Bulimia Nervosa

Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Bulimia nervosa is an eating disorder characterised by repeated episodes of uncontrolled overeating (binges) followed by compensatory weight loss behaviours.

Features include:

  • Excessive preoccupation with body weight and shape.
  • Undue emphasis on weight in self-evaluation.
  • Feeling of lack of control over eating.
  • Compensatory weight control mechanisms which can be:
    • Self-induced vomiting.
    • Fasting.
    • Intensive exercise.
    • Abuse of medication such as laxatives, diuretics, thyroxine or amfetamines.
  • The incidence of bulimia nervosa is estimated to be 10-15 per 1,000 females per year.
  • Lifetime prevalence in women is thought to be about 2%[3].
  • It occurs across all socio-economic groups. It is more common in western societies.
  • It occurs in ten times as many females as males, although incidence in men is believed to be increasing.
  • It is more common in adolescence and young adulthood.
  • Many with bulimia do not seek treatment[4].
  • Exact prevalence figures are difficult to ascertain, owing to the numbers who do not seek medical help, the lack of country-specific data, and the crossover with binge eating disorder (BED)[5]. In this separate condition there is bingeing behaviour but without the compensatory purging. Possibly because of the difference in clinical and lay understanding about the meanings of the terms, results based on questionnaire surveys have been variable.

Risk factors[1]

Development of bulimia nervosa appears to be multifactorial and difficult to ascertain. Apart from female gender, potential risk factors include:

  • Parental and childhood obesity.
  • Family dieting.
  • Family history of eating disorders (high heritability shown).
  • A history of severe life stresses and possibly sexual or physical abuse.
  • Parental and premorbid psychiatric disorder or substance misuse.
  • Parental problems, such as high expectations, low care and overprotection, and disruptive events in childhood such as parental death and alcohol dependency.
  • Early experiences of criticism regarding eating habits or body weight.
  • Perceived pressure to be thin (from cultural or family sources).
  • Recreational pressure (models, jockeys, ballet dancers, athletes).
  • Early menarche.
  • Premorbid characteristics such as perfectionism, anxiety, obsessional traits, low self-esteem, emotionally unstable personality disorder (formerly borderline personality disorder), difficulty in resolving conflict. 

History

The history often dates back to adolescence. The core features include:

  • Regular binge eating. Loss of control of eating during binges. (In order to fulfil diagnostic criteria for the Diagnostic and Statistical Manual of Mental Disorders fifth edition (DSM-5), binge eating should occur, on average, at least once a week for three months.)
  • Attempts to counteract the binges - eg, vomiting, using laxatives, diuretics, dietary restriction and excessive exercise.
  • Body mass index (BMI) is maintained above 17.5 kg/m2.
  • Preoccupation with weight, body shape and body image. Self-evaluation is unduly based on body weight and shape.
  • Preoccupation with food and diet. This is often rigid or ritualistic and deviations from a planned eating programme cause distress. The affected person therefore starts to avoid eating with others and becomes isolated.

Physical symptoms may occur including:

  • Bloating and fullness.
  • Lethargy.
  • Heartburn and reflux.
  • Abdominal pain.
  • Sore throat and dental problems due to vomiting.

Mood disturbance and anxiety are common, as are low self-esteem, and self-harm. Severe comorbid conditions may be present - eg, depression and substance abuse.

Examination

Physical examination is usually normal and is mainly aimed at excluding medical complications such as dehydration or dysrhythmias (induced by hypokalaemia).

Examination must include height and weight (and calculation of the BMI) and blood pressure. In severe cases signs may be present:

  • Salivary glands (especially the parotid) may be swollen.
  • There may be oedema if there has been laxative or diuretic abuse.
  • Russell's sign may be present (calluses form on the back of the hand, caused by repeated abrasion against teeth during inducement of vomiting).
  • There may be erosion of dental enamel due to repeated vomiting.
  • Binge eating disorder: more common than bulimia in men (although still less common than in women) and affects a wider age range.
  • Sporadic bingeing in other psychiatric disorders - eg, depression.
  • Anorexia nervosa with bulimic features.
  • Other forms of eating disorder which can be difficult to classify - known as unspecified feeding or eating disorder (UFED) or eating disorder not otherwise specified (EDNOS)[6].
  • Medical causes of bingeing or vomiting.
  • These are usually normal apart from serum potassium, which is often low.
  • Renal function and electrolytes should be checked in view of frequent self-induced vomiting.

People with suspected bulimia nervosa should be referred immediately to a community-based, age-appropriate specialist eating disorder service for assessment and management. However, primary care has a significant role to play in patient management and support. The great majority of patients with bulimia nervosa can be treated as outpatients. There is a very limited role for the inpatient treatment of bulimia nervosa. This is primarily concerned with the management of suicide risk or severe self-harm, or for low serum potassium.

Management in adults

Guidelines from the National Institute for Health and Care Excellence (NICE) recommend that as a first step, patients should be encouraged to follow an evidence-based bulimia-focused guided self-help programme, with direct encouragement and support from healthcare professionals. Individual eating-disorder-focused cognitive behavioural therapy (CBT-ED), a specifically adapted form of CBT, should be offered to adults with bulimia nervosa if self-help is ineffective or not an option. The course of treatment is usually 20 sessions over 20 weeks, often with twice-weekly sessions initially.

Management in young people under the age of 18 years

NICE guidelines recommend bulimia-nervosa-focused family therapy as first-line management. This involves 18-20 sessions over six months with a therapist and involves the family in supporting and monitoring, and encouraging regular eating and reducing compensatory behaviours. If this is ineffective or not an option then the alternative is individual CBT-ED. This typically involves 18 sessions over six weeks, initially with more frequent sessions. Some sessions would involve the person's parent(s) or carer(s).

Pharmacological

NICE guidelines currently recommend that medication should not be offered as a sole treatment for bulimia. The evidence review found no evidence that pharmacological therapy is effective. Comorbid mental health problems may require pharmacological treatment.

Evidence

The evidence base for optimal treatment of bulimia nervosa remains weak[8]. Cochrane reviews seem to demonstrate efficacy of CBT, although quality of evidence is noted to be variable[9].

General medical aspects

There may be a need for management of physical aspects:

  • Patients with bulimia nervosa who are vomiting frequently or taking large quantities of laxatives (especially if they are also underweight) should have their fluid and electrolyte balance assessed frequently. If electrolyte disturbance is detected, it is usually sufficient to focus on eliminating the behaviour responsible.
  • Recommend regular dental reviews and dental hygiene (eg, rinse the mouth after vomiting).
  • Reduce laxatives slowly.
  • Screen for osteoporosis.

For those with bulimia and diabetes, collaboration is required with the person, the diabetes team and the family. Sugars and ketones may need close monitoring, and be aware of the possibility of insulin misuse. Monitor potassium carefully.

  • Haematemesis, and metabolic complications (eg, hypokalaemia), following excessive self-induced vomiting.
  • Dental erosions.
  • There may be painless enlargement of the salivary glands, tetany and seizures.
  • Around 10-15% go on to develop anorexia[1].

Up to 80% of people with bulimia make a complete recovery with treatment, although figures vary widely. If recovery has not occurred within five years, they are more likely to progress to a chronic course.

The risk of death is significantly lower than that with anorexia nervosa and is estimated at about 0.4%, which is due to the slight increase in suicide.

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  1. Eating disorders; NICE CKS, October 2014 (UK access only)
  2. Harrington BC, Jimerson M, Haxton C, et al; Initial evaluation, diagnosis, and treatment of anorexia nervosa and bulimia nervosa. Am Fam Physician. 2015 Jan 1 91(1):46-52.
  3. Smink FR, van Hoeken D, Hoek HW; Epidemiology, course, and outcome of eating disorders. Curr Opin Psychiatry. 2013 Nov 26(6):543-8. doi: 10.1097/YCO.0b013e328365a24f.
  4. Treasure J, Claudino AM, Zucker N; Eating disorders. Lancet. 2010 Feb 13 375(9714):583-93.
  5. Kessler RC, Berglund PA, Chiu WT, et al; The prevalence and correlates of binge eating disorder in the World Health Organization World Mental Health Surveys. Biol Psychiatry. 2013 May 1 73(9):904-14. doi: 10.1016/j.biopsych.2012.11.020. Epub 2013 Jan 3.
  6. Dingemans AE, van Furth EF; EDNOS is an eating disorder of clinical relevance, on a par with anorexia and bulimia nervosa. Tijdschr Psychiatr. 2015 57(4):258-64.
  7. Eating disorders: recognition and treatment; NICE Guideline (May 2017)
  8. Bailey AP, Parker AG, Colautti LA, et al; Mapping the evidence for the prevention and treatment of eating disorders in young people. J Eat Disord. 2014 Feb 3 2:5. doi: 10.1186/2050-2974-2-5. eCollection 2014.
  9. Hay PP, Bacaltchuk J, Stefano S, et al; Psychological treatments for bulimia nervosa and binging. Cochrane Database Syst Rev. 2009 Oct 7 (4):CD000562. doi: 10.1002/14651858.CD000562.pub3.
Author:
Dr Mary Harding
Peer Reviewer:
Dr Jacqueline Payne
Document ID:
1894 (v26)
Last Checked:
24 July 2017
Next Review:
23 July 2022

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. Patient Platform Limited has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.