case study about anorexia

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

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

• Simone Daugaard Hemmingsen   ORCID: orcid.org/0000-0001-6789-7105 1 , 2 , 3 , 4 , 5 ,
• Mia Beck Lichtenstein   ORCID: orcid.org/0000-0002-7885-9187 6 , 7 ,
• Alia Arif Hussain   ORCID: orcid.org/0000-0002-1011-5165 8 , 9 ,
• Jan Magnus Sjögren   ORCID: orcid.org/0000-0003-2060-1914 8 , 9 &
• René Klinkby Støving   ORCID: orcid.org/0000-0002-4255-5544 1 , 2 , 3 , 4 , 5  

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

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

Case presentation

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

Conclusions

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

Trial registration

ClinicalTrials.gov, NCT02502617 . Registered 20 July 2015.

Peer Review reports

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

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

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

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

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

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

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

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

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

The psychopathological profile of the patient

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

Qualitative observations

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

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

Neuropsychological findings

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

Memory performance on WMS-III

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

Cognitive flexibility on D-KEFS and WCST

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

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

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

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

WAIS-IV processing speed

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

d2-R test of attention

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

Discussion and conclusions

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

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

Impaired cognitive flexibility

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

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

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

Cognitive adaptation in anorexia nervosa

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

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

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

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

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

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

Availability of data and materials

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

Abbreviations

• Anorexia nervosa

Intelligence quotient

Body mass index

The Beck Depression Inventory II

The Eating Disorder Inventory 3

The Wechsler Memory Scale III

The Wechsler Adult Intelligence Scale IV

The Processing Speed Index

The Delis-Kaplan Executive Function System

The Wisconsin Card Sorting Test Revised and Expanded

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

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

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Acknowledgements

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

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

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

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Hemmingsen, S.D., Lichtenstein, M.B., Hussain, A.A. et al. Case report: cognitive performance in an extreme case of anorexia nervosa with a body mass index of 7.7. BMC Psychiatry 20 , 284 (2020). https://doi.org/10.1186/s12888-020-02701-1

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Am Fam Physician. 2015;91(1):46-52

A more recent article on eating disorders in primary care is available.

Patient information : See related handout on eating disorders , written by the authors of this article.

Eating disorders are life-threatening conditions that are challenging to address; however, the primary care setting provides an important opportunity for critical medical and psychosocial intervention. The recently published Diagnostic and Statistical Manual of Mental Disorders , 5th ed., includes updated diagnostic criteria for anorexia nervosa (e.g., elimination of amenorrhea as a diagnostic criterion) and for bulimia nervosa (e.g., criterion for frequency of binge episodes decreased to an average of once per week). In addition to the role of environmental triggers and societal expectations of body size and shape, research has suggested that genes and discrete biochemical signals contribute to the development of eating disorders. Anorexia nervosa and bulimia nervosa occur most often in adolescent females and are often accompanied by depression and other comorbid psychiatric disorders. For low-weight patients with anorexia nervosa, virtually all physiologic systems are affected, ranging from hypotension and osteopenia to life-threatening arrhythmias, often requiring emergent assessment and hospitalization for metabolic stabilization. In patients with frequent purging or laxative abuse, the presence of electrolyte abnormalities requires prompt intervention. Family-based treatment is helpful for adolescents with anorexia nervosa, whereas short-term psychotherapy, such as cognitive behavior therapy, is effective for most patients with bulimia nervosa. The use of psychotropic medications is limited for anorexia nervosa, whereas treatment studies have shown a benefit of antidepressant medications for patients with bulimia nervosa. Treatment is most effective when it includes a multidisciplinary, team-based approach.

Eating disorders have traditionally been classified into two well-established categories. They are anorexia nervosa and bulimia nervosa. 1 Additionally, many patients have been classified as having the residual category of eating disorder not otherwise specified. 2 Revisions in the recently published Diagnostic and Statistical Manual of Mental Disorders , 5th ed., (DSM-5) may facilitate more specific eating disorder diagnoses. 3 , 4 The DSM-5 includes a diagnostic category for binge-eating disorder, which is characterized by a loss of control and the feelings of guilt, shame, and embarrassment. The disorder is not associated with self-induced vomiting or other compensatory behaviors; hence, patients are typically overweight or obese. Other feeding and eating disorders in the DSM-5 include pica, rumination disorder, and avoidant/restrictive food intake disorder. 3 This article focuses on anorexia nervosa and bulimia nervosa.

The DSM-5 diagnostic criteria for anorexia nervosa ( Table 1 3 ) are similar to the previous DSM-IV criteria with respect to behavioral and psychological characteristics involving restriction of food intake resulting in low body weight, intense fear of gaining weight or becoming fat, and disturbance of body image. 1 , 3 Notably, the DSM-5 criteria do not refer to a specific degree of weight loss required for the diagnosis, but instead provide guidelines for specifying the severity of weight loss. As in the DSM-IV, the new criteria specify two diagnostic types of anorexia nervosa (restricting type and binge eating/purging type). In a significant revision to previous criteria, diagnosis of anorexia nervosa no longer requires the presence of amenorrhea.

Bulimia nervosa involves the uncontrolled eating of an abnormally large amount of food in a short period, followed by compensatory behaviors, such as self-induced vomiting, laxative abuse, or excessive exercise. The main update in the DSM-5 criteria for bulimia nervosa ( Table 2 3 ) is a decrease in the average frequency of bingeing and purging from twice to once a week. 4

Prevalence and Etiology

Bulimia nervosa affects four to six out of 200 females in the United States. Anorexia nervosa is much less common, with a lifetime prevalence of one out of 200 females in the United States. Approximately 95% of persons with an eating disorder are 12 to 25 years of age. Although 90% of patients with an eating disorder are female, the incidence of diagnosed eating disorders in males appears to be increasing. 5

The etiology of eating disorders is unknown and probably multifactorial. Environmental influences include societal idealizations about weight and body shape. Parenting style has been discounted as a primary cause of eating disorders. However, parenting style, household stress, and parental discord may contribute to anxiety and personality traits that are risk factors for an eating disorder. An emphasis on success and external rewards may lead to overly high expectations. Children may then try to be successful with something they can control: regulating what they eat and how they look. Sexual assault or abuse has not been associated with anorexia nervosa but may be a risk factor for bulimia nervosa. 6

There is increasing evidence of biologic risk factors for eating disorders. Twin studies and other research suggest a genetic link. 7 Eating disorders have been associated with abnormal neurotransmitter systems involving serotonin and dopamine. 8 , 9 The role of hormones such as ghrelin, leptin, and oxytocin has also been investigated. 10

Clinical Presentation

Table 3 includes clinical signs of eating disorders. 11 – 13 Patients with eating disorders may often comment about being “fat” or not liking their body shape. Weight loss with anorexia nervosa may go unnoticed for some time, particularly when patients wear baggy clothes or extra layers. Patients with anorexia nervosa commonly restrict their diet to vegetables, fruit, and diet products, and often skip meals altogether. They develop mealtime rituals, such as cutting food into tiny pieces, patting liquid off with napkins, or picking food apart. Although anorexia nervosa has been associated with some cognitive deficits as demonstrated on neuropsychological tests, many patients maintain good cognitive function and verbal fluency even when malnourished. 14

Patients with eating disorders often engage in excessive physical activity despite bad weather, illness, or injury. A study found that approximately one-third of patients hospitalized for anorexia nervosa reported excessive (i.e., obligatory, obsessive, or driven) exercise during the three months before admission. 15

Patients with bulimia nervosa may arrange complex schedules to accommodate episodes of binge eating and purging, often accompanied by frequent trips to the bathroom. In addition to excessive exercise, other methods of weight control include abuse of laxatives or diuretics. Frequent self-induced vomiting can contribute to parotitis, stained teeth or enamel erosions, and hand calluses.

As cachexia progresses, patients with anorexia nervosa lose strength and endurance, move more slowly, and demonstrate decreased performance in sports. Overuse injuries and stress fractures can occur. Bradycardia, orthostatic hypotension, and palpitations may progress to potentially fatal arrhythmias. Epigastric pain and a bloating sensation are common. Laxative abuse causes hemorrhoids and rectal prolapse. Severe hypoglycemia may lead to seizures. Wounds heal poorly. Endocrine symptoms in anorexia nervosa include hypothermia (feeling cold), delayed onset of menses or secondary amenorrhea, and osteopenia progressing to osteoporosis. 11 , 12

More than one-half of patients with eating disorders meet criteria for a current or past episode of major depression. 16 Anorexia nervosa is associated with an increased risk of suicide, with the suicide standardized mortality ratio estimated to be as high as 31 in one meta-analysis. 17 Other associated psychiatric disorders include obsessive-compulsive disorder, obsessive-compulsive personality disorder, social phobia, anxiety disorders, substance use disorders, and personality disorders. Psychological symptoms include heightened emotional arousal, reduced tolerance of stress, emotional dysregulation, social withdrawal, and self-critical perfectionistic traits. 3

Screening for Eating Disorders

Annual health supervision examinations and preparticipation sports physicals are ideal screening opportunities. In addition to weight, height, and body mass index measurements, a screening tool such as the SCOFF questionnaire ( Table 4 18 ) can be used. 11 , 12 , 18 The SCOFF questionnaire has been validated only in adults but suggests an approach that can also be used with children. 12

Initial Evaluation

The first priority in the evaluation of patients with eating disorders is to identify emergency medical conditions that require hospitalization and stabilization. Before the patient is weighed, a urine sample should be obtained to assess specific gravity for hydration status, pH level, ketone level, and signs of kidney damage. Weight, height, body mass index, and body temperature should be recorded. Because patients may wear extra clothes or hide heavy items to exaggerate their weight, they should be weighed wearing only underwear and a hospital gown. An attendant or parent may have to be present while they change. Clinicians may consider having patients face away from the scale so that they do not know their weight. Blood pressure should be recorded with orthostatic vital signs.

Electrocardiography and laboratory studies such as urinalysis with specific gravity, complete blood count, complete metabolic panel, amylase and lipase measurement, phosphorous and magnesium measurement, and thyroid function tests (thyroid-stimulating hormone, thyroxine, free triiodothyronine) should be performed promptly. 11 , 12 Less urgent testing, such as bone density testing, can be deferred.

Family physicians can fill a central role in the monitoring and treatment of patients with eating disorders. A psychotherapist or psychiatrist usually is involved. Eating disorder specialists, often with backgrounds in psychiatry or adolescent medicine, are ideally involved but may not be available in some locations. A dietitian can help select nutritious and calorie-rich foods. For youth, it is critical to involve their schools. Most states require formal 504 plans that spell out special accommodations, such as snack breaks in class or allowances for missed school, to allow equal educational opportunities for students with medical disabilities.

Treatment success may be dependent on developing a therapeutic alliance with the patient, involvement of the patient's family, and close collaboration within the treatment team. Additional online resources for the treatment team, patient, and family are listed in eTable A .

Treatment should be individualized based on symptom severity, course of illness, psychiatric comorbidity, availability of psychosocial/familial support, patient motivation for undergoing treatment, regional availability of specialized treatment programs, and medical stability. Indications for hospitalization include significant electrolyte abnormalities, arrhythmias or severe bradycardia, rapid persistent weight loss in spite of outpatient therapy, and serious comorbid medical or psychiatric conditions, including suicidal ideation. 11 , 12 Table 5 includes the American Academy of Pediatrics criteria for inpatient treatment. 19 After the patient is stabilized at a local hospital, his or her condition or comorbidities may necessitate transfer to a facility specializing in eating disorder inpatient care.

The focus of initial treatment for patients who have anorexia nervosa with cachexia is restoring nutritional health, with weight gain as a surrogate marker. Feeding tubes may be needed in severe cases when the patient has a high resistance to eating. Refeeding syndrome can occur in a malnourished individual when a rapid increase in food intake results in dramatic fluid and electrolyte shifts, and is potentially fatal. Thus, hospitalization should be considered for initial treatment of any seriously malnourished patient to allow for daily monitoring of key markers such as weight, heart rate, temperature, hydration, and serum phosphorus level. 20

Nutritional Intervention and Weight Restoration . Patients with anorexia may eat only 500 kcal a day, whereas the average daily caloric requirement for a sedentary adolescent is 1,800 kcal for females and 2,200 kcal for males. 21 A reasonable initial target for weight restoration is 90% of the average weight expected for the patient's age, height, and sex. 12 , 22 Growth charts are available from the Centers for Disease Control and Prevention at http://www.cdc.gov/growthcharts/charts.htm . Initiation or resumption of menses is an important marker of biologic health in females. In one report, 86% of females with anorexia nervosa who achieved the 90% body mass index goal resumed menses within six months. 22 The patient's pre–eating disorder weight history may help in determining a target body mass index. For growing adolescents, the goal weight may need to be adjusted every three to six months. Weight gain may not begin until caloric intake significantly exceeds sedentary requirements. Strenuous physical activity and sports should be restricted.

Nutritional guidance focuses on healthy food intake and regaining the energy needed to resume activities. Although calorie counting is important, it generally should not be discussed with the patient. Daily menus should include three full meals and a structured snack schedule that is monitored by parents or the school nurse. A multivitamin plus vitamin D and calcium supplements are recommended.

Psychotherapy . Psychotherapy is the foundation for successful treatment of an eating disorder. Family-based treatment (the Maudsley method) is one of the more promising approaches for adolescents with anorexia nervosa. 23 – 25 Goals of psychotherapy include reduction of distorted body image and dysfunctional eating habits, return to social engagement, and resumption of full physical activities. 26 Family members need support and help learning how to care for the patient. Clinical trials have shown significant improvement in bulimia nervosa with cognitive behavior therapy and interpersonal psychotherapy. 27 Group therapy is used in many eating disorder treatment programs. Alternate adjunctive therapies such as equine therapy (based on the idea that caring for horses through grooming and other interactions is healing) may hold promise, although they are not evidence-based therapies. 28 Mindfulness practices such as meditation and yoga benefit patients with anxiety and may provide low-energy physical activity. 29

Medications . Studies have shown only limited benefit of medications in the treatment of anorexia nervosa. Antidepressants, including selective serotonin reuptake inhibitors (SSRIs), may help mitigate symptoms of depression and suicidal ideation in patients with anorexia nervosa. However, they have not proved beneficial in facilitating weight restoration or preventing relapse. 30 , 31 Although case reports and recent preliminary studies have suggested a role for atypical antipsychotics such as olanzapine (Zyprexa), controlled studies have not demonstrated significant benefit in patients with anorexia nervosa. 11 , 32 – 35 Larger placebo-controlled studies will be needed to evaluate this approach. If psychotropic medications are attempted, the patient should be closely monitored, possibly in an inpatient or residential setting, and supervised by a psychiatrist or eating disorder specialist.

In patients with bulimia nervosa, studies have suggested SSRIs may be beneficial in decreasing the frequency of binge eating and purging. 35 – 37 Thus, the addition of an SSRI might be considered for patients who are not responding to an initial trial of psychotherapy and for patients with major depression or another comorbid disorder responsive to antidepressant medications.

Although approximately one-half of patients with anorexia nervosa fully recover, about 30% achieve only partial recovery, and 20% remain chronically ill. 38 Anorexia nervosa has the highest mortality rate of any mental health disorder, with an estimated all-cause standardized mortality ratio of 1.7 to 5.9. 39 , 40 The prognosis for bulimia nervosa is more favorable, with up to 80% of patients achieving remission with treatment. However, the 20% relapse rate represents a significant clinical challenge, and the disorder is associated with an elevated all-cause standardized mortality ratio of 1.6 to 1.9. 39 , 40

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What next for eating disorder genetics? Replacing myths with facts to sharpen our understanding

• Laura M. Huckins   ORCID: orcid.org/0000-0002-5369-6502 1 , 2 , 3 , 4 , 5 , 6 ,
• Rebecca Signer 1 , 2 , 3 ,
• Jessica Johnson 1 ,
• Ya-Ke Wu 7 , 8 ,
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• Cynthia M. Bulik   ORCID: orcid.org/0000-0001-7772-3264 8 , 11 , 12  

Molecular Psychiatry volume  27 ,  pages 3929–3938 ( 2022 ) Cite this article

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• Psychiatric disorders

Substantial progress has been made in the understanding of anorexia nervosa (AN) and eating disorder (ED) genetics through the efforts of large-scale collaborative consortia, yielding the first genome-wide significant loci, AN-associated genes, and insights into metabo-psychiatric underpinnings of the disorders. However, the translatability, generalizability, and reach of these insights are hampered by an overly narrow focus in our research. In particular, stereotypes, myths, assumptions and misconceptions have resulted in incomplete or incorrect understandings of ED presentations and trajectories, and exclusion of certain patient groups from our studies. In this review, we aim to counteract these historical imbalances. Taking as our starting point the Academy for Eating Disorders (AED) Truth #5 “Eating disorders affect people of all genders, ages, races, ethnicities, body shapes and weights, sexual orientations, and socioeconomic statuses”, we discuss what we do and do not know about the genetic underpinnings of EDs among people in each of these groups, and suggest strategies to design more inclusive studies. In the second half of our review, we outline broad strategic goals whereby ED researchers can expand the diversity, insights, and clinical translatability of their studies.

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Over the past decade, substantial progress has been made in understanding the genetic etiology of anorexia nervosa (AN) and related eating disorders (EDs). Global collaborative efforts have yielded large-scale linkage, and later, genome-wide associations studies [ 1 , 2 , 3 , 4 ], revealing the first genome-wide significant loci [ 1 ] and 53 genes associated with AN across tissues [ 5 ]. These studies have led to new insights and hypotheses about the etiopathology of AN including evidence of psychiatric and metabolic risk factors [ 1 ]; shared genetic etiology with metabolic, anthropometric, and psychiatric traits [ 1 ]; and evidence for clinical consequences of predicted aberrant AN-gene expression [ 5 ]. Similar analyses of other EDs are underway. However, substantial unanswered questions remain about the biological mechanisms underlying AN and EDs; this gap in our understanding is a key contributor to the lack of effective, personalized treatments. ED science faces an uphill battle in replacing decades of myths, misunderstandings, and stereotypes about the presentation, demographics, symptoms, and etiopathology of EDs. Moreover, these misconceptions are subtly embedded in the research questions that have contributed to fundamental knowledge in the field and have influenced the populations we recruit and study.

To contextualize ED genetic research, we take as a starting point an aspirational document prepared and disseminated (available in 34 languages) by the Academy for Eating Disorders (AED), titled the Nine Truths About Eating Disorders [ 6 ]. Ongoing ED research is addressing several of the AED truths [ 7 ]. We focus on AED Truth #5 “Eating disorders affect people of all genders, ages, races, ethnicities, body shapes and weights, sexual orientations, and socioeconomic statuses” to illustrate how inclusivity in genetic research can contribute to a more comprehensive understanding of the full spectrum of EDs and ultimately revolutionize our understanding of this disease cluster.

AED Truth #5 directly counters many of the stereotypes that have hindered ED science. Dissecting this truth illustrates the importance of broad representation to prevent biased or distorted understanding of the causes and impact of EDs. The failure to acknowledge the diversity of individuals affected by EDs has led to narrow definitions of disease and diagnostic criteria, and consequently incomplete assessments of disease characteristics, risk factors, and etiology. Accordingly, individuals who fall outside of these parameters (i.e., those who are not young, thin, affluent white women) have been excluded from research and even from treatment. Stereotypes propagated by the media as well as the medical profession have contributed to under-detection and under-treatment of individuals with EDs who do not conform to these expectations. Under-detection, under-diagnosis, and under-referral for specialist treatment have been documented in men [ 8 , 9 ], in people of color [ 10 , 11 , 12 , 13 , 14 ], in older individuals [ 15 ], in the LGBTQIA+ community [ 16 , 17 , 18 ], and in individuals living in larger bodies [ 19 ]. Failure to include these communities truncates our observations of risk factors and symptoms of EDs to a narrow slice of the affected population. Without representation, we cannot begin to understand the full spectrum of risk, and the mechanisms underlying EDs.

Expansion of genetic studies to include diverse presentations of EDs, and to capture the full spectrum of symptoms, behaviors, and outcomes that characterize EDs will yield increased power for discovery overall, but, more importantly, may also yield insights into specific genetic underpinnings of different facets of the disorders. Analytical approaches that can identify symptom-specific associations and account for potential biases can help reshape the understanding of EDs in the minds of researchers, clinicians, and the general public. In the Section “Background”, we outline what is known about EDs across the various groups referenced in AED Truth #5, and highlight existing genetic studies in these groups. In the Section “Large-scale approaches to address diversity in ED genetics”, we propose strategies for enhancing genetic research to advance the science of EDs.

EDs affect people of all genders and sexual orientations

ED research, diagnoses, treatment guidelines, and public attention have overwhelmingly focused on women and girls. Although men might be included in studies, numbers are often too small to warrant analysis or to generate confident conclusions (Fig.  1 ). Although EDs occur within and across gender and sexual orientation spectra [ 8 , 16 , 17 , 18 , 20 ], the underlying genetic and environmental risk factors may be very different within and across groups, necessitating specialized screening, prevention, and treatment. In this review, we use ‘sex’ to refer to categorical variables including ‘male’ and ‘female’ as defined in the original studies, and ‘gender’ to refer to socially constructed behaviors and identities, rather than biological attributes [ 21 , 22 ].

Data include all genetic studies from 1980–2021. Studies where sex or race/ethnicity were not recorded are included in ‘all’. Studies with at least one male participant are included in ‘male and female sexes included’; studies with at least one non-European participant are included in ‘includes non-Europeans’. We caution that, for many of these studies, numbers of males/non-Europeans are very small.

EDs in boys and men

According to a recent large meta-analysis, the gender ratio for AN is estimated to be 7:1 [ 23 ], for bulimia nervosa (BN) ~3.2:1 [ 23 ], and for binge-eating disorder (BED) 2.8:1 [ 23 ]. The lifetime prevalence of EDs was 8.4% for women and 2.2% for men around the world, based on an analysis of 94 articles with ED diagnoses from 28 countries (e.g., Argentina, Brazil, Canada, China, Finland, Germany, Italy, Japan, and Portugal) [ 23 ]. Globally, the lifetime prevalence of AN was 1.4% for women and 0.2% for men; BN was 1.9% for women and 0.6% for men; and BED was 2.8% for women and 1.0% for men [ 23 ]. These figures reflect diagnostic criteria developed based on clinical presentation in women and likely underestimate the prevalence in men. For example, whereas women (in Western countries) address their underlying “drive for thinness” and concern with weight and shape by focusing on being thin and losing weight, men tend to show more concern for building lean muscle [ 24 ] and express that drive via reducing body fat percentage or striving for muscle definition. Compensatory behaviors also differ, with women being more likely to engage in self-induced vomiting and diuretic/laxative use, whereas men are more likely to exercise excessively and take anabolic steroids or supplements to pursue their ideal body shape [ 25 ]. In addition, the long history of EDs being considered a female disorder increases hesitancy and shame in males decreasing help-seeking [ 24 ], and hinders detection by clinicians who do not include EDs on the differential for male patients [ 9 ].

EDs in the LGBTQIA+ population

LGBTQIA+ individuals report increased prevalence of psychiatric disorders, including all EDs [ 16 , 17 , 18 ], due at least in part to the systematic discrimination, harassment, and violence they experience [ 16 , 17 , 18 , 26 ]. Watson, et al. [ 17 ], found that “enacted stigma” (the collective experience of systematic discrimination) was associated with multiple disordered eating phenotypes such as binge eating, fasting, and vomiting. Subsequent studies have confirmed internalized trans- and homophobia as risk factors for EDs [ 26 ]. Underlying facets of body image and shape concerns as risk factors for EDs may differ dramatically between transgender and cisgender individuals [ 26 , 27 ]. Alignment with specific gender presentations may present as a key motivation for disordered eating [ 26 , 27 , 28 , 29 ]; for example, the desire to suppress menstruation through restriction and excessive exercise has been observed in transgender men [ 27 , 30 ].

What we know and do not know about ED genetics relative to gender and sexual orientation

Genetic studies have identified both shared and distinct genetic risk factors across sexes. For example, female relatives of men with AN have an elevated crude relative risk of AN (20.3) [ 31 ], implying at least some shared genetic risk. However, studies comparing same- and opposite-sex twins found that only 50% of the genetic risk for ED behaviors was shared between the sexes, with females having a higher loading of genetic risk [ 32 ]. Heritability patterns also differ developmentally: twin studies of boys and young men estimate ~50% heritability across pre-pubescence, adolescence, and into adulthood; whereas, heritability among girls and young women was undetectable (~0%) until puberty, reaching 50% only in adulthood [ 33 ]. More recent studies have leveraged genetic correlation analyses to examine sex-specific relationships between AN and anthropometric traits. For example, AN and body fat percentage (BF%) are more highly genetically correlated among females than among males [ 34 , 35 ], and partitioned heritability analyses of SNP-h 2 showed that BF% female was significantly enriched for CNS tissue while BF% male was enriched for adipose tissue [ 35 ].

No explicit research exists on the genetic risk of EDs among LGBTQIA+ individuals, though we can reasonably assume that many of the same genetic influences on EDs are acting on these individuals as cisgender and heterosexual individuals, although environmental risk factors may differ. What is essential for ED genetic studies is that these individuals are included and unique risk factors that contribute to their experience of EDs are considered and assessed.

It is overly simplistic to conclude that AN and anthropometric traits have different genetic risk factors between men and women. Such an interpretation ignores the historical bias in ED research. Because diagnostic guidelines were developed and tailored to the presentation of EDs in women and girls, assessment instruments likely have differential accuracy and sensitivity according to sex and gender [ 36 ]. Moreover, heritability and expression of a trait do not occur in a vacuum. Diagnosis of a disorder (and consequent inclusion in research) is representative not just of genetics and downstream biology, but of a constellation of social and environmental exposures, including ED risk factors, but also vigilance of caregivers and clinicians to ED symptoms, and access to appropriate treatment. Similarly, studies of anthropometric traits will likely be confounded by gendered societal pressure for thinness, such that women are exposed to higher rates of bullying, shame, and pressure to lose weight. These factors might account for the brain-specific heritability of body fat percentage in women [ 34 ]. Such considerations are key to introducing equity into studies of EDs, and will be notable throughout our discussions not just of gender, but of race and ethnicity, age of onset, and socio-economic status. Finding ways to address, account for, or remove these factors will be key to furthering our understanding of EDs.

EDs affect people of all races and ethnicities

Ed prevalence across races and ethnicities.

The limited available data from population-based studies report few racial or ethnic differences in the prevalence of EDs among adults, although results are inconsistent. Nationally representative studies in the US report no significant racial or ethnic differences in the prevalence of AN, BN, or BED [ 8 ], although more recent studies report significantly lower lifetime prevalence of AN among Black and Hispanic/Latinx participants [ 37 ], higher prevalence of BN among Hispanic/Latinx adolescents [ 38 ], and higher prevalence of general ED pathology among American Indian/Alaskan Native and Hispanic/Latinx college students [ 39 ]. There have been few representative, population-based studies of ED prevalence outside of the U.S., Europe, and Australasia. The World Health Organization World Mental Health surveys reported prevalence estimates for BN and BED from 14 countries, including Columbia (0.4% BN, 0.9%, BED), Brazil (2.0% BN, 4.7% BED), Mexico (0.8% BN, 1.6% BED), Romania (0.0% BN, 0.2% BED), Belgium (1.0% BN, 1.2% BED), France (0.7% BN, 1.7% BED), Germany (0.3% BN, 0.5% BED), Italy (0.1% BN, 0.7% BED), the Netherlands (0.9% BN, 0.9% BED), New Zealand (1.3% BN, 1.9% BED), Northern Ireland (0.5% BN, 1.5% BED), Portugal (0.8% BN, 2.4% BED), Spain (0.7% BN, 0.8% BED), and the U.S. (1.0% BN, 2.6% BED) [ 40 ]. A 2013 review of prevalence investigations of EDs included studies from the World Mental Health surveys, the U.S., Western Europe, Latin America, South Korea, and New Zealand. The authors reported that the pooled prevalence of lifetime EDs was higher among Western countries (1.29%) compared to the South Korean sample (0.21%) [ 41 ]. A review of epidemiological studies of EDs in African countries found that most included relatively small community or student samples. No cases of AN were reported. The pooled prevalence of BN was 0.87%, and the pooled prevalence of Eating Disorders Not Otherwise Specified was 4.45% [ 42 ].

Furthermore, studies have reported differing prevalence of component symptoms of binge eating, purging, body dissatisfaction, and fear of weight gain across races and ethnicities. For example, Asian men and women with EDs tend to exhibit lower fear of fatness [ 43 , 44 , 45 ], a key DSM-5 diagnostic criterion, as well as higher levels of thin ideal internalization compared to European Americans and African Americans [ 46 ], possibly influencing ED prevalence estimates among Asian men and women.

Detection and referral and assessment of EDs in diverse populations

Differences in prevalence estimates may reflect that people of color are less likely to be diagnosed with an ED, to seek treatment, and to be referred for specialist treatment [ 10 , 13 , 14 ]. As outlined in the section on gender and sexual orientation, historical biases in ED research have yielded diagnostic schema and treatment guidelines based on very specific presentations. Diagnoses and guidelines may disproportionately address clinical features expected in a prototype white cisgender female patient, reducing applicability across racial and ethnic groups. Similarly, cultural differences in environmental exposures and racial/ethnic differences in ED symptomatology are rarely captured by existing ED assessments. Studies using established assessments are able to say whether individuals report standard symptoms, but inadequately address unique symptoms or risk factors that may characterize the illnesses across diverse groups—again potentially hampering knowledge and perpetuating health disparities.

What we know and do not know about ED genetics relative to race and ethnicity

It is widely known that complex trait genetics has focused overwhelmingly on individuals of European ancestry [ 47 , 48 ], including over 90% of individuals in psychiatric genetics GWAS [ 49 ]. Large GWAS of non-Europeans (e.g., the PAGE consortium [ 50 ]) have enabled trans-ancestry fine-mapping and led to discovery of novel disease-associated genes, even using substantially smaller sample sizes [ 50 , 51 ]. Although relatively underpowered, multi-ancestry sequencing studies of schizophrenia indicate that rare variant burdens are similar across ancestries [ 52 ]. The success of cross-ancestry GWAS and sequencing studies in these traits shows the promise of trans-ancestry fine-mapping loci using diverse cohorts and may increase the likelihood that causal variants can be found [ 49 , 50 , 51 ]. Although early work on candidate genes, genome-wide microsatellite studies, and replications emerged from Japan [ 2 , 53 , 54 ], subsequent AN GWAS have been restricted to European-ancestry populations. Although large diverse samples are not yet available in EDs, this is poised to change as the ED Working Group of the Psychiatric Genomics Consortium (PGC-ED) has highlighted diversification of samples and engagement of international researchers as a priority [ 55 ].

EDs affect individuals across the lifespan

EDs affect people of all ages [ 15 ], although symptoms, presentation and prevalence may change over the lifespan. As with gender and race, a historical focus on a specific presentation (i.e., young girls and women) may have introduced age bias into diagnostic criteria, assessment instruments, and treatment guidelines. Across the lifespan, disparate genetic and environmental risk factors may underlie superficially similar ED behaviors. Investigating genetic factors underlying motivations and emotions related to EDs, as well as specific behaviors and anthropometric phenotypes across the lifespan may provide novel insights into the psychiatric and metabolic causes and mechanisms underlying EDs.

EDs in youth

Disordered eating behaviors occur in young children, but can differ in clinical presentation. For example, “avoidant/restrictive food intake disorder (ARFID)” [ 56 ] occurs in 1.5–3.2% of children and adolescents [ 57 , 58 ], and is characterized by food restriction for a variety of non-weight related reasons, including sensory sensitivities (e.g., texture aversions), fear of choking or vomiting (i.e., phobic avoidance), or low interest in food and low appetite [ 59 ]. The restriction associated with ARFID does not include fear of weight gain or body dysmorphia [ 59 ] as in AN. Similarly, loss-of-control eating (LOC), a clear precursor to binge eating [ 60 ] occurs in more than one quarter of children with overweight or obesity [ 61 ], and is characterized by feeling unable to control what or how much one is eating [ 62 , 63 ]. Although both ARFID and LOC can occur alone, they also commonly co-occur with other psychiatric disorders. The risk of LOC is elevated in children with ADHD [ 64 ], anxiety [ 65 , 66 ], and in children who have experienced weight-related bullying [ 67 ], and the risk of ARFID is elevated among children with autism spectrum disorder [ 68 ], and vice-versa [ 69 ]. Moreover, both LOC and ARFID exhibit complex relationships with metabolic factors: for example, youth with LOC who showed greater anxiety had higher leptin levels [ 65 ] and more frequent metabolic syndrome [ 66 ]. The extent to which these childhood presentations are precursors for later AN, BN, and BED is not entirely clear; however, ongoing developmental research aims to characterize developmental continuities and discontinuities in EDs.

EDs in midlife and beyond

EDs that occur in midlife and beyond can represent persistent cases, relapsing cases in individuals with initial onset in childhood or adolescence, or most uncommonly, new onset cases [ 70 ]. The requirement for an extremely low BMI in AN diagnosis likely biases toward a younger cohort, as BMI naturally increases with age [ 71 , 72 ], perhaps explaining patterns of earlier AN incidence (peaking at 16 [ 73 ]) compared to Other Specific Feeding and Eating Disorder (OSFED; peak 18–30 [ 73 ]). Further, inclusion of amenorrhea in diagnostic criteria naturally biases clinicians towards people who menstruate i.e., missing pre-pubertal and post-menopausal females and males. EDs do, however, occur in midlife and beyond. In fact, Eating Disorder Examination-Questionnaire (EDE-Q) scores among women do not decline until after age 54, whereas scores in men peak at ages 55–64 [ 74 ]. Further, 15.7% of respondents aged 40–60 have clinically meaningful EDE-Q scores [ 75 ], and 13% of women aged 50+ report at least one core ED symptom [ 76 ]. Moreover, familiar factors are cited as contributors, including self-esteem [ 75 , 77 ], body dissatisfaction [ 78 , 79 ], BMI [ 79 , 80 ], perfectionism [ 78 ], and societal pressure for thinness [ 78 ].

What we know and do not know about ED genetics across the lifespan

Little is known about the genetic risk factors underlying ED onset at different ages. A recent GWAS examined genetic etiology of AN age-of-onset, and compared early onset (defined as <13 years of age) to typical-onset AN [ 81 ]. Distinct genetic risk factors were associated with early onset compared to typical onset, including a potentially causal correlation between younger age at menarche and early onset, and associations between typical age of onset and a range of anthropometric traits [ 81 ]. No explicit research exists on the genetics of age-of-onset in other EDs; nor have any studies to our knowledge investigated the genetics of later onset AN. However, given the shared and distinct features of EDs across the lifespan, including age-diverse samples will be essential to capture context- and developmentally-specific differences in environmental and genetic risk factors.

EDs affect individuals across socioeconomic groups

EDs affect individuals at all socioeconomic status (SES) levels. However, individuals with lower SES are less likely to receive screening or treatment for EDs and thus remain underrepresented among clinical samples [ 82 ], particularly in the U.S. Although early findings suggested that AN was associated with higher SES [ 83 ], a more recent systematic review of U.S. and Europe community and population-based studies concluded that EDs are not disorders of affluence [ 84 ]. Further, in a cohort of two million men and women in Sweden, a country with free or low-cost healthcare, an ED diagnosis was associated with parent education but not income after adjusting for education, suggesting that SES was not systematically associated with seeking healthcare for EDs [ 85 ]. Little is known regarding associations between EDs and SES in non-Western countries, likely due to the paucity of prevalence studies as discussed earlier. For example, in the 2010 Global Burden of Disease study, regions other than North American had poor coverage of epidemiological data on EDs [ 86 ]. In the aforementioned World Mental Health surveys, only one country (Columbia) was considered low-income, while the other 13 countries were upper-middle to high-income [ 40 ]. However, this study did not statistically compare prevalence across countries. In a study of National Health Insurance data from Taiwan, which includes 99% of the Taiwanese population, findings indicated that the incidence and prevalence of EDs had increased over the previous decade. However, estimates were lower than those obtained from community samples, suggesting that factors other than treatment affordability may have impacted treatment-seeking in this sample [ 87 ].

Other factors related to lower SES may be associated with increased risk for EDs. Some studies in U.S. samples have found evidence that food insecurity or insufficiency is associated with BED and BN [ 88 , 89 ], while stress and childhood adversity are associated with ED symptoms, further underscoring the need to ensure that individuals across the SES spectrum are represented in ED studies and treatment settings [ 90 , 91 ].

What we know and do not know about ED genetics and SES

Indicators of SES, including education, social deprivation, and household income, have heritable components [ 92 ], and studies have revealed genetic correlations between SES and psychiatric disorders [ 93 ]. A recent study found that SES was positively genetically correlated with AN [ 94 ]. Partitioning out the genetic SES variance resulted in reduced genetic variation for AN, and reduced genetic cross-trait associations among psychiatric disorders [ 94 ]. These results emphasize the importance of controlling for SES in order to reduce bias in estimates of genetic variance. A twin study revealed that neighborhood disadvantage was associated with increased disordered eating in girls across all stages of pubertal development, and the expected pubertal increases in genetic influences on disordered eating were only observed in girls from advantaged backgrounds [ 95 ]. Genetic influences on disordered eating were potentiated much earlier for girls living in disadvantaged contexts, suggesting interplay between genetic risk and SES.

EDs affect individuals of all body shapes and weights

Disproportionate attention to AN has obscured the fact that EDs occur in individuals of all body shapes and sizes. Although low BMI is required for a diagnosis of AN, BN can occur in individuals across the BMI spectrum, and BED occurs in individuals with typical and higher weight bodies. The DSM-5 now recognizes atypical AN (AAN) in which individuals meet all diagnostic criteria for AN including weight loss but do not present with low weight [ 20 , 96 ]. AAN has been associated with poor nutritional and medical status secondary to weight loss [ 97 ], poor quality of life [ 98 ], premorbid overweight and obesity [ 99 ], and history of weight-based teasing [ 100 ]. Despite this, individuals with AAN are less likely than those with AN to be screened for and to receive treatment [ 101 , 102 ]. Considerably more work is required to understand the full array of presentations of AAN across the diverse populations highlighted in this review.

What we know and do not know about ED genetics relative to body shape and weight

Genetic research has addressed body shape and weight in three ways. First, GWAS have highlighted shared genetic factors between AN and body shape and weight, including negative genetic correlations between AN and body fat percentage ( r  = −0.36), fat mass ( r  = −0.33), BMI ( r  = −0.32), waist to hip ratio (r = −0.2), hip circumference ( r  = −0.2) and waist circumference ( r  = −0.24) [ 1 ], suggesting that many of the same genes that increase risk for AN also contribute to these anthropometric traits. However, existing GWAS have focused exclusively on AN in individuals with low BMIs, leaving individuals with EDs in larger bodies unstudied (although such studies are underway). Second, applying polygenic risk scores (PRS) in biobank data demonstrates that AN-PRS are associated with weight loss, even among adults who have never been diagnosed with AN [ 103 ]. Further, while AN, BN, and BED have similar psychiatric trait associations, they diverge in their associations with metabolic and anthropometric traits [ 104 ]. Although AN and anthropometric measures are negatively correlated, BED is significantly positively associated with several body shape and weight measures, suggesting that BMI-associated genomic variants are broadly relevant for all three EDs, but may act in opposite directions [ 104 ]. Third, phenome-wide association studies (PheWAS) showed that AN-genes are associated with anthropometric traits (including lowest recorded weight and weight change over time) in a clinical cohort with no history of AN; further, AN-gene associations with chronic pain, substance use and cholesterol levels were mediated by BMI [ 5 ].

In addition, genetic research has the potential to shed light on the extent to which restrictive EDs in individuals with larger bodies (i.e., AAN) are genetically similar to AN. Comparing GWAS of AN and AAN could inform nosology and shed light on whether it is actually appropriate (from a genetic perspective) to label this presentation as a form of AN. Divergent results could inform whether AN and AAN share the same underlying genetics and only differ in BMI or represent genetically distinct syndromes.

Large-scale approaches to address diversity in ED genetics

In the Section “Background”, we outlined ways in which stereotypes and misconceptions have biased our understanding of and research on EDs. Here, we suggest five overarching foci to improve the applicability of genetic research on EDs to the full spectrum of afflicted individuals (Fig.  2 ).

Here we diagram the broad goals and specific actions we propose to address and the current challenges in eating disorder research. More detailed descriptions of the challenges and recommended actions are addressed in this review.

Broader and more inclusive recruitment

As there is no guarantee that the same genetic and environmental factors influence risk for EDs across demographic groups, innovative practices are essential to ensure representation of individuals of diverse ancestry, gender and sexual orientation, age, SES, and body sizes. Strategies to recruit and retain diverse participants have been discussed in detail elsewhere [ 105 ], but several core points warrant emphasis. First, participants report that seeing themselves represented in study personnel and in recruitment materials and websites increases interest in participation. Likewise, participants who share their personal stories about being from a minoritized group and suffering from an ED can help reduce shame and encourage participation. A clear explanation of why representation is important can also help potential participants decide to volunteer. Many fear that researchers desire for inclusivity is simply to tick a demographic checkbox, but feel more inclined to participate when they learn that their participation will contribute to ensuring that any treatments that emerge from the science will be relevant to others who share their background. Understanding the actual downstream implications of participation can be a powerful incentive to join a study. Finally, engaging participants in the process from the earliest phases of study design (i.e., co-design [ 106 ]) and providing regular updates about the study progress (websites, blogs) creates a sense of ownership and community that allows participants to feel like part of a larger team.

Building capacity

The ED research workforce is overwhelmingly white, which is also true for the ED genetics workforce. Building capacity to diversify the workforce has to start early in the educational trajectory. Recruiting interested individuals into science, technology, engineering and mathematics (STEM) as early as middle school (~ages 11–14) and engaging them in research related to eating, body composition, nutrition, psychology, psychiatry, and EDs will ensure a more diverse workforce in the future. Moving away from a purely sociocultural theory of ED etiology will engage more individuals interested in science (including genetics) and encourage more research on the biology of EDs.

Restructuring diagnostic guidelines and disease nosology

A recurring theme in Part 1 was the extent to which the narrow focus on young white thin females with AN in both research and in lay circles has shaped and biased the diagnostic schema, instruments, and research conclusions in the ED field. This restricted perspective has considerable downstream implications—from individuals outside of this stereotype who are neither detected nor referred for treatment, to who volunteers to participate in studies, to the conclusions that are drawn from samples that are mostly of European ancestry. The bias is compounding because any findings from these samples only serve to reinforce existing stereotypes about disease prevalence and presentation. Failure to include people of color and of size, other genders, and children and older people in our research studies severely limits our understanding. Moving the field forward will require a careful reconsideration of disease nosology and treatment guidelines. Guidelines should be restructured to consider differing presentations, behaviors, environmental risk factors, and psychological drivers, bearing in mind that many of the marginalized identities discussed in this review are intersectional, meaning that diagnostic criteria need to be flexible and applicable simultaneously to many different groups and presentations.

Researchers should also attend to nomenclature used outside of the DSM and ICD that often emerges from traditional and social media to describe dysfunctional eating behavior. Popular terms like disordered eating, body dysmorphia, food addiction, orthorexia, and relative energy deficiency in sport (previously female athlete triad) often capture trends in the population that describe what people are actually experiencing. The breadth in naming and lack of parallel to current treatment guidelines presents a variety of challenges. First, by using the above terms in the medical literature without defined criteria, we exacerbate challenges in clinical translation, as findings related to disordered eating might not easily be applied to a patient with AN or BN presenting to clinic. Second, we may unknowingly exclude historically marginalized groups who might find one of the above terms to be more representative of their lived experience. For example, if an individual identifies with a diagnosis of body dysmorphia, but researchers only recruit patients with atypical AN, we may miss including that participant and others like them. Lastly, the ED field suffers from chronic underfunding due in part to a dilution of recognition of the true prevalence of the disorders and resulting public health impact [ 107 ]. By addressing the many names and experiences lived with ED we can improve treatment access to the public and improve funding and discovery in research.

Success in this area will require a multi-pronged approach. First, the creation and deployment of more broadly useful screening tools and questionnaires should include opportunities to describe symptoms and behaviors falling outside stereotyped expectations for each condition; should not include BMI stratification or BMI-based inclusion/exclusion criteria; and should be appropriate cross-culturally.

Researchers should also explore alternative or additional phenotyping approaches that rely on observed behaviors, specific symptoms, and digital phenotyping. Other examples include electronic-health record-based phenotype inference [ 108 , 109 , 110 ] or analysis of specific reported symptoms and behaviors from population and biobank studies. However, we caution that these approaches are also susceptible to bias; creating phenotype algorithms without first interrogating any assumptions and implicit biases risks automating inequalities [ 11 , 111 ]. For example, a previous study used 18 ICD codes to identify potential AN cases in a large healthcare system [ 71 ], selecting positive cases for further chart review. However, 6/18 codes related or referred to menstruation (despite the demonstrated ineffectiveness of amenorrhea as a diagnostic criterion [ 112 , 113 , 114 , 115 ]), substantially biasing the sample towards people who menstruate.

Researchers should leverage insights from genetic studies to reshape disease nosology. Novel analytical approaches such as pathway-based PRS, transcriptomic imputations, and incorporating electronic and longitudinal health records afford researchers an unprecedented opportunity to study disease on an individual rather than population level. Such analyses might allow researchers to infer molecular subtypes of disease, identifying for example clinically-relevant subgroups associated with specific molecular signatures. Alternatively, these analyses might reveal that clinically distinct presentations are not rooted in genetic differences, rather stemming from societal or environmental exposures. Any assessment of environmental risk factors or correlates must account for the broad range of experiences that individuals with EDs from diverse backgrounds might have. Beyond the historical focus on the societal thin ideal, space must be made for assessing main effects of group-specific or shared factors (e.g., weight-based stigmatization or discrimination, food insufficiency, teasing and bullying, race-based discrimination) as well as gene x environment interplay. Understanding these disparate presentations, behaviors and symptoms will also represent a significant step towards personalizing treatment options, effectively identifying interventions and therapies that match specific symptoms and behaviors.

More sophisticated analytical approaches to refine phenotype-genotype associations

Although there are substantial insights to be gained from larger, more inclusive GWAS of AN, it is imperative that we expand our analytical approaches, adopting cutting edge statistical techniques in order to more fully elucidate the genetic architecture of EDs. Elegant and intentional study design may increase our power to understand disease as much as increasing sample size.

Substantial attention should be paid to approaches that can identify shared and distinct associations between ED diagnoses, or within disorders between subtypes. Explicit comparison of cases between psychiatric disorders has previously been shown to elucidate disorder-specific genic associations [ 116 ]. As such, genetic studies that compare and contrast AN and BN, for example, might increase our power to detect genetic correlates of shared and distinct symptoms and behaviors. These studies might include joint analysis across subtypes; case-case GWAS that explicitly compare individuals with different ED subtypes; PRS or LDScore approaches, or next generation analytical approaches such as genomic structural equation modeling (SEM). Further, these studies may also bring us closer to clinical utility: the diagnostic challenge for a clinician is rarely ‘whether’ an individual will develop a disorder: rather, the challenge is to identify the correct diagnosis among several similar possibilities, or to predict disease prior to onset. For this goal, differentiating AN from BN will be more useful than AN from controls.

Researchers should also investigate the role of potentially clinically relevant endophenotypes. For example, comparing genetic risk factors across the lifespan may elucidate relationships with specific biological pathways and mechanisms. Studies of younger cohorts may reveal the role of metabolic and hunger/satiety dysregulation in AN, whilst examining ED onset in older cohorts may elucidate specifically the role of psychiatric pathways. Investigating these groups may also yield insights into the role of hormones associated with menarche and menopause to ED pathology through BMI and/or body dissatisfaction [ 117 ]. A secondary analysis of a genome-wide association study of AN with 9,335 cases and 31,981 controls found that early-onset AN was significantly genetically correlated with younger age at menarche, and Mendelian randomization analysis supported a causal link between younger age at menarche and early-onset AN [ 81 ]. Further work needs to be completed to determine the hormonal relationship between estrogen fluctuations, appetite and satiety hormones, BMI, body satisfaction, and psychiatric phenotypes.

Researchers should also undertake approaches that can identify clinical consequences of genetic associations. For example, phenome-wide association studies (PheWAS) test for associations between genetic risk factors and the full patient phenome, including diagnostic records, reactions to medications, substance use/abuse, and longitudinal trajectories. These approaches might be particularly useful in disentangling whether specific comorbidities occur due to genetic pleiotropy (i.e., shared genetic underpinnings), healthcare pleiotropy (i.e., due to common mis-diagnosis, or as common ‘stops’ on a diagnostic trajectory), or due to diagnostically meaningful overlap.

Expand insights beyond genotype, towards biology and environmental interactions

Approaches that rely on genotype alone will ultimately be limited in the potential for translational and clinical insights. A full dissection of potential functional genomics approaches and integrative analyses is outside the scope of this review, and indeed has been explored in detail elsewhere [ 118 , 119 , 120 , 121 , 122 ]. However, we caution that researchers must consider factors beyond genetics in their interpretations of GWAS and consequent associations. Failure to consider the biological, environmental, and societal contexts under which genetic studies are conceived, recruited, and analyzed risks mis-interpreting or over-interpreting the relevance of our findings, and potentially entrenching bias and stereotypes throughout our research. Put simply, expanding our samples and approaches will be pointless if we do not also consider carefully all the implications of our findings.

We should be wary of over-interpreting differential heritability, correlations, or relative lack of genome-wide associations between two groups. For example, it might be tempting to interpret differential heritability between sexes as explaining sex differences in ED diagnoses. However, genetic associations are only as good as the phenotypes we provide; researchers should consider that phenotyping instruments might have differential power; diagnostic contamination might occur at different rates; disease severity might be substantially different between groups; and study participation rates may differ dramatically. If indeed researchers identify true sex-specific effects (or other differential associations across groups) that are not confounded by diagnostic differences, it is important not to default to assumptions of genetic essentialism [ 22 ]. Instead, the next step must be to consider how these interact with biology and environment to cause disease; for example, considering the effects of specific variants on hormone biology, age at menarche, or related factors that might influence ED development. Understanding the role of these environmental contexts will be key in pinpointing appropriate treatments in differing life stages and contexts, and perhaps in understanding why some treatments are less effective in certain patient groups.

Consideration of the impact of societal factors is also essential. These may include exposure to stress and early life adversity; access to therapy and/or healthcare; access to healthy foods and opportunities for exercise; and support networks of family and friends. On the surface these factors are not genetic; however, it is likely that they correlate with genetic factors, as evidenced for example by recent GWAS of SES [ 94 , 123 ] and loneliness [ 124 ]. Most obviously, healthcare access differs substantially among countries, and will likely influence disease trajectory, diagnostic rates, and study participation. Even within countries, systemic racism prevents equal access to early life support, healthcare services and referrals to specialists, and may increase exposure to a variety of disease risk factors [ 11 , 12 , 111 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 ]. These factors may confound our studies, with the degree of confounding significantly correlated with genetic factors. As such, we might expect our GWAS and genetic studies to be differentially powered across ancestries, as increased environmental risks in one group might decrease our ability to detect genetic associations [ 11 ]. These issues should be borne in mind when interpreting GWAS associations and underscore the need to collect large and diverse GWAS samples.

Finally, we note that expanding inclusion within our studies is vital to equity in research and clinical care. The ability to participate in studies and research, and access to the findings and benefits of that research, should be equally available to all. Increasing diversity will inarguably increase our insight and understanding of ED biology, and indeed of psychiatric disease genetics more broadly; however, the goal of inclusion and equity alone is a sufficient motivator. Research conclusions that emerge from the study of a narrow and privileged subset of individuals with EDs and the treatment approaches they generate overestimate our actual understanding of disease and further perpetuate already damaging health disparities. This work is both hard and expensive, but must be a priority to replace myths with facts and to sharpen our understanding of EDs.

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LMH is supported by NIMH (R01MH118278; R01MH124839); NIEHS (R01ES033630); the Klarman Family Foundation (2019 Eating Disorders Research Grants Program); the Seaver Family Foundation. JJ is supported by the NIMH (R01MH118278) and the Klarman Family Foundation (2019 Eating Disorders Research Grants Program). RS is supported by the Klarman Family Foundation (2019 Eating Disorders Research Grants Program). CMB is supported by NIMH (R01MH120170; R01MH124871; R01MH119084; R01MH118278; R01 MH124871); Brain and Behavior Research Foundation Distinguished Investigator Grant; Swedish Research Council (Vetenskapsrådet, award: 538-2013-8864); Lundbeck Foundation (Grant no. R276-2018-4581). YKW reports funding from International Society of Nurses in Genetics (ISONG).

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Laura M. Huckins, Rebecca Signer & Jessica Johnson

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Huckins, L.M., Signer, R., Johnson, J. et al. What next for eating disorder genetics? Replacing myths with facts to sharpen our understanding. Mol Psychiatry 27 , 3929–3938 (2022). https://doi.org/10.1038/s41380-022-01601-y

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• Katie Nicholls ,
• Nicola Boggis ,
• Nikila Pandya
• Department of Paediatrics , Maidstone and Tunbridge Wells NHS Trust , Kent, Aylesford , UK
• Correspondence to Dr Katie Nicholls, katie.nicholls2{at}nhs.net

Eating disorders in the form of anorexia and bulimia are becoming increasingly common in young adults and children. Most of the patients are initially seen by their general practitioner (GP) and it may take several months before the facts are pieced together and an underlying eating disorder is identified. However, other medical conditions, albeit rare, should be considered when assessing these young adults as potentially missing them can lead to devastating consequences. This case highlights how a 15-year-old girl who presented to her GP with a history suggestive of an eating disorder and had a body mass index below the 0.4th centile, in fact had classical symptoms and clinical signs of primary adrenal failure, or Addison's disease.

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Anorexia nervosa: a case study

• PMID: 1052188
• DOI: 10.1159/000286995

D.R., a single 19-year-old female experiencing anorexia nervosa, was admitted to a mental health center inpatient unit weighing 64 lb, approximately 54 lb underweight, with liver, kidney, and pancreas damage. D.R. was hospitalized for 59 days. Treatment consisted of utilizing a hierarchy of reinforcements in the form of privileges mutually agreed upon between patient and therapist, psychodynamic and supportive psychotherapy, and involvement in the ward milieu therapeutic program. All privileges had to be earned. Access to food was controlled by the staff. For pounds gained privileges were granted, for pounds lost privileges were curtailed. Dynamically, D.R.'s eating behavior was viewed as an unconscious spite and revenge reaction toward her parents as well as an attempt to elicit attention. At the time of discharge D.R. weighed 104.5 lb. Prior to discharge D.R. agreed that if her weight dropped below 100 lb she would return for readmission. Five months later D.R.'s weight stabilized between 102 and 104 lb. Two years later, D.R.'s weight remains at that level. The study cautions against using solely a behavior modification approach in the treatment of anorexia nervosa.

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Incidence, prevalence and mortality of anorexia nervosa and bulimia nervosa

Annelies e. van eeden.

a Parnassia Psychiatric Institute, The Hague, The Netherlands

b University of Groningen, University Medical Center Groningen, Department of Psychiatry, Groningen, The Netherlands

Daphne van Hoeken

Hans w. hoek.

c Columbia University, Mailman School of Public Health, Department of Epidemiology, New York, New York, USA

Purpose of review

To review the recent literature on the epidemiology of anorexia nervosa and bulimia nervosa in terms of incidence, prevalence and mortality.

Recent findings

Although the overall incidence rate of anorexia nervosa is considerably stable over the past decades, the incidence among younger persons (aged <15 years) has increased. It is unclear whether this reflects earlier detection or earlier age of onset. Nevertheless, it has implications for future research into risk factors and for prevention programs. For bulimia nervosa, there has been a decline in overall incidence rate over time. The lifetime prevalence rates of anorexia nervosa might be up to 4% among females and 0.3% among males. Regarding bulimia nervosa, up to 3% of females and more than 1% of males suffer from this disorder during their lifetime. While epidemiological studies in the past mainly focused on young females from Western countries, anorexia nervosa and bulimia nervosa are reported worldwide among males and females from all ages. Both eating disorders may carry a five or more times increased mortality risk.

Anorexia nervosa and bulimia nervosa occur worldwide among females and males of all age groups and are associated with an increased mortality risk.

INTRODUCTION

This review aims to provide an overview of the recently published studies on the epidemiology of anorexia nervosa and bulimia nervosa. It is an update of previous reviews on this subject in this journal [ 1 – 3 ]. For a review of the epidemiology of binge eating disorder, see Keski-Rahkonen in this issue [ 4 ]. 

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Epidemiological studies provide information about the distribution (who, when and where) of disorders in a defined population and its trends over time. For eating disorders, there are some methodological problems regarding epidemiological research. Eating disorders are relatively rare in the community and help seeking is often avoided or delayed, for example for reasons of denial (particularly in anorexia nervosa) or stigma and shame (particularly in bulimia nervosa). These factors make general population studies on eating disorders costly and ineffective. Several strategies have been used to beat this problem, in particular the use of psychiatric case registers and other medical record-based studies. We must bear in mind that the results of these studies are an underestimation of the occurrence of eating disorders in the community, because not all patients will seek help, will be detected by their general practitioner or be referred to healthcare services. Moreover, different rates over time could be due to different case detection systems and diagnostic criteria, increased awareness leading to earlier detection and referral, and broader availability of treatment facilities, instead of a true increase in occurrence [ 1 , 5 ].

To review the literature, we searched for articles published in English using Medline/PubMed , Embase, PsycINFO and Google Scholar, using several key terms relating to epidemiology, anorexia nervosa and bulimia nervosa. We also checked the reference lists of the articles that we found for any additional articles missed by the database search.

Incidence is the number of new cases of a disorder in a population over a specified period of time (usually 1 year). The incidence rate of eating disorders is commonly expressed per 100 000 persons per year (100 000 person-years). The study of newly developed cases of an eating disorder provides clues to unravel its etiology [ 6 ]. It is noteworthy that healthcare register-based incidence rates represent the situation at the moment of detection, which is likely to be later than the moment of disorder onset.

Incidence of anorexia nervosa

Martinez-Gonzalez et al. [ 7 ▪ ] conducted a systematic review and meta-analysis of 31 published studies from 1980 to 2019 on the incidence of anorexia nervosa in females, mainly from Western countries. The incidence rates varied widely depending on the methodology, population and diagnostic criteria used. They reported on the incidence rates of only three population-based studies: 120 per 100 000 person-years among Swedish females aged 20–32 years [ 8 ], 200 per 100 000 person-years among Spanish females between the age of 12 and 22 years [ 9 ] and 270 per 100 000 person-years in Finnish twin females aged 15–19 years [ 10 ]. The pooled incidence rate of studies based on outpatient healthcare services (8.8 per 100 000 person-years; 95% confidence interval, CI: 7.8–9.8) was higher than that of hospital admissions (5.0; 95% CI 4.9–5.1) [ 7 ▪ ]. Compared to these all-age rates, the pooled incidence rates were higher for females aged 10–29 years, both in outpatient healthcare services [63.7 per 100 000 person-years (95% CI 61.2–66.1)] and in hospital admissions [8.1 (95% CI 7.6–8.5)] [ 7 ▪ ]. Furthermore, for healthcare register-based studies the incidence rates of anorexia nervosa showed a significant increase over time, especially in outpatient healthcare services. This does not necessarily mean a true increase in the occurrence of anorexia nervosa, as it could represent improved public awareness, detection and treatment rates over time.

Few studies have examined the incidence of anorexia nervosa in the general population; a limitation also encountered in the systematic review by Martinez-Gonzalez et al. [ 7 ▪ ]. The most recent study by Silen et al. [ 11 ▪ ] assessed the incidence rate of anorexia nervosa between the ages of 10 and 20 years according to the Diagnostic and Statistical Manual of Mental Disorders 5th Ed. (DSM-5) criteria in Finnish twins born between 1983 and 1987, yielding an incidence rate of anorexia nervosa of 320 (95% CI 230–440) per 100 000 person-years in the total group, 580 (95% CI 430–810) per 100 000 person-years among females and 30 (95% CI 10–310) per 100 000 person-years among males. These rates are higher than the rates in females described by Martinez-Gonzalez et al. [ 7 ▪ ]. This might be due to the use of the ‘broader’ DSM-5 criteria for anorexia nervosa by Silen et al. [ 11 ▪ ], and to the fact that twins may share genetic and environmental risk factors for anorexia nervosa, leading to a potential overestimation.

Population-based incidence rates are much higher than those derived from primary care and healthcare facilities, reflecting the selection filters on the pathways to (psychiatric) care [ 5 ]. Studies in general practices present incidence rates at the earliest stage of detection within the healthcare system. There have been no recent publications on all age groups in primary care since the previous review in this journal [ 1 ], that included a Dutch primary care study [ 12 ] which examined new cases with anorexia nervosa in a large representative sample of the Dutch population. The overall incidence rate of anorexia nervosa in Dutch females and males of all ages in primary care was fairly constant during three decades: in 1985–1989 it was 7.4 (95% CI 5.6–9.7) per 100 000 person-years, in 1995–1999 7.8 (95% CI 6.0–10.1) and in 2005–2009 6.0 (95% CI 4.3–8.1) [ 12 ]. Although no new studies have been published on incidence rates of anorexia nervosa in the total primary care population, Wood et al. [ 13 ▪ ] investigated 11- to 24-year-olds in England and found stable incidence rates between 2004 and 2014 (27.4 per 100 000 person-years; 95% CI 26.0–29.0). Demmler et al. [ 14 ] studied the incidence rate of eating disorders (all combined) in general practices in the UK since 2008, and reported a slight decline. The authors ascribe this finding to a decreasing trend in incidence of bulimia nervosa and a stable level of anorexia nervosa incidence, but they did not report rates per eating disorder diagnosis. Another primary care study among 10- to 19-year-olds in the UK reported an increased incidence rate in the age group of 13–16 years for all eating disorders combined, comparing 2018 rates to those in 2003 [ 15 ]. It is unclear whether this reflects a true increase in incidence or a shifting in age at detection.

The study of Reas and Ro [ 16 ▪ ], which was included in the meta-analysis by Martinez-Gonzalez et al. [ 7 ▪ ], described recent time trends in the incidence of anorexia nervosa in persons aged 10–49 years, using secondary care data of the Norwegian National Patient Register. The overall incidence rates for males and females combined were stable (differences nonsignificant) from 2010 to 2016, both for narrowly defined anorexia nervosa (18.8–20.4 per 100 000 person-years) and for broadly defined anorexia nervosa (33.2–39.5 per 100 000 person-years). They were also stable per sex for narrowly defined anorexia nervosa: in females 36.3–42.3 per 100 000 person-years, and in males 2.2–4.0 per 100 000 person-years; and for broadly defined anorexia nervosa: in females 63.3–79.1 per 100 000 person-years, and in males 4.4–5.9 per 100 000 person-years. The male to female ratio was found to be 1 : 13 for narrowly defined anorexia nervosa and 1 : 14 for broadly defined anorexia nervosa. This is in accordance with other studies showing considerably lower incidence rates for males, usually by more than a factor of 10, in comparison to females [ 11 ▪ , 12 ]. The incidence of anorexia nervosa according to DSM-5 criteria in 8- to 17-year-olds was examined in secondary care services in the UK and Ireland [ 17 ]. The overall incidence rate was 13.7 (95% CI 12.9–14.5) per 100 000 person-years; in females it was 25.7 (95% CI 24.1–27.3) and in males 2.3 (95% CI 1.8–2.8).

In females, the highest incidence rate of anorexia nervosa is around the age of 15 [ 11 ▪ , 12 , 17 ]. Several studies report a remarkable increase in the incidence of anorexia nervosa among girls aged 10–14 years [ 16 ▪ , 17 ]. Although most research has been performed in young females, some studies report incident anorexia nervosa cases in later life as well [ 12 , 16 ▪ ]. It is noteworthy that the peri-menopausal period has been suggested as another high-risk period in female life for the onset or recurrence of eating disorders [ 18 , 19 ]. In males, findings regarding the peak period of anorexia nervosa onset are less clear. While some studies have shown comparable [ 11 ▪ ] or a somewhat higher (age 16) peak age of onset [ 17 ], others found lower peak ages of 12–13 years [ 20 ] in comparison to females.

In summary, recent studies on time trends show fairly stable incidence rates for anorexia nervosa in the last decades [ 12 , 16 ▪ ], although some healthcare register-based studies suggest an increase in the incidence of anorexia nervosa [ 7 ▪ ], which might be explained by greater public awareness, better detection and the use of broader diagnostic criteria. Incidence rates in males are found to be lower, usually by more than a factor 10, in comparison to females [ 11 ▪ , 16 ▪ ]. The rates in males should be interpreted as an underestimation because of underdetection due to a double stigma: the stigma of having a psychiatric disorder, and an additional stigma of suffering from a ‘female-specific’ disorder [ 21 ]. Finally, the finding that the incidence of anorexia nervosa is increasing in younger girls (<15 years) has important implications for future research into risk factors [ 22 ], the development of prevention programs for younger subjects, and the planning of healthcare services.

Incidence of bulimia nervosa

Few studies have investigated the incidence of bulimia nervosa. In the population cohort study of Finnish twins born in the 1980 s, the incidence rate of DSM-5 bulimia nervosa between 10 and 20 years of age was 100 (95% CI 60–190) per 100 000 person-years overall, and 180 (95% CI 110–340) per 100 000 person-years in females [ 11 ▪ ]. These population-based DSM-5 rates of bulimia nervosa are higher than DSM-IV rates for females aged 10–19 years identified in Dutch primary care (range 20.5–22.0 per 100 000 person-years) [ 12 ], partly because of the use of broader DSM-5 criteria in the Finnish study [ 11 ▪ ], but moreover because of the fact that only a small proportion of community ‘cases’ present to (primary) care [ 3 , 5 ]. It is of note that the Finnish study [ 11 ▪ ] investigated the incidence rate between 10 and 20 years of age, which only partly covers the peak age period of 15 to 29 years suggested by other studies [ 12 , 16 ▪ ].

The Dutch primary care study showed a significant decrease in the all-age incidence rate of bulimia nervosa according to DSM-IV criteria over three decades: in 1985–1989 it was 8.6 (95% CI 6.7–11.0), in 1995–1999 6.1 (95% CI 4.5–8.2) and in 2005–2009 3.2 (95% CI 2.0–4.9) per 100 000 person-years [ 12 ]. The English primary care study in 11- to 24-year-olds also showed a significant decline in the incidence rate of bulimia nervosa between 2004 and 2014 (incidence rate ratio: 0.5; 95% CI 0.3–0.7) [ 13 ▪ ]. Also, Demmler et al. [ 14 ] explained their all-age finding of a slight decrease in the incidence rate of all eating disorders combined in primary care to a declining trend in incidence of bulimia nervosa.

Findings of the Norwegian National Patient Register study [ 16 ▪ ] support a significant decline in overall incidence rates of bulimia nervosa in secondary care between 2010 and 2016, both in narrowly defined bulimia nervosa [2010: 18.5 per 100 000 person-years (95% CI 16.9–20.2); 2016: 16.1 (95% CI 14.6–17.2)] and in broadly defined bulimia nervosa (2010: 29.4 per 100 000 person-years (95% CI 27.4–31.5); 2016: 26.9 (95% CI 24.9–28.8). A significant decrease in incidence rates was found in all age groups, except for a trend of an increase among girls aged 10–14 years, suggesting a shift to earlier ages of onset or detection. The peak incidence was among females aged 20–29 years. In males, the incidence rates were low and stable over time, ranging between 0.9 and 1.6 for narrowly defined bulimia nervosa, and ranging between 1.7 and 2.5 for broadly defined bulimia nervosa. The male to female ratio was found to be 1 : 24 for narrowly defined bulimia nervosa and 1 : 26 for broadly defined bulimia nervosa. Incident cases of bulimia nervosa also occur in later life [ 12 , 16 ▪ ].

In conclusion, there is a decline in incidence rates of bulimia nervosa over time. The peak age of incidence ranged between 15 and 29 years. Studies of incidence in males are scarce, but the rates are found to be much lower than in females.

Incidence of anorexia nervosa and bulimia nervosa in non-Western countries

Most epidemiological studies on eating disorders have been conducted in Western countries. Although studies assessing the epidemiology of eating disorders in non-Western countries are still scarce, we will highlight the most recent findings. Two Taiwanese studies [ 23 ▪ , 24 ] used national health insurance claim data to investigate the epidemiology of eating disorders between 2001 and 2013 in 10- to 49-year-old persons. In comparison to Western countries, the overall anorexia nervosa incidence rate in Taiwan is very low (1.1–1.3 per 100 000 person-years), but stable over time. Regarding bulimia nervosa, the incidence rates in Taiwan among females increased in the years up to 2009 [21.6 (95% CI 17.8–25.4) per 100 000 person-years] and then decreased [16.3 (95% CI 12.8–19.8) per 100 000 person-years] [ 24 ], following the trend in changes in incidence of Western countries, although a decade later. The incidence in Taiwan differs from that in Western countries in terms of older age at detection of anorexia nervosa and bulimia nervosa (20–29 years) and an increase in incidence among adults rather than adolescents [ 23 ▪ , 24 ]. This last finding aligns with findings of increasing numbers of persons in midlife with incident eating disorders in Western countries [ 19 ].

A study using data and methodology from the Global Burden of Disease (GBD) Study 2017 [ 25 ] reported increasing incidence rates of anorexia nervosa and bulimia nervosa from 1990 to 2017 in China, which is in contrast with the stable (anorexia nervosa) and decreasing (bulimia nervosa) rates in Western countries, but in line with the general trend of an increase in rates in all psychiatric diagnoses in China. Because of methodological issues related to the low prevalence and lack of global coverage of epidemiological studies for eating disorders, GBD calculations on these data must be interpreted with caution [ 26 , 27 ]. In this case [ 25 ], study results were difficult to check because 15 of the 39 publications from which data were included had been published in Chinese. From the abstracts of the included studies it would appear that in at least 26 of the 39 publications no formal eating disorder diagnosis had been applied, and that none of the studies addressed incidence. This casts doubts on the validity of the findings.

Prevalence is the proportion of cases in a population present at a certain point or interval in time. The point prevalence is the prevalence at a specific date (point) in time. The 12-month prevalence is the prevalence over an interval of a year. The lifetime prevalence is the proportion of the population that has had the disorder at any moment in life up to the moment of registration. In general, lifetime prevalence rates are higher than point and 12-month prevalence rates, especially when assessed in older populations. Prevalence indicates the demand for care and is therefore useful in the planning of healthcare facilities. Many studies have assessed the prevalence of anorexia nervosa and bulimia nervosa. In this review, we focus on recently published systematic reviews and meta-analyses, supplemented by recently published population-based studies that have not been included in the described reviews and meta-analyses.

Prevalence of anorexia nervosa

Galmiche et al. [ 28 ] have performed an extensive systematic review of 94 studies published between 2000 and 2018 that addressed the prevalence of formally diagnosed eating disorders in the general population. They explained the high variability of prevalence rates by the use of different diagnostic instruments [most commonly used: Structured Clinical Interview for DSM (13%), Composite International Diagnostic Interview (12%) and Eating Disorder Examination (11%)], diagnostic criteria [DSM-IV (78%), DSM-5 (14%) and DSM-III-R (4%)] and clinical investigation methods [face-to-face interview (51%), paper-and-pencil questionnaire (27%) or online or by telephone (22%)]. Weighted means were constructed from the prevalence rates and the population size of each study included, but were most likely not stratified for age. No confidence intervals were provided, only minimum-maximum ranges of the prevalence rates. The authors themselves conclude that the small number of studies makes it difficult to estimate weighted mean sex ratios. These limitations hamper the interpretation of some findings that are at odds with previous literature, in particular for point prevalence and 12-month prevalence rates. We therefore reproduce only the ranges of lifetime prevalence rates of anorexia nervosa, which were 0.1% to 3.6% in females and 0% to 0.3% in males.

Another systematic review and meta-analysis by Qian et al. [ 29 ] included 33 studies published between 1990 and 2020 on the prevalence of anorexia nervosa in the population. All studies combined, an overall lifetime prevalence rate of 0.2% (95% CI 0.06–0.3) was found. In studies applying DSM-5 criteria (18%; all in Western countries) a higher overall lifetime prevalence rate was found [0.9% (95% CI 0.7–1.1)]. This is in line with previous research showing an increase in anorexia nervosa prevalence rates when applying DSM-5 criteria, in comparison to rates according to DSM-IV criteria [ 30 , 31 ]. Lifetime prevalence rates in males and females (Table ​ (Table1) 1 ) were in the lower range of the rates described in the review of Galmiche et al. [ 28 ]. This could be explained by a large proportion of studies that had been conducted in Asia (40%) with very large sample sizes and much lower rates compared to Western countries, and the broader period studied (1984–2017) with especially lower prevalence rates before 2000 [ 29 ]. That is in contrast to findings described in a previous review in this journal [ 1 ] and to the notion that anorexia nervosa rates in Asian countries have been increasing in recent years and that they currently appear to be comparable to, or even higher than, those in Western countries [ 32 – 34 ]. In the review by Qian et al. [ 29 ], 6 of the 33 studies included had been published in Chinese and so the results were difficult to evaluate. However, there seems to be a lack of population-based studies using formal diagnostic interviews and applying DSM (-III-R, -IV, or -5) or International Classification of Diseases 10th Ed. (ICD-10) criteria. In Asia ‘non fat-phobic’ presentations of anorexia nervosa are common. In the DSM-5 the possibility of ‘persistent behaviour that interferes with weight gain’, which would apply to nonfat phobic presentations, is added to the DSM-IV B-criterium ‘intense fear of gaining weight or becoming fat’. Thus, the replacement of DSM-IV by DSM-5 criteria for anorexia nervosa will ultimately lead to higher rates among Asian people.

Overview of recently published studies on prevalence rates. Studies are grouped by design and listed in chronological order

CI, confidence interval; NR, not reported; SD, standard deviation; SE, standard error.

In their systematic review, Lindvall Dahlgren, Wisting and Ro [ 35 ] focused specifically on the prevalence of DSM-5 defined anorexia nervosa in the general population. Nineteen studies published until 2017 were included. Lifetime prevalence rates for anorexia nervosa in females differed according to the study method; 1.7–3.6% in studies with two-stage design and 0.8–1.9% in interview-based studies. Point prevalence rates in females ranged from 0.06% to 1.2%, predominantly assessed with self-reports.

Since this systematic review [ 35 ], several studies [ 11 ▪ , 36 ▪▪ , 37 , 38 ▪ , 39 – 43 ] have been published that investigated prevalence according to DSM-5 criteria. The prevalence rates reported in these recent studies are shown in Table ​ Table1 1 and are largely in line with those reported in the review. However, the population-based study of Finnish twins born in the 1980 s [ 11 ▪ ], in which the whole sample was diagnostically interviewed, found higher lifetime prevalence rates for anorexia nervosa: 6.2% (95% CI 4.6–8.3) in females and 0.3% (95% CI 0.08–1.3) in males. Suggested explanations for the higher rate found among females were the twin nature of the study, the thorough anorexia nervosa assessment and Finnish socio-cultural characteristics favouring a drive for thinness. Only 55% of the females identified with anorexia nervosa in the study reported that they had been diagnosed in real life by a healthcare professional.

Although epidemiological studies have mainly focused on the traditionally known high-risk group of young females, it has been shown in recent years that anorexia nervosa is prevalent among older persons as well [ 18 , 19 ]. The highest lifetime prevalence rates are found in adults, because of the accumulation of anorexia nervosa first emerging in the peak age period of adolescence [ 44 ] combined with incidence later in adulthood. A longitudinal, population-based study among Polish males showed that anorexia nervosa was prevalent in all age groups (10–80 + years) [ 45 ]. Although a decrease in point prevalence among females over a 30-year follow-up period was found, with no anorexia nervosa cases by age 50 [ 46 ▪ ], the 12-month prevalence rate in 40- to 50-year-old females was still 0.2% in another study [ 36 ▪▪ ].

Prevalence of bulimia nervosa

The three previously discussed systematic reviews and meta-analyses [ 28 , 29 , 35 ] also reported prevalence rates for bulimia nervosa. The lifetime prevalence rates for bulimia nervosa ranged from 0.3% to 4.6% in females and from 0.1% to 1.3% in males in the extensive systematic review by Galmiche et al. [ 28 ]. As discussed previously, we refrain from reproducing the 12-month and point prevalence rates they report for methodological reasons.

Qian et al. [ 29 ] reported an overall lifetime prevalence rate for bulimia nervosa of 0.6% (95% CI 0.3–1.0). This review included a relatively large (40%) proportion of Asian studies. For bulimia nervosa the lifetime prevalence in Western countries was 7.3 times higher than that in Asian countries. The lifetime prevalence rates in females and males (Table ​ (Table1) 1 ) were close to the rates described by Galmiche et al. [ 28 ]. The pooled overall lifetime prevalence rate rose up to 1.4% (95% CI 0.0–6.3), when using only studies that applied DSM-5 criteria (18%; all in Western countries) [ 29 ]. Other studies supported this increase [ 30 , 31 ], which could be explained by the lower required frequency of binge eating and compensatory behaviour in DSM-5 compared to DSM-IV.

Lindvall Dahlgren et al. included only studies that had applied DSM-5 criteria and found few studies on bulimia nervosa, but the authors reported preliminary evidence for an increase in bulimia nervosa prevalence [ 35 ]. Two two-stage studies reported a point prevalence rate of 0.6% in females [ 30 , 48 ]. The lifetime prevalence rate was found to be 2.6% among females in one interview-based study [ 49 ]. In self-report studies, point prevalence rates ranged from 0.5% to 8.7% in females.

Since these systematic reviews, several studies on the prevalence of DSM-5 defined bulimia nervosa [ 11 ▪ , 36 ▪▪ , 37 , 38 ▪ , 40 – 43 , 47 ▪▪ ] have been published in recent years. Among females, lifetime prevalence rates around 2.3% (range 2.1–2.6%) were consistently found [ 11 ▪ , 36 ▪▪ , 42 , 47 ▪▪ ], which gives further support for an increase in bulimia nervosa prevalence since the introduction of DSM-5 criteria. Only one study in a large population-based sample of US adults [ 38 ▪ ] reported a substantially lower lifetime prevalence rate [0.5% (Standard Error 0.06)] in females. Possible explanations for this low rate are the use of lay interviewers rather than clinicians and the use of a questionnaire that has not been validated for eating disorder diagnoses. The combination of these factors could lead to underreporting, especially in the case of bulimia nervosa where stigma and shame around bingeing and purging play an important role.

Few recent studies reported on prevalence in males. The results were in the same order as found in the systematic reviews [ 28 , 29 ], with lifetime prevalence rates ranging between 0.1% and 1.2% [ 11 ▪ , 38 ▪ , 47 ▪▪ ]. In males like in females [ 36 ▪▪ , 46 ▪ ], bulimia nervosa does occur in all age groups up to the age of 80, although the prevalence declines after age 30 [ 45 ].

The preliminary evidence for an increase in prevalence of bulimia nervosa in population-based studies is noteworthy in the face of decreasing incidence rates in primary and secondary care. One possible explanation is that people who have a lower frequency of binge eating and compensatory behaviour (meeting DSM-5 but not DSM-IV criteria, i.e. once a week) seek help less often than those who have this behaviour more often, and thus are less often included in care-based studies. Future research is needed to clarify this apparent discrepancy.

Mortality could be described as an incidence rate in which the event being measured is death. The crude mortality rate (CMR) is the number of deaths within the study population over a specified period. The standardized mortality ratio (SMR) is the ratio of observed deaths in the study population versus that of expected deaths in the population of origin. For comparison reasons the SMR is preferred, because the CMR is not standardized for age and sex. Mortality is often used as an indicator of the severity of a disorder.

In a previous review in this journal [ 27 ], it has been reported that both anorexia nervosa and bulimia nervosa were associated with significantly increased mortality rates. In comparison to age-matched and sex-matched people in the general population, the mortality risk was around two times higher in people followed up after outpatient treatment for anorexia nervosa, or after any treatment for bulimia nervosa. In people followed up after inpatient treatment for anorexia nervosa, the mortality risk was even over five times higher. Since this previous review, a few new studies have been published.

In a landmark meta-analysis of worldwide eating disorder mortality rates by Arcelus et al. [ 50 ] the CMR of anorexia nervosa patients was 5.1 deaths per 1000 person-years (95% CI 4.0–6.1). The SMR was 5.9 (95% CI 4.2–8.3), i.e. an almost 6 times increased risk. In a recent study, after 5 years follow-up the SMR of anorexia nervosa inpatients with (complications of) severe malnutrition was found to be as high as 15.9 (95% CI 11.6–21.4) [ 51 ]. This study population was probably more severely affected than most of the study populations included in the meta-analysis [ 50 ]. For bulimia nervosa, Arcelus et al. reported a CMR of 1.7 per 1000 person-years (95% CI 1.1–2.4) and a SMR of 1.9 (95% CI 1.4–2.6) [ 50 ]. Recently, in a large 12-year follow-up study a higher mortality risk was found in females after inpatient treatment for bulimia nervosa compared to similar-age females hospitalized for pregnancy-related events [adjusted hazard ratio 4.7 (95% CI 2.1–10.8)] [ 52 ]. This difference could be even larger when compared to the general population. Iwajomo et al. investigated mortality after hospitalization for an eating disorder (anorexia nervosa, bulimia nervosa or eating disorder not otherwise specified) in a Canadian population-based cohort [ 53 ▪ ]. Although results were not presented for each eating disorder separately, the total SMR was five times higher compared to the general population [SMR 5.1 (95% CI 4.8–5.3)]. Rates were higher for males [SMR 7.2 (95% CI 6.6–8.0)] compared to females [SMR 4.6 (95% CI 4.3–4.9)]. This is in line with other recent studies that also found higher mortality rates among males: in people treated for bulimia nervosa in secondary mental healthcare services an overall SMR of 2.5 (95% CI 1.5–4.0) was reported, with significantly higher rates among males compared to females [crude hazard ratio 5.4 (95% CI 1.8–16.5)] [ 54 ]. In another study on hospitalization for anorexia nervosa, in-hospital mortality in males was more than twice that for females [odds ratio 2.4 (95% CI 1.5–3.8)] [ 55 ]. However, in a study directly comparing males and females from the same hospital, from the same treatment period and for the same follow-up period, no significant differences in SMR were found for anorexia nervosa or for bulimia nervosa [ 56 ▪ ], which might be due to the relatively small sample size of males. The SMRs for each sex-group [ 57 , 58 ] have already been described in the previous review [ 27 ]. While there were no significant differences in mortality rates, males with anorexia nervosa or bulimia nervosa did die sooner in comparison to females with anorexia nervosa or bulimia nervosa [ 56 ▪ ].

In summary, recent findings accentuate high mortality rates for anorexia nervosa and bulimia nervosa, with highest rates among those who received inpatient treatment for anorexia nervosa. Although results are still inconclusive, the suggestion that males have a probably higher mortality risk than females underscores the clinical relevance of detecting and treating anorexia nervosa and bulimia nervosa in males.

Anorexia nervosa and bulimia nervosa occur among females and males of all age groups worldwide and are associated with an increased mortality risk. The trend of a decreasing peak age at incidence has implications for future research into risk factors, the development of earlier prevention programs and planning of treatment services. Besides the well-known risk group of young females from Western countries, the occurrence of anorexia nervosa and bulimia nervosa in males, older persons and non-Western countries highlights the need for further research in these groups. Moreover, improved awareness will lead to earlier detection and treatment in these groups that suffer from an extra stigma of a ‘young, Western, female-specific’ psychiatric disorder.

Acknowledgements

The authors would like to thank Judith Offringa for her editorial assistance.

Financial support and sponsorship

Conflicts of interest.

There are no conflicts of interest.

REFERENCES AND RECOMMENDED READING

Papers of particular interest, published within the annual period of review, have been highlighted as:

• ▪ of special interest
• ▪▪ of outstanding interest

• Open access
• Published: 20 August 2024

Views and experiences of eating disorders treatments in East Asia: a meta-synthesis

• See Heng Yim 1 , 2 &
• Ulrike Schmidt 1 , 2  

Journal of Eating Disorders volume  12 , Article number:  120 ( 2024 ) Cite this article

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Introduction

Although there have been qualitative meta-syntheses on experiences of eating disorders treatments, there is a paucity of syntheses specifically examining the perspectives and experiences of eating disorders treatments (ED) in East Asia (EA). Such synthesis could facilitate a better understanding of culture-specific perspectives and experiences. This review complements a quantitative scoping review published on ED treatments in EA (Yim & Schmidt, 2023), where most interventions reviewed focused on cognitive behavioural therapy (CBT) and internet interventions. The present meta-synthesis summarises stakeholders’ views on treatments and to synthesise clinical and research recommendations.

A systematic search of five databases and a citation search were conducted to identify relevant studies and data were analysed using thematic synthesis. Out of the 301 studies found, a total of 12 papers were included in the analysis.

A diverse range of treatments, such as family therapy, paediatric/psychiatric inpatient care, CBT, and counselling, were discussed. Three overarching themes were identified: Delineating Physical and Psychological Recovery; ‘I am not alone in this battle’; and Barriers to Change. The themes further delve into the various obstacles to recovery, including financial concerns and limited access to professionals and services. Culture-specific factors include family obligations and promoting family harmony. Balancing interdependence and independence from one’s family, as well as understanding family body ideals versus broader societal body ideals, are important considerations in ED interventions.

Some themes paralleled other qualitative syntheses, highlighting improved family relationships, perceived authoritarianism in treatments, and financial barriers. The review extends beyond the previous findings, revealing nuanced factors like family roles, cultural values, and norms. Clinical recommendations include incorporating family context in treatment and considering cultural influences on body image ideals. Capacity building through telemedicine and increased training is essential for advancing ED treatment in East Asia. Continued research is needed to better understand and treat people affected by ED in EA.

Plain English Summary

Research on eating disorders (EDs) treatment mainly focuses on Western countries, with little exploration of experiences in East Asia. To fill this gap, we reviewed 12 studies on the perspectives of individuals, families and clinicians regarding EDs treatments in East Asia. Our synthesis identified three main themes:

Physical and Psychological Recovery : Effective treatment needs to address both physical and mental aspects of recovery.

Finding Support – ‘I am not alone in this battle’ : Many individuals find strength in knowing they are not alone.

Barriers to Change : Obstacles like financial difficulties, limited EDs knowledge from professionals, and cultural factors can hinder recovery.

Cultural-specific factors such as family obligations and maintaining family harmony can impact on treatment motivation and effectiveness. Balancing family’s wishes/ interdependence and personal aspirations/ independence can also be a challenge. Our findings highlight the need for culturally sensitive treatments. Expanding telemedicine and increasing provider training can also help overcome treatment barriers. In conclusion, understanding cultural and contextual factors is essential for developing effective support systems and improving ED treatment outcomes in East Asia.

Eating disorders (EDs) research has been historically centred in the Global North. However, in the past decade, more attention has been paid to non-WEIRD (Western, Educated, Industrial, Rich, Democracies) populations. Reviews report an increasing incidence of EDs in regions in East Asia (EA), where the prevalence of EDs may now be comparable to that reported in North America or Europe [ 1 ]. Young females are seen as an at-risk population for developing EDs in almost every country in EA. The exceptions include North Korea, because as of 2023, there have been no studies conducted in that country. There is also no epidemiological study on EDs in Mongolia [ 2 ]. Chen et al. [ 2 ] also report that in China, the prevalence of binge eating disorder (BED) exceeds that of bulimia nervosa (BN), with both being higher than the prevalence of anorexia nervosa (AN).

Different cultural factors have been hypothesised to contribute to the development and maintenance of EDs. Previous studies suggest that self-construal, which refers to how individuals define themselves in terms of independence from or interdependence with others, could influence treatment seeking when experiencing psychological distress [ 3 ]. Asians, who often endorse collectivistic values and exhibit interdependent self-construal, may articulate treatment goals in terms of benefiting their family. Another relevant concept is family harmony, particularly emphasised in ethnic Chinese culture, the largest ethnic group in EA. Values such as promoting interpersonal and family harmony and ‘saving face’ are seen as important and may affect help-seeking behaviours [ 4 ]. Contemporary EA societies face conflicting collectivistic and individualistic values where people grapple with bicultural contextual forces. Negotiating these conflicting value systems can lead to identity conflict, potentially serving as risk factors for body dissatisfaction and disordered eating [ 5 ]. Dysfunctional psychological individuation, the process of developing a sense of self and transitioning from hierarchical to symmetrical (more equal relationship between equal adults) parent-child relationships, is linked to the development of mental health conditions [ 6 ]. Additionally, values such as filial piety may hinder the process of individuation from the family [ 7 ].

Body image disturbance has been a core diagnostic criterion in the West. Research on body image dissatisfaction in EA has been mixed. Sing Lee [ 8 ] identified the presence of non-fat-phobic AN in EA, differentiating from the EDs phenotype in the West. Other studies have consistently identified high drive of thinness and body dissatisfaction in countries such as China [ 9 ] and South Korea [ 10 ]. Whilst earlier studies suggested that Westernisation is a factor in body image disturbance in EA [ 11 ], other researchers have challenged these findings. A 12-month prospective study found that Asian women reported more pressure and body comparison from social media depictions from Asian media when compared to Western media, suggesting that Asian media influences were more salient [ 12 ]. Other cross-cultural studies identified that Chinese American students have less body dissatisfaction than other American students [ 13 ]. That said, the impact of Westernisation may be reflected in the racialisation of body, where Asian Americans may be more distressed by certain body parts such as the shape of their eyes/nose, or their breast size [ 14 ]. Although it is difficult to directly compare East Asians living in the diaspora or as international students with those East Asians that are residing in their home countries, the research findings point to the nuanced influence of Westernisation on body ideals.

Policy, alongside cultural norms, can significantly influence individuals’ mental health and recovery. China’s historical One Child Policy (OCP) has been a focal point of research, examining how the policy led to an imbalanced gender ratio in China with more males than females, as well as how being an only child may impact social development compared to having siblings. Some studies suggest that only children may exhibit more self-centred and competitive behaviours [ 15 ], others report contradictory findings. For instance, Settles et al. [ 16 ] referenced the heightened pressure from parents onto their only children to excel academically, equating academic success with overall success [ 16 ]. Additionally, the systemic devaluation of females is evident, as seen in Zhejiang Province, China, where couples were allowed a second child only if the first child was a girl.

Yim & Schmidt [ 17 ] conducted a systematic scoping review on psychological treatments for EDs in EA. Compared to Europe and North America, there were significantly fewer EDs intervention studies. Out of the 18 published studies, most were feasibility or uncontrolled studies, but they generally showed good intervention acceptability and positive effects on ED symptoms. Notably, cognitive therapies were the predominant approach used, with family therapy largely absent in the literature despite being a first-line treatment for EDs in countries like the UK [ 18 ]. Qualitative studies in EA can complement quantitative findings. For instance, [ 7 ] described a culturally-adapted family therapy model based on the Micucci [ 19 ] approach. This model views the family’s response to the illness as a symptomatic cycle and aims to address family conflicts, including marital issues, which distinguishes it from ED-focused family therapies like Family-based treatment (FBT) and the Maudsley model (FT-ED). Additionally, the model focuses on promoting individuation of the young person from their family. Tan et al. [ 20 ] described the most helpful family involvement in the Asian context would be maternalistic, where family is a supportive, caring and loving, rather than paternalistic, which is seen as taking control of the decisions. Yim & Schmidt [ 17 ] also reported structural adaptations of EDs treatments such as having shortened treatment sessions for practical reasons, where healthcare is not free and specialist centres are far away in some regions in EA.

Qualitative synthesis provides a richer understanding that goes beyond understanding the effects of interventions on symptoms, and include stakeholders’ views, perceptions and experiences of treatments. To our knowledge, there is no qualitative synthesis of EDs treatment experiences nor professionals’ views of ED treatments in EA. A previous synthesis looked at experiences of family-based treatment (FBT) for AN among adolescents [ 21 ]. Themes such as relinquishing control ambivalently (initial treatment resistance, authoritative care), improved family relationships, and failure to address family issues were identified. Such synthesis can facilitate a better understanding of culture-specific perspectives of all stakeholders, which may lay a foundation for hypothesis-generation and testing in future EDs interventions research. Hence, the aim of this review is to synthesise the views and experiences of patients, families and healthcare professionals of EDs treatments in EA, with a particular focus on the cultural aspects influencing treatments.

The search was conducted according to the Enhancing Transparency in Reporting the synthesis of Qualitative research (ENTREQ) statement [ 22 ]. The search strategy was devised in consultation with a specialist librarian, and included both a database and citation search. Four English databases were comprehensively searched: Embase, Global Health, Ovid Medline, APA PsycINFO (any time till June 2024). As researcher SHY also understands Chinese, the Chinese research database was also searched ( https://oversea.cnki.net/kns/defaultresult/index ) with the search term eating disorders (饮食/进食失调) using subject headings search. Search terms were (eating disorder* or bulimia or anorexia or binge eating or disordered eating or ARFID or Avoidant Restrictive Food Intake Disorder) AND (China or Hong Kong or Taiwan or Macau or Macao or Mongolia or Japan or Korea or Chinese or Taiwanese or Mongolian or Japanese or Korean or east Asia or east Asian or far east) AND (qualitative or interview). Keyword search and subject heading search together with title/abstract search was done (see supplementary info for an example of search string).

Inclusion criteria .

Peer-reviewed qualitative studies on the views, experiences or perceptions of EDs interventions, from service providers, patients, or families in East Asia. Regions in East Asia include China, Hong Kong, Japan, Macau, Mongolia, North Korea, South Korea and Taiwan (Asia Society, https://asiasociety.org/countries-regions/east-asia ).

Articles published in English or Chinese.

Exclusion criteria .

Studies on the East Asian diaspora.

Descriptive studies or single case study without a clear qualitative data collection and analysis methodology, clinical opinion papers.

Books, dissertations, conference abstracts.

Data analysis and extraction

Screening and deduplication were done on Rayyan software [ 23 ]. Thomas and Harden [ 24 ] thematic synthesis method was chosen for its suitability in understanding people’s views and experiences of EDs treatments to inform clinical practice, as opposed to developing theories or models like grounded theory. As no previous reviews existed in this area, integrating existing studies in a review was crucial for informing future clinical practice and research. Unlike quantitative meta-analysis, which focuses on prediction, this method emphasises interpretive explanations. In this study approach, although the data search was systematic, the purpose of study inclusion was purposive rather than exhaustive, aiming for conceptual understanding rather than data saturation. SHY independently conducted the screening of the texts and discussed any uncertainties with US.

The analysis proceeded in several steps. Firstly, the first author, SHY, familiarised herself with the papers. Themes and all participants’ quotes from both the Results and Discussion sections of each paper were then extracted and coded line-by-line using QSR NVivo [ 25 ]. Additional information such as participant demographics, diagnosis, and research method were also extracted to preserve study context. Codes were then grouped and categorised inductively based on their meanings, with attention paid to draw out culture-specific themes. The free codes were grouped together hierarchically in NVivo and printed out where annotations were made by hand to help generate themes. The analytical theme generation process aimed to extend beyond the original study themes and was reviewed by the second author.

Quality assessment

The methodological quality of the included studies was assessed using the appraisal tool CASP Qualitative Studies Checklist (Critical Appraisal Skills Programme, 2018) (Table  1 ). The ten appraisal questions focus on research design, recruitment method, data collection, researcher/participant relationship, ethical considerations, data analysis, clarity of findings, and importance/value of the research. The authors of the checklist did not recommend scoring up the results but instead emphasised using the appraisal tool qualitatively. SHY completed the CASP and this was checked by US. The quality of the studies did not particularly impact on the theme generation, but instead provides context for the overall analysis.

Reflexivity

It is important to be aware of researchers’ biases and positionality in qualitative analysis. SHY is Chinese by ethnicity and was born and raised in Hong Kong. She completed her undergraduate and postgraduate studies in the UK and works in the National Health Service in the UK as a clinical psychologist, where intrinsically western and white-orientated models were taught and practiced. Therefore, she is aware of her background where on the one hand, she understands culture-specific issues in some parts on EA, on the other hand, she is in a slightly detached position professionally and geographically. US is a UK-trained psychiatrist who is originally from Germany and has extensive experience in EDs. She approached the research topic and data from the point of view of an EDs expert as well as using her experience of treating EDs patients from East Asia in the UK as well as collaborating with East Asian researchers. She is aware of her positionality as a White European woman and this allows her to discuss the cultural differences between East and West with SHY.

A total of 12 studies were included. However, two of the studies (Ma and Lai, 2006; Ma, 2008) were based on the same cohort of participants. In one of these papers, the research focus was on perceived treatment effectiveness, and in the other on experiences of treatment. Figure  1 shows the PRISMA chart. None of the Chinese language studies were qualitative studies on experiences of EDs interventions and hence all included studies were in English. Table  2.1 & 2.2 shows a summary of the study characteristics and extracted settings and themes. Overall, most studies examined people with AN except for [ 26 ] who included people with BN, purging disorder and night eating disorder, and [ 27 ] who included BN. One study examined parents’ views and perceptions of help for AN in Hong Kong [ 28 ], and two studies examined professionals’ views and perceptions of treating young people with AN in Taiwan [ 29 ]; [ 30 ]. The mean age of the participants interviewed was below age 30 for all patient-related studies. All studies were conducted in Chinese-speaking (Cantonese and Mandarin) regions of EA. The majority of the patients interviewed identified as females – one out of 69 participants in total across all studies identified as male.

PRISMA flowchart

Three main themes were identified.

Theme 1. Delineating physical and psychological recovery

People with lived experience of EDs described how treatment ‘ was helpful but [they were] not symptom free ’ ( [ 26 ]. In particular, participants often described the distinction between physical health and their psychological health, suggesting that recovery involves both components and that (inpatient) treatments seem to only support physical recovery. A participant noted, ‘ the only positive impact was physical health , others (were) all negative; but without that I would have already died.’ [ 31 ]. Another participant concurred, ‘I did not find the staff helped me with my anxieties about my weight…I was not helped psychologically , it was all about the physical improvements’ [ 28 ]. However, without psychological recovery, participants described their symptoms worsened post-discharge. For example, participant said ‘I think it [bingeing and purging becoming even worse after discharge] might be because I have gained lots of weight during the period of receiving inpatient care , but I could not psychologically accept it…thus…I started to fast badly , and after a while , my bingeing emerged and my urge to eat got even stronger.’ [ 28 ]. This view was shared among professionals as well. One dietician in Taiwan reflected that “ We should study psychology. Anorexia is not only physical’ [ 29 ].

On the other hand, there are other participants who described a full recovery (‘ [I] live like a normal person’ [ 28 ].

Theme 2. ‘I am not alone in this battle’

This theme includes three pairs of relational dyads – the patients in relation to their families, their therapists, and their peers.

Sub-theme 2.1. The dialectics of interdependence and independence

In the included studies, it appears that certain cultural values of interdependence and filial piety may provide a fertile ground for EDs to develop. As a participant (person with an ED) put it,

‘I wanted to have some freedom from my parents but I didn’t want to go against them. Their control/protection was benign , good for me , but it’s seamless and suffocating. I just need some space to make my own choice. Anorexia was part of my identity because eating and weight are the only things I have control over’ [ 4 ].

Mealtimes are seen as a non-negotiable duty especially if the older family members prepare the dishes. As mentioned by a Taiwanese woman with lived experience of an ED: ‘ mealtime was held to be sacred , reflecting the Chinese belief that eating works towards preserving harmony , cohesion , and unity in the family. Grandmother’s cooking and food serving signified her devotion to , and affection for , her children. The entire family was , in turn , expected to reciprocate their grandmother’s gesture by observing filial piety and obeying her rules about food and meals’ [ 4 ].

For some participants, the need to obey senior family members, fulfil family duties, and prioritise others’ needs may suppress their own needs and lead to internal conflicts: ‘ I should get more involved with my parent’s business , care more about how they feel and what they want’ [ 4 ]. The researchers speculated that this may also relate to traditional Chinese culture, where males are more valued than females, and daughters feel the need to live up to the family’s expectations when they are an only child. In these situations, healing involves individuation from interdependence and exploring self-identity to prevent relapse [ 32 ]. This quote illustrates this point: ‘ as I started seeing myself independent from my mum , I became more comfortable and no longer felt inferior to her… my bingeing and purging frequency reduced.’ [ 4 ]. Another participant from the same study described moving out of the family home as a turning point towards EDs recovery [ 4 ].

Nevertheless, the cultural value of interdependence can also serve as a protective and motivating factor towards recovery. Instead of citing personal reasons for recovery, some participants described their motivation to get better for their parents, influenced by the cultural value of ‘saving face’: ‘ … My anorexia was a face-losing thing…I felt like becoming too much a burden…I was eager to become normal again…so that I could save face for my parents’ [ 4 ]. When a participant looked back on the recovery, one discussed the cultural value that emphasises ‘the body is given by the parents’: ‘ I vomited the money you earned…. I hurt the body you have given me…again and again’ [ 26 ].

Similarly, recognising that the family will unconditionally accept them regardless of whether they manage to meet their parents’ expectations, can also be motivating. One participant described how her family will always stand by her side,

‘I really decided to walk out of this eating disorder swamp. I felt that , no matter what , my parents would love me , even when I’m vomiting and when I am the ugliest. Perhaps they couldn’t understand me , but because that’s me , they would accept this person unconditionally’ [ 26 ].

Therapy provides a space for the family to ‘ have a deeper chat’ and to facilitate a greater understanding of each other, improving the family relationships. This includes both the parent-child dyad as well as sibling dyad:

‘The therapist did not talk much about eating in treatment. She worked on the family relationships. Let’s understand her work in this way. With the onset of the illness , the family must have problems and the family relationship must be damaged… when our communication improved and our relationships were repaired , we became more harmonious and the child would listen to other parents.’ [ 27 ]. ‘In fact , I can see that both my brother and sister want to help me , but I can’t accept the way they help me…now I can see that they just want to give some ideal solutions to me. ’ [ 33 ].

Some studies emphasise the role of the father and increasing paternal presence (e.g., [ 27 ]). Traditionally, it is assumed that mums are responsible for domestic matters as well as the children’s wellbeing. As a mum put it, ‘[the child’s] father is a CEO of a huge company and I don’t want to upset him. I want him to concentrate his energy and time on work. I told him about my difficulty only when I could no longer handle it’ [ 27 ]. A father reflected on his guilt towards not caring for his daughter: ‘… I should stay behind to take more care of her’ [ 27 ]. Therapy plays a pivotal role in fostering and enhancing the father’s presence, while also illuminating the daughter’s longing for paternal care. In a case study, Lily, a participant, reported that her improved relationship with her father facilitated a return to normal and regular eating habits. As a result of therapy, her father began dedicating more time to the family, acknowledging that he previously prioritised rest over spending time with family. In another scenario where the individual’s father had passed away, the therapist emerged as a dependable father figure, providing invaluable support and understanding [ 4 ].

Subtheme 2.2. Clinician as a trusted and safe base

Both clinicians and patients described important common factors in therapy such as calm, patience and building trust. In the paediatric wards, the nurses mentioned “ You must take the time to establish a relationship with her. She is willing to rely on you , and she is willing to tell you where the problem is .” [ 29 ]. A patient mentioned ‘the therapist has really good temper. No one can stand to talk to me so long , except my mother , including my brother and sister. And her tone makes me think that she’s a person I can trust.’ [ 34 ]. Developing a safe base allows the families to then explore more difficult topics. Studies describe the use of the word ‘ as a bridge’ to recount the role of therapist in treatment:

‘She made me feel confident. We began to trust her (the therapist). We felt that she can help us. With that trust in mind , I feel free to disclose my feelings honestly…my body weight dropped and I was very frightened….I had no confidence and was very fearful. She (the therapist) looked at me with a warm smile and in a firm tone , said that she had confidence in me and I could make it’ [ 34 ].

Subtheme 2.3. Relating to peers with EDs

References to sharing and comparing EDs behaviours, such as sharing purging techniques, were noted [ 28 ]. For instance, one participant described observing peers using their iPad to calculate meal calories and researching diets online to lose weight after discharge. In the analysis, the authors hypothesised that due to the historical One-Child Policy in China, being on the ward might be the participants’ first time living with peers away from their families. They wondered whether some of the group dynamics of cooperation and conflict might be attributed to the lack of experience of living with siblings.

On the other hand, positive aspects from peers were also noted, such as finding people to talk to: ‘I had been keeping this secret (my ED) for an extremely long time without finding somebody to talk to’ as well as reducing vomiting behaviours due to others reporting to the nurses [ 31 ].

Theme 3. Barriers to change

Four aspects of barriers were described: financial, structural, coercive practice and cultural.

Subtheme 3.1. ‘I am wasting my family’s money’

One participant mentioned, “Psychotherapy or counselling would cost me 400/500 yen (approximately 70 USD) per session. I am still a student and don’t have much money. I thought I could follow self-help resources and treat myself” [ 26 ]. While she expressed an individual perspective, others described, “We are not wealthy as a family,” indicating a family-oriented viewpoint among the participants. For instance, one participant discussed how their family did not consider finances a barrier to treatment:

‘…I can see that my family doesn’t care about money when compared to my health , and my sister also wastes her study time to keep on seeing the therapist every week. Now I can see that they all treat me very , very well , and want me to be healthy again.’ [ 32 ].

Subtheme 3.2. Unavailable professionals and services

Participants were dissatisfied by the lack of specialist services, as well as the lack of knowledge of EDs among healthcare professionals. This is evident in terms of the short period of time they are being seen for:

‘The diagnostic process involved me describing my situation and the doctor asking me more questions…diagnosed me with bulimia nervosa. The whole process took about 6 to 7 minutes. It was very short and nonspecific. I feel my condition was not taken seriously.’ [ 26 ].

The scarcity of specialist services was mentioned by multiple participants. One of them said, ‘ treatment resources are only available at big hospitals’ in mainland China [ 26 , 35 ]. In Hong Kong, parents described how difficult it was to find therapists that are knowledgeable about AN:

‘I really don’t know where you could find family therapists that specialise in treating anorexia in Hong Kong… in foreign countries , there is usually a team which put strong emphasis on family support and teamwork , and such kind of support is totally unavailable in Hong Kong’ [ 28 ].

The lack of knowledge among professionals can also lead to patients and families feeling invalidated. A doctor mentioned that amenorrhoea could be stress-related and could be a common gynaecological issue, or patients were told to use willpower to overcome their EDs. Parents expressed feeling blamed:

‘During the consultation , we were scolded by the psychiatrist [in A & E]. Have I done anything wrong? He told me that my daughter was well-behaved but I left her in other people’s care. Hey , I have to work! I have already tried my best to find something that is suitable for my daughter.’ [ 28 ].

These experiences by parents are echoed by professionals in Taiwan, who acknowledged their treatment knowledge gap:

One physician said, “ Our care for anorexia is taught by the attending physician one by one , from the intensive care unit to the ward care , and then to the outpatient care. In fact , education is carried out during the follow-up process and the ward rounds. This kind of education only means that the few people who are cared for know how to take care of them. Nurses still don’t know how to care of them” [ 29 ].

The other gap acknowledged was the lack of awareness of non-AN EDs. In a study where a hypothetical vignette of a female who vomits and binges were presented, researchers noted that almost every clinician in the study specified AN rather than BN [ 35 ].

Subtheme 3.3. Coercive practice

Coercive practices, particularly within inpatient settings, were reported, involving the use or threat of restraints and nasogastric (NG) tubes. For instance, a nurse mentioned that even the visible presence of an NG tube could be employed as a form of coercion [ 29 ]. Describing their own experience as a former inpatient, one individual expressed deep distress regarding witnessing physical restraints [ 28 ]. Such experiences resulted in negative treatment experiences, with participants recounting psychological trauma and nightmares related to their inpatient care [ 28 ]. In outpatient family therapy, mothers described feeling like a ‘villain’ and needing to force feed their child [ 28 ]. In view of such practices, participants expressed that such treatment compelled them to act against their desires, and they doubted its efficacy in addressing their weight-related fears [ 32 ].

Subtheme 3.4. Converging and diverging cultural ideals

While thin ideals are often valued in EA cultural norms, there are also contrasting views that perceive thinness as a Western ideal. Participants in the study perceived being chubby as the ideal in Chinese culture, as one individual expressed: “In our culture, being chubby should mean pretty and lucky. My first memory of the really thin women were western models and movie stars…my mum always said they are ugly” [ 4 ]. This contradicts the thinness ideal highlighted in other studies (e.g. 11). Interestingly, exposure to the actual environment in the West helped correct participants’ perceptions of body ideals, which proved beneficial to their recovery:

‘[the participant] highlighted that these cross-cultural exposures and experiences living abroad had enabled and empowered her to challenge the stereotyped images of beauty portrayed and perpetuated by western media… “after I moved to the US , I realised that people here do not look like those in the movies…” ’ [ 4 ].

Study quality

Most studies used adequate qualitative methodologies. The main quality issues identified include not mentioning ethical considerations, lacking researcher reflexivity, lacking details regarding the analytic steps, and that in some studies (e.g. where family therapy was the treatment modality), the analysing researcher was also the treating therapist, which may introduce bias (see Table  1 for more detail).

The 12 studies included in the review generated three analytical themes in response to our research question on people’s experiences of treatment in East Asia (Table  3 ). Cultural aspects relating to people’s experiences were considered when identifying themes.

A diverse range of treatment was described - including family therapy, paediatric/ psychiatric inpatient care, cognitive behavioural therapy, and faith-based counselling. This contrasts with the systematic quantitative scoping review by Yim & Schmidt [ 16 ], where CBT and internet interventions were the main treatments in focus. Some of the themes share similarities to other qualitative syntheses on AN treatment such as improved family relationships as well as the perceived authoritarianism and control in treatments [ 18 ], and the use of restraints and NG tube in inpatient wards. Similar to the findings from Yim & Schmidt [ 16 ], participants also directly mentioned financial barriers and the unavailability of specialist professionals/ services.

The current review goes beyond the cultural adaptations described in Yim and Schmidt [ 16 ]. More nuanced factors such as family roles, cultural values and norms were shared by participants, which can be important issues to be addressed in therapy. With respect to policy, the historical One Child Policy (OCP) in mainland China was mentioned in Wu and Harrison [ 28 ] where they hypothesised that this could potentially impact the interpersonal dynamics in inpatient settings. This was not mentioned in other studies in Yim & Schmidt’s [ 16 ] review. Whether or not the OCP affects the social literacy of single children is under debate, as the single child will still be interacting with peers at school [ 15 ]. This is also potentially confounded by the nature of EDs where body comparison is part of the symptomatic behaviour. It is difficult to disentangle the relative influences on people’s negative experiences in inpatient treatments. In contrast, the impact of OCP is wide-ranging and other impacts may influence the development or maintenance of an eating disorder. OCP has led to an imbalanced sex ratio with more males to females in China and having one child only may be seen as a deprivation of one’s reproductive choice. This also adds to the pressure of looking after one’s elderly parents without the support of other siblings. At the same time, single children (especially girls) faced immense pressure to excel, and are enrolled in multiple tutorials and extracurricular activities [ 16 ]. The pressure to achieve, in addition to preserving the family’s ‘face’, may contribute to the development of an ED [ 26 ]. Relating to the negative aspects of peer influence in EDs wards, it would be useful to explore if similar issues were found in group therapies. Future studies could also explore how single children versus non-single children perceive group or residential treatments (i.e. where there are the same rules for all).

Collectivist culture, where family harmony and ‘saving face’ are esteemed [ 4 ], can present a complex dynamic. Whilst this cultural value may impede help-seeking due to stigma, participants also noted that it functions as a motivator for getting better. Another significant cultural value is Filial Piety, where researchers speculate it may hinder patient’s individuation process [ 7 ]. The necessity for individuation becomes evident as participants highlighted pivotal moments in their ED recovery, such as moving out of the family home or moving abroad for studies [ 4 ]. Initially, participants with EDs struggled with parental expectations and prioritised family wishes over personal aspirations. For some, their EDs may serve the function of creating distance/ challenging parental control or wishes without overtly going against them [ 4 ]. This is potentially compounded by cultural beliefs favouring men over women, leading girls to internalise feelings of inferiority. Balancing familial and individual needs emerges as a central focus in EDs therapy for them. However, similar to other culture-specific values, filial piety can potentially also be a protective factor, motivating patients to comply with parental directives and attend therapy. The idea of interdependent self-construal is pertinent here [ 14 ]. Patients described relational motives to recovery, such as ‘I am “vomiting” your money and your love’. The process of individuation also includes maintaining family connections. Echoing findings by Medway and Rhodes [ 18 ], some family therapy studies in East Asia (e.g., [ 27 ] underscore the reorganisation of family dynamics and roles, often with increased paternal involvement. Yim & Schmidt [ 17 ] speculated that CBT was preferred to family therapy due to most parents working full-time in East Asia. This sentiment is reflected in some parents’ statements like ‘Hey, I have to work!’ However, the present review suggests that the benefits of family therapy are being recognised for restructuring family dynamics and roles, as well as increasing communications and bonding. This is evidenced in the theme ‘I am not alone in this battle’, where family relationships are perceived as improved, and families come together and the patient did not feel judged or uncared for by their parents. This agrees with Tan et al’s [ 20 ] view of using a maternalistic approach in treating ED patients in Asia.

Clinical recommendations

This review, along with Yim and Schmidt (2023), identified treatment, training and research gaps for EDs in EA. We propose the following clinical implications and recommendations:

EDs conceptualisation in EA

Clinicians in EA need to have greater awareness of EDs in general, especially EDs other than AN [ 35 ]. Although our combined reviews show that individual treatment approaches seem to be the norm in EA, it will be useful to include the family context as part of the formulation and treatment planning.

Clinicians should have an awareness of how culture relates to one’s formulation of an ED whilst attending to individual differences. Some examples of culturally informed treatment planning may include harnessing the interdependence and cultural norms of ‘sacred’ family meals as an act of care rather than the family being cast in the role of a ‘villain’. It may be appropriate to consider both interdependent, relational motivators and goals, in addition to personal goals towards recovery, paying attention to the process of individuation whilst maintaining connectedness.

The role of body image

Body image ideals appear to be another conflicting value. On the one hand, studies mentioned how thin ideals are pervasive in EA (e.g. 13), which could be an influence from Westernisation. On the other hand, participants described being ‘chubby’ as being valued [ 4 ]. Whilst there may be generational differences in body ideals, it could also create a sense of internal conflicts if young people’s perceived ideals are different from those of their parents. With the conflicting findings from the studies regarding the relative influence of Western and Asian media (e.g. [ 12 ]), it is important for clinicians to consider a multidimensional conceptualisation of body image and not to make assumptions around the body ideals that the individual is influenced by. Moreover, it may be important to include the family’s perception and ideals of the person’s weight and shape.

Capacity building

The advancement of telemedicine can facilitate better more in-depth training of medical professionals on understanding and treating EDs (e.g. see [ 36 ], as well as increasing the affordability and accessibility of treatments, and also capacity building of evidence-based EDs treatments in EA. It is recommended that journal special issues, conference themes on culture and EDs, or special interest groups/ clinical research networks on EDs in East Asia/for East Asians should be organised to facilitate knowledge and skills exchange.

Limitations

All the included studies are conducted in the Chinese (Mandarin and Cantonese)-speaking regions in EA. Our search strategy did not include grey literature which is a limitation. Some researchers may argue that qualitative studies are context specific and a synthesis of such findings may de-contextualise them. Whilst the aim of this review is not to provide generalisability, it is worth acknowledging that in terms of context transferability, people’s experiences and views in other regions such as Japan and Korea are unknown. It may be that relevant papers were written in the respective languages and therefore not found in our search. Nevertheless, the settings and populations of the included studies were listed in Tables  2.1 and 2.2 , which could assist in the interpretation of the transferability of the findings.

Research recommendations

Most of the EDs study participants experienced AN in the studies, and little is known about the experiences of people with BN, BED, or the relatively newer ARFID diagnosis in the region. This is especially pertinent as the prevalence of BED and BN is higher than that of AN in China [ 2 ].

The prevailing models of treating AN in the West such as ED-focused family approaches for adolescents, are also an underexplored area, so we could not identify whether there are differences in people’s experiences or perceived effectiveness of an ED-focused therapy versus the modified Micucci’s model. The concept of non-fat phobic AN was not mentioned in the studies. Moreover, the studied populations were relatively young (most of them were under 30). Future research on older individuals with EDs in EA would be valuable.

Gender is another key area that needs to be addressed. Across all the included studies, only one patient identified as male. Given most of the studies identified were conducted in China, and that China has a larger male to female ratio, the finding is therefore somewhat surprising. It is difficult to understand how gender and its intersection with aspects of EA culture may influence treatment experiences.

In terms of methodology, it is important for future research to consider researchers bias and reflexivity to increase transparency, credibility and research rigor.

Given that professionals may perceive EDs as a gastrointestinal or gynaecological issue, it is likely that EDs are under-detected within those specialities. Future explorations of specific cultural factors and the relative influence of different body ideals are needed, and understanding the unique cultural struggles of the East Asian Diaspora versus East Asians residing in their home countries.

Data availability

No datasets were generated or analysed during the current study.

Abbreviations

Eating disorder(s)

Anorexia Nervosa

Bulimia Nervosa

Binge Eating Disorder

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Acknowledgements

Ulrike Schmidt receives funding from the National Institute for Health and Care Research (NIHR) Maudsley Biomedical Research Centre (BRC) and by the Medical Research Council/Arts and Humanities Research Council/Economic and Social Research Council Adolescence, Mental Health and the Developing Mind initiative as part of the EDIFY program, Grant/Award Number: MR/W002418/1.

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SHY designed and planned the review with supervision from US. SHY performed the search and extracted the data, and data interpretation was performed by SHY and US. SHY wrote the manuscript with support and supervision from US. All authors reviewed the manuscript.

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Yim, S.H., Schmidt, U. Views and experiences of eating disorders treatments in East Asia: a meta-synthesis. J Eat Disord 12 , 120 (2024). https://doi.org/10.1186/s40337-024-01070-4

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Received : 25 April 2024

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DOI : https://doi.org/10.1186/s40337-024-01070-4

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