Eating Disorders: What We Know About Their Epidemiology, Causes, and Complications

AUTHORS:

James J. Burns, MD, MPH, FAAP
University of Florida, College of Medicine

REVIEW ARTICLE | PUBLISHED SUMMER 2025 | Volume 45, Issue 3

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Abstract

Adolescents with eating disorders presenting to primary care pediatric offices can be a challenging clinical problem to address. Clinicians should be able to identify the various types of eating disorders by applying DSM-5-TR criteria for Anorexia Nervosa(AN) (including the restricting and binge-purging subtype), Atypical Anorexia Nervosa (AAN), Bulimia Nervosa (BN), Binge Eating Disorder (BED), Avoidant Restrictive Food Intake Disorder (ARFID), and Other Specified Feeding and Eating Disorders (OSFED). Old theories that eating disorders occur because of faulty parenting have been refuted. Knowing the risk factors and how a combination of genetic, sociocultural, psychological, and biological factors contributes to the development of eating disorders can help the provider convey to the patient and their family an understanding of these at-times puzzling disorders and potentially alleviate guilt that this is their fault. Individual vulnerabilities likely combine with environmental triggers leading to the cognitive and behavioral characteristics found in patients presenting with an eating disorder. Fascinating studies are developing a greater insight into the complexity of eating disorders and hold potential keys to management. The clinician should be aware of the potential complications seen in patients with eating disorders involving many organ systems, including cardiovascular, endocrine, nutritional, gastrointestinal, hepatic, pulmonary, cerebral, hematologic, and renal. Electrolyte abnormalities and specific vitamin and mineral deficiencies can be seen. Bone development can be adversely affected. Higher rates of mortality are seen. Co-morbid psychiatric disorders, including suicidality, depression, and anxiety, occur more frequently with eating disorders. This review provides a comprehensive introduction to the definition, epidemiology, etiology, and complications of eating disorders.

Introduction

Eating disorders are very common, with approximately 5% of females experiencing Anorexia Nervosa (AN), Bulimia Nervosa (BN), or Binge Eating Disorder (BED) by age 20.1. They may present with a broad spectrum of symptoms, making identification a challenging task for the busy clinician at times.

With an annual estimated cost of $64.7 billion in the United States and a mortality rate among mental health problems second only to opiate overdose, the impact of these conditions is immense.2 Clinicians must be aware of eating disorders, diagnose them early, and ensure the provision of appropriate care. Frequently, patients with eating disorders are unnecessarily subjected to extensive diagnostic evaluations to rule out organic etiologies for their symptoms. Several clinical references provide the clinician with guidance on best practices.3-8 There are five main types of eating disorders, including AN, BN, BED, Avoidant Restrictive Food Intake Disorder, and OSFED as defined in the Diagnostic and Statistical Manual, Fifth Edition, Text Revision (DSM-5-TR).9

This paper aims to define the types of eating disorders and describe the epidemiology, pathophysiology, clinical features, and complications. Paul Robinson will discuss how to assess patients in the office, and Jasmine Reese and her team at Johns Hopkins All Children’s will discuss the various options for managing patients. Of note, most patients with eating disorders can be managed as outpatients using Family-Based Therapy.

Definition and Description of Eating Disorders

Anorexia Nervosa (AN)

AN is a condition where the patient restricts calorie intake for at least three months, leading to low body weight. Calorie restriction is typically less than 1,000 calories and can often be as low as 600-700 calories or less per day. Accompanying this is a disturbance in body image that affects their view of self. They usually deny they are underweight but rather feel that they are too heavy and fail to understand how low weight is a serious health risk. Additionally, they have an intense fear of gaining weight even though they are malnourished. There are two subtypes of AN, including restrictive and binge-purging.

Patients with AN frequently weigh themselves, overestimate food calories, and often perform self-checks in the mirror. They wear baggy clothes to hide their thin body. Athletes with AN may over-exercise, even when sick, injured, or in poor weather conditions. These exercises may be done in secret in the middle of the night and are compulsive, with feelings of guilt if they skip a day.7 Anorexic behaviors are ego-syntonic, and patients feel restricting is making them healthier and, in their mind, is a good thing.

Low weight criteria in children and adolescents as defined in the DSM-5-TR, is body mass index (BMI) less than the 5th percentile. Additional guidance is found in the Society for Adolescent Health and Medicine position paper, which characterizes malnutrition based on percent median BMI as mild (80-90%), moderate (70-79%), or severe (<70%).3 Of note, the consensus is that admission to the hospital is generally indicated for a BMI ≤75% of the median BMI (see other criteria below).

In adults, low weight criteria as defined in DSM-5-TR are a BMI <18.5-19 kg/m2 for the diagnosis of AN. Further classification includes mild (BMI 17-19 kg/m2), moderate (BMI 16-16.9 kg/m2), severe (BMI 15-15.9 kg/m2), and extreme (BMI <15 kg/m2).

Atypical AN (AAN), listed in the DSM-5-TR9 in the OSFED category, is a condition where the patient meets the criteria for AN but does not yet meet the requirements for low weight. These patients are at risk for many of the complications, as patients meeting the full criteria for AN, and this category appears to be more common than AN. Weight loss, which is a significant feature, can be categorized as mild (5%), moderate (7.5%), severe (10%), or when the time frame is known as moderate (5% in one month, 7.5% in 3 months, 10% in 6 months or 20% in 1 year), severe (>5% in one month, >7.5 % in 3 months or >10% in 6 months, >20% in one year).3 There are often strong anorexia thinking patterns with AAN, and patients may have delays in diagnosis because of their normal weight, allowing restricting behaviors to become well-established. The new DSM-5-TR9 adds that individuals with atypical AN may experience many of the physiological complications associated with AN.

Amenorrhea has been removed from diagnostic criteria for AN as per DSM-5-TR9, but is frequently present. Also, the return of menses can be a valuable measure of physiologic recovery.

There are two other conditions with potentially overlapping features to anorexia: the relative energy deficiency in sports (RED-S), formerly called the “Female Athletic Triad,” and orthorexia nervosa. RED-S is seen in athletes with osteoporosis, disordered eating, and an imbalance in calories eaten vs. calories burned. In females, there is amenorrhea.10 Orthorexia nervosa, as described in a recent consensus statement11, pertains to an individual who obsesses over food quality, resulting in potential nutritional deficiencies.

Although not included in the DSM-5-TR9, a new category of severe AN, named AN-PLUS, has been recently coined. The “PLUS” mnemonic refers to P-poor quality of life, L-Lack of treatment response, U-unstable medically, and S-severe symptoms. This category describes a treatment-resistant form of AN that presents unique clinical challenges and ethical dilemmas.12

Bulimia Nervosa (BN)

BN is defined by DSM-5-TR9 as recurrent episodes of binge eating, with food intake much higher than usual over a 2-hour time frame, and feeling a lack of control over eating. Additionally, BN involves compensating behaviors after the binge, including self-induced vomiting, misuse of laxatives, diuretics, enemas, fasting, and, as with anorexia, inappropriate exercising. In BN, these behaviors occur at least once a week for the previous three months. Again, as in AN, self-evaluation is influenced by body shape and weight, and patients with BN seek weight loss as a goal. In many cases, weight is in the normal or overweight range.

There are four categories of severity based on the frequency of binging/purging behavior with mild 1-3, moderate 4-7, severe 8-13 episodes, and extreme >14 episodes per week. Examples of unambiguously significant episodes of binge eating might include four bagels with spread, one box of cereal, a whole box of graham crackers, or six bananas.7

Bulimic behavior is ego-dystonic; that is, patients feel shame and self-recrimination. There may be triggers for binge eating, such as depressed feelings, stress, fasting, and boredom.9 The most common compensatory behavior involves self-induced vomiting with instruments such as toothbrushes or fingers. Ipecac, historically used to induce emesis for overdose poisoning, with known cardiotoxic effects, is sometimes used and can be ordered online. As with anorexia, the patient may overexercise. Many of the behaviors of BN are done in secret. Between binge-purge cycles, the patient may fast or attempt to eat healthy, low-calorie foods.

Eighty percent of patients with BN have one or more co-morbid psychiatric conditions, including depression, bipolar disorder, obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), anxiety, substance abuse, and borderline personality disorders (cluster B). As with atypical anorexia, patients who have symptoms of bingeing and purging at a frequency of less than once per week or for less than three months fit into the OSFED category, as do patients with purging without bingeing. Patients with BN are more impulsive and may shoplift, steal, and sexually act out, compared to patients with anorexia nervosa.6

Binge Eating Disorder (BED)

BED is now a formally recognized eating disorder in DSM-5-TR.9 BED is where the patient has binge eating at least once a week for three months without purging or other compensatory behaviors. Bingeing is defined the same as BN, i.e., large amounts of food with a sense of loss of control of overeating. However, there is no compensatory behavior. The degree of severity is the same as with bulimia and is defined by the number of binge-eating episodes per week. As with bulimia, there is marked shame and distress with the behaviors (ego-dystonic), and there are often triggers for the binge. BMI is usually normal or overweight. A person who has binge eating less than once per week for less than three months is placed in the OSFED category.

Avoidant Restrictive Food Intake Disorder (ARFID)

ARFID is a condition in which a patient fails to maintain adequate weight and avoids food due to at least one of the following: 1) Lack of interest in eating, 2) Sensory characteristics of food, such as textures, smells, color, or taste, and 3) Concern about the consequences of eating, such as choking, vomiting, and abdominal pain. About 14% of inpatients with eating disorders have ARFID. Patients may need to rely on enteric tubes or oral supplements. There are no body image issues with ARFID, and there is no desire to lose weight or fear of gaining weight. Many patients state they wish to gain weight. Patients with ARFID have more concomitant autistic disorders, attention deficit and hyperactivity disorder (ADHD), and anxiety.

Patients with ARFID have low body weight that is usually not as low as that of AN patients. Additionally, weight loss in ARFID tends to be more chronic rather than the dramatic, extreme weight loss seen in AN. Families with ARFID patients may try to accommodate their child’s or teen’s food preferences, perpetuating significant restrictions on diet choices.

Two other feeding and eating disorders that will not be a primary focus of this review are pica and rumination. Patients with Pica have recurrent episodes of eating nonfood substances. Pica can be caused by organic causes such as iron deficiency or lead poisoning. Pica may lead to complications such as bezoars. Adolescents with developmental disabilities, autism, or other mental health issues such as OCD or schizophrenia may exhibit pica. Patients with Rumination disorder regurgitate their food. They may then re-chew, swallow, or spit the food out. There is no underlying medical cause for this. Rumination behavior may be a category of self-stimulation seen in autistic or developmentally disabled children.9

Epidemiology of Eating Disorders

The epidemiology of eating disorders varies considerably depending on the population sampled, the year the study was conducted, the research methods employed, and the diagnostic definitions used. There is likely a tendency to underestimate prevalence due to patients with eating disorders not seeking help for their disorder.

Lifetime prevalence, defined as the estimated number of adolescents who have experienced an eating disorder at some point in their lifetime, was found to be 5.7% among females and 1.2% among males in a Dutch cohort study of 1,584 adolescents aged 11-19. Additionally, the lifetime prevalence of DSM-5-TR9-diagnosed eating disorders was as follows: AN: 1.7% in females, 0.1% in males; BN: 0.8% in females, 0.1% in males; BED: 2.3% in females,0.7% in males; and OSFED: 0.6% in females, 0.3% males.13 A systematic review found a 0.3% to 15.5% prevalence in non-clinical adolescent samples for ARFID.14 Most studies generally agree with these statistics.

However, a prospective Finnish population-based twin study that followed 1,347 adolescents from 12 to 22 years of age, found the lifetime prevalence of having any eating disorder was 17.9% in females and 2.4% in males. The lifetime prevalence rates for subcategories of eating disorders were as follows: AN, 6.2% in females and 0.3% in males; BN, 2.4% in females and 0.16% in males; and BED, 0.6% in females and 0.3% in males. These unexpectedly high rates remained high, controlling for potential factors such as the twin population and location. This study is likely a more accurate reflection of the true epidemiology of eating disorders because it was prospective, long-term, and used more precise diagnostic tools.15

As noted above, eating disorders are less common among men, accounting for an estimated 10% of AN, 25% of BN, and 33% of BED cases.6 ARFID rates were similar for men and women. When associated with autism, men had higher rates of ARFID.9 The onset of eating disorders varies by type, with AN onset in late childhood and early adolescence, BN and BED onset in late adolescence and young adulthood, and ARFID onset in childhood.16 All socioeconomic and racial categories are affected by eating disorders, with higher rates seen in LGBTQ adolescents.17 There is some evidence that Hispanic youth with eating disorders are underrecognized.17,18 Data indicate that rates of referrals and hospitalizations have been increasing both before and since the COVID-19 pandemic.19-21

Additionally, perinatal risk factors have been found to be related to eating disorders, including prematurity, increasing parental ages, multiple births, C-sections, and congenital malformations of the mouth.22,23 AN and BN may be seen more commonly in certain sports such as gymnastics, running, wrestling, dance, and modeling.24

Etiology of Eating Disorders

Multiple factors contribute to eating disorders, including genetic, environmental, psychological, sociocultural, and biological factors. Much has yet to be clarified, and in many circumstances, it is challenging to determine which findings are a primary factor in the etiology or the consequences of the disordered eating behaviors.

Genetic: In a study of 1,831 relatives of 504 probands with eating disorders, there was an 11.3-fold relative risk of AN for female relatives of a proband with AN and a 12-fold relative risk of AN when the proband had BN. Also, there was a 4.2 relative risk of BN for female relatives of a proband with AN and a 4.4 relative risk of BN if the proband had BN.

Twin studies indicate that the proportion of AN attributable to genetic factors ranges from 16% to 74% for AN, 28% to 83% for BN, and 39% to 45% for BED.25,26 A sizable Swedish twin study showed a genetic correlation with AN of 57% for strictly defined AN, 62% for BN, and 60% of the genetic effects of AN and BN may be shared.27

Genome-wide association studies have also added substantial knowledge. Eight significant loci were identified in AN through a genome-wide association study involving 16,992 individuals with a history of AN and 55,525 controls. Also, genetic correlations were seen with OCD, depression, anxiety, schizophrenia, physical activity, and educational attainment.28 Another genome-wide association study found common genetic variants in 20%. There was one significant locus on chromosome 12. This is a region that is also associated with type 1 diabetes and autoimmune disorders. There were no genome-wide associations between eating disorders and obesity, as well as insulin or glucose levels.29 Genome-wide association studies are ongoing for other eating disorders.25

Sociocultural Environment: Eating disorders may be influenced by environments where physical appearance is overvalued, such as at school and by family.30 Teasing from peers may set in motion body dissatisfaction and dieting behaviors. It is estimated that 60-70% of high school girls are dieting. Earlier studies indicating that dysfunctional families led to anorexia have not been borne out. They are more likely related to the stress that having a teen with an eating disorder places on a family. However, child abuse has been found to correlate with increased rates of eating disorders.31,32

Media exposure is associated with body image dissatisfaction. Girls who want to look like characters on TV shows were twice as likely to be constant dieters or to have purging behaviors.33 Reading girls’ magazines doubles the risk of eating disorders.34. Social comparison is associated with higher body dissatisfaction. A study by Becker in Fiji found higher ‘EAT’ scores and an increase in purging after the introduction of Western television.35 Studies have shown a correlation between social media usage and disordered eating cognitions and behaviors.36 Fifty studies in seventeen countries indicate that social media usage may lead to eating disorders by inducing social comparison, thin/fit ideal internalization, and self-objectification.37

Psychological: Temperament characteristics of patients with AN include perfectionism, obsessionality, reward dependence, negative affectivity, and neuroticism.23,26,30,38

Cognitive problems associated with AN include set-shifting difficulties (defined as a component of executive function that involves flexible thinking and the ability to multitask), rigid thinking, difficulties adapting to change, and problems with poor central coherence (a bias toward processing details at the expense of the broader context).39 Conditioned learning may be a factor similar to what is seen in the cerebral mechanisms of addiction. Exposure to low-calorie foods, activities, and thin body images is perceived as abnormally rewarding.40 Dieting may also be a significant trigger for the onset of AN.23,30,41

In the Minnesota starvation experiment conducted in 1945 by Ancel Keys, research was conducted on normal conscientious objectors to determine the physical and mental effects of starvation and how to manage these effects. This was done to address the anticipated large number of starving people from WWII. The researchers found many behaviors/characteristics of starvation were similar to those seen in eating disorder patients, including an obsession with food, anxiety, irritability, eating rituals, cutting food into small pieces, holding food in their mouths, and taking a long time to eat. With refeeding, many of the mental issues improved. This implies that behaviors seen in AN may result from the physiological effects of malnutrition.42

Biological: Fascinating research is being conducted to elucidate the neurobiology of eating disorders. Many neuropeptides are being discovered that regulate food intake. The list is ever-growing and includes appetite stimulants such as neuropeptide Y, agouti protein, melanin-concentrating hormone, ghrelin, phosphine, and adiponectin, as well as appetite suppressants including leptin, spexin, kisspeptin, oxytocin, nesfatin-1, GLP-1, amylin, and peptide YY. Some are made in the hypothalamus, some in adipose tissue, some in the pancreas, and some in the stomach and intestine.

Additionally, functional magnetic resonance imaging in patients with AN appears to reveal dysregulation of neural activation throughout the entire brain. It is theorized that multiple parts of the brain may be involved in behavioral features of AN. Studies have found that altered activation of the front-striatal and limbic circuits are involved with reduced activity in lower brain regions. Limbic circuits were found to be inhibited by inputs from the cognitive areas such as the dorsolateral prefrontal cortex and parietal cortex, suggesting dysregulation that could explain restricted eating.43 Studies have investigated the reward circuits, which may be altered in AN, BN, and BED. Serotonergic and dopaminergic pathways are also believed to be involved.44,45

Gastrointestinal hormones, including ghrelin, an appetite stimulant secreted by the stomach, were elevated in AN. It appears that a central nervous system resistance to ghrelin develops in AN, which is felt to be due to an alteration in the reward circuitry. Peptide YY is an appetite suppressant released by the distal intestine in response to caloric intake. Levels of peptide YY are elevated in patients with AN, which may contribute to reduced intake. Agouti-related peptide, another mediator that increases appetite and decreases metabolism, is found in higher amounts in AN. Restricted eating may be due to inaccurate hunger signals (anterior insula) or decreased neural sensitivity to the reward value of food taste during hunger (dorsal striatum, frontostriatal circuits). Another area of study is the role of the gut microbiome, which may be a factor in eating disorders.45 Clearly, further study is needed.

Complications of Eating Disorders

Virtually every organ system is affected by eating disorders. Lower BMI correlates with medical complications.23 Several references provide a comprehensive discussion of these complications.5-7,23,46,47

Mortality rates for AN are estimated to be 5.6% per decade.48 Suicide may account for as much as 20% or more of deaths in AN.49,50 Mortality in anorexia may be due to fatal dysrhythmias from low phosphorus, low potassium, hypoglycemia, and cardiac etiologies. Standard mortality ratios compared to normal populations were 4.7-5.9 for AN and 1.9-2.3 for BN.49,51 Suicide risk is 18 times greater in AN than in controls. In both AN and BN, 25%-33% have suicidal ideation, and similar rates have attempted suicide. Suicide ideation in BED was found in 25%.9

The heart is affected by having an eating disorder, with bradycardia being found in nearly all AN patients. This may degenerate into sinus pauses, junctional rhythm, premature ventricular contractions, and then more malignant life-threatening arrhythmias. This is alleviated with nutritional recovery. A reduced ventricular ejection fraction is observed in 15%. With AN, left ventricular mass and cardiac output are reduced. Heart failure may be seen as a consequence of refeeding, dehydration, anemia, and pericardial effusion.52 Mitral valve prolapse and pericardial effusion can also be seen. Myocardial fibrosis, which has been associated with sudden death, was seen in 23% of 40 patients with AN and 0% in controls.53 Some references cite QTc prolongation as a feature of AN and a mechanism of malignant arrhythmias and, potentially, sudden cardiac death. However, more recent large meta-analyses and cohort studies have not found any prolongation of the QTc interval.54,55 Additionally, prolonged QTc in AN patients is not associated with arrhythmias or mortality. If QTc is prolonged, it should be evaluated for potential secondary causes rather than assuming AN is the cause. The sinus pauses and bradyarrhythmia may be more related to sudden death than prolonged QTc.23 Patients with eating disorders have hypotension, especially seen with upright posture. As noted above, low potassium or phosphorus can lead to sudden cardiac death, as can refeeding syndrome. Finally, patients may attempt to cause vomiting by ingesting ipecac, which can lead to emetine cardiotoxicity.

Eating disorders can affect the endocrine system, leading to decreased IGF-1 and increased GH levels due to GH receptor resistance. The GnRH pulse generator is not functioning normally in AN, leading to pre-pubertal levels of FSH and LH, which can lead to pubertal delay, amenorrhea, short stature, and decreased bone calcium during a critical time in adolescence. Although reduced T3 and T4 levels can be seen in AN, they do not indicate thyroid hormone deficiency. Instead, they represent the “euthyroid sick syndrome” from the effects of malnutrition. Elevated glucocorticoid levels are seen in response to starvation, which stimulates gluconeogenesis and can decrease bone calcium. Glucose levels are low in AN and may be associated with sudden death. This may be due to liver injury or glycogen depletion. Increased cortisol and GH increase glucose in starvation, providing some adaptation.

Hyponatremia, a common finding, may be due to purging or syndrome of inappropriate antidiuretic hormone (SIADH). It can also be seen in patients who water load to increase weight before weigh-ins. Additionally, central diabetes insipidus can occur, leading to hypernatremia due to defects in the release of vasopressin. This may become clinically relevant with fluid restrictions.

Bone mineralization is lower in AN.23 This is felt to be due to several hormonal and nutritional factors. This may not be completely reversible. Males and females with AN are at risk for low bone mineral density. This is seen mainly in restricting eating disorders. Adolescence is a critical period for bone density development, with approximately 95% of calcium being deposited in bone by age 19. In females, decreased estrogen levels lead to increased bone reabsorption. In males, low testosterone levels are associated with reduced bone mineral density (BMD). Other factors include GH resistance and elevated cortisol levels. Low calcium and vitamin D intake also contribute to low bone density. Low BMD is associated with spondylolysis in gymnasts and dancers, as well as tibial stress fractures in runners. This risk persists for decades.

Also, with weight loss in AN, hypothermia is often seen. This may be due to a reduced basal metabolic rate, inadequate body insulation, and hypoglycemia. Attempts to counteract this include stimulating non-shivering thermogenesis, which manifests as hyperactive behaviors.56

Due to poor intake, iron deficiency, hypophosphatemia, hypomagnesemia, hypokalemia, low zinc, and various vitamin deficiencies, including Vitamin C, can be present. Especially concerning may be thiamine deficiency, which can cause Wernicke’s encephalopathy or Korsakoff psychosis. Copper, selenium, vitamin B12 (cobalamin), and vitamin B9 (folate) levels may be too low. Zinc deficiency can present with abdominal pain, alopecia, anorexia, blepharitis, corneal opacities, delayed wound healing, depression, dermatitis, diarrhea, dysarthria, impaired taste, fever, glossitis, growth retardation, hypogonadism, immune dysfunction, impaired concentration, intention tremor, nervousness, night blindness, nystagmus, paronychia, pica, and stomatitis. Protein levels are often preserved in AN due to a minimally adequate intake of lean meat.

Hypophosphatemia may occur during binge eating episodes or in refeeding syndrome in malnourished patients during the process of increasing caloric intake, where phosphorus is shifted from the blood into cells. In a study of 374 severely malnourished patients with AN, 64.3% were zinc deficient, 54.2% were vitamin D deficient, 37.1% were copper deficient, 20.5% were selenium deficient, 15% were vitamin B1 (thiamine) deficient, 4.7% were vitamin B12 deficient, and 8.9% were folate deficient.57

Most patients with AN have gastrointestinal (GI) complaints. There can be problems with severe constipation, nausea, abdominal pain, vomiting, heartburn, dysphagia, reflux, and bloating. Gastroparesis leads to early satiety, reflux, and decreased eating. These many symptoms were found to be more related to somatization than eating disorder severity. If the patient is severely malnourished with significant abdominal discomfort, it is worth evaluating them for superior mesenteric artery syndrome or median arcuate ligament syndrome.

AN can affect the liver, leading to hypoglycemia. Elevated liver enzymes can result from fatty liver during refeeding. Additionally, liver ischemia, autophagy, and apoptosis of hepatic cells may occur. Furthermore, there are higher rates of pancreatitis associated with AN.

Complications of purging, as seen with AN or the binge-purging subtype of AN, include complaints of dizziness, heartburn from gastroesophageal reflux, dysphagia, bloating, and abdominal pain. Physical findings may include orthostatic hypotension, palatal scratches, a loss of the gag reflex, esophageal dysmotility, salivary gland enlargement, subconjunctival hemorrhage, dental enamel erosion, abrasions on the dorsum of the hand (Russel sign), rupture of the esophagus (Boerhaave’s syndrome), upper GI bleeding from Mallory-Weiss tears of esophagus, and pancreatitis. Abuse of laxatives might lead to damage to the colon and rectal prolapse.

Edema can occur, especially when purging is discontinued. Purging can lead to dehydration, hypokalemic alkalosis from vomiting, hypomagnesemia and hypophosphatemia, and hypochloremia. Laxatives may cause hyperchloremic acidosis because the bicarbonate secreted by the pancreas is trapped by magnesium and sulfates and excreted into the stool.

AN often affects the pulmonary system, including weak respiratory muscles, dyspnea, reduced pulmonary capacity, and emphysematous changes. The patient may experience aspiration pneumonia due to vomiting when purging behaviors occur. Pneumothorax or pneumomediastinum can occur from purging (Boerhaave syndrome) or with severe malnutrition (the Macklin effect, which involves alveolar rupture due to increased interalveolar pressure and low vascular pressure).

There are effects of anorexia on the brain, including impairment in thinking/learning, problems with attention, concentration, problem-solving, psychomotor slowing, and lack of insight. Thus, it is imperative that nutritional recovery is begun before attempts at meaningful psychotherapy, which may not be effective in starvation.

The bone marrow is replaced with a thick mucopolysaccharide substance, resulting in low WBC, anemia, and thrombocytopenia. Iron, B12, and folate deficiency may also potentially cause anemia. The sedimentation rate should be low; if it is high, it should raise suspicion of an undiagnosed inflammatory disorder.

Reproductively, amenorrhea occurs in 84% of females with AN. There is also an increased likelihood of miscarriage, preterm birth, neonatal microcephaly, small for gestational age, and perinatal mortality. Interestingly, teens with eating disorders have higher rates of pregnancy than their same-aged peers23.

Skin findings in eating disorders include lanugo, dry skin, brittle nails, acrocyanosis, carotenemia, and edema. In addition, there are deficits in wound healing.

Renal findings may include kidney stones from vitamin D excess, sterile pyuria, poor concentration, edema, decreased GFR, elevated BUN, and alkaline urine. Prerenal and renal failure may also be seen.

Comorbid psychiatric disorders can occur in patients with eating disorders. With ARFID, there are increased rates of anxiety disorder, OCD, autism, ADHD, and intellectual disability. With AN, there may be bipolar, depressive, and anxiety disorders, and alcohol use disorders, especially if there is purging. In BN, there are frequent comorbid mental health disorders, including depression, bipolar disorder, anxiety, borderline personality disorders, and substance use disorders (especially alcohol or stimulant use disorders being found in 30% of BN patients). In BED, there are similar rates of comorbid mental health problems as is seen in AN or BN. The most common being major depressive disorder and alcohol use disorder.9

Conclusion

Eating disorders are being seen with increasing frequency in pediatric practices. Clinicians must recognize the five unique presentations, including anorexia nervosa, bulimia nervosa, binge eating disorder, avoidant restrictive food intake disorder, other specified feeding and eating disorders, and their variants, such as atypical anorexia nervosa. They are due to genetic, sociocultural, psychological, and biological factors. The clinician should be aware of the significant complications seen in patients with eating disorders involving most organ systems. Electrolyte abnormalities, bone development deficiency, and increased rates of mortality are commonly seen. Comorbid psychiatric disorders, including suicidality, depression, and anxiety, occur more frequently with eating disorders.

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Disclosure: Author reports no conflict of interest.