Binge-Eating Disorder

Detailed Diagnostic Criteria

Detailed diagnostic criteria are taken from the Diagnostic Statistical Manual, 4th edn. (DSM-IV).

  1. Recurrent episodes of binge eating. An episode of binge eating is characterized by both (1) Eating, in a discrete period of time, a large amount of food that is larger than most people would eat in a similar period of time and circumstance and (2) A sense of lack of control over eating during the episode
  2. The binge eating episodes are associated with at least three of the following:
    1. Eating much more rapidly than normal
    2. Eating until feeling uncomfortably full
    3. Eating large amounts of food when not feeling physically hungry
    4. Eating alone because of being embarrassed by how much one is eating
    5. Feeling disgusted with oneself, depressed, or feeling very guilty after overeating
  3. Marked distress regarding binge eating.
  4. Binge eating occurs at least 2 days a week for 6 months.
  5. The binge eating is not associated with the regular use of inappropriate compensatory behaviors (eg, purging, fasting, excessive exercise) and does not occur exclusively during the course of anorexia nervosa or bulimia nervosa.

Prevalence of Eating Disorders

 According to Keel (2005) and Wilson, Grilo & Vitousek (2007), the prevalence of eating disorders is as follows:

  • 3 % of adults
  • Higher in obese persons

Typical Course of Eating Disorders

Keel (2005), Steinhausen (2002) and Wilson, Grilo & Vitousek (2007) describe the typical onset and course of eating disorders:

  • Onset: usually either childhood or late adolescence/early adulthood
  • Individuals who seek treatment are typically older than anorexia or bulimia patients
  • Individuals tend to be significantly overweight and obese

Etiology: What Causes Eating Disorders?

There is no single cause of eating disorders but rather they result from multiple influences—social, psychological, developmental, biological, and genetic.

Genetic factors

  • Twin Studies look at Heritability (a percentage representing how much genes contribute to the development of an eating disorder in a particular group of people):
    • Bulimia = 54%. Bullik et al (2001) found evidence of bulimia susceptibility on chromosome 10
    • Anorexia =  52%. Grice et al. (2002) found evidence of anorexia susceptibility on chromosome 1
    • Binge-Eating =  41%.  (Striegel-Moore & Bulik, 2007)
    • Evidence suggests that eating disorders are likely the result of the combined influence of many genes, not just a single gene.
  • Family studies examine the prevalence of eating disorders within groups of genetically related individuals. They have found that:
    • Biological relatives of individuals with Anorexia and Bulimia are 7 to 12 times more likely to have an eating disorder than the general population.
    • Family members of an individual with an eating disorder are 2 to 3.5 times more likely to suffer from bipolar or unipolar depression.
    • Family members of an individual with bulimia have a 3-4 times higher risk for substance abuse.

Psychological, behavioral, physiological and cultural factors

Keel (2005) and Striegel-Moore & Bulik (2007) describe a range of psychological, behavioral, physiological and cultural factors associated with the development of eating disorders:

  • Personality
    • Anorexia: high levels of perfectionism and constraint, higher levels of negative emotion (i.e. depression and anxiety)
    • Bulimia: high levels of impulsiveness and poor emotional regulation, higher levels of negative emotion (i.e. depression and anxiety)
  • Behavior
    • Dieting behavior and initial weight loss is positively reinforced through compliments and attention; increasing value and using foods as rewards can reinforce binges.
    • The experience of eating can become a punishing experience, due to physical discomfort, anxiety, shame over eating, and shame over one’s body/shape.
  • Cognition
    • Those with anorexia or bulimia pay more attention to information about food and body weight/shape than those without an eating disorder.
    • Dichotomous thinking (or black-and-white thinking) – foods get classified as good/bad; losing weight = good, gaining weight = bad.
    • Cognitive rigidity – individuals continue with a specific course of action, without reevaluating it consequences.
    • These cognitions may reflect a consequence of an eating disorders and don’t necessarily predate the onset of an eating disorder.
  • Physiology
    • Low or abnormal Serotonin (5-HT)
    • Serotonin plays a role in eating and weight regulation.
    • Even after recovery some functioning of serotonin is still abnormal, suggesting that a serotonin abnormality may predispose certain individuals to the development of an eating disorder.
  • Culture/Society
    • Western culture’s emphasis on thinness is internalized leading to body dissatisfaction, dieting, and restriction which then leads to over-eating in some individuals.
    • For females: widespread objectification of the female body teaches girls and women that they are valued only for their looks.

Treatment

Many individuals with eating disorders never receive any form of treatment. Why is this?

Treatment is more likely when an individual has more severe symptoms, impaired psychosocial functioning (i.e. problems at school, home, or job) or a personality disorder or mood disorder (Keel, 2005). 

Inpatient Treatment

  • Spend 24 hours per day in treatment
  • Controlled environment, close monitoring, intensive therapy
  • Patients are often either underweight or purging frequently or suicidal, but very often treatment centers encourage patients to begin treatment as inpatients in order to break their cycle.

Outpatient Treatment

  • Day programs, evening programs, or intensive group and individual therapy that occurs weekly, biweekly, or monthly
  • Day programs involve 2 or 3 monitored meals and snacks and group therapy, but there is less medical monitoring and patients spend evenings and nights at home. 

Cognitive-Behavioral Treatment

  • A empirically supported directive therapy that is organized around the theory that disorders are composed of reinforced behaviors to which there are healthier alternatives and irrational beliefs that need to be elicited, challenged, and replaced
  • Shown to be particularly effective with bulimia and binge-eating disorder, but similar results are lacking for anorexia.
    • In 30-50% of Bulimia cases it eliminates binge-eating and purging
    • Over 50% of Binge Eating Disorder individuals recover with this treatment

Medication

  • Antidepressants and mood stabilizers have been used to treat Anorexia, Bulimia, and Binge Eating Disorder, particularly when used to address simultaneous disorders such as depression, bipolar disorder, and anxiety disorders.

More information

Web-Based Resources

References

  • Diagnostic and statistical manual of mental disorders, 4th ed: DSM-IV. Washington, D.C. American Psychiatric Association Press.
  • “American Public Opinion on Eating Disorders: A Poll Conducted on Behalf of the National Eating Disorders Association (NEDA),” GMI Inc., March 2005.
  • Becker, A.E., Grinspoon, S.K., Klibanski, A., & Herzog, D.B. (1999).  Eating disorders. The New England Journal of Medicine, 340(14), 1092-98.
  • Bulik, C.M., Devlin, B., Bacanu, S., Thorton, L., Klump, K.L., Fichter, M.M. & et al. (2001). Significant linkage on chromosome 10p in families with bulimia nervosa. American Journal of Human Genetics, 72, 200-207.
  • Fairburn, C.G. & Harrison, P.J. (2003). Eating disorders. The Lancet, 361, 407-416.
  • Franko, D.L. & Keel, P.K. (2006). Suicidality in eating disorders: Occurrence, correlates, and clinical implications.  Clinical Psychology Review, 26, 769-782.
  • Grice, D.E., Halmi, K.A., Fichter, M.M., Strober, M., Woodside, D.B., Treasure, J.T. & et al. (2002).  Evidence for a susceptibility gene for anorexia nervosa on chromosome 1.  American Journal of Human Genetics, 70, 787-92.
  • James I. Hudson, Eva Hiripi, Jr., Harrison G. Pope, and Ronald C. Kessler (2007) "The Prevalence and Correlates of Eating Disorders in the National Comorbidity Survey Replication," Biological Psychiatry, February, pp. 348-358.
  • Keel, P.K. (2005). Eating Disorders. Upper River Saddle: Pearson Prentice Hall.
  • Mitchell, J.E., Pomeroy, C., Adson, D.E.  (1997).  Managing medical complications.  In Garner, D.M. & Garfinkel, P.E. (Eds.), Handbook of Treatment for Eating Disorders (2nd ed.; pp. 383-393).  New York, NY: Guilford Press.
  • NEDA (2006)  “NEDA college poll finds nearly 20% have struggled with eating disorder,” press release accessed at www.nationaleatingdisordersassociation.org.
  • Steinhausen, H. (2002). The outcome of Anorexia Nervosa in the 20th century. American Journal of Psychiatry, 159(8), 1284-1293.
  • Striegel-Moore, R.H. & Bulik, C.M. (2007).  Risk factors for eating disorders. American Psychologist, 62(3), 181-198.
  • Wilson, G.T., Grilo, C.M., & Vitousek, K.M. (2007).  Psychological treatment of eating disorders.  American Psychologist, 62(3), 199-216.