives a search for food, eating, and makes food more rewarding. This is a well-known fact because starvation activates brain circuits that motivate eating.

One group of women had been diagnosed with AN, but were in remission (RAN); the other group did not have AN. The RAN group showed reduced neural activation to taste stimulation in the brain’s anterior insula and reduced connectivity between the right anterior and mid-dorsal insula and ventral caudal putamen.

This circuitry involves connected regions that are important for recognizing the feeling of hunger. This circuit typically would drive us to want to eat when we are starving or deprived of food. Most people report that hunger increases the reward and pleasure of food, and thus drives the motivation to eat.

Individuals with AN, however, tend to have a disconnect in this process. Anorexia Nervosa patients are obsessed with food, yet do not eat. Failure to launch this food reward circuit in people with AN may be a key to AN restrictive eating and severe weight loss in persons.

Anorexia Nervosa may be a disease where perceptions of hunger persist in a vacuum disconnected the motivation to eat. Patients with AN describe increased discomfort, anxiety, and panic when they eat, even when they are starving. Profound anxiety may contribute to starvation because it impairs the ability to start eating.

Bulik and others published in Nature Genetics the most extensive genetics study on the disease, analyzing the genomes of nearly 17,000 people with Anorexia and more than 55,000 people without. Eight risk loci for anorexia nervosa were identified that were predictive of other psychiatric disorders, a low BMI, and metabolic derangement.

This study showed that there was also a link to the ability to metabolize fats and sugars [7]. Who knows what this means other than the metabolic problems in AN could be produced by a biological predisposition.

Researchers identified other patterns of genetic associations similar to those found in other psychiatric illnesses, including OCD and depression. We had suspected that the brain’s reinforcement systems might reinforce disordered eating very early on and thought similarities to substance use disorders might offer a clue and endogenous opioid-dopamine targets.

There may be genetic and risk profile similarities between Anorexia and Bulimia Nervosa [8], which relate to genetics, reward deficiency, and early bad learning. Early starvation or dieting might be a trigger like teen cigarette smoking, early-onset binge drinking, or illicit drug use triggers .

Concluding Remarks

Psychedelic medicine [9] trials are also underway for mescaline, psilocybin, nitrous oxide, and others for depression and PTSD. Treatments for SUDs have changed dramatically over this time as well.

Reward deficiency syndrome [10] has been proposed to explain some of the patients with SUDs and brain circuits involved in naturally occurring pleasure and SUD related hijacking. Animal models for SUD have been quite good at predicting treatments, and many are currently in use. TMS [11], DBS [12], and even Vaccines based on these models may be the next for SUDs.

Many of these novel treatment approaches may be helpful in Anorexia Nervosa, Bulimia Nervosa , and other eating disorders.

1. https://www.npr.org/2013/02/04/171080334/remembering-karen-carpenter-30-years-later

2. https://en.wikipedia.org/wiki/History_of_anorexia_nervosa

3. Watson, H.J., Yilmaz, Z., Thornton, L.M. et al. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa. Nat Genet 51, 1207–1214 (2019). https://doi.org/10.1038/s41588-019-0439-2

4. Mitchell JE, Peterson CB. Anorexia Nervosa.N Engl J Med. 2020 Apr 2;382(14):1343-1351. doi: 10.1056/NEJMcp1803175

5. Murray S, Tulloch A, Gold MS, Avena NM Hormonal and neural mechanisms of food reward, eating behaviour and obesity. Nat Rev Endocrinol. 2014 Sep;10(9):540-52. doi: 10.1038/nrendo.2014.91. Epub 2014 Jun 24.

6. Kaye WH, Wierenga CE, Bischoff-Grethe A, Berner LA, Ely AV, Bailer UF, Paulus MP, Fudge JL. Neural Insensitivity to the Effects of Hunger in Women Remitted From Anorexia Nervosa. Am J Psychiatry. 2020 Mar 12

7. Watson, H.J., Yilmaz, Z., Thornton, L.M. et al. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa. Nat Genet 51, 1207–1214 (2019). https://doi.org/10.1038/s41588-019-0439-2

8. Yao, S., Larsson, H., Norring, C., Birgegård, A., Lichtenstein, P., DʼOnofrio, B., . . . Kuja-Halkola, R. (2019). Genetic and environmental contributions to diagnostic fluctuation in anorexia nervosa and bulimia nervosa. Psychological Medicine, 1-8. doi:10.1017/S0033291719002976

9. https://www.jns-journal.com/article/S0022-510X(20)30051-4/fulltext Chi T, Gold JA. A review of emerging therapeutic potential of psychedelic drugs in the treatment of psychiatric illnesses. J Neurol Sci. 2020 Apr 15;411:116715. doi: 10.1016/j.jns.2020

10. Blum K, Baron D, McLaughlin T, Gold MS.Molecular neurological correlates of endorphinergic/dopaminergic mechanisms in reward circuitry linked to endorphinergic deficiency syndrome (EDS). J Neurol Sci. 2020 Apr 15;411:116733. doi: 10.1016/j.jns.2020.116733. Epub 2020 Feb 14

11. https://niaaa.scienceblog.com/67/rehabilitating-the-addicted-brain-with-transcranial-magnetic-stimulation/

12. https://www.sciencealert.com/surgeon-attempting-deep-brain-stimulation-as-last-resort-for-opioid-addict

About the Author:

Dr. Gold was the first Faculty from the College of Medicine to be selected as a University-wide Distinguished Alumni Professor and served as the 17th University of Florida’s Distinguished Alumni Professor. Learn more about Mark S. Gold, MD

The opinions and views of our guest contributors are shared to provide a broad perspective of eating disorders. These are not necessarily the views of Eating Disorder Hope, but an effort to offer a discussion of various issues by different concerned individuals.

We at Eating Disorder Hope understand that eating disorders result from a combination of environmental and genetic factors. If you or a loved one are suffering from an eating disorder, please know that there is hope for you, and seek immediate professional help .

Published on May 7, 2020. Reviewed & Approved on May 7, 2020, by Jacquelyn Ekern MS, LPC

Published on EatingDisorderHope.com

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Answer some general questions about how you feel about food, your current eating habits, how you feel after you eat, and other indicators of an eating disorder.

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Not All Black Girls Know How to Eat

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50 Must-Read Books About Eating Disorders

Emily Martin

Emily has a PhD in English from the University of Southern Mississippi, MS, and she has an MFA in Creative Writing from GCSU in Milledgeville, GA, home of Flannery O’Connor. She spends her free time reading, watching horror movies and musicals, cuddling cats, Instagramming pictures of cats, and blogging/podcasting about books with the ladies over at #BookSquadGoals (www.booksquadgoals.com). She can be reached at [email protected].

View All posts by Emily Martin

According to the National Eating Disorder Association , eating disorders affect over 70 million people worldwide. Those numbers seem to be rising as well, due to the increased impact media has on our everyday lives. Thankfully, there are plenty of books about eating disorders out there that document the struggles of this issue in ways that are both enlightening and empowering. Here some of the best options for books about eating disorders out there, across several genres.

**Please note that the following titles might be triggering for those currently suffering or recovering from eating disorders.**

Memoirs About Eating Disorders

Not all black girls know how to eat   by stephanie covington armstrong.

Stephanie Covington Armstrong does not fit the stereotype of a woman with an eating disorder. She grew up poor and hungry in the inner city. Foster care, sexual abuse, and overwhelming insecurity defined her early years. But the biggest difference is her race: Stephanie is black.

In this moving first-person narrative, Armstrong describes her struggle as a black woman with a disorder consistently portrayed as a white woman’s problem. Trying to escape her self-hatred and her food obsession by never slowing down, Stephanie becomes trapped in a downward spiral. Finally, she can no longer deny that she will die if she doesn’t get help, overcome her shame, and conquer her addiction to using food as a weapon against herself.

unbearable lightness : A story of loss and gain by portia de rossi

Portia de Rossi weighed only 82 pounds when she collapsed on the set of the Hollywood film in which she was playing her first leading role. This should have been the culmination of all her years of hard work—first as a child model in Australia, then as a cast member of one of the hottest shows on American television. On the outside she was thin and blond, glamorous and successful. On the inside, she was literally dying.

In this remarkable and beautifully written work, Portia shines a bright light on a dark subject. A crucial book for all those who might sometimes feel at war with themselves or their bodies, Unbearable Lightness is a story that inspires hope and nourishes the spirit.

brave girl eating: A Family’s Struggle with anorexia by harriet brown

In Brave Girl Eating, the chronicle of a family’s struggle with anorexia nervosa, journalist, professor, and author Harriet Brown recounts in mesmerizing and horrifying detail her daughter Kitty’s journey from near-starvation to renewed health. Brave Girl Eating is an intimate, shocking, compelling, and ultimately uplifting look at the ravages of a mental illness that affects more than 18 million Americans.

loud in the house of myself: memoir of a strange girl   by stacy pershall

Stacy Pershall grew up as an overly intelligent, depressed, deeply strange girl in Prairie Grove, Arkansas, population 1,000. From her days as a thirteen-year-old Jesus freak through her eventual diagnosis of bipolar disorder and borderline personality disorder, this spirited memoir chronicles Pershall’s journey through hell and her struggle with the mental health care system.

hunger: A Memoir of (my) body   by roxane gay

New York Times  bestselling author Roxane Gay has written with intimacy and sensitivity about food and bodies, using her own emotional and psychological struggles as a means of exploring our shared anxieties over pleasure, consumption, appearance, and health. As a woman who describes her own body as “wildly undisciplined,” Roxane understands the tension between desire and denial, between self-comfort and self-care. In  Hunger,  she casts an insightful and critical eye on her childhood, teens, and twenties—including the devastating act of violence that acted as a turning point in her young life—and brings readers into the present and the realities, pains, and joys of her daily life.

With the bracing candor, vulnerability, and authority that have made her one of the most admired voices of her generation, Roxane explores what it means to be overweight in a time when the bigger you are, the less you are seen.  Hunger  is a deeply personal memoir from one of our finest writers, and tells a story that hasn’t yet been told but needs to be.

please eat…: A mother’s struggle to free her teenage son From anorexia   by Bev Mattocks

Bright, popular and a star on the rugby pitch, 15-year-old Ben had everything he could want. But then food-loving Ben began to systematically starve himself. At the same time, his urge to exercise became extreme. In a matter of months Ben lost one quarter of his bodyweight as he plunged into anorexia nervosa, an illness that threatened to destroy him.

Please eat…:A mother’s struggle to free her teenage son from anorexia  is his mother’s heart-breaking yet inspirational account of how she watched helplessly as her son transformed into someone she didn’t recognise, physically and mentally. It also describes how, with the help of his parents and therapist, and through his own determination, Ben slowly began to recover and re-build his life.

the body tourist by dana lise shavin

In this moving and funny memoir that spans the six years following the author’s purported recovery from anorexia, Dana Lise Shavin offers a candid and ultimately optimistic window into the mindset and machinations of a mental illness whose tentacles reached deep into her life, long after she was considered “cured.”

While many writers have written candidly and eloquently about their struggles with depression, addictions, and eating disorders, those stories usually conclude once there is progress toward recovery. Beyond recovery—whether from addiction, illness, the death of a loved one, or divorce—there is another story, one that is about how we re-join the world, and, in the living years that follow the darkness, pursue a life that is creative, engaged, and deeply felt in one’s body.

how to disappear completely by kelly osgood

She devoured their memoirs and magazine articles, committing the most salacious details of their cautionary tales to memory—how little they ate, their lowest weights, and their merciless exercise regimes—to learn what it would take to be the very best anorectic. When she was hospitalized for anorexia at fifteen, she found herself in an existential wormhole: how can one suffer from something one has actively sought out? Through her own decade-long battle with anorexia, which included three lengthy hospitalizations, Osgood harrowingly describes the haunting and competitive world of inpatient facilities populated with other adolescents, some as young as ten years old.

With attuned storytelling and unflinching introspection, Kelsey Osgood unpacks the modern myths of anorexia, examining the cult-like underbelly of eating disorders in the young, as she chronicles her own rehabilitation.  How to Disappear Completely  is a brave, candid and emotionally wrenching memoir that explores the physical, internal, and social ramifications of eating disorders and subverts many of the popularly held notions of the illness and, most hopefully, the path to recovery.

lesbian crushes and bulimia: A diary on how i acquired my eating disorder by natasha holme

In 1989, nineteen-year-old Natasha is obsessively in love with her former teacher, Miss Williams. The tattoo she flashes around says so. Natasha meets Alex, a girl her own age, who questions her about the tattoo. An awkward romance is born. In this real-life teenage diary, Natasha records her panic at a looming LESBIAN relationship. To lose some excess fat, she starves herself of food…whilst working in a chip shop. And just to make sure she’s gay, Natasha drags five boys into bed in the space of a week, a sin for which the sexuality police threaten to kick her out of the university Lesbian and Gay Society. In this coming out story and love story, Natasha struggles with clumsy attempts at heterosexuality, the sickening effects of weight loss techniques, disapproving shaven-headed lesbians, and sexual harassment in the chip shop.

it was me all along by andie mitchell

All her life, Andie Mitchell had eaten lustily and mindlessly. Food was her babysitter, her best friend, her confidant, and it provided a refuge from her fractured family. But when she stepped on the scale on her twentieth birthday and it registered a shocking 268 pounds, she knew she had to change the way she thought about food and herself; that her life was at stake.

It Was Me All Along  takes Andie from working class Boston to the romantic streets of Rome, from morbidly obese to half her size, from seeking comfort in anything that came cream-filled and two-to-a-pack to finding balance in exquisite (but modest) bowls of handmade pasta. This story is about much more than a woman who loves food and abhors her body. It is about someone who made changes when her situation seemed too far gone and how she discovered balance in an off-kilter world. More than anything, though, it is the story of her finding beauty in acceptance and learning to love all parts of herself.

this mean disease: growing up in the shadow of my mother’s anorexia nervosa   by daniel becker

In the first book written by the child of someone who died from an eating disorder, Daniel Becker shows us the heartbreaking details of his mother’s anorexia nervosa—her unrelenting obsession with food and her inability to nourish herself. His earliest memory of her is watching as she packs her suitcase for the first of numerous hospitalizations. From the observations of that confused child to his realization of helplessness as an adult, Daniel conveys the inner world of an anorectic and her family. He provides an intimate portrayal of how he, his father and his two brothers each struggled to balance their loyalty to Mom against the increasing awareness that only by separating from her could they ensure their own survival. In the end, Daniel must come to terms with his mother’s slow demise and begin to lead a life out from under the shadow of her illness.

wasted: a memoir of anorexia and bulimia by marya hornbacher

Why would a talented young woman enter into a torrid affair with hunger, drugs, sex, and death? Through five lengthy hospital stays, endless therapy, and the loss of family, friends, jobs, and all sense of what it means to be “normal,” Marya Hornbacher lovingly embraced her anorexia and bulimia—until a particularly horrifying bout with the disease in college put the romance of wasting away to rest forever. A vivid, honest, and emotionally wrenching memoir,  Wasted  is the story of one woman’s travels to reality’s darker side—and her decision to find her way back on her own terms.

how to murder your life by Cat marnell

At twenty-six, Cat Marnell was an associate beauty editor at  Lucky , one of the top fashion magazines in America—and that’s all most people knew about her. But she hid a secret life. She was a prescription drug addict. She was also a “doctor shopper” who manipulated Upper East Side psychiatrists for pills, pills, and more pills; a lonely bulimic who spent hundreds of dollars a week on binge foods; a promiscuous party girl who danced barefoot on banquets; a weepy and hallucination-prone insomniac who would take anything— anything —to sleep.

This is a tale of self-loathing, self-sabotage, and yes, self-tanner. It begins at a posh New England prep school—and with a prescription for Attention Deficit Disorder medication Ritalin. It continues to New York, where we follow Marnell’s amphetamine-fueled rise from intern to editor through the beauty departments of  NYLON ,  Teen Vogue ,  Glamour , and  Lucky . We see her fight between ambition and addiction and how, inevitably, her disease threatens everything she worked so hard to achieve.

Teen Books About Eating DIsorders

Just listen by sarah dessen.

Last year, Annabel was “the girl who has everything”—at least that’s the part she played in the television commercial for Kopf’s Department Store.

This year, she’s the girl who has nothing: no best friend because mean-but-exciting Sophie dropped her, no peace at home since her older sister became anorexic, and no one to sit with at lunch. Until she meets Owen Armstrong.

Tall, dark, and music-obsessed, Owen is a reformed bad boy with a commitment to truth-telling. With Owen’s help, maybe Annabel can face what happened the night she and Sophie stopped being friends.

wintergirls by laurie halse anderson

Lia and Cassie are best friends, wintergirls frozen in matchstick bodies, competitors in a deadly contest to see who can be the skinniest. But what comes after size zero and size double-zero? When Cassie succumbs to the demons within, Lia feels she is being haunted by her friend’s restless spirit.

Tiny pretty things   by sona charaipotra and dhonielle clayton

Gigi, Bette, and June, three top students at an exclusive Manhattan ballet school, have seen their fair share of drama. Free-spirited new girl Gigi just wants to dance—but the very act might kill her. Privileged New Yorker Bette’s desire to escape the shadow of her ballet-star sister brings out a dangerous edge in her. And perfectionist June needs to land a lead role this year or her controlling mother will put an end to her dancing dreams forever. When every dancer is both friend and foe, the girls will sacrifice, manipulate, and backstab to be the best of the best.

massive by julia Bell

“I’m fat,” I hear myself saying. I look in the mirror. My face has gone hot and red; I feel like I’m going to explode. “I’m fat.” It sizzles under my skin, puffing me up, pushing me out, making me massive.

Weight has always been a big issue in Carmen’s life. How could it not? Her mom is obsessed with the idea that thin equals beautiful, thin equals successful, thin equals the way to get what you want. Carmen knows that as far as her mom is concerned, there is only one option: be thin.

When her mother sweeps her off to live in the city, Carmen finds that her old world is disappearing. As her life spirals out of control Carmen begins to take charge of the only thing she can—what she eats. If she were thin, very thin, could it all be different?

monkey taming by judith fathallah

When Jessica was thirteen years old, she met the Monkey. The Monkey lived inside her: a driving, fiery voice telling her that thinness was the only way. The only way to be safe, to be good, to be acceptable and above all, to escape from the cold, looming threat of approaching adulthood. Jessica listened to the Monkey, and it consumed her.

This is the illuminating story of a teenage girl’s wanderings in darkness: the spiral down into madness, the terrible realities of an adolescent psychiatric unit, and the stark choice that she must either tame her monster—or die.

fat chance by lesléA newman

A diary records a year in the life of Judi Leibowitz as she dreams of becoming the thinnest girl in the eighth grade and struggles to control her unending battle with calories, food, pounds, and bulimia.

paperweight by meg haston

Seventeen-year-old Stevie is trapped. In her life. In her body. And now in an eating disorder treatment center on the dusty outskirts of the New Mexico desert.

Life in the center is regimented and intrusive, a nightmare come true. Nurses and therapists watch Stevie at meal time, accompany her to the bathroom, and challenge her to eat the foods she’s worked so hard to avoid.

Her dad has signed her up for sixty days of treatment. But what no one knows is that Stevie doesn’t plan to stay that long. There are only twenty-seven days until the anniversary of her brother Josh’s death—the death  she  caused. And if Stevie gets her way, there are only twenty-seven days until she, too, will end her life.

Paperweight  follows seventeen-year-old Stevie’s journey as she struggles not only with a life-threatening eating disorder, but with the question of whether she can ever find absolution for the mistakes of her past…and whether she truly deserves to.

the hanged man by francesca lia block

After the death of her father, Laurel is haunted by a legacy of family secrets, hidden shame, and shattered glass. Immersing herself in the heady rhythms of a city that is like something wild, caged, and pacing, Laurel tries to lose herself. But when she runs away from the past, she discovers a passion so powerful, it brings her roundabout and face-to-face with the demons she wants to avoid.

nothing by robin friedman

“Sometimes trees can look healthy on the outside, but actually be dying inside. These trees fall unexpectedly during a storm.” For high school senior Parker Rabinowitz, anything less than success is a failure. A dropped extracurricular, a C on a calc quiz, a non-Jewish shiksa girlfriendone misstep, and his meticulously constructed life splinters and collapses. The countdown to HYP (Harvard, Yale, Princeton) has begun, and he will stay focused. That’s why he has to keep it a secret. The pocketful of breath mints. The weird smell in the bathroom. He can’t tell his achievement-obsessed father. He can’t tell his hired college consultant. And he certainly can’t tell Julianne, the “vision of hotness” he so desperately wants to love. Only Parker’s little sister Danielle seems to notice that he’s withering away.

falling into place by amy zhang

On the day Liz Emerson tries to die, they had reviewed Newton’s laws of motion in physics class. Then, after school, she put them into practice by running her Mercedes off the road. Why did Liz Emerson decide that the world would be better off without her? Why did she give up? The nonlinear novel pieces together the short and devastating life of Meridian High’s most popular junior girl. Mass, acceleration, momentum, force—Liz didn’t understand it in physics, and even as her Mercedes hurtles toward the tree, she doesn’t understand it now. How do we impact one another? How do our actions reverberate? What does it mean to be a friend? To love someone? To be a daughter? Or a mother? Is life truly more than cause and effect? Amy Zhang’s haunting and universal story will appeal to fans of Lauren Oliver, Gayle Forman, and Jay Asher.

believarexic by Jj johnson

Jennifer can’t go on like this—binging, purging, starving, and all while trying to appear like she’s got it all together. But when she finally confesses her secret to her parents and is hospitalized at the Samuel Tuke Center, her journey is only beginning.

As Jennifer progresses through her treatment, she learns to recognize her relationship with food, and friends, and family—and how each is healthy or unhealthy. She has to learn to trust herself and her own instincts, but that’s easier than it sounds. She has to believe—after many years of being a believarexic.

Adult Fiction

She’s come undone by wally lamb.

Meet Dolores Price. She’s 13, wise-mouthed but wounded, having bid her childhood goodbye. Stranded in front of her bedroom TV, she spends the next few years nourishing herself with the Mallomars, potato chips, and Pepsi her anxious mother supplies. When she finally orbits into young womanhood at 257 pounds, Dolores is no stronger and life is no kinder. But this time she’s determined to rise to the occasion and give herself one more chance before she  really  goes under.

binary star by sarah gerard

With luminous, lyrical prose, Binary Star is an impassioned account of a young woman struggling with anorexia and her long-distance, alcoholic boyfriend. On a road trip circumnavigating the United States, they stumble into a book on veganarchism, and believe they’ve found a direction.

Binary Star is an intense, fast-moving saga of two young lovers and the culture that keeps them sick (or at least inundated with quick-fix solutions); a society that sells diet pills, sleeping pills, magazines that profile celebrities who lose weight or too much weight or put on weight, and books that pimp diet secrets or recipes for success.

behind closed doors by b.a. Paris

Everyone knows a couple like Jack and Grace. He has looks and wealth; she has charm and elegance. He’s a dedicated attorney who has never lost a case; she is a flawless homemaker, a masterful gardener and cook, and dotes on her disabled younger sister. Though they are still newlyweds, they seem to have it all. You might not want to like them, but you do. You’re hopelessly charmed by the ease and comfort of their home, by the graciousness of the dinner parties they throw. You’d like to get to know Grace better.

But it’s difficult, because you realize Jack and Grace are inseparable.

Some might call this true love. Others might wonder why Grace never answers the phone. Or why she can never meet for coffee, even though she doesn’t work. How she can cook such elaborate meals but remain so slim. Or why she never seems to take anything with her when she leaves the house, not even a pen. Or why there are such high-security metal shutters on all the downstairs windows.

Some might wonder what’s really going on once the dinner party is over, and the front door has closed.

restricted: A novel of half Truths by jennifer Kinsel

Restricted  takes readers into the mind of a nineteen-year-old girl named Erin. Brought on by the obsession over weight and calories, and fueled by low self-esteem, she falls victim to an eating disorder. The world she enters is a world where thoughts are overrun by fears, lies are no longer fiction, and reality is miles away. The healthy nineteen year old that used to be is replaced by a weaker girl unable to keep up with her peers. Erin’s distorted thinking and actions eventually take a toll on her body and mind. In order to get better, change is the only option. The journey told starts during the height of the sickness and follows Erin through the many challenges and lessons of treatment. In order to start her process in recovery, she must face her greatest fear: herself. Based on the author’s own experiences, Erin’s story is not unique. There are millions around the world who are living her story, still struggling to find their way.

handle with care by jodi picoult

Every expectant parent will tell you that they don’t want a perfect baby, just a healthy one. Charlotte and Sean O’Keefe would have asked for a healthy baby, too, if they’d been given the choice. Instead, their lives are made up of sleepless nights, mounting bills, the pitying stares of “luckier” parents, and maybe worst of all, the what-ifs. What if their child had been born healthy? But it’s all worth it because Willow is, funny as it seems, perfect. She’s smart as a whip, on her way to being as pretty as her mother, kind, brave, and for a five-year-old an unexpectedly deep source of wisdom. Willow is Willow, in sickness and in health.

Everything changes, though, after a series of events forces Charlotte and her husband to confront the most serious what-ifs of all. What if Charlotte had known earlier of Willow’s illness? What if things could have been different? What if their beloved Willow had never been born? To do Willow justice, Charlotte must ask herself these questions and one more. What constitutes a valuable life?

the passion of alice by stephanie grant

After an episode of heart failure, Alice arrives in the eating disorder clinic of Seaview Hospital, where she detachedly watches a circus unfold…starring her perfectionist mother, Syd (“she’d been a synchronized swimmer in college”), her counselors (“the therapists are like tuning forks for epiphanies”), and the resident anorexics, bulimics, and compulsive eaters. But it is newcomer Maeve Sullivan, at once raucous and tender, with her fleshy body and hedonistic appetites, who turns Alice’s adventure beyond her own distorted looking glass into a new perception of herself—and who wakens an attraction that touches Alice’s soul and changes her life forever.

anthologies

Body outlaws: rewriting the rules of beauty and body image ,  edited by ophira edut.

Pick up a magazine, turn on the TV, and you’ll find few women who haven’t been fried, dyed, plucked, or tucked. In short, you’ll see no body outlaws. The writers in this groundbreaking anthology reveal a world where bodies come in all their many-splendored shapes, sizes, colors, and textures. In doing so, they expand the national dialogue on body image to include race, ethnicity, sexuality, and power—issues that, while often overlooked, are intimately linked to how women feel about their bodies. Body Outlaws offers stories by those who have chosen to ignore, subvert, or redefine the dominant beauty standard in order to feel at home in their bodies.

feed me! Writers dish about food, eating, weight, and body image ,  edited by harriet brown

In our appearance-obsessed society, eating is about much more than hunger and sustenance. Food inspires pleasure and anxiety, shame and obsession. We are constantly judged on how we look, so we’ve come to judge ourselves (and others) on what and how we eat. Exploring the bonds between appetite and remorse, hunger and longing, satisfaction and desire, this anthology is for every woman who’s ever felt guilty about eating dessert, or gushed over a friend’s weight loss, or wished she had a different body.

going hungry: writers on desire, self-denial, and overcoming anorexia ,  edited by kate taylor

Here, collected for the first time, 19 writers describe their eating disorders from the distance of recovery, exposing as never before the anorexic’s self-enclosed world. Taking up issues including depression, genetics, sexuality, sports, religion, fashion and family, these essays examine the role anorexia plays in a young person’s search for direction. Powerful and immensely informative, this collection makes accessible the mindset of a disease that has long been misunderstood.

things i’ll never say , edited by anne angel

A baby no one knows about. A dangerous hidden identity. Off-limits hookups. A parent whose problems your friends won’t understand. Everyone keeps secrets—from themselves, from their families, from their friends—and secrets have a habit of shaping the lives around them. Acclaimed author Ann Angel brings together some of today’s most gifted YA authors to explore, in a variety of genres, the nature of secrets: Do they make you stronger or weaker? Do they alter your world when revealed? Do they divide your life into what you’ll tell and what you won’t? The one thing these diverse stories share is a glimpse into the secret self we all keep hidden.

non-fiction/self-help Books About Eating Disorders

Goodbye ed, hello me   by jenni schaefer.

Jenni Schaefer and Ed (eating disorder) are no longer on speaking terms, not even in her most difficult moments. In her bestseller,  Life Without Ed,  Jenni learned to treat her eating disorder as a relationship, not a condition-enabling her to break up with Ed once and for all. In  Goodbye Ed, Hello Me  Jenni shows you that being fully recovered is not just about breaking free from destructive behaviors with food and having a healthy relationship with your body; it also means finding joy and peace in your life.

healing your hungry heart by joanna poppink

10 million people in the U.S., including 1 in 5 women, suffer from eating disorders. While this issue has long been associated with teenage girls, doctors are now reporting that a growing number of women are also developing these disorders later in life or have hidden these problems for years. For women in their thirties, forties, fifties, and beyond, issues of loss from divorce, death, and empty nest syndrome as well as marriage and career pressures can trigger an eating disorder.

Psychotherapist Joanna Poppink offers a comprehensive and effective recovery program for women with eating disorders, based on her thirty-year professional practice treating adults with anorexia, bulimia, and binge eating. She shares her personal struggles with bulimia, along with stories from a wide-range of clients she has counseled. Poppink primarily addresses women who have been suffering with eating disorders for years while they manage their careers, marriages, and families.

the eating disorder sourcebook by carolyn costin

Anorexia, bulimia, binge eating, exercise addictions…these disorders can be devastating, but they are in no way unbeatable. Therapist Carolyn Costin, herself recovered from anorexia, brings three decades of experience and the newest research in the field together, providing readers with the latest treatments, from medication and behavioral therapy to alternative remedies.

does every woman have an eating disorder?   by stacey m. Rosenfeld

Does every woman have an eating disorder? It’s a bold question but one that must be asked. Why is it that today’s women—successful students, career women, wives, and mothers—are struggling more than ever with food and weight? Even those who don’t suffer from a clinical eating disorder seem to have some sort of issue around food and weight.

We live in a culture of culinary abundance but are taught to do whatever it takes to shrink our flesh. From an early age, women are bombarded with messages regarding what size and shape they should be, a campaign that takes a toll on their relationship with food, their self-esteem, and their health.

It’s hard to go a day without seeing an advertisement for a new diet product, overhearing a conversation about weight between colleagues or a plan of attack between friends as they brace themselves for dining out, or reading a headline about our nation’s obesity crisis.

the sacred bombshell handbook of self-love   by abiola abrams

The Sacred Bombshell Handbook of Self-Love is your passport to become the woman you were born to be. If you’ve been looking for a sign, this is it. Love-Body-Spirit™ coach, advice columnist, and motivational speaker Abiola Abrams reveals 11 self-worth secrets with assignments to awaken your feminine energy, reclaiming the word “bombshell” to mean a woman who deliciously embodies her mind, body, spirit—and joy.

Abiola’s transformational coaching is buoyed by her Guyanese family lessons and overcoming personal challenges from disordered eating to a “failed” marriage. If you have everything going for you, except what you really want, this journey is for you.

Self-love is sacred. Being empowered is your “femergetic” birthright. Consider this your playbook to activate your Big, Brave, Brazen, Bombshell Breakthrough Life!

a hunger so wide and so deep: a multi-racial view of women’s eating problems by becky w. thompson

The first of its kind, A Hunger So Wide and So Deep challenges the popular notion that eating problems occur only among white, well-to-do, heterosexual women. Becky W. Thompson shows us how race, class, sexuality, and nationality can shape women’s eating problems. Based on in-depth life history interviews with African-American, Latina, and lesbian women, her book chronicles the effects of racism, poverty, sexism, acculturation, and sexual abuse on women’s bodies and eating patterns.

A Hunger So Wide and So Deep dispels popular stereotypes of anorexia and bulimia as symptoms of vanity and underscores the risks of mislabeling what is often a way of coping with society’s own disorders. By featuring the creative ways in which women have changed their unwanted eating patterns and regained trust in their bodies and appetites, Thompson offers a message of hope and empowerment that applies across race, class, and sexual preference.

gaining: the truth about life after eating disorders by aimee liu

Aimee Liu, who wrote Solitaire , the first-ever memoir of anorexia, in 1979, returns to the subject nearly three decades later and shares her story and those of the many women in her age group of life beyond this life-altering ailment. She has extensively researched the origins and effects of both anorexia and bulimia, and dispels many commonly held myths about these diseases with the persuasive conclusion that anorexia is a result of personality. Using her own experience and the stories of many recovering anorexics she’s interviewed, Liu weaves together a narrative that is both persuasive in argument and compelling in personal details.

unbearable weight: feminism, western culture, and the body   by susan bordo

“ Unbearable Weight  is brilliant. From an immensely knowledgeable feminist perspective, in engaging, jargonless (!) prose, Bordo analyzes a whole range of issues connected to the body—weight and weight loss, exercise, media images, movies, advertising, anorexia and bulimia, and much more—in a way that makes sense of our current social landscape—finally! This is a great book for anyone who wonders why women’s magazines are always describing delicious food as ‘sinful’ and why there is a cake called Death by Chocolate. Loved it!”―Katha Pollitt, Nation columnist and author of  Subject to Debate: Sense and Dissents on Women, Politics, and Culture  (2001)

fasting girls: the history of anorexia nervosa by joan jacobs brumberg

Winner of four major awards, this updated edition of Joan Jacobs Brumberg’s  Fasting Girls  presents a history of women’s food-refusal dating back as far as the sixteenth century. Here is a tableau of female self-denial: medieval martyrs who used starvation to demonstrate religious devotion, “wonders of science” whose families capitalized on their ability to survive on flower petals and air, silent screen stars whose strict “slimming” regimens inspired a generation. Here, too, is a fascinating look at how the cultural ramifications of the Industrial Revolution produced a disorder that continues to render privileged young women helpless. Incisive, compassionate, illuminating,  Fasting Girls  offers real understanding to victims and their families, clinicians, and all women who are interested in the origins and future of this complex, modern and characteristically female disease.

French toast for breakfast: declaring peace with emotional eating   by mary anne cohen

This is a warm and compassionate guide to understanding the emotions that underlie eating problems: shame, anger, guilt, sexual difficulties, and the fear of success. Clearly written for people concerned about food and weight issues, it is intended to help readers see food as their friend and nourisher, not their enemy. French Toast For Breakfast is filled with practical exercises, dialogues from actual therapy sessions, straight-forward answers to common questions, an in-depth comparison of treatment options, and a look at relapse—how to prevent it and what to do if it occurs. It also includes a unique questionnaire to help readers determine which path to peace is best for them.

you remind me of you by eireann corrigan

For three years, Eireann Corrigan was in and out of treatment facilities for her eating disorders. By the time she graduated high school, her doctors said she was going to die if things didn’t change. That July, her high school boyfriend attempted suicide. In one gunshot moment, everything was altered. In a striking and vivid voice, Eireann Corrigan recounts these events, finding meaning in the hurt, humor in the horror, and grace in the struggle that life demands. You Remind Me of You is a testament to the binding ties of love and pain, and the strange paths we take to recovery.

the glimmering room  by cynthia cruz

Fierce and fearless, The Glimmering Room beckons readers down into the young speaker’s dark underworld, and because we are seduced by Cruz’s startling imagery and language rich with “Death’s outrageous music,” we follow willingly. Peopled with “ambassadors from the Netherworld”—the orphaned and abused, the lost and addicted—Cruz leads us through this “traveling minstrel show / Called girlhood—” which is at once tragic and magical.

a hunger: poems  by lucie brock-broido

Ranging from the mundane to the ethereal, the themes of Brock-Broido’s first collection are interesting and sometimes startling. The poems range from those concerned with time, especially the conjunction of the past and the future; those influenced by things or places specifically American, poems that appear vaguely autobiographical; and those based on actual historical or contemporary events, usually involving, and often narrated by, a child.

how to (un)cage a girl   by francesca Lia block

Told in three parts and covering subjects such as anorexia, rape, self-loathing, love, and loss,  How to (Un)cage A Girl  is a celebration of girls and women in a three part poetry collection that is powerful, hopeful, authentic, and universal.

graphic novels

Ink in water by lacy j. davis.

As a young artist living in Portland, Lacy Davis’s eating disorder began with the germ of an idea: a seed of a thought that told her  she just wasn’t good enough . And like ink in water, that idea spread until it reached every corner of her being. This is the true story of Lacy’s journey into the self-destructive world of multiple eating disorders. It starts with a young and positive Lacy, trying to grapple with our culture’s body-image obsession and stay true to her riot grrrl roots. And while she initially succeeds in overcoming a nagging rumination about her body, a breakup with a recovering addict starts her on a collision course with anorexia, health food obsession, and compulsive exercise addiction. At the request of her last real friend, she starts going to a twelve-step Overeaters Anonymous course, only to find that it conflicts with her punk feminist ideology.

Blending bold humor, a healthy dose of self-deprecation, vulnerability, literary storytelling, and dynamic and provocative artwork by illustrator Jim Kettner,  Ink in Water  is an unflinching, brutally honest look into the author’s mind: how she learned to take control of her damaging thoughts, redirect her perfectionism from self-destructive behaviors into writing and art, and how she committed herself to a life of health, strength, and nourishment.

Of course, while books about eating disorders can be helpful and therapeutic, if you or someone you know is suffering from disordered eating or any related disorders, please get help beyond the written word. If you are in the U.S., the contact helpline for the National Eating Disorder Association is (800) 931-2237. Also consider speaking to a therapist, in person or online.

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

Jane miskovic-wheatley.

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

2 Sydney Local Health District, Sydney, Australia

Emma Bryant

Shu hwa ong, sabina vatter.

3 Healthcare Management Advisors, Melbourne, Australia

Stephen Touyz

Sarah maguire, associated data.

Not applicable—all citations provided.

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

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

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

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

Supplementary Information

The online version contains supplementary material available at 10.1186/s40337-023-00801-3.

Plain language summary

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

Introduction

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

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

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

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

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

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

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

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

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

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

ED, particularly AN, have long been associated with an increased risk of mortality. The current review summarises best available evidence exploring this association. Several factors complicate these findings including a lack of consensus on definitions of remission, recovery and relapse, widely varying treatment protocols and research methodologies, and limited transdiagnostic outcome studies or syntheses such as meta-analyses. Table ​ Table1 1 provides a summary of outcomes reported by studies identified in this review. There is considerable heterogeneity in the reported measures.

Summary of patient outcomes including predictors and mediators by eating disorder diagnosis

NB—Figures reported in the table for BN and BED are results from systematic review, which differentiated between treatment completer and intent to treat analysis [ 22 ]

*Any ED covers Feeding and/or Eating Disorders Not Otherwise Specified, OSFED

Overall outcomes

A good outcome for a person experiencing ED symptomatology is commonly defined as either remission or no longer meeting diagnostic criteria, as well as improved levels of psychosocial functioning and quality of life [ 28 , 29 ]. However, such a comprehensive approach is rarely considered, and there is no consensus on a definition for recovery, remission, or relapse for any of the ED diagnoses [ 30 , 31 ]. To contextualise this variation, definitions and determinants for these terms are presented in Table ​ Table2 2 .

Sample of definitions of relapse, remission, and recovery in eating disorder research

NB—Ordered by diagnostic group then follow-up period. Where authors referred to definitions from a previous study, references included

a EDE Eating disorder examination

b %EBW Percent expected body weight for age, gender, and height

c EAT Eating Attitudes Test (EAT-26)

d EDE-Q Eating Disorder Examination—Questionnaire

e PSR Psychiatric Status Rating

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

Remission, recovery, and relapse

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

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

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

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

Diagnostic crossover

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

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

Anorexia nervosa (AN)

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

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

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

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

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

Bulimia nervosa (BN)

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

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

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

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

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

Binge eating disorder (BED)

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

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

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

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

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

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

EDNOS, OSFED and UFED

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

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

Avoidant/Restrictive Food Intake Disorder (ARFID)

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

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

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

Community outcomes

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

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

Factors relating to outcomes

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

Age of presentation

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

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

Clinical features and co-occurring conditions

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

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

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

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

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

Psychosocial, environmental and health factors

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

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

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

Treatment factors

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

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

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

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

Self-esteem, self-compassion, and motivation

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

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

Relapse prevention programs

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

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

Online relapse prevention programs

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

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

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

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

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

Standardised, weighted, and crude mortality

AN is consistently described as having the highest mortality rate of the ED, but actual rate difference varies between studies. A summary of Standardised Mortality Ratios across studies is presented in Table ​ Table3. 3 . SMRs from a meta-analysis suggest that measured mortality of AN is approximately three times as high as for other ED diagnoses, and in a UK study of ED patients ( n  = 1892) accessing services between 1992 and 2004, the SMR for AN was almost five times higher than other ED [ 127 ]. This is consistent with other research (a meta-analysis summarising 41 studies) reporting people with AN were 5.2 [3.7–7.5] times more likely to die prematurely from any cause [ 128 ]. A longitudinal study ( n  = 246) found SMR of AN to be only twice as high compared to BN, but still 6.5 times the rate expected in the general population [ 49 ].

Standardised mortality rate by eating disorder diagnosis across included studies

*Mortality rate is reported by per 1000 person-year

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

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

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

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

Years of life lost/years lived with disability

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

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

Risk factors

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

Cause of death

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

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

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

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

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

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

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

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

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

Key findings

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

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

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

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

Strengths and limitations

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

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

Acknowledgements

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

Abbreviations

Author contributions.

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

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

Availability of data and materials

Declarations.

Not applicable.

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

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Contributor Information

Phillip aouad, sarah barakat, robert boakes.

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

Leah Brennan

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

Susan Byrne

6 School of Psychology, Perth, Western Australia Australia

Belinda Caldwell

7 Eating Disorders Victoria, Victoria, Australia

Shannon Calvert

8 Perth, Australia

Bronny Carroll

David castle.

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

Ian Caterson

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

Belinda Chelius

11 Eating Disorders Queensland, Brisbane, QLD Australia

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

Simon Clarke

13 Westmead Hospital, Sydney, NSW Australia

Janet Conti

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

Lexi Crouch

15 Brisbane, Australia

Genevieve Dammery

Natasha dzajkovski, jasmine fardouly.

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

Carmen Felicia

17 University of Sydney, Sydney, NSW Australia

John Feneley

18 New South Wales Health, Sydney, NSW Australia

Amber-Marie Firriolo

Nasim foroughi, mathew fuller-tyszkiewicz.

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

Anthea Fursland

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

Veronica Gonzalez-Arce

Bethanie gouldthorp.

21 Hollywood Clinic, Ramsay Health Care, Perth, Australia

Kelly Griffin

Scott griffiths.

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

Ashlea Hambleton

Amy hannigan.

23 Queensland Eating Disorder Service, Brisbane, QLD Australia

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

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

Phillipa Hay

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

Francis Kay-Lambkin

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

Michael Kohn

28 Westmead Hospital, Sydney, Australia

Eyza Koreshe

Isabel krug, jake linardon, randall long.

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

Amanda Long

30 Exchange Consultancy, Redlynch, NSW Australia

Sloane Madden

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

Danielle Maloney

Sian mclean.

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

Thy Meddick

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

Deborah Mitchison

Richard o’kearney.

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

Roger Paterson

35 ADHD and BED Integrated Clinic, Melbourne, VIC Australia

Susan Paxton

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

Melissa Pehlivan

Genevieve pepin.

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

Andrea Phillipou

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

Judith Piccone

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

Rebecca Pinkus

Bronwyn raykos.

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

Paul Rhodes

Elizabeth rieger, sarah-catherine rodan, karen rockett, janice russell.

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

Haley Russell

Fiona salter.

42 Ramsay Health Care, Perth, Australia

Susan Sawyer

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

Beth Shelton

44 National Eating Disorders Collaboration, Victoria, Australia

Urvashnee Singh

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

Sophie Smith

46 Sydney, Australia

Evelyn Smith

Karen spielman, sarah squire.

47 The Butterfly Foundation, Sydney, Australia

Juliette Thomson

Ranjani utpala, lenny vartanian, andrew wallis.

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

Warren Ward

49 Department of Psychiatry, University of Queensland, Brisbane, Australia

Sarah Wells

50 University of Tasmania, Hobart, TAS Australia

Eleanor Wertheim

Simon wilksch.

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

Michelle Williams

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

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Books About Anorexia: Must-Reads To Overcome It [Top 10] [2024 Update]

What are good books on eating disorders – and specifically, anorexia nervosa? On this page you will find the best self-help books on anorexia and how to overcome it. We cover both children’s and adult books on this topic, featuring research, advice and true stories. Read along…

Interesting and poignant books on anorexia

Because many people do not yet know much about what anorexia nervosa is exactly, we have made an overview of some of the most read books about anorexia. The list consists of books for parents of children with an eating disorder, books with personal stories, and books with tips and tools to help you overcome this condition.

We start our recommendations with the top 10 best books about Anorexia of all time. This list has been updated this year, including all the recent titles.

The updated top 10 list: the best books about anorexia

Going hungry.

19 People who have experienced (or are experiencing) anorexia have decided to share their story in this book. This is a unique way to learn about this eating disorder.

8 Keys to Recovery from an Eating Disorder: Effective Strategies from Therapeutic Practice and Personal Experience (8 Keys to Mental Health)

If you never had an eating disorder or knew someone who did, it can be tricky to understand what goes on inside of the mind and body. Carolyn Costin and Gwen Schubert Grabb tell you what strategies work to recover from an eating disorder.

Help Your Teenager Beat an Eating Disorder, Second Edition 

Teenagers can be focused on their looks too much and this can, at some point, lead to an eating disorder. What parents can do to help their child recover from the disorder is laid out perfectly in this book.

Recover Your Perspective: A Guide To Understanding Your Eating Disorder and Creating Recovery Using CBT, DBT, and ACT

An eating disorder will not only affect your body, but also your mind. Understanding what goes on inside of you will help you deal with your eating disorder. Certain techniques can be very effective during your time of recovery.

Talking to Eating Disorders: Simple Ways to Support Someone With Anorexia, Bulimia, Binge Eating, Or Body Ima ge Issues

If you are not the one who suffers from the eating disorder, it can be hard to provide support. This book shows you what you can do and what you shouldn’t do.

I hope this finds you well

We love this book, because of the message you get from the poems. Life is not always easy, and it can be filled with confusion, heartbreak, and other emotions that could lead to an eating disorder. This book can be your companion on your journey of recovery.

By Their Side: A Resource for Caretakers and Loved Ones Facing an Eating Disorder

When you are in the middle of something, it can be hard to see that there is a way out. Support from the people that surround you can be key to you getting better when experiencing the effects of an eating disorder. This book is for those who want to take care of someone with an eating disorder.

Eating Disorders Anonymous: The Story of How We Recovered from Our Eating Disorders

We recommend this book because of the 12 steps it shares on how to recover from an eating disorder. Our second reason to read this book, is the experiences that are shared by others who faced an intense road of recovery from their eating problems.

When Your Teen Has an Eating Disorder: Practical Strategies to Help Your Teen Recover from Anorexia, Bulimia, and Binge Eating

Eating disorders can be manifested in different ways. Once you have discovered your child suffers from an eating disorder, you want to know what to do to help its recovery. The strategies in this book will provide you with information on what you can do for your child.

The Inside Scoop on Eating Disorder Recovery

A book that comes from personal experience is always more impressive, and the humor that is used in this book will help you understand and deal with an eating disorder and show you how to recover.

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About The Author

Ron Koster MSc

Thank you so much for reading the book recommendations on Top 10 Book Awards. My name is Ron - master in international research journalism - and I am appoined as editor-in-chief. Now it is your turn. Underneath, you can tell us which books also belong in this list, according to you. Give us the title and the reason why you think the book belongs there. I am reading your comment with great pleasure.

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We love books

Our book awards and overviews originate from our love for reading books. Together with our editors, we gather the best books around the world. These recommendation lists are based on our verdict, news paper reviews, our editor’s picks and sales numbers.

Do you know a book that should be added to the list you are viewing now? You are welcome to add your recommendation underneath this page via the comments.

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How did we select our top 10 our criteria for awarding these books.

In order to select & award our top 10 books, we paid careful attention to the following criteria:

• The quality of the texts: is it well written?
• Sales numbers & the popularity of the book.
• Newspaper reviews: has it been received well?
• The amount of good examples and imagery in the book.
• The amount of good and practical knowledge about the subject.
• The number of years of experience that the author has about the topic.
• Reader reviews: how much did the worldwide audience love this book?
• Our personal opinion: we let our editors read the book thoroughly and we asked them: does it appeal to you?
• The actuality of the book: are the tips and informational bits in this book dated or still relevant for modern day readers?

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