Eating disorders

Eating disorders are psychological conditions characterized by abnormal eating habits, disturbed body image, and, in most of these disorders, weight loss. Adolescent girls and young women are most commonly affected. Individuals with anorexia nervosa are preoccupied with their weight, body image, and a desire to be thin. Self-imposed restriction of calories, excessive exercising, or purging (e.g., laxative use) result in pronounced and potentially fatal weight loss. Bulimia nervosa is characterized by recurrent binge eating followed by measures to compensate for overeating (e.g., self-induced vomiting) driven by a fixation on body weight and shape. However, the BMI in individuals with bulimia nervosa is typically normal or elevated. Individuals with binge eating disorder have binge eating episodes but do not take measures to control their weight. Unlike in individuals with anorexia nervosa or bulimia nervosa, there is no fixation on body weight and shape, and patients are often overweight. Pica is an eating disorder characterized by the appetite for and ingestion of nonnutritive substances (e.g., hair, clay, mud). First-line treatment for all conditions is cognitive behavioral therapy (CBT). All eating disorders, except for pica, are associated with an increased risk of mood disorders, anxiety disorders, and personality disorders and often have a chronic, relapsing disease course, with various outcomes from complete recovery, symptom fluctuation and relapses to progressive deterioration.

Epidemiology ^[1][2]

• Prevalence
  • Female: 0.3%–1%
  • Men: 0.1%
• Age
  • Peak: 10–25 years of age
  • Bimodal distribution at 13–14 and 17–18 years of age
• Sex: : ♀ > ♂ (10:1)

Etiology

The etiology of anorexia nervosa is multifactorial and not entirely understood. Several factors are thought to contribute to the development of the disease:

• Genetic factors: There is a higher concordance of anorexia nervosa in identical twins than in fraternal twins.
• Neurobiological factors: a disorder of the endogenous reward system
• Psychiatric factors: associated with obsessive-compulsive disorder, anxiety disorders, mood disorders, and personality disorders
• Psychosocial factors
  • Traumatization
  • Poor ability to handle/resolve conflicts
  • Difficulty establishing autonomy and gaining control (e.g., separation from parents)
  • High-pressure careers and sports (e.g., modeling, ballet, gymnastics, wrestling )
  • Unrealistic standards of beauty

Features ^[3]

• Significant deliberate reduction in body mass (as measured by BMI) using strategies that include restrictive eating, purging, and excessive exercise
• Fear of weight gain motivates compensatory behavior that promotes weight loss, even if the patient already has low body weight.
• Body image disturbance
  • Excessive concern about weight and body shape, despite being considerably underweight
  • Lack of awareness of the seriousness of low body weight

Subtypes

• Restricting type
  • No binge eating or purging over a 3-month period
  • Suggests weight loss is achieved by excessive dieting, exercise, or fasting
• Binge-eating/purging type
  • Presence of binge eating or purging over a 3-month period
  • Suggests weight loss is achieved by vomiting, diuretic and laxative abuse, or enemas

Severity based on BMI

• Patients ≤ 20 years of age: BMI below the 10^thpercentile for sex and age is considered the threshold for being underweight. ^[4]
• Patients > 20 years of age
  • Mild: BMI 17–18.4 kg/m²
  • Moderate: BMI 16–16.99 kg/m²
  • Severe: BMI 15–15.99 kg/m²
  • Extreme: BMI < 15 kg/m²

Additional clinical features

• CNS
  • Hypothermia
  • Cortical pseudoatrophy with enlargement of the subarachnoid space → possible organic psychosyndrome → disturbed concentration and memory, changes in personality
  • Seizures
• Endocrine disorders
  • Stress hormones: ↑ cortisol, ↑ adrenaline
  • Thyroid: euthyroid sick syndrome, hypothyroidism
  • Secondary amenorrhea; (severe weight loss suppresses the hypothalamic-pituitary-gonadal axis → hypogonadotropic hypogonadism)
  • Impaired glucose tolerance
• Heart: : hypotension, cardiac arrhythmia (bradycardia), cardiac atrophy, mitral valve prolapse
• Bones: : secondary osteoporosis and stress fractures
• Skin and hair: dry skin, wound healing disorders, hair loss, lanugo body hair, Russell sign
• Salivary glands: : sialadenosis with dystrophy
• Teeth: caries and perimylolysis due to frequent vomiting

Diagnostics ^[4]

• History (see features above)
• Physical exam: : BMI < 18.5 in adults ^[5]
• Laboratory findings
  • Electrolyte imbalances: ↓ potassium , ↓ sodium, ↓ chloride, ↓ phosphate, ↓ magnesium, ↑ bicarbonate (metabolic alkalosis)
  • ↓ Glucose , pathological tolerance of low glucose levels
  • Liver enzymes: ↑ AST/ALT
  • ↑ Serum α-amylase
  • Renal function parameters: ↓ creatinine
  • Lipids: ↑ cholesterol
  • Proteins: hypoproteinemia, hypoalbuminemia
  • CBC: pancytopenia

Laboratory findings normalize following adequate treatment and weight gain.

Treatment ^[6]

• Psychotherapy (first-line)
  • Cognitive behavioral therapy
  • Psychodynamic psychotherapy
• Pharmacotherapy: may be added as adjunctive therapy in severe disease
  • Antidepressants
  • Olanzapine
• Nutritional support
  • Goal: Monitor weight gain, provide nutritional education, and support healthy eating habits.
  • Indications for hospitalization
    • BMI < 15 kg/m2 or < 70% ideal body weight
    • Unstable vital signs
      • Hypothermia (< 35.5°C or 96° F)
      • Bradycardia (< 40 bpm)
      • Hypotension (systolic blood pressure < 80 mm Hg) or symptoms of lightheadedness
    • Acute medical complications (e.g., syncope, seizures, pancreatitis, liver failure)
    • Arrhythmia
    • Hypoglycemia
    • Marked dehydration and electrolyte disturbances
    • Severe refeeding syndrome
  • Contract governing medical treatment: agreement between the patient and caregivers on target weight development and daily number of meals (usually 3–5 meals/day, 500–1000 g weight gain/week)

Refeeding syndrome

• Definition: a condition caused by rapid reinitiation of normal nutrition in a chronically malnourished patient
• Pathophysiology: very rapid increase in daily food intake in severely malnourished patients can cause massive insulin release → increased displacement of magnesium, potassium, and phosphate (shift from extracellular to intracellular) → ↓ phosphate, ↓ potassium, ↓ magnesium (serum levels)
• Clinical features
  • Edema
  • Tachycardia (torsades de pointes)
  • Seizures
  • Ataxia
  • Rhabdomyolysis
• Treatment: electrolyte substitution
• Prophylaxis: : monitor electrolyte levels, limit initial dietary intake to 1000–1500 kcal/day

Prognosis

Anorexia nervosa is a chronic, relapsing disease course with various outcomes (complete recovery, symptom fluctuation and relapses, progressive deterioration).

• Mortality
  • Mortality rate: 5.1 deaths per 1,000 person-years ^[7]
  • Most commonly due to severe cachexia/starvation, cardiac failure, or suicide
• Increased risk of comorbidities ^[8]
  • Mood disorders (e.g., depression, bipolar disorder)
  • Anxiety disorders (e.g., generalized anxiety disorder, social anxiety disorder)
  • Personality disorders
  • Obsessive-compulsive disorder
  • Growth retardation
• Increased risk during pregnancy
  • Miscarriage or premature birth
  • Intrauterine growth retardation
  • Hyperemesis gravidarum
  • Postpartum depression

Individuals with eating disorders may switch from one disorder to another or show merging of symptoms, especially following treatment of one disorder.

Anorexia nervosa is associated with a high mortality rate because of associated medical complications (e.g., arrhythmia, bradycardia) and the high rate of suicide among individuals with the disease.

The antidepressant bupropion lowers the seizure threshold. It is, therefore, contraindicated in individuals with eating disorders who are at an increased risk of developing seizures secondary to dehydration and electrolyte imbalances!

Epidemiology ^[2][9]

• Prevalence
  • Female: 0.3%–1%
  • Men: 0.1%
• Peak age: 20–24 years of age
• Sex: ♀ > ♂ (> 90% of affected individuals are young women)

Etiology

• The etiology of bulimia nervosa is multifactorial and not entirely understood. For factors, see also “Etiology” in anorexia nervosa above.
• Obesity during childhood and early puberty

Features ^[3]

• Recurrent binge eating
• Recurrent compulsive behavior to counteract weight gain
  • Self-induced vomiting after binge eating (most frequent)
  • Laxative abuse
  • Transient starvation periods
  • Other weight-loss measures
• Binge eating and compulsive compensatory behavior both occur at least once a week over a 3-month period.
• Sense of self-worth pathologically influenced by the perception of physical appearance (body weight and shape)
• Binging and purging do not occur exclusively during episodes of anorexia nervosa.

Additional clinical features ^[10]

• Teeth: caries and perimylolysis due to frequent vomiting
• Gastrointestinal tract
  • Esophagitis and/or gastritis
  • Esophageal/gastric lacerations (Mallory-Weiss syndrome)
  • Bilateral parotid gland swelling (sialadenosis)
• Skin
  • Calluses on the knuckles (Russell sign)
  • Dry skin and brittle nails
• Cardiovascular symptoms
  • Cardiac arrhythmias
  • Hypotension
• CNS: seizures

Diagnostics ^[4]

• History (see features above)
• Physical exam: BMI is normal or slightly elevated (≥ 18.5 kg/m² or ≥ 10^thpercentile for pediatric patients)
• Laboratory findings
  • ↓ Potassium, ↓ sodium, ↓ chloride, and ↓ calcium
  • ↑ Blood pH (metabolic alkalosis)
  • Possible ↑ serum α-amylase

Treatment

• Psychotherapy (first-line): : cognitive behavioral therapy
• Nutritional support: Provide nutritional education and support healthy eating habits.
• Pharmacotherapy: Selective serotonin reuptake inhibitors (e.g., fluoxetine) may help decrease binging/purging cycles. ^[11]

Prognosis

The disease course is chronic with relapses.

• Mortality: 2–8 times higher than the general population ^[7]
• Increased risk of psychological comorbidities ^[8]
  • Most common: depression, anxiety, and panic disorders (particularly social phobias)
  • Attention deficit hyperactivity disorder
  • Alcohol and drug addiction or abuse

Bulimia nervosa can transition to anorexia nervosa and vice versa.

Epidemiology ^[2]

• Prevalence: most common eating disorder in adults in the US (∼ 2–5% of general population)
• Peak age: early adulthood to middle age
• Sex: ♀ > ♂

Etiology ^[12]

The etiology of binge eating disorder is multifactorial and not entirely understood. For factors, see also “Etiology” in anorexia nervosa above.

• Genetic factors (family history is common)
• Strict dieting and having access to preferred binge foods
• Psychological issues (e.g., poor body self-image, stress, childhood bullying)

Features ^[3]

• Recurrent binge eating: eating a portion of food disproportionately larger than what an average individual would eat in a similar time span (e.g., two hours) and under similar circumstances
• No purging behavior
• Feeling of lack of control over the amount of food consumed with at least three of the following properties:
  • Eating faster than normal
  • Eating until uncomfortably full
  • Eating large amounts when not hungry
  • Eating alone because of embarrassment regarding eating habits
  • Feeling of disgust and/or guilt after eating
• Binge eating behavior occurs at least once a week over a 3-month period.

Additional clinical features ^[12]

• Pronounced obesity at a young age is common.
• No weight loss measures (no vomiting, no laxative use)
• Often associated with hyperlipidemia, metabolic syndrome, type 2 diabetes, and cardiovascular disease

Treatment

• Psychotherapy (first-line) ^[13]
  • Guided self-help based on cognitive behavioral therapy (CBT)
  • Interpersonal psychotherapy
• Pharmacological therapy: may be added if CBT alone is ineffective
  • SSRIs: help to reduce binge eating impulse
  • Lisdexamfetamine or topiramate; : indicated in patients who do not respond to treatment with SSRIs to reduce weight gain from binge eating and impulsive behavior
  • Methylphenidate: to reduce binge eating episodes ^[14]

Prognosis

• Chronic, relapsing disease course
• Increased risk of psychological comorbidities (e.g., depression)

Individuals with binge eating disorder may be experiencing emotional distress about their binge eating, but not about their weight or appearance.

Epidemiology ^[2]

• Prevalence: highest in children, during pregnancy, and in individuals with certain psychiatric comorbidities (see “Etiology” below)
• Sex: ♀ = ♂

Etiology

The etiology is not entirely understood. Pica is associated with:

• Nutritional deficiencies (iron deficiency, zinc deficiency)
• Pregnancy
• Low socioeconomic status
• Psychosocial trauma (e.g., due to maternal deprivation): pica has been suggested to provide temporary comfort to individuals who have experienced emotional trauma ^[15]
• Intellectual/developmental disability
• Autism spectrum disorder
• Dementia
• Schizophrenia

Features ^[3]

• An eating disorder characterized by the appetite for and ingestion of nonnutritive substances (e.g., hair, clay, soil, ice, paint chips)
• Persistent ingestion of nonnutritive substances for > 1 month that is inappropriate for developmental age and not part of culturally or socially normative practice.

Complications

• Lead poisoning from paint ingestion
• GI complications
  • Bowel obstruction
  • Bowel perforation
  • Bacterial or parasitic infections

Diagnosis

• The diagnosis of pica should only be made if eating behavior is inappropriate for the patient's developmental age and, in the context of personality or neurocognitive disorders, sufficiently severe to qualify as an additional clinical entity.
• The diagnosis is not made if the eating behavior is rooted in accepted cultural or social practices.

Treatment

• Behavioral interventions and nutritional rehabilitation (first-line)
• Pharmacotherapy: SSRIs (second-line) ^[16]