The Diagnosis and Treatment of Anorexia Nervosa in Childhood and Adolescence

Abstract

Background

Anorexia nervosa (AN) is a serious disease with a lifetime prevalence of up to 3.6% in women and 0.3% in men. Abnormally low weight and the associated starvation partly account for its somatic and mental manifestations.

Methods

This review is based on publications retrieved by a selective search concerning AN in childhood and adolescence.

Results

The peak age of onset of AN is 15.5 years. The frequency of inpatient treatment for AN rose by 40% during the COVID pandemic, indicating the importance of environmental factors; the heritability of AN is estimated at 0.5. The ICD-11 sets the threshold for AN-associated underweight at the fifth percentile for age of the body mass index, as long as the remaining diagnostic criteria are met. The main goal of the multiprofessional treatment of AN is the return to normal body weight, which is a central prerequisite for regaining somatic and mental health. The mean duration of AN is 3.4 years, and approximately two-thirds of patients recover from the disease over the long term.

Conclusion

Marked weight loss in childhood and adolescence can trigger AN in the presence of a predisposition to this disease. Patients and their families should receive psychoeducation regarding the symptoms of starvation and their overlap with those of AN. Important objectives are to shorten the duration of the illness, minimize mortality and the risk of chronic illness, and to identify pharmacological approaches to treatment.

Anorexia nervosa (AN) begins in late childhood to young adulthood. It is characterized by underweight that is not explicable by constitutional underweight, medical factors, or a lack of food. It is characterized by an exaggerated preoccupation with one‘s own figure and body weight, intense fear of gaining weight or becoming fat, and behaviors that prevent weight gain. The affected persons express little or no fear of impaired physical or mental health as a consequence of being underweight (1).

The onset of anorexia nervosa.

Anorexia nervosa (AN) begins in late childhood to young adulthood. It is characterized by underweight that is not explicable by constitutional underweight, medical factors, or a lack of food.

In an international, systematic epidemiological review, the lifetime prevalence of AN was up to 3.6% in women and 0.3% in men (2). A meta-analysis revealed peak onset at age 15.5 years; 18% of all patients had already received a diagnosis of AN by age 14, and 55% by 18 (3).

The sufferers’ health is usually impaired for many years, with major adverse effects on their emotional, social, and cognitive development. Body image disturbances and weight phobia are known to be risk factors for the development of AN (e1), but an adequate understanding of the early warning signs or the initial, subsyndromal signs of disease in AN is still lacking (4). AN carries a serious prognosis (e2).

Typical features of anorexia nervosa.

• exaggerated preoccupation with one‘s own body weight

• fear of weight gain

• little or no fear of the risk to health from excessive weight loss

Prolonged inadequate energy intake leads to starvation. Somatic and psychological adaptations occur, including behavioral changes that increase the likelihood of survival of the starved organism (5). A wide range of humoral factors are involved. A subphysiological decrease in the serum level of the hormone leptin, which is mainly produced in adipocytes, is thought to be an essential hormonal signal for the gradual somatic and psychological adaptation to starvation (5, 6). Knowledge about this adaptation is indispensable for an understanding of the manifestations, comorbidities, course, and treatment of AN. In particular, psychological manifestations are often directly attributed to AN, yet there is often an overlap (Table 1): starvation (itself a consequence of AN) is a contributing cause of many of the psychological manifestations of AN.

Table 1. Anorexia nervosa (AN) and starvation: comparison of mental manifestations (abbreviated version).

	Anorexia nervosa	Starvation (Minnesota Starvation Study) (e30)*
Mental preoccupation with food	Persistent, barely suppressible; agonizing quality of experience, associated with weight phobia, cooking for others, watching cooking videos, reading recipes	Food is a central theme; frustrated by constant thoughts of eating; observing and hoarding food, giving food away, collecting recipes
Eating behavior	Slow/ritualized eating, fear of food, manipulations (e.g. hiding food, drinking large amounts of water instead of eating)	Eating slowly/very deliberately; mostly alone, otherwise in silence, drinking more; mass of food increased by adding water
Appetite/Hunger	Heterogeneous, rapid satiety and feeling of fullness; detection problematic (denial or inability to perceive internal hunger and satiety signals); dependent on extent/duration of starvation	Some are hungry all the time. At the end of the starvation period, 59% said they were hungry most of the time
Other mental findings	At the beginning possibly improved/balanced mood, increased performance/increased ambition. With progression, tiredness, exhaustion, possibly physical hyperactivity, social withdrawal, depression, mental rigidity/compulsiveness. Decrease in concentration and memory, loss of libido, decline in spontaneity/creativity	Fatigue, depression, apathy; nervousness, inner restlessness, emotional instability, irritability; decline in interests, humor, physical activity, decision-making ability, judgment, and libido; slow speech, shuffling gait, change in the sense of time that is experienced as unpleasant, impaired concentration and short-term memory
Effects of weight gain	Slow decrease in mental preoccupation with food/body weight, depression, rigidity and compulsiveness; desire for social contact increases. Frequent persistence of body image disorders and urge to be thin. Depressiveness and AN-related cognitions and emotions may intermittently increase with realimentation. Potential appearance of binge eating attacks	Psychological recovery only after months. Mood improvement proportional to the amount of calories consumed. Slow increase in libido, increase in feelings of hunger with binge eating, nausea/vomiting. Irrational fear of not having enough food. Initially, worsening of the psychological findings was encountered in a subgroup.

*The Minnesota Starvation Experiment (e30), conducted in 1945, involved 32 volunteers (conscientious objectors) who lost 25% of their initial weight in 24 weeks.

The subsequent realimentation phase lasted twelve weeks, but this was not sufficient to enable all participants to regain their former weight.

The subjects were examined somatically and psychologically throughout.

Learning objectives

This article should enable the reader to:

• know the prevalence, risk factors, diagnostic evaluation, and common comorbidities of AN, its treatment (including with drugs), and key figures relating to the usual course of anorexia nervosa in children and adolescents;

• understand adaptation to starvation and its implications for psychological findings in patients with AN;

• be familiar with the clinical symptomatology of atypical anorexia nervosa;

• be aware of the tasks confronting physicians who care for young patients with anorexia nervosa and their relatives.

Etiology

Genetic risk factors

The relative risk of an eating disorder in first-degree female relatives of index cases, compared to normal controls, is 11 (7). Heritability, as measured in twin studies, is 0.5–0.6 (8, e3); genes thus account for 50–60% of the variance. The known genetic correlations reflect comorbidities that are evident in clinical experience (e.g., obsessive-compulsive disorder and depression). A correlation with schizophrenia and a possible link to delusional body image disturbances have also been reported (8). The polygenic predisposition to AN overlaps with underweight and low fat mass, a high level of physical activity, a high educational level, and a variety of metabolic phenotypes (e.g., low fasting insulin and leptin levels and high HDL cholesterol). These complex genetic overlaps, collectively termed a “metabopsychiatric disorder,” set AN apart from other mental disorders (8). These correlations may, however, be partly or wholly due to underweight being a criterion for the diagnosis of AN. Many premorbidly obese adolescents with AN-like manifestations whose BMI does not drop below the 5^th centile as required for the diagnosis of AN, even after they have lost a large amount of weight, are given a DSM-5 diagnosis of atypical AN and are therefore not represented in genetic studies of AN (e4, e5).

The prevalence of anorexia nervosa.

In an epidemiological review, the lifetime prevalence of AN was up to 3.6% in women and 0.3% in men. A meta-analysis revealed peak onset at age 15.5 years; 18% of all patients had already received a diagnosis of AN by age 14, and 55% by 18.

Environmental risk factors

The COVID-19 pandemic revealed the importance of environmental factors. Elevated incidence and hospitalization rates were observed in a number of countries, as was a more rapid progression of the manifestations of AN (e6, 9). In Germany, the hospitalization rate per 100 000 children and adolescents rose from 5.38 in 2019 to 7.48 in 2021 (10).

In a predisposed individual, weight loss or weight stagnation and, in particular, a decrease in fat mass must take place at a critical age in order to trigger AN (or a relapse of AN) (5). Patients may go on a diet in order to lose weight, live more healthily, or lessen their environmental impact by means of vegetarianism or veganism. Fat mass reduction can also be initiated by intense physical activity (e.g., workouts). The role of (social) media as a co-trigger, mediator and amplifier for disordered eating and excessive exercise behavior is debated (e7). Weight loss can also be induced by critical/unmanageable life events and other psychosocial or sociocultural triggers (e8). In some cases, AN may follow weight loss that has occurred, for example, because of an infection, food abstinence after surgery, or depression. Such factors are distinct from disease-intensifying or disease-maintaining factors such as positive comments from others regarding the initial weight loss, the need to remain in control, stress or the defense against stress, and dysfunctional cognition (e8).

Risk factors for anorexia nervosa.

• Genetic: heritability 0.5 to 0.6 in twin studies.

• Environmental: weight loss or weight stagnation; critical or unmanageable life events

Diagnostic evaluation

The diagnosis of AN is based, on the one hand, on the finding of underweight and, on the other hand, on the presence of specific thought patterns and behaviors (see diagnostic criteria according to DSM-5 and ICD-11, eTable 1; the tasks of the physician relating to the diagnostic evaluation are listed in Box 1 (for details, see the eBox).

eTable 1. Comparison of the ICD-11 and DSM-5 diagnostic criteria for anorexia nervosa (1, e37–e39).

ICD-11 criteria	DSM-5 criteria
Significantly low body weight for the individual’s height, age and developmental stage that is not due to another health condition or to the unavailability of food. A commonly used threshold is body mass index (BMI) less than 18.5 kg/m2 in adults and BMI-for-age under 5th percentile in children and adolescents. Rapid weight loss (e.g. more than 20% of total body weight within 6 months) may replace the low body weight guideline as long as other diagnostic requirements are met.	A. Restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health. Significantly low weight is defined as a weight that is less than minimally normal or, forchildren and adolescents, less than that minimally expected.
Children and adolescents may exhibit failure to gain weight as expected based on the individual developmental trajectory rather than weight loss. Low body weight is accompanied by a persistent pattern of behaviors to prevent restoration of normal weight, which may include behaviors aimed at reducing energy intake (restricted eating), purging behaviors (e.g. self-induced vomiting, misuse of laxatives), and behaviors aimed at increasing energy expenditure (e.g. excessive exercise), typically associated with a fear of weight gain.	B. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight.
Low body weight or shape is central to the person‘s self-evaluation or is inaccurately perceived to be normal or even excessive.	C. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.
The subtype should be additionally specified:
Anorexia nervosa with significantly low body weight Anorexia nervosa with significantly low body weight meets all definitional requirements for anorexia nervosa, with BMI between 18.5 kg/m 2 and 14.0 kg/m² for adults or between the fifth percentile and the 0.3 percentile for BMI-for-age in children and adolescents.
Anorexia nervosa with significantly low body weight, restricting pattern Anorexia nervosa with significantly low body weight, restricting pattern refers to individuals who meet the definitional requirements of anorexia nervosa with significantly low body weight and who induce weight loss and maintain low body weight through restricted food intake or fasting alone or in combination with increased energy expenditure (such as through excessive exercise) but who do not engage in binge eating or purging behaviors.	Restricting type During the last 3 months, the individual has not engaged in recurrent episodes of binge eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas). This subtype describes presentations in which weight loss is accomplished primarily through dieting, fasting, and/or excessive exercise.
Anorexia nervosa with significantly low body weight, binge-purge pattern Anorexia nervosa with significantly low body weight, binge-purge pattern refers to individuals who meet the definitional requirements of anorexia nervosa with significantly low body weight and who present with episodes of binge eating or purging behaviors. These individuals induce weight loss and maintain low body weight through restricted food intake, commonly accompanied by significant purging behaviors aimed at getting rid of ingested food (e.g. self-induced vomiting, laxative abuse or enemas). This pattern also includes individuals who exhibit binge eating episodes but do not purge.	Binge-eating/purging type During the last 3 months, the individual has engaged in recurrent episodes of binge eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas)
Anorexia Nervosa with significantly low body weight, unspecified
Anorexia nervosa with dangerously low body weight Anorexia nervosa with dangerously low body weight meets all definitional requirements for anorexia nervosa, with BMI under 14.0 kg/m² in adults or under the 0.3rd percentile for BMI-for-age in children and adolescents. In the context of anorexia nervosa, severe underweight status is an important prognostic factor that is associated with a high risk of physical complications and substantially increased mortality.
Anorexia nervosa with dangerously low body weight, restricting pattern
Anorexia Nervosa with dangerously low body weight, binge-purge pattern
Anorexia Nervosa with dangerously low body weight, unspecified
Anorexia Nervosa in recovery with normal body weight	Partial remission Criterion A has not been met for a long period of time, while either criterion B or criterion C is still met.
	Complete remission None of the diagnostic critieria have been met for a long period of time.
Other specified anorexia nervosa	Atypical anorexia nervosa All of the diagnostic criteria for AN are met, but the body weight is in the normal or supranormal range despite marked weight loss.
Anorexia nervosa, unspecified

Box 1. The physician’s tasks in suspected anorexia nervosa and case management*¹.

• History-taking from the patient and caregivers

  • weight history

  • current eating behavior

  • physical activity

  • mental and physical findings

• Further tasks of the physician on initial presentation

  • physical examination

  • mental status examination

  • determination of height, weight, and BMI

  • laboratory tests

  • further diagnostic evaluation if necessary

  • set a weight target*²

• Case management over the course of treatment

*¹ This is an abbreviated version; for more extensive information, see eTable 2

*² to be continually adapted to age and height; a weight corridor of 2–3 kg may be appropriate in order to take account of physiological fluctuations in weight

BMI, body mass index

eBox. The physician’s tasks in suspected anorexia nervosa and case management.

History-taking from patient and caregivers

• Procedure

  • joint and separate discussion with patient and parents/guardians/others

• Weight history

  • weight and age prior to initial weight loss; lowest weight remembered since the start of the eating disorder (and age at that time); recent weight loss or fluctuations; change in clothing style (smaller sizes, constantly wearing loose clothing); prior pediatric documentation of weight, height and BMI

• Nutritional behavior:

  • current eating habits (e.g. portion sizes, skipping meals, eating alone only, calorie counting, vegan/vegetarian diet), current food intake/fluid intake (e.g. ”What did you eat and drink yesterday? Is it similar on other days?”); binge eating, (self-induced) vomiting, taking laxatives

• Physical activity

  • desire for body or health optimization (increase in sporting activity, workout videos), inner restlessness; ask specifically about activity (e.g. in hours per day, distances in km); is the activity experienced as a compulsion?

• Mental abnormalities

  • constant preoccupation with food and weight (consider that the patient may be reluctant to disclose information due to shame/fear); cooking for family members; interest in recipes and food- and eating-related online videos

  • body image disturbance and weight phobia (may be denied out of shame/fear); possible questions: „How do you feel about your weight compared to your peers? Do you think a certain part of your body is too fat? Are you afraid of gaining weight?“

  • Lack of awareness of the health threat by starvation

  • perfectionism, rigidity, increased focus on performance (e.g. increasing the time spent on homework)

  • depression: restriction of interests, sadness, social withdrawal, hopelessness, suicidal tendencies, sleep disturbance, tiredness/exhaustion, loss of spontaneity and creativity

  • other psychiatric comorbidity (e.g. obsessive-compulsive disorder, anxiety disorder)

• Physical abnormalities (see also physical examination)

  • circulatory problems (e.g. syncope), shivering, primary or secondary amenorrhea (note: if the patient is taking an oral contraceptive, do not misconstrue discontinuation bleeding as menstruation), duration of amenorrhea, hair loss, vomiting, other diseases (e.g. type 1 diabetes mellitus, inflammatory bowel disease, celiac disease, premorbid overweight/obesity)

Other tasks of the physician on the initial presentation of the disease

• physical examination, pulse and blood pressure measurement; in case of bradycardia (HR < 45), nocturnal heart rate determination (e.g. by long-term ECG) to rule out a dangerous nocturnal bradycardia (HR ≤ 35). Determine body temperature, check for foot and leg edema and superficial cuts. Indicators of prolonged vomiting: Inflammation of the oral mucosa, cavities, and swelling of the salivary glands in front of/under the ear (“hamster cheeks”), under the tongue, calluses on fingers. Tanner stage

  • psychological findings in the light of the exploratory discussion and mental abnormalities revealed by history (see above)

  • laboratory testing (electrolytes, phosphate, hepatic and pancreatic amylase, kidney values, complete and complete blood count, serum leptin level if necessary (starvation ≤ 2 ng/mL; rarely higher))

  • if clinically necessary, further diagnostic testing (e.g. ECG, sonography to rule out pleural or pericardial effusions, cranial MRI to rule out brain lesions)

  • determination of current BMI and BMI percentile (e40). For online BMI percentile determination, see for example www.bkk24.de/lbl/ratgeber-gesundheit/artikel-lesen/bmi-rechner-fuer-kinder.html.

  • determination of the target BMI or target weight according to the 25th BMI age percentile (the target weight should be set higher in the case of premorbid overweight/obesity)

  • if the patient is in critical condition, direct transfer to the responsible children’s hospital or child and adolescent psychiatry department

Tasks over the course of treatment

• maintain contact with the patient and family: at the beginning, arrange a weekly meeting of 10 minutes, build up motivation for weight gain (discuss the advantages and disadvantages of AN with the patient, explain the health threat); if necessary, build up motivation for inpatient treatment, be prepared for psychological deterioration/crises, brief documentation of the psychological findings

• draw up a contract with weekly weight gain targets (e.g. 300 grams/week); (partial) inpatient treatment in the event of non-compliance

• at first, weekly standardized weight checks (if necessary twice a week if at risk); in the medium term, height checks additionally to adjust target BMI

• parent education regarding compliance with regular food intake (3 main meals and 3 snacks)

• laboratory tests, physical examination, pulse and blood pressure measurements depending on initial findings and progression

• case management involving outpatient and, if necessary, inpatient medical and psychotherapeutic staff and nutritionists; support the family in their search for psychotherapists experienced in treating AN, for nutritional advice, and for hospitals.

BMI, body mass index; EKG, electrocardiography; HR, heart rate;

MRI, magnetic resonance imaging

Weight criterion

According to the DSM-5, underweight in children and adolescents is operationalized as a body mass index (BMI; kg/m²) lying below the 5th sex-specific age percentile for BMI (1). Some patients display no clear loss of weight; rather, body weight remains fairly constant over time and the BMI gradually drops below the 5th age percentile as the individual ages and grows in height. It is pointed out in both the DSM-5 and the ICD-11 that the 5th percentile criterion is not meant to imply a sharp boundary between normal and abnormal. The ICD-11 alternatively permits a diagnosis of AN after rapid, marked weight loss (> 20% of body weight over 6 months); thus a patient who was overweight and then developed AN may, in fact, be of normal weight.

Body image disturbance/weight phobia

In addition to being underweight, most patients also have a body image disturbance and weight phobia. They consider themselves too fat overall or in certain parts of their body. The DSM-5 (1) allows a diagnosis to be made even if these cognitions are not present, provided that the eating and exercise behaviors preclude the physiological need for weight gain.

Central event in the onset of anorexia nervosa.

An initial significant weight loss is considered to trigger the onset of anorexia nervosa. Weight loss can occur for a variety of reasons.

Differential diagnosis

Diagnostic difficulties may arise because of hidden abnormal eating behavior or weight loss. It is, therefore, essential that a medical history should also be taken from the patient’s parents or other people close to her or him. Other mental disorders that can cause weight loss, such as avoidant or restrictive eating disorder (e9), bulimia nervosa, emetophobia (pathological fear of vomiting), obsessive-compulsive disorder, depressive episodes, and psychoses, should be ruled out in the differential diagnosis. Infection, autoimmune disease (e.g., encephalitis), neoplasia, and endocrine disease (e.g. Addison‘s disease) can rarely simulate AN.

Constitutionally underweight healthy persons are occasionally wrongly diagnosed with AN. A detailed exploration in constitutionally thin, healthy children in the lowest percentile range will, however, reveal the following:

• a long-term weight history in the lowest percentile range,

• a relatively unremarkable food intake in quantity and quality,

• no body image disturbance or weight phobia, and

• often, first-degree relatives who were also underweight at that age.

Differential diagnosis.

A history from a parent, guardian, or someone else who is close to the patient is essential. Other mental disorders that can cause weight loss must be ruled out in the differential diagnosis, including bulimia nervosa, emetophobia, obsessive-compulsive disorder, depressive episodes, and psychoses.

Subclassification

Both the DSM-5 and the ICD-11 further classify AN into a restrictive type and a binge-eating/purging type. The restrictive type dominates in adolescence (> 80%) (11, 12). The DSM-5 classifies remission as either partial or total, while the ICD-11 contains a separate diagnosis of anorexia nervosa in remission. These subclassifications take into account the fact that the return of normal weight is not a sufficient criterion for recovery: amenorrhea, body image disturbances, or the desire to lose weight may persist. Atypical AN according to the DSM-5 (in which the underweight criterion is not met) has become more common in recent years.

Atypical anorexia nervosa.

Atypical anorexia nervosa, according to the DSM-5, is characterized by lack of fulfillment of the weight criterion, possibly because of a high starting weight before weight loss.

Laboratory diagnostic testing

The blood tests listed in the eBox and eTable 3 should be carried out when AN is diagnosed and over the course of the disease. The serum leptin level informs about the patient’s fat mass and the extent of neuroendocrine starvation. Leptin measurement can also be helpful if patients deny the manifestations of the disease despite clinical evidence (AN is likely with subnormal leptin levels) (13). In severely starved individuals, serum leptin becomes undetectable with standard assays. Constitutional underweight is usually associated with a leptin level in the (low) normal range.

Premorbid history and the onset of the eating disorder

Premorbid social anxiety, compulsions, perfectionism, and/or ambition are frequently found (14). These personality traits in particular contribute to the intensive and prolonged pursuit of intentional behavioral changes (e.g. dieting, increasing fitness). Major depression, anxiety and obsessive-compulsive disorders can begin before AN. According to studies, patients with AN, in contrast to those with atypical AN according to DSM-5, are more likely to be underweight from the age of 2 to 4 (15, 16). The average premorbid BMI of hospitalized patients in Germany was also below the median (eTable 2). A small subgroup of people with AN had other eating disorders before developing AN (e10).

eTable 2. Baseline data of hospitalized patients with anorexia nervosa (AN) and atypical AN (one diagnostic criterion not met) from the German Anorexia Nervosa Registry with the participation of 16 hospitals (August 2014 to February 2019; 469 patients). Modified according to (12, e12, e41).

Characteristics	On admission	On discharge
Age in years (mean ± SD; range) (12)	15.17 ± 1.64; 8.9–18.9
BMI in kg/m² (mean ± SD; range) (12)	15.4 ± 1.5; 11.6–20.7	18.3 ± 1.43; 13.6–22.9
Premorbid BMI in kg/m² (mean ± SD) Premorbid BMI-SDS Premorbid BMI age percentile (e11)	19.7 ± 2.8 −0.36 ± 0.89 ≈36
Restrictive type Binge-eating/purging type Atypical anorexia nervosa (12)	80% 6% 14%
Duration of treatment in weeks (mean ± SD; range) (12)		17.21 ± 8.64; 0.0–61.0
Severity classification according to ICD-11 (n = 404; without atypical anorexia nervosa)
– significantly low weight (BMI percentile ≥ 0.3) – dangerously low weight (< 0.3rd percentile) (12)	50% 50%
Duration of illness before admission in weeks	51 ± 45
Reasons frequently given (by parents) for hospitalization (multiple answers possible) (e41)	low weight: 65% too little food: 52% rapid weight loss: 46% depressive mood: 26% medical/psychotherapeutic advice: 23%

BMI, body mass index; SD, standard deviation; SDS, standard deviation scores

Many patients retrospectively associate initial weight loss with improved performance and mood as well as an increased sense of control (e11). As weight loss continues, the clinical picture changes: patients are unable to gain weight on their own or can only do so with a major effort (e12). Persistent hunger becomes a chronic stressor (Tabelle 1) (5). Patients sometimes set an even lower target weight and are usually severely impaired by eating disorder-specific cognitions, including constant mental preoccupation with food and weight. Their memory and concentration may be impaired.

Comorbidities and clinically relevant accompanying manifestations

Comorbidities.

Comorbid mental disorders—in particular depression, anxiety disorders and obsessive-compulsive disorder—are found in more than half of inpatients.

Comorbid mental disorders, in particular depression, anxiety and obsessive-compulsive disorder, are found in more than half of inpatients (11, 17). Depression can be a consequence of starvation (Table 1) and often improves after weight gain. The clinical picture of depression in AN differs from other forms of depression in adolescence. For example, suicidal ideation was three times more common in individuals with AN and comorbid depression than in persons with depression but no comorbid eating disorder (46% vs. 14%). On the other hand, depressed patients with AN attempted suicide less frequently than other depressed adolescents (1% vs. 39%; e13). The symptoms of comorbid OCD are sometimes closely interwoven with those of an eating disorder (e.g. compulsive washing due to fear/disgust of food). Some sufferers have delusional cognitions (e.g. calorie intake via ointments).

30–80% of patients display increased physical activity (18), e.g., sports and/or marked physical restlessness. Motivations for such behavior include the fear of weight gain and the mood-stabilizing effect of physical activity. Many patients experience physical hyperactivity as a compulsion. Studies in animals and human beings have found evidence that this hyperactivity is triggered by a subphysiological level of leptin secretion (18). Patients with hyperactivity nevertheless experience tiredness and exhaustion (e14).

Typical accompanying manifestations.

30–80% of patients display increased physical activity, e.g., sports and/or marked physical restlessness. Motivations for such behavior include the fear of weight gain and the mood-stabilizing effect of physical activity. Many patients experience physical hyperactivity as a compulsion.

Treatment

Key components of treatment.

• psychoeducation

• monitoring of weight gain

• improvement of the mental and physical state

• involvement of the family

Essential components of the treatment of AN are psychoeducation, the initiation and monitoring of weight gain, improvement of mental and physical condition, a multidisciplinary networked approach, and involvement of the family (19). The aim is to normalize eating behavior, treat the physical consequences of disordered eating and underweight, improve the underlying difficulties on an emotional, cognitive and interactional level, and enable social integration and catching up on missed steps in development (20).

Nutritional therapy, target weight, and exercise therapy

All guidelines emphasize rapid weight restoration as a central treatment goal (19–21). Weight restoration is a prerequisite for mental and physical recovery and an improved quality of life (19). Depressiveness, preoccupation with food (22), and restrictive eating behavior all diminish during inpatient realimentation; body image disturbances, drive for thinness, and mental fixation on weight diminish to a lesser extent (11). The German guideline recommendations for weight gain are 200–500 g in the outpatient setting and 500–1000 g per week in the inpatient setting (20). In recent studies, no refeeding syndrome was observed in severely malnourished adults (BMI <13 kg/m²; [e15]) or adolescents (BMI <15 kg/m²; [23]) during realimentation with an initially higher/normocaloric calorie count (e.g., 2000 kcal/d from the start of treatment, with increasing energy intake if weight gain is insufficient) under close clinical laboratory monitoring (phosphate, calcium, potassium, magnesium) and, if necessary, phosphate and thiamine supplementation. Hypophosphatemia and other electrolyte imbalances are the most important manifestations of this severe metabolic derailment (24). At the same time, 2000 kcal/d were needed at the start of treatment in order to achieve a weight gain of 700 g/week (23). Even with constant weight gain, the improvement of starvation-related psychopathology requires an individually varying period of several weeks (Table 1). As the energy requirement for adequate weight gain can be over 3000 kcal/d in some phases, energy-dense foods are recommended. Gastrointestinal complaints (bloating, nausea, abdominal pain, flatulence, constipation) often occur before or at the beginning of refeeding but subside as weight restoration progresses (e16).

Target weight.

The initial target weight for hospital discharge is usually the 25th BMI percentile. In the case of habitually lower premorbid BMI percentiles, a lower target can also be set, but not below the 10th percentile. The premorbid BMI percentile and, in girls, the menarche/return of menstruation in the intermediate term provide a guide to healthy body weight.

Psychotherapy.

Psychotherapy should accompany realimentation. It increases motivation in the starvationstage; later, individual issues increasingly come to the fore; the final emphasis is on relapse prevention.

The initial weight goal for discharge from inpatient treatment is usually the 25th BMI percentile (20). In the case of habitually lower premorbid BMI percentiles, a lower weight target can also be set, but in the authors‘ opinion not below the 10th BMI percentile. The premorbid BMI percentile and, in girls, the menarche/return of menstruation in the intermediate term provide orientation for determining the individual healthy body weight. While, in some female patients, menstruation already recommences during realimentation, in others it may not do so even after the target weight has been reached. In addition to an adequate body fat percentage (e17) and sufficient leptin secretion (6), prerequisites to the resumption of menstruation also include the return of the ovaries and uterus to normal size after their starvation-induced reduction (e18).

For many years, physical exercise was not recommended for patients with AN during realimentation. Today, specialized institutions successfully integrate moderate sports and exercise interventions (Table 2 [e19, 25]), also to reduce the risk of osteoporosis. To improve bone density, calcium and vitamin D are orally substituted in patients with vitamin D deficiency up to the 10th BMI percentile, although the transdermal application of 17-beta-estradiol appears to be more effective. Supplementation of other demonstrated micronutrient deficiencies (vitamins, zinc, selenium) is advisable (20). The benefit of hormone replacement therapy with estradiol or progesterone is debated (20, 21). In older adolescents (bone age ≥ 15 years) who do not gain weight and have a bone density Z-score of 2.0 or less, a 17-beta-estradiol patch and oral progesterone can be considered, in consultation with pediatricians (26).

Table 2. Efficacy studies on the treatment of children and adolescents with anorexia nervosa.

First author	Year	Study design	Intervention	Findings	Remarks
Psychotherapy
Monteleone et al. (e31)	2022	systematic meta-review	various interventions*	FT superior to CG (improvement in disease severity and body weight)	disease: 3 RCTsweight: 4 RCTs
Zeeck et al. (e32)	2018	network meta-analysis	psychotherapeutic interventions	no superiority with respect to weight gain of any specific approach	8 studies, 10 treatments
Treatment setting
Herpertz-Dahlmann et al. (e33)	2014	RCT	DCS after 3 weeks of FIT vs. FIT	comparable BMI 12 months after either DCS or FIT (mean difference in favor of DCS, 0.46 kg/m2)	DCS on wards with extensive and specific experience in the treatment of eating disorders
Exercise intervention
Dittmer et al. (25)	2020	RCT	manual-based intervention vs. ST	more marked reduction of physical hyperactivity (z = −2.81; p = 0.005; effect size = −0.3) than with ST	no difference in other outcomes related to anorexia nervosa
Realimentation
Garber et al. (e34) Golden et al. (e35)	2021	RCT	HCR (initial 2 000 kcal/d) vs LCR (initial 1 400 kcal/d)	HCR: safe, shorter time to medical stabilization (HR 1.67; 95% CI [1.1; 2.5], p = .01) and shorter treatment (±4 days); no difference between HCR and LCR with respect to 12-month remission rates (p = 0.42) or rehospitalization rates (p = 0.84)	caveat: realimentation should be carried out in a highly specialized setting with close medical monitoring; the typical duration is 12 days
Pharmacotherapy
Han et al. (e36)	2022	meta-analysis	olanzapine vs. placebo	BMI difference at 3–9 months: 0.7 kg/m2 (95% CII [–0.4; 1.7], p = 0.21)	3 studies (n = 65), of which only 1 was an RCT (n = 20)

95% CI, 95% confidence interval; BMI, body mass index; CG, control group; CI, confidence interval; DCS, day clinic setting;

FIT, full inpatient treatment; FT, family therapy; HCR, high-calorie realimentation; HR, hazard ratio; kcal/d, kilocalories/day; LCR, low-calorie realimentation; RCT, randomized controlled trial; ST, standard treatment; vs., versus.

* Behavioral therapy, cognitive-behavioral therapy for eating disorders (CBT-ED), family therapy, interpersonal psychotherapy, Maudsley model for adults with anorexia nervosa‘, mixed or non-specific psychotherapy, multidisciplinary care, psychodynamic-oriented psychotherapy, psychoeducation‘, sports therapy and pharmacological treatments. Comparison therapies: specific medication or psychological intervention (active), ST, placebo, waiting list (WL) or no treatment (NT), ST mixed with WL/NT, mixed active treatment and WL/NT

Psychotherapy and treatment settings

Aside from realimentation, psychotherapy is a further major element of treatment in the German clinical practice guidelines, which are now being updated (20). In the starvation stage, supportive psychotherapy is used to increase motivation and provide reassurance regarding the (usually unfounded) fear of excessive weight gain. After this, individual issues increasingly come to the fore. Finally, the focus is on relapse prevention.

Initially, the least restrictive setting for outpatient treatment is indicated: both the patient and her/his parents should be involved, and therapy should be provided by a psychotherapist who is experienced in the treatment of eating disorders under medical supervision. The patient should be hospitalized for treatment if not enough weight is gained, or, obviously, in case of an imminent threat to life. The length of inpatient treatment in Germany ranged from 3 to 6 months (eTable 2; [e20]). Treatment teams should be experienced in dealing with patients with AN. On the basis of evidence from 9 RCTs, Anglo-American guidelines (19, 21) recommend manual-based, eating-disorder-specific, family-centered procedures (FBT/FT-AN), with close involvement of parents in therapy carried out by specially trained therapists, as the first line of treatment. FBT/FT-AN is practically unavailable to date in Germany. Promising results were obtained in two recent pilot studies of home treatment (27) and FBT (28) as two different means of shortening the 3- to 6-month-long inpatient treatments (29) in Germany (e20). The findings of both pilot studies now need confirmation in RCTs of adequate size.

Pharmacotherapy

No drug has been approved for the treatment of AN. Antidepressants, including serotonin reuptake inhibitors, are nevertheless used clinically despite the lack of evidence for their effectiveness (30). Comorbid depression may fail to respond to antidepressant treatment because of a starvation-dependent pathogenesis. Evidence for the benefit of antipsychotic drugs in AN is largely lacking as well (31, 32), yet they are commonly used to facilitate weight gain and to reduce tension, AN-specific cognitions, and physical hyperactivity.

There have been small-scale RCTs investigating the use of cannabinoids (e21) and ghrelin agonists (e22) for appetite enhancement. A feasibility study with psilocybin (10 adults) appears promising (e23). In recent case studies, recombinant leptin (metreleptin) has been used for the off-label treatment of severe AN in adolescents and adults, under the assumption that leptin deficiency induces mental manifestations of starvation (18, 33, 34).

Pharmacotherapy.

No drug has been approved for the treatment of AN. Antidepressants are nevertheless used clinically despite the lack of evidence for their effectiveness. The potential benefit of cannabinoids, ghrelin agonists, psilocybin, and metreleptin is currently being studied.

Medical case management and disease course

Aside from making the initial diagnosis, physicians in private practice have an important role in psychoeducation on the medical consequences of AN, motivating patients to undergo treatment, and somatic management (35), including risk assessment in children and adolescents with AN, with the involvement of their parents or legal guardians. Medical treatment and follow-up should be individually adapted to the ongoing medical assessment (Box 1, Box 2, eBox, eTable 3). Patients can be motivated to undergo treatment through repeated discussion; for some patients, the parents will need to be educated to understand that there is an urgent need for treatment. Patients often become more willing to participate in a personal discussion if they are asked to identify positive aspects of their illness. A subsequent stage of the discussion can then address its negative aspects, including the patient’s depressive mood, social withdrawal, and family disputes about eating (and, possibly, exercise) behavior. In acute, severe AN, the patient’s thoughts and feelings may be dominated by the eating disorder to such an extent that they appear delusional (e24). Discussions with medical staff then revolve exclusively around the desire to eat less and lose weight. In this situation, a persistent appeal to reason, with exhortation to eat more, is unhelpful and may well exacerbate anxiety and stress. The German clinical practice guideline (20) recommends actively calling patients in for regular follow-up under standardized conditions while remaining aware of possible weight manipulation, which should be understood as a symptom of the disease.

Box 2. Parameters relevant for assessment of somatic risk*.

• Body weight

  • BMI percentile

  • absolute BMI

  • speed of weight loss

• Eating and drinking habits

  • fluid intake; dehydration

  • calorie content of ingested food

• Cardiovascular parameters

  • resting heart rate

  • systolic/diastolic blood pressure

  • ECG

  • QTc

  • syncope

• Other somatic parameters

  • body temperature

  • laboratory findings

The assessment of the somatic risk (and, in particular, the selection of the proper setting for treatment) requires an individualized combined evaluation of all relevant parameters in the context of the patient’s general condition, recent course, and physical and mental functionality. If an individual parameter is markedly abnormal (e.g. hypokalemia), there may be an urgent need for action. Inpatient treatment is indicated in the event of clinically relevant danger to self or others.

* Details and reference values: eTable 3

BMI, body mass index; EKG, elektrocardiography;

QTc, QT interval corrected for frequency

eTable 3. Parameters whose combined values are relevant to the assessment of somatic risk.

	No/mild risk			Potential moderate risk			potential acute/severe risk
Body weight
BMI percentiles	≥ 5th BMI perentile			1st to 4th BMI percentile			< 1st bmi percentile
Absolute BMI values (kg/m2)	5th percentile			1st to 4th percentile			<1st percentile
	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 14.5 14.9 15.3 15.7 16.3 16.8 17.4 18.0	Girls 14.2 14.7 15.3 16.0 16.7 17.3 17.8 18.2	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 13.7–14.4 14.0–14.8 14.3–15.2 14.8–15.6 15.3–16.2 15.8–16.7 16.4–17.3 17.0–17.9	Girls 13.4–14.1 13.7–14.6 14.3–15.2 15.0–15.9 15.7–16.6 16.3–17.2 16.8–17.7 17.2–18.1	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 13.6 13.9 14.2 14.7 15.2 15.7 16.3 16.9	Girls 13.3 13.6 14.2 14.9 15.6 16.2 16.7 17.1
The speed of weight loss	stable weight			weight loss of 500 g to < 1 kg/week for at least 3 consecutive weeks with existing underweight (< 5th bmi percentile)			weight loss of ≥ 1 kg/week for at least 3 consecutive weeks with existing underweight (< 5th bmi percentile)
Eating and drinking behavior
Fluid intake and dehydration	little or no reduction of fluid intake, possible mild dehydration, possible dry mouth or risk of developing dehydration with a trend toward negative fluid balance			markedly reduced fluid intake or cessation of fluid intake for 12–24 hours. Moderate dehydration: reduced diuresis, dry mouth, normal skin turgor, mild tachypnea/tachycardia			severe dehydration or cessation of fluid intake for > 24 hours. Severe dehydration: reduced diuresis, dry mouth., reduced skin turgor, sunken eyes, tachypnea/tachycardia, peripheral edema
Cessation of food intake	< 12 hr in a day			12–24 hrs			> 24 hrs
Cardiovascular parameters
Resting heart rate	z-score > –1			z-score -1 to -4			z-score < –4
Average of 2-3 daytime measurements	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 68 67 66 64 63 62 61 59	Girls 70 69 68 67 65 64 64 63	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 47–67 45–66 44–65 42–63 41–62 40–61 38–60 37–58	Girls 48–69 47–68 46–67 44–66 43–64 42–63 41–63 40–62	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 46 44 43 41 40 39 37 36	Girls 47 46 45 43 42 41 40 39
Systolic blood pressure	z-score > –1			z-score -1 to -4			z-score < –4
(mmHg); repeated measurements	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 97 99 101 103 106 109 111 113	Girls 98 99 101 103 104 104 105 106	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 80–96 81–98 83–100 84–102 86–105 88–108 89–110 98–112	Girls 79–97 80–98 82–100 83–102 83–103 84–103 85–104 85–105	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 79 80 82 83 85 87 88 89	Girls 78 79 81 82 82 83 84 84
Diastolic blood pressure	z-score > –1			z-score -1 to -4			z-score < –4
(mmHg); repeated measurements	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 57 58 59 60 61 62 63 64	Girls 57 58 59 60 61 62 62 63	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 38–56 39–57 39–58 39–59 40–60 41–61 40–62 42–63	Girls 39–56 40–57 40–58 41–59 42–60 42–61 42–61 41–62	Age (years) 10.5 11.5 12.5 13.5 14.5 15.5 16.5 17.5	Boys 37 38 38 38 39 40 40 41	Girls 38 39 39 40 41 41 41 42
EKG, QTc	< 460 ms (girls) < 450 ms (boys) without any other relevant abnormality in the ECG			< 460 ms (girls) < 450 ms (boys) without any other relevant abnormality in the ECG			> 460 ms (girls) 450 ms (boys) and/or a relevant ECG abnormality not related to the QTc
Syncope (history of)	at most mild or rare dizziness; no presyncope or syncope			dizziness, presyncope, at most one syncope			repeated syncopal episodes
Further somatic parameters
Body temperature	> 36.0 °C			< 36.0 °c–35.5 °c			< 35.5 °c
Laboratory tests	normal values of phosphate, sodium, potassium, albumin, glucose, transaminases, leukocytes, and hemoglobin (repeated determinations depending on condition and course)			deviations from normal values that are still within the limits at right; close monitoring required			hypophosphatemia < 0.8 mmol/l hyponatremia < 125 nmol/l hypokalemia < 2.5 mmol/l hypoalbuminemia < 30 g/l hypoglycemia < 3 mmol/l transaminases > 3 times the normal value leukocytes < 2/nl hemoglobin < 10 g/l

The assessment of somatic risk (and any choice of treatment setting that is made as a result) is generally not possible on the basis of individual parameters but rather requires consideration of the combination of all parameters in view of the patient‘s general condition, recent course, and physical and mental functionality. However, especially severe abnormalities of even a single parameter (e.g. hypokalemia) may call for urgent action. If there is clinically relevant danger to self or others,hospitalization is indicated.

Parts of the table are based on the risk stratification for young patients with eating disorders in the report of the Royal College of Psychiatrists (e42). It was adapted to the German healthcare system by incorporating the German S3 guideline (20) and clinical pediatric/child and adolescent psychiatric expertise. For the calculation of the percentiles and z-values for BMI. blood pressure and heart rate, nationally representative reference data from the German Health Interview and Examination Survey for Children and Adolescents (KiGGS) were used (e43. e44). The percentiles and z-values for blood pressure were presented in this publication for height at the 50th percentile. Explanation: z-scores of -1, -2, -3, and -4 correspond to the 15.9, 2.3, 0.1, and 0.003 percentiles.

BMI, body mass index; ECG, electrocardipography; hr, hour; ms, millisecond; QTc, frequency-corrected QT interval

Medical case management.

Medical treatment and follow-up should be individually adapted to the ongoing medical assessment. Patients can be motivated to undergo treatment through repeated discussion; some patients’ parents will need to be educated to understand that there is an urgent need for treatment.

25% of patients were readmitted to the hospital within one year of their initial inpatient treatment (e25). Psychological problems that were already present before AN, such as anxiety disorders, depression, or an emotionally unstable personality accentuation, may re-emerge after successful realimentation. The transition from adolescence to adulthood poses potential risks because of a potentially inadequate transition to care by non-pediatric physicians, combined with the sudden attainment of legal age. The parents or guardians of a child or adolescent whose welfare is at risk can apply to the family court for a closed placement in accordance with §161b of the German Civil Code (BGB); from age 18 onward, this is only possible if the patient presents an acute danger to herself/himself, or to others (Mental Illness Act). Medicolegal guardianship should be considered in some cases and should ideally be applied for before the individual’s 18th birthday.

The duration of illness.

In an 18-year longitudinal outcome study including 51 adolescent patients, the mean duration of AN was 3.4 years.

There are no standardized, internationally accepted criteria for remissions of AN (36). In an 18-year longitudinal outcome study including 51 adolescent patients, the duration of AN was 3.4 ± 2.4 years (mean ± standard deviation) (37). In a recent meta-analysis of 109 studies that included 10,644 adolescent and adult patients with AN, body weight normalized in 45% of over 72.8 ± 76.8 months of observation. At 10 years and beyond, 67% recovered from AN, with recovery defined as the absence of eating disorder symptoms or a “good” outcome on established scales (e.g., the Morgan-Russell scale; [38]). Subclinical abnormalities, such as mild eating disturbances, increased perfectionism and compulsiveness (e26), and an increased risk of other mental disorders, especially anxiety disorders and depression (e27), often persist after recovery. The lethality of AN is evident in long-term studies of adults: in a German 25-year longitudinal study of adults who had been hospitalized for AN, 97 (7.6%) of the 1271 study participants died (39). A meta-analysis revealed a standardized mortality ratio of 5.86 for AN, which was the highest among all mental disorders (40), with deaths rarely occurring before age 18. Common causes of death are suicide and complications of starvation. Childhood-onset AN has been reported to have both a better and a worse prognosis (e28 and e29, respectively).

Mortality.

A meta-analysis revealed a standardized mortality ratio of 5.86 for AN, which was the highest among all mental disorders (40). Common causes of death are suicide and complications of starvation.

Overview and perspectives

AN is among the more severe mental illnesses of childhood and adolescence; it endangers physical health through starvation. Early detection and early intervention are essential. The higher prevalence of AN in females has not yet been adequately explained. In the near future, internationally accepted remission criteria will need to be defined; if possible, the course of the disease should be shortened, the risks of chronification and of death should be reduced, and an understanding should be gained of whether and how weight loss in adolescence (be it intentional or unintentional) can transform into AN. If it is found that certain drugs can counteract the central adaptation to starvation and thereby alleviate the starvation-related manifestations of AN, their use might markedly improve the outcome of AN. The putative benefit of leptin supplementation has yet to be confirmed in randomized and controlled trials.

Patients should be taught about the complex physical and mental changes induced by starvation and their improvement once normal weight is restored; psychoeducation about these matters can strengthen their motivation to gain weight. In the hospital setting, normocaloric realimentation can be provided from the outset under close supervision. Treatment settings should be reconsidered; appropriate outpatient and day-treatment facilities should be made more widely available in accordance with best professional practice so that each patient can receive individually optimized treatment. There is a need for stronger coordination of the diagnostic procedures and treatments that are offered in pediatrics and child and adolescent psychiatry. The efficacy of FBT, FT-AN, and home treatment should be investigated in RCTs in Germany; if the findings are positive, these procedures should be recommended in the next update of the German clinical practice guidelines. Further study is needed on the benefits and risks of psychoactive drugs and the potential definability of a prognostically valid prodromal stage in which preventive treatment might be provided.

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Only one answer is possible per question. Please select the answer that is most appropriate.

Question 1

The lifetime prevalence of anorexia nervosa in women and men is 3.6% and 0.3%, respectively. How many of these patients receive a diagnosis of anorexia nervosa by age 18?

1. 15%;

2. 40%;

3. 55%;

4. 70%;

5. 90%

Question 2

What are important and scientifically proven risk factors for the development of anorexia nervosa?

1. genetics, peer-group influences, and parental personality traits

2. environmental factors, individual personality traits, and socioeconomic status

3. genetics, environmental factors, and individual personality traits

4. genetics, parental personality traits, and individual personality traits

5. peer-group influences, individual personality traits, and socioeconomic status

Question 3

According to ICD-11, what event is considered to be the overriding central factor in the development of anorexia nervosa?

1. marked initial weight loss, for any of a variety of reasons

2. an unresolved traumatic event in childhood

3. increased exercise in weight-focused sports

4. orientation towards the Western ideal of beauty

5. the desire to protect the environment through a sustainable lifestyle

Question 4

What disease entity is an important element of the differential diagnosis of anorexia nervosa?

1. social behavior disorder

2. obsessive-compulsive disorder

3. metabolic syndrome

4. chronic skin diseases

5. reactive attachment disorder of childhood

Question 5

What is the reason for the special importance in the diagnostic evaluation of history-taking from the parents, guardians, or other persons close to the child or adolescent patient with anorexia nervosa who have insight into her or his eating behavior?

1. The extent of weight phobia can usually only be clearly determined by third parties.

2. Eating behavior at home should never be discussed with the patients themselves.

3. Parents often play an important supportive role during the acute phase of the illness.

4. Patients often give unreliable information about their own eating behavior as a consequence of their illness.

5. Family conflicts in eating situations can only be adequately assessed by taking a history from third parties.

Question 6

What disease is the most common comorbidity in patients with anorexia nervosa?

1. diabetes;

2. Crohn’s disease;

3. depression

4. specific phobias;

5. psychosis

Question 7

Which of the following is considered a central goal of treatment both in the German guidelines and in the English-language guidelines for the treatment of anorexia nervosa?

1. weight restoration;

2. psychoeducation;

3. insight into the illness

4. social integration;

5. medication

Question 8

What is the average duration of illness in adolescents with anorexia nervosa?

1. 3 months;

2. 6 months;

3. 12 months;

4. 3.4 years;

5. 6.8 years

Question 9

Which statement about starvation in anorexia nervosa is correct?

1. Most of the mental manifestations of anorexia nervosa precede starvation.

2. Inpatient weight restitution leads to marked improvement in psychological symptoms within two weeks.

3. Starvation can be terminated promptly by the intravenous administration of serotonin reuptake inhibitors.

4. Starvation is causally involved in the development of the mental and physical manifestations of anorexia nervosa.

5. High leptin levels are held to be a marker for the onset of starvation.

Question 10

Which of the following descriptions fits atypical anorexia nervosa?

1. The underweight criterion is not met because the initial weight was relatively high.

2. There is a body image disturbance and the patient feels too thin.

3. The patient is to be classified as in partial remission on a psychological level.

4. The patient‘s laboratory values are consistently unremarkable.

5. The patient does not exhibit weight phobia and would like to gain weight.