Bulimia Nervosa

Bulimia Nervosa is an eating disorder characterized by recurrent episodes of binge eating, compensatory behaviors to prevent weight gain, and self-evaluation that is significantly influenced by body shape and weight.

Epidemiology
  • The 12-month prevalence in young females is 1 to 1.5%, with a peak in older adolescence and young adulthood.[1]
  • Bulimia affects females significantly more than males (10:1).[2]
Prognosis
  • Bulimia nervosa commonly begins in adolescence or young adulthood and onset before puberty or after age 40 is uncommon.
  • Binge eating most common starts during or after an episode of dieting to lose weight.
  • For many individuals, symptoms remit with or without treatment, but treatment improves outcomes.
    • Periods of remission lasting longer than 1 year are associated with better long-term outcome.[3]
  • There is an elevated risk for mortality, and the CMR (crude mortality rate) for bulimia nervosa is nearly 2% per decade (vs. 5% for anorexia nervosa).
    • Individuals are also at increased risk for suicide.
Psychiatric Comorbidity
  • The conversion from initial bulimia nervosa to anorexia nervosa happens in a minority of cases (between 10 to 15%). Individuals who do cross-over to anorexia nervosa typically revert back to bulimia nervosa or have multiple occurrences of switching back and forth between these disorders.
    • A proportion of individuals with bulimia nervosa will continue to binge eat but no longer engage in inappropriate compensatory behaviours, and thus their symptoms will only meet criteria for binge-eating disorder or other specified eating disorder. Diagnosis should be based on the current (i.e. - past 3 months) clinical presentation.
  • There is an increased frequency of depressive symptoms (e.g. - low self-esteem) and depressive disorders in individuals with bulimia nervosa.
  • The lifetime prevalence of substance use, particularly alcohol or stimulant (in an attempt to control appetite and weight) use, is at least 30%.[4]
  • A substantial percentage of individuals with bulimia nervosa also have borderline personality disorder.[5]
Medical Comorbidity
  • Menstrual irregularity and/or amenorrhea can occur in females.
  • Fluid and electrolyte disturbances (e.g. - hyponatremia) from purging behaviours can sometimes cause serious medical complications.
  • Rare but potentially fatal complication include gastroesophageal rupture, and cardiac arrhythmias.
  • Individuals who chronically use laxatives to purge may become dependent and have constipation.[6]
Risk Factors
  • Stressful life events, childhood obesity, early pubertal maturation, childhood sexual or physical abuse, social anxiety disorder, weight concerns, low self-esteem, depressive symptoms, and anxiety in childhood can increase the risk for bulimia nervosa.[7]
  • Internalization of a thin body ideal has been found to increase risk for developing weight concerns, which increases the risk for bulimia nervosa.
  • There may be genetic vulnerabilities for bulimia as well.
Cultural
Criterion A

Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:

  1. Eating, in a discrete period of time (e.g. - within any 2-hour period), an amount of food that is definitely larger than what most individuals would eat in a similar period of time under similar circumstances.
  2. A sense of lack of control over eating during the episode (e.g. - a feeling that one cannot stop eating or control what or how much one is eating).
Criterion B

Recurrent inappropriate compensatory behaviours in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise.

Criterion C

The binge eating and inappropriate compensatory behaviours both occur, on average, at least once a week for 3 months.

Criterion D

Self-evaluation is unduly influenced by body shape and weight.

Criterion E

The disturbance does not occur exclusively during episodes of anorexia nervosa.

Specifiers

Specify if:

  • In partial remission: After full criteria for bulimia nervosa were previously met, some, but not all, of the criteria have been met for a sustained period of time.
  • In full remission: After full criteria for bulimia nervosa were previously met, none of the criteria have been met for a sustained period of time.

Severity Specifier

Specify if: The minimum level of severity is based on the frequency of inappropriate compensatory behaviours (see below). The level of severity may be increased to reflect other symptoms and the degree of functional disability.

  • Mild: An average of 1 to 3 episodes of inappropriate compensatory behaviours per week.
  • Moderate: An average of 4 to 7 episodes of inappropriate compensatory behaviours per week.
  • Severe: An average of 8 to 13 episodes of inappropriate compensatory behaviours per week.
  • Extreme: An average of 14 or more episodes of inappropriate compensatory behaviours per week.
  • An “episode of binge eating” is defined by the DSM-5 as eating, in a discrete period of time, an amount of food that is definitely larger than what most individuals would eat in a similar period of time under similar circumstances. This is a determination that is contextual and requires subjectivity of clinician judgment.[8]
  • Some individuals do not report a feeling of loss of control but instead say they have abandoned any efforts to control their eating. This can be considered as “loss of control” under the DSM-5 criteria.[9]
  • The most common triggers for binge eating episodes include negative affect (emotions), interpersonal stressors; dietary restraint; negative feelings related to body weight, body shape, and food; and boredom
  • Binge eating usually occurs in secrecy or individuals will try to make it inconspicuous.
    • During binges, individuals tend to eat foods they would otherwise avoid, will eat until they are painfully or uncomfortably full.[10]
  • The most common inappropriate compensatory behaviour is vomiting.[11]
    • Individuals may use fingers or instruments to stimulate the gag reflex. Overtime, individuals may be able to vomit at will. Other purging behaviors include the misuse of laxatives and diuretics.[12]
  • Outside of the episodes of bingeing, individuals will restrict their total caloric consumption and preferentially select low-calorie foods while avoiding foods that they perceive to be fattening or likely to trigger a binge.[13]

Eating Disorder Scales

Name Rater Description Download
Eating Disorder Diagnostic Scale (EDDS) Patient A 22-item self-report scale for individuals between 13 to 65 years old that screens for anorexia nervosa, bulimia nervosa, and binge-eating disorder. Link
    • Individuals whose binge-eating behaviour occurs only during episodes of anorexia nervosa are given the diagnosis anorexia nervosa, binge-eating/purging type. These individuals should not be given the additional diagnosis of bulimia nervosa.
    • Individuals with an initial diagnosis of anorexia nervosa who then binge and purge but whose presentation no longer meets the full criteria for anorexia nervosa, binge-eating/purging type (e.g. - when weight is normal according to BMI), a diagnosis of bulimia nervosa should be given only when all criteria for bulimia nervosa have been met for at least 3 months.[14]
    • The other key differences between bulimia nervosa and anorexia nervosa is that:
      • A diagnosis of bulimia nervosa should not be given when the disturbance occurs only during episodes of anorexia nervosa.
      • Individuals with bulimia are typically within the normal weight or overweight range (BMI >18.5 and <30 in adults).[15]
    • Individuals who binge eat but do not engage in repeated, inappropriate compensatory behaviors should have a diagnosis of binge-eating disorder considered instead.[16]
    • In neuropsychiatric disorders such as Kleine-Levin syndrome, there is also disturbed eating behaviour. However, the characteristic feature of bulimia nervosa, concern and self-evaluation with body shape and weight, are not present.
    • Overeating is common in major depressive disorder, with atypical features (atypical depression). However, there is no inappropriate compensatory behaviors and they do not exhibit the excessive concern with body shape and weight characteristic of bulimia nervosa. If criteria for both disorders are met, both diagnoses should be given.
    • Binge-eating behaviour makes up part of the impulsive behaviours seen in borderline personality disorder. If the criteria for both borderline personality disorder and bulimia nervosa are met, both diagnoses should be given.[17]

Various laboratory abnormalities can be present:[18]

  • Fluid and electrolyte abnormalities (hypokalemia, hypochloremia, and hyponatremia)
  • Loss of gastric acid through vomiting may produce a metabolic alkalosis (elevated serum bicarbonate)
  • Frequent purging through laxative and diuretic abuse can cause metabolic acidosis.
  • Mildly elevated levels of serum amylase (from increase in the salivary isoenzyme)
  • ECG may show cardiac arrhythmias (due to hypokalemia)

Thus, standard investigations include:

  • CBC, electrolytes, extended electrolytes, renal function (Cr, eGFR, BUN), albumin level, serum amylase, liver function (AST, ALT, GGT), cholesterol, and an electrocardiogram.
  • Oral examination may reveal permanent loss of enamel (in particular lingual surfaces of the front teeth) from recurrent vomiting, dental carries, and salivary gland and parotid gland hypertrophy
    • Perioral irritation, and oral ulcers may also be noticeable
  • Hand examination may reveal calluses on the back of hand (from repeated contact with teeth)
  • Dermatological exam may reveal petichiae
  • A cardiac exam may be warranted to assess for arrhythmias, edema, and decreased volume status.
  • Gastrointestinal exam may reveal non-focal abdominal pain, abdominal bloating, signs of constipation. Rarely some individuals may have signs or symptoms of esophageal tears, or gastric rupture. Chronic use of laxatives may also result in constipation and/or rectal prolapse.[19]

Various forms of psychotherapy have been found to be effective for treatment of bulimia, including:[20][21]

  • Individual therapy (CBT, IPT, behavioural, and psychodynamic approaches)
  • Group therapy (CBT, IPT, supportive, and psychodynamic approaches)
  • Family and couples self-help, online resources, 12 step programs
Recommended Reading

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  • Antidepressant medications have been shown to be helpful (can reduce binge eating and purging) in treating bulimia, including selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine.
    • This may be based on elevating central 5-hydroxytryptamine levels.
    • Thus, SSRIs can be used for particularly difficult binge-purge cycles that do not respond to psychotherapy alone.
  • Combination of CBT and fluoxetine has highest remission rates compared to either treatment alone.
  • Imipramine, desipramine, trazodone, and monoamine oxidase inhibitors (MAOIs) have also been investigated but are less frequently used.
  • Medication is helpful in patients with comorbid depressive disorders and bulimia nervosa.
  • Bupropion is contraindicated due to increased seizure risk in individuals in eating disorders.[22]

Eating Disorder Guidelines

Guideline Location Year PDF Website
International Comparison (Curr Opin Psychiatry) International 2017 - Link
Canadian Clinical Practice Guidelines (Children and Adolescents) Canada 2020 - Link
National Institute for Health and Care Excellence (NICE) UK 2017 - Link
American Psychiatric Association (APA) USA 2006, 2012 - Guideline (2006)
Guideline Watch (2012)
Quick Reference
For Providers
Articles
Research
1) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
2) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
3) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
4) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
5) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
6) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
7) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
8) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
9) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
10) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
11) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
12) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
13) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
14) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
15) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
16) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
17) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
18) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
19) American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA.
20) Yager, Joel, et al. Practice guideline for the treatment of patients with eating disorders. American Psychiatric Association, 2006. Third Edition