Eating disorders in children, adolescents, and young adults


Eating disorders are severe conditions that affect children, adolescents, and young adults with increasing frequency. These disorders carry a high medical and psychiatric morbidity, with a standardized mortality ratio for anorexia nervosa (AN) of 6 and for bulimia nervosa (BN) of 2.


Eating disorders are severe conditions that affect children, adolescents, and young adults with increasing frequency.1 These disorders carry a high medical and psychiatric morbidity, with a standardized mortality ratio for anorexia nervosa (AN) of 6 and for bulimia nervosa (BN) of 2.2 Similar

to BN, the standardized mortality ratio for eating disorder not otherwise specified (EDNOS) is also 2.2 Often it is the pediatrician who will have the first interaction with a patient showing symptoms consistent with an eating disorder. The pediatrician, therefore, has an important role to play in the identification and management of eating disorders in children, adolescents, and young adults. This article reviews the epidemiology of eating disorders; updates the reader on the revised diagnostic criteria for eating disorders; and discusses identification and principles of management, focusing on those issues particularly pertinent to the pediatrician.

Eating disorders are predominantly found in girls and women with a female-to-male ratio of 9:1.3 Onset usually begins during adolescence, with the highest risk group being girls aged from 15 to 19 years.4 In recent years, an increasing prevalence has been seen in minority populations and in younger age groups. Athletes, diabetics, and obese adolescents are particularly vulnerable.5-7 Disturbances of body image and diet are less prevalent in young men than in young women. Nevertheless, it is more common than generally believed: Approximately 10% of cases of AN and BN are young adolescent men.8 In addition, presenting symptoms of eating disorders in boys may include intense bodybuilding, the use of anabolic steroids, and preoccupation with body shape and musculature.

The diagnostic criteria for eating disorders have recently been revised.9 In addition to AN and BN, the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), now includes binge-eating disorder (BED) and avoidant/restrictive food intake disorder (ARFID), as well as other categories. The core features of AN are restriction of energy intake leading to a significantly low body weight for developmental stage, body image distortion, preoccupation with shape, and fear of gaining weight. In contrast to DSM-IV, the 85% of expected body weight (EBW) threshold and amenorrhea have both been removed as requirements for the diagnosis of AN. Core features for BN include cycles of binge eating with consumption of large amounts of food with loss of control followed by inappropriate compensatory behaviors such as self-induced vomiting, use of laxatives, diuretics, diet pills, or excessive exercise. Patients with BN are usually of normal weight, but their weight can be high or low. In contrast to DSM-IV, in which the frequency of binging and purging to meet criteria for BN was twice a week for 3 months, in DSM-5 the frequency of those episodes has been reduced to once a week.

Binge-eating disorder describes a condition in which patients binge but do not use inappropriate compensatory behaviors. The new diagnostic category ARFID describes patients who restrict their caloric intake but who do not have body image distortion or fear of gaining weight. They avoid foods based on texture or color and they can have concerns about aversive consequences of eating, such as choking or vomiting. Although the DSM-5 has expanded the number of diagnostic categories, the number of patients with disordered eating behaviors far exceeds the number of patients with an eating disorder.


Female athlete triad

Although it is not listed as among the DSM-5 criteria for an eating disorder, the female athlete triad refers to a condition characterized by reduced energy availability, menstrual dysfunction, and reduced bone mineral density (BMD) in women athletes. The energy deficit may be intentional and accompanied by an eating disorder, or it may be unintentional when the athlete underestimates the energy requirements for her sport. An energy deficit can even occur at a stable weight. Among US high school and collegiate athletes, the prevalence of the triad is low (up to 1.2%). However, the prevalence of the individual components of the triad is much higher, with 23.5% of women athletes experiencing menstrual dysfunction and 18.2% exhibiting disordered eating.10


Typical presentations to the pediatrician are primarily related to weight-control behaviors (including food restriction, binging, purging, laxative abuse, and excessive exercise) and the effects of malnutrition (Tables 1, 2). A child or adolescent can present with failure to gain expected weight during a period of growth or may even present with frank growth retardation and pubertal delay. Female adolescents and young adults may present with primary or secondary amenorrhea.

Strategies for office-based screening are outlined in Table 3. Screening tools are available for the pediatrician, for example the Eating Attitudes Test or the SCOFF (Sick, Control, One stone, Fat, Food) questionnaire (Table 4).11,12 Many practices and clinics employ confidential questionnaires that screen for a variety of risk and resilience behaviors, including questions related to eating disorders. For adolescents and young adults, it is important to interview the patient alone in addition to interviewing him/her with a parent. History should include questions about recent weight changes including maximum and minimum weight and weight at which menses were lost; changes in eating habits; and symptoms related to malnutrition. Other pertinent information should include a detailed menstrual history including confidential sexual history; a 24-hour dietary recall including measurements of food items consumed; and information on the amount, intensity, and duration of exercise. It is important to ask about preoccupation with shape and weight; distortion in body image; and binging or purging behaviors. Denial or secrecy is common, and frequently there are discrepancies between the history provided by the patient and that provided by a parent.

The physical examination should include measurement of height and weight obtained with the patient dressed in a hospital gown, post voiding. Body mass index (BMI) should be calculated (weight in kg ÷ by height in m2) and plotted on the Centers for Disease Control and Prevention growth charts. In a child or adolescent, the BMI percentile should be determined for age, sex, and height and compared with prior growth charts. Other medical diagnoses should be considered and excluded, including thyroid disease, inflammatory bowel disease, or celiac disease. Initial workup should include a complete blood cell count; erythrocyte sedimentation rate; serum electrolytes; calcium; magnesium; phosphorus; glucose; liver function tests; kidney function; urinalysis; triiodothyronine (T3); thyroxine (T4); and thyroid-stimulating hormone. For those who are amenorrheic, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and estradiol should be obtained. A testosterone level can be obtained in boys.



Medical complications

Medical complications can affect almost every organ system (Table 2). Growth retardation, pubertal delay or arrest, and impaired acquisition of peak bone mass may all occur as well as menstrual irregularities in women and decreased erections in men.

Energy imbalance is considered to be the leading factor disrupting the hypothalamic-pituitary-gonadal axis. Reduced pulse frequency of gonadotropin-releasing hormone results in low LH, FSH, and low estradiol or testosterone levels. In adolescent girls, energy imbalance may explain to some degree the fact that in up to 20% of cases of patients with AN, amenorrhea can occur before weight loss.13

Amenorrhea can persist after weight restoration in women with AN. Conversely, menses can resume in some despite low body weight. A recent study demonstrated that AN presents a high heritability and that polymorphisms in genes coding the estrogen receptors alpha and beta have been shown to be associated with AN.14 Menstrual dysfunction, however, can occur across all eating disorder subtypes. Dietary restriction and excessive exercise are associated with amenorrhea, whereas binge eating, vomiting, and appetite suppressant abuse are associated with oligomenorrhea or normal menses.15 Clinical variables associated with menstrual disturbances include vomiting, low dietary fat intake, and low body weight.

Eating disorders are associated with reduced BMD and increased fracture risk.16 Adolescence is an important time for bone mass acquisition and malnutrition can interrupt that process. In women, the degree of reduction in BMD is directly related to the duration of amenorrhea and degree of malnutrition. Bone mass density can increase with weight gain and resumption of menses, but it may not return to normal.17,18 Reduced BMD is also a finding in adolescent boys with AN.19

Hypokalemia is the most common electrolyte abnormality in AN.20 Metabolic alkalosis occurs in patients who vomit or abuse diuretics. Laxative abuse can cause acidosis. Hyponatremia is often due to excessive water ingestion or diuretic misuse. Urea and creatinine are generally low, and normal concentrations may mask dehydration or renal dysfunction. Abnormalities of liver enzymes are predominantly characterized by elevation of aminotransferases, which may occur before or during nutritional rehabilitation.

Refeeding syndrome describes a potentially lethal shift in electrolytes due to an increased secretion of insulin during refeeding. Cellular uptake of phosphorus can lead to hypophosphatemia within 4 days of refeeding and can precipitate sudden cardiac failure and arrhythmias. Reduced concentrations of free T4 and total T3 and elevated cortisol levels are frequently seen in patients with AN. Hypoglycemia is common. Hypercholesterolemia is a common finding, but its significance in relation to cardiovascular risk is uncertain. Albumin levels are usually normal. Finally, other abnormalities include hyperamylasemia, hypercarotenemia, and elevated creatine kinase.20



Principles of management

Treatment is best provided by a multidisciplinary team consisting of a physician, nutritionist, psychotherapist, and/or psychiatrist.1,21 Collaboration between all professionals involved in the patient’s care is important.

The pediatrician can be the physician member of the team or can refer the patient to a team of eating disorders specialists. Part of the evaluation will be to assess for psychiatric comorbidity. If the pediatrician elects to be the physician member of the team, management should include monitoring of weight, vital signs, and medical stability on a regular basis, sometimes even weekly if needed. Indications for hospitalization include electrolyte disturbances; severe malnutrition (weight, <75% EBW); bradycardia (<50 bpm during the day or <45 bpm at night); hypotension; or orthostasis. A weight gain of 1 to 2 lb weekly as an outpatient in malnourished patients is a reasonable goal. Many providers limit exercise during the initial treatment phase.

A dual-energy x-ray absorptiometry scan should be considered for all patients with AN or EDNOS and for women who have been amenorrheic for longer than 6 months to assess for low BMD. In adolescent women, oral estrogen-progestin is not effective in increasing BMD, likely because of the suppressive effects of oral estrogen on insulin-like growth factor 1, and because hormonal contraception is not recommended for treatment of low bone mass.22,23 Hormonal contraception can also mask resumption of menses, which is an important marker for determining recovery. The most important intervention is to restore menstrual function through improved nutrition.24

Adequate calcium intake is essential and vitamin D is necessary for calcium absorption. An estradiol level higher than 30 pg/mL is predictive of resumption of menses within 3 to 6 months.13

The role of psychotropic medications for treatment is limited. The evidence of efficacy is mostly weak or moderate. There is support for the use of antidepressants, however, particularly high-dose fluoxetine in BN.25

Family-based therapy (FBT) has been shown to be an effective evidence-based treatment for adolescents with AN and BN.26,27 There are 3 phases of FBT with distinct goals: Phase 1 is weight restoration; phase 2 focuses on returning control over eating back to the adolescent; and phase 3 focuses on adolescent development and treatment termination. The role of the pediatrician in FBT is to function as a consultant to the parents and primary therapist, to monitor for medical stability, and to offer guidance and feedback to the patient and family.28



Children, adolescents, and young adults with eating disorders can present to the pediatrician with a variety of symptoms including weight loss, vomiting, growth retardation, pubertal delay, and amenorrhea. In an adolescent girl who has lost weight, is exercising excessively, or is engaging in unhealthy weight control behaviors, an eating disorder should be suspected. Management is best conducted by a multidisciplinary team. Weight restoration and resolution of the cognitive distortions regarding shape and weight are the main goals of treatment.

In girls and young women, weight restoration is accompanied by resumption of spontaneous menses, and in boys and young men, it results in the normalization of testosterone levels. Hormone replacement therapy is not recommended to treat amenorrhea or low BMD in girls and women because it has not been shown to be effective in increasing bone mass and masks resumption of spontaneous menses. Family-based therapy is an effective form of psychological treatment in children and adolescents with AN. The role of the pediatrician is to serve as a consultant to the family, therapist, and patient and to monitor for medical stability.



1. Rosen DS; American Academy of Pediatrics Committee on Adolescence. Identification and management of eating disorders in children and adolescents. Pediatrics. 2010;126(6):1240-1253.

2. Arcelus J, Mitchell AJ, Wales J, Nielsen S. Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-analysis of 36 studies. Arch Gen Psychiatry. 2011;68(7):724-731.

3. Herpertz-Dahlmann B. Adolescent eating disorders: definitions, symptomatology, epidemiology and comorbidity. Child Adolesc Psychiatr Clin N Am. 2009;18(1):31-47.

4. Smink FR, van Hoeken D, Hoek HW. Epidemiology of eating disorders: incidence, prevalence and mortality rates. Curr Psychiatry Rep. 2012;14(4):406-414.

5. Sim LA, Lebow J, Billings M. Eating disorders in adolescents with a history of obesity. Pediatrics. 2013;132(4):e1026-e1030.

6. Pinhas-Hamiel O, Levy-Shraga Y. Eating disorders in adolescents with type 2 and type 1 diabetes. Curr Diab Rep. 2013;13(2):289-297.

7. Neithercott T. Body wars. Skipping meals, purging food, avoiding insulin--the scary world of eating disorders and diabetes. Diabetes Forecast. 2013;66(3):48-53.

8. Rosen DS. Eating disorders in adolescent males. Adolesc Med. 2003;14(3):677-689, viii.

9. Attia E, Becker AE, Bryant-Waugh R, et al. Feeding and eating disorders in DSM-5. Am J Psychiatry. 2013;170(11):1237-1239.

10. Javed A, Tebben PJ, Fischer PR, Lteif AN. Female athlete triad and its components: toward improved screening and management. Mayo Clin Proc. 2013;88(9):996-1009.

11. Mintz LB, O'Halloran MS. The Eating Attitudes Test: validation with DSM-IV eating disorder criteria. J Pers Assess. 2000;74(3):489-503.

12. Morgan JF, Reid F, Lacey JH. The SCOFF questionnaire: assessment of a new screening tool for eating disorders. BMJ. 1999;319(7223):1467-1468.

13. Golden NH, Jacobson MS, Schebendach J, Solanto MV, Hertz SM, Shenker IR. Resumption of menses in anorexia nervosa. Arch Pediatr Adolesc Med. 1997;151(1):16-21.

14. Ramoz N, Versini A, Gorwood P. Anorexia nervosa and estrogen receptors. Vitam Horm. 2013;92:141-163.

15. Poyastro Pinheiro A, Thornton LM, Plotonicov KH, et al. Patterns of menstrual disturbance in eating disorders. Int J Eat Disord. 2007;40(5):424-434.

16. Golden NH. Osteoporosis in anorexia nervosa. Expert Rev Endocrinol Metabol. 2010;5(5):723-732.

17. Miller KK, Lee EE, Lawson EA, et al. Determinants of skeletal loss and recovery in anorexia nervosa. J Clin Endocrinol Metab. 2006;91(8):2931-2937.

18. Bachrach LK, Guido D, Katzman D, Litt IF, Marcus R. Decreased bone density in adolescent girls with anorexia nervosa. Pediatrics. 1990;86(3):440-447.

19. Misra M, Katzman DK, Cord J, et al. Bone metabolism in adolescent boys with anorexia nervosa. J Clin Endocrinol Metab. 2008;93(8):3029-3036.

20. Winston AP. The clinical biochemistry of anorexia nervosa. Ann Clin Biochem. 2012;49(pt 2):132-143.

21. Golden NH, Katzman DK, Kreipe RE, et al; Society for Adolescent Medicine. Eating disorders in adolescents: position paper of the Society for Adolescent Medicine. J Adolesc Health. 2003;33(6):496-503.

22. Strokosch GR, Friedman AJ, Wu SC, Kamin M. Effects of an oral contraceptive (norgestimate/ethinyl estradiol) on bone mineral density in adolescent females with anorexia nervosa: a double-blind, placebo-controlled study. J Adolesc Health. 2006;39(6):819-827.

23. Golden NH, Lanzkowsky L, Schebendach J, Palestro CJ, Jacobson MS, Shenker IR. The effect of estrogen-progestin treatment on bone mineral density in anorexia nervosa. J Pediatr Adolesc Gynecol. 2002;15(3):135-143.

24. BergstrÓ§m I, Crisby M, EngstrÓ§m AM, et al. Women with anorexia nervosa should not be treated with estrogen or birth control pills in a bone-sparing effect. Acta Obstet Gynecol Scand. 2013;92(8):877-880.

25. Hay PJ, Claudino AM. Clinical psychopharmacology of eating disorders: a research update. Int J Neuropsychopharmacol. 2012;15(2):209-222.

26. Lock J, Le Grange D, Agras WS, Moye A, Bryson SW, Jo B. Randomized clinical trial comparing family-based treatment with adolescent-focused individual therapy for adolescents with anorexia nervosa. Arch Gen Psychiatry. 2010;67(10):1025-1032.

27. le Grange D, Crosby RD, Rathouz PJ, Leventhal BL. A randomized controlled comparison of family-based treatment and supportive psychotherapy for adolescent bulimia nervosa. Arch Gen Psychiatry. 2007;64(9):1049-1056.

28. Katzman DK, Peebles R, Sawyer SM, Lock J, Le Grange D. The role of the pediatrician in family-based treatment for adolescent eating disorders: opportunities and challenges. J Adolesc Health. 2013;53(4):433-440.


Dr Martin is a clinical fellow in the Division of Adolescent Medicine, Department of Pediatrics, Lucile Packard Children's Hospital, Palo Alto, California, and Stanford University School of Medicine, California. Dr Golden is chief, Division of Adolescent Medicine, and Marron and Mary Elizabeth Kendrick Professor of Pediatrics, Stanford University School of Medicine, California. The authors have nothing to disclose in regard to affiliations with or financial interests in any organizations that may have an interest in any part of this article.

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