|Classification and external resources|
|Patient UK||Bulimia nervosa|
Bulimia nervosa is an eating disorder characterized by binge eating and purging, or consuming a large amount of food in a short amount of time followed by an attempt to rid oneself of the food consumed (purging), typically by vomiting, taking a laxative, diuretic, or stimulant, and/or excessive exercise, because of an extensive concern for body weight.
The term bulimia comes from Greek βουλιμία boulīmia, "ravenous hunger", a compound of βοῦς bous, "ox" and λιμός, līmos, "hunger"; literally, bulimia nervosa means disease of hunger affecting the nervous system. Bulimia nervosa was named and first described by the British psychiatrist Gerald Russell in 1979.
Some individuals may tend to alternate between bulimia nervosa and anorexia nervosa. Bulimia is also commonly accompanied with fasting over an extended period of time. These dangerous, habit-forming practices occur while the sufferer is trying to keep their weight under a self-imposed threshold. It can lead to potassium loss and health deterioration, with depressive symptoms that are often severe and lead to a high risk of suicide. Bulimia nervosa is considered to be less life-threatening than anorexia; however, the occurrence of bulimia nervosa is higher. Bulimia nervosa is nine times more likely to occur in women than men. Up to 1% of women have bulimia nervosa.
Many individuals with bulimia nervosa also have an additional psychiatric disorder. Common comorbidities are mood disorders, anxiety, impulse control, and substance-misuse disorders. Patients with bulimia nervosa often have impulsive behaviors involving overspending and sexual behaviors as well as having family histories of alcohol and substance abuse, mood and eating disorders.
The majority, about 80 to almost 90 percent of individuals with bulimia are women. However, males do develop the disorder and some studies suggest that the prevalence among males is higher than previously believed.
Among women, adolescents are the most at risk. A survey of 496 adolescent girls reported that more than 12 percent experienced some form of eating disorder by the time they were 20.
Over the years the size and weight of the average woman has increased with improved nutrition, but there has also been an increased message from the media to be thin. The media projects a thin ideal rather than a healthy ideal, and this causes women and young girls to work toward having a thin body even if it means purging.
These cycles often involve rapid and out-of-control eating, which may stop when the bulimic is interrupted by another person or the stomach hurts from over-extension, followed by self-induced vomiting or other forms of purging. This cycle may be repeated several times a week or, in more serious cases, several times a day and may directly cause:
- Chronic gastric reflux after eating
- Dehydration and hypokalemia caused by frequent vomiting
- Electrolyte imbalance, which can lead to cardiac arrhythmia, cardiac arrest, and even death
- Esophagitis, or inflammation of the esophagus
- Boerhaave syndrome, a rupture in the esophageal wall due to vomiting
- Oral trauma, in which repetitive insertion of fingers or other objects causes lacerations to the lining of the mouth or throat
- Gastroparesis or delayed emptying
- Mallory-Weiss tears
- Enlarged glands in the neck, under the jaw line
- Peptic ulcers
- Calluses or scars on back of hands due to repeated trauma from incisors
- Constant weight fluctuations are common
The frequent contact between teeth and gastric acid, in particular, may cause:
- Severe dental erosion
- Perimolysis, or the erosion of tooth enamel
- Swollen salivary glands
- Constant vomiting can lead to gastroesophageal reflux
These are some of the many signs that may indicate whether someone has bulimia nervosa:
- fixation on number of calories consumed
- fixation on and extreme consciousness of weight
- low self-esteem
- low blood pressure
- irregular menstrual cycle
- constant trips to the bathroom
As with many psychiatric illnesses, delusions can occur with other signs and symptoms leaving the person with a false belief that is not ordinarily accepted by others.
People with bulimia nervosa may also exercise to a point that excludes other activities.
Bulimics are much more likely than non-bulimics to have an affective disorder, such as depression or general anxiety disorder: A 1985 Columbia University study on female bulimics at New York State Psychiatric Institute found 70% had suffered depression some time in their lives (as opposed to 25.8% for adult females in a control sample from the general population), rising to 88% for all affective disorders combined. Another study by the Royal Children's Hospital in Melbourne on a cohort of 2,000 adolescents similarly found that those meeting at least two of the DSM-IV criteria for bulimia nervosa or anorexia nervosa had a sixfold increase in risk of anxiety and a doubling of risk for substance dependency. Some sufferers of anorexia nervosa exhibit episodes of bulimic tendencies through purging (either through self-induced vomiting or laxatives) as a way to quickly remove food in their system. Bulimia also has negative effects on the sufferer's dental health due to the acid passed through the mouth from frequent vomiting causing acid erosion, mainly on the posterior dental surface.
The onset of bulimia nervosa is often during adolescence, between 13 and 20 years of age, and many cases have previously suffered obesity, with many sufferers relapsing in adulthood into episodic binging and purging even after initially successful treatment and remission. Bulimia nervosa may affect up to 1% of young women and after 10 years of diagnosis, half will recover fully, a third will recover partially, and 10–20% will still have symptoms.
Adolescents with bulimia nervosa are more likely to have self-imposed perfectionism and compulsivity issues in eating compared to their peers. This means that the high expectations and unrealistic goals that these individuals set for themselves are internally motivated rather than by social views or expectations.
Bulimia nervosa can be difficult to detect, compared to anorexia nervosa, because bulimics tend to be of average or slightly above or below average weight. Many bulimics may also engage in significantly disordered eating and exercising patterns without meeting the full diagnostic criteria for bulimia nervosa. The diagnostic criteria utilized by the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) published by the American Psychiatric Association includes repetitive episodes of binge eating (a discrete episode of overeating during which the individual feels out of control of consumption) compensated for by excessive or inappropriate measures taken to avoid gaining weight. The diagnosis is made only when the behavior is not a part of the symptom complex of anorexia nervosa and when the behavior reflects an overemphasis on physical mass or appearance.
There are two sub-types of bulimia nervosa:
- Purging type bulimics self-induce vomiting (usually by triggering the gag reflex or ingesting emetics such as syrup of ipecac) to rapidly remove food from the body before it can be digested, or use laxatives, diuretics, or enemas.
- Non-purging type bulimics (approximately 6–8% of cases) exercise or fast excessively after a binge to offset the caloric intake after eating. Purging-type bulimics may also exercise or fast, but as a secondary form of weight control.
As with anorexia nervosa, there is evidence of genetic predispositions contributing to the onset of this eating disorder. Abnormal levels of many hormones, notably serotonin, have been shown to be responsible for some disordered eating behaviours. Brain-derived neurotrophic factor (BDNF) is under investigation as a possible mechanism.
There is evidence that sex hormones may influence appetite and eating in women, and the onset of bulimia nervosa. Studies have shown that women with hyperandrogenism and polycystic ovary syndrome have a dysregulation of appetite, along with carbohydrates and fats. This dysregulation of appetite is also seen in women with bulimia nervosa. In addition, gene knockout studies in mice have shown that mice that have the gene encoding estrogen receptors have decreased fertility due to ovarian dysfunction and dysregulation of androgen receptors. In humans, there is evidence that there is an association between polymorphisms in the ERβ (estrogen receptor β) and bulimia, suggesting there is a correlation between sex hormones and bulimia nervosa.
Bulimia has been compared to drug addiction, though the empirical support for this characterization is limited. However, people with bulimia nervosa may share dopamine D2 receptor-related vulnerabilities with those with substance abuse disorders.
Dieting, a common behaviour in bulimics, is associated with lower plasma tryptophan levels. Decreased tryptophan levels in the brain, and thus the synthesis of serotonin, increases bulimic urges in currently and formerly bulimic individuals within hours.
Media portrayals of an 'ideal' body shape are widely considered to be a contributing factor to bulimia. In a 1991 study by Weltzin, Hsu, Pollicle, and Kaye, it was stated that 19% of bulimics undereat, 37% of bulimics eat an amount of food that is normal for an average human being, and 44% of bulimics overeat. A survey of 15- to 18-year-old high school girls in Nadroga, Fiji, found the self-reported incidence of purging rose from 0% in 1995 (a few weeks after the introduction of television in the province) to 11.3% in 1998.
Through the cognitive and socio-cultural perspectives, indications towards the origin of bulimia nervosa can be established. Fairburn et al.’s cognitive behavioral model of bulimia nervosa provides a chief indication of the cause of bulimia through a cognitive perspective, while the “thin ideal” is particularly responsible for the etiology of bulimia nervosa through a socio-cultural context.
When attempting to decipher the origin of bulimia nervosa in a cognitive context, Fairburn et al.’s cognitive behavioral model is often considered the golden standard. Fairburn et al.’s model discusses the process in which an individual falls into the binge-purge cycle and thus develops bulimia. Fairburn et al. argue that extreme concern with weight and shape coupled with low self esteem will result in strict, rigid, and inflexible dietary rules. Accordingly, this would lead to unrealistic restricted eating, which may consequently induce an eventual “slip” where the individual commits a minor infraction of the strict and inflexible dietary rules. Moreover, the cognitive distortion due to dichotomous thinking leads the individual to binge. The binge subsequently should trigger a perceived loss of control, promoting the individual to purge in hope of counteracting the binge. However, Fairburn et al. assert the cycle repeats itself, and thus consider the binge-purge cycle to be self-perpetuating.
In contrast, Byrne and Mclean’s findings differed slightly from Fairburn et al.’s cognitive behavioral model of bulimia nervosa in that the drive for thinness was the major cause of purging as a way of controlling weight. In turn, Byrne and Mclean argued that this makes the individual vulnerable to binging, indicating that it is not a binge-purge cycle but rather a purge-binge cycle in that purging comes before binging. Similarly, Fairburn et al.’s cognitive behavioral model of bulimia nervosa is not necessarily applicable to every individual and is certainly reductionist. Everyone differs from another, and taking such a complex behavior like bulimia and applying the same one theory to everyone would certainly be invalid. In addition, the cognitive behavioral model of bulimia nervosa is very cultural bound in that it may not be necessarily applicable to cultures outside of the Western society. To evaluate, Fairburn et al.’s model and more generally the cognitive explanation of bulimia nervosa is more descriptive than explanatory, as it does not necessarily explain how bulimia arises. Furthermore, it is difficult to ascertain cause and effect, because it may be that distorted eating leads to distorted cognition rather than vice versa.
When exploring the etiology of bulimia through a socio-cultural perspective, the “thin ideal internalization” is significantly responsible. The thin ideal internalization is the extent to which individuals adapt to the societal ideals of attractiveness. Studies have shown that young females that read fashion magazines tend to have more bulimic symptoms than those females who do not. This further demonstrates the impact of media on the likelihood of developing the disorder.  Individuals first accept and “buy into” the ideals, and then attempt to transform themselves in order to reflect the societal ideals of attractiveness. J. Kevin Thompson and Eric Stice claim that family, peers, and most evidently media reinforce the thin ideal, which may lead to an individual accepting and “buying into” the thin ideal. In turn, Thompson and Stice assert that if the thin ideal is accepted, one could begin to feel uncomfortable with their body shape or size since it may not necessarily reflect the thin ideal set out by society. Thus, people feeling uncomfortable with their bodies may result in suffering from body dissatisfaction, and may develop a certain drive for thinness. Consequently, body dissatisfaction coupled with drive for thinness is thought to promote dieting and negative affects, which could eventually lead to bulimic symptoms such as purging or binging. Binges lead to self-disgust which causes purging to prevent weight gain.
A study dedicated to investigating the thin ideal internalization as a factor of bulimia nervosa is Thompson’s and Stice’s research. The aim of their study was to investigate how and to what degree does media effect the thin ideal internalization. Thompson and Stice used randomized experiments (more specifically programs) dedicated to teaching young women how to be more critical when it comes to media, in order to reduce thin ideal internalization. The results showed that by creating more awareness of the media’s control of the societal ideal of attractiveness, the thin ideal internalization significantly dropped. In other words, less thin ideal images portrayed by the media resulted in less thin ideal internalization. Therefore, Thompson and Stice concluded that media affected greatly the thin ideal internalization. Papies showed that it is not the thin ideal itself, but rather the self association with other persons of a certain weight that decide how someone with bulimia nervosa feels. People that associate themselves with thin models get in a positive attitude when they see thin models and people that associate with overweight get in a negative attitude when they see thin models. Moreover it can be taught to associate with thinner people.
There is little data on the prevalence of bulimia nervosa in general populations. Most studies conducted thus far have been on convenience samples from hospital patients, high school or university students. These have yielded a wide range of results: between 0.1% and 1.4% of males, and between 0.3% and 9.4% of females. Studies on time trends in the prevalence of bulimia nervosa have also yielded inconsistent results. According to Gelder, Mayou and Geddes (2005) bulimia nervosa is prevalent between 1 and 2 percent of women aged 15–40 years. Bulimia nervosa occurs more frequently in developed countries and in cities, with study finding that bulimia is five times more prevalent in cities than in rural areas. There is a perception that bulimia is most prevalent amongst girls from middle-class families, however in a 2009 study girls from families in the lowest income bracket studied were 153 percent more likely to be bulimic than girls from the highest income bracket.
There are higher rates of eating disorders in groups involved in activities which idealize a slim physique, such as dance, gymnastics, modeling, cheerleading, running, acting, swimming, diving, rowing and figure skating. Bulimia is thought to be more prevalent among Caucasians, however a more recent study showed that African-American teenage girls were 50 percent more likely than white girls to exhibit bulimic behavior, including both binging and purging.
There are two main types of treatment given to those suffering with bulimia nervosa; psychopharmacological and psychosocial treatments.
There are several empirically supported psychosocial treatments for bulimia nervosa. Cognitive behavioral therapy (CBT), which involves teaching clients to challenge automatic thoughts and engage in behavioral experiments (for example, in session eating of "forbidden foods") has demonstrated efficacy both with and without concurrent antidepressant medication. Research suggests that cognitive-behavioral therapy (CBT) is the most effective psychotherapeutic treatment for bulimia nervosa. One exception was a study that suggested that interpersonal psychotherapy (IPT) might be as effective as CBT, although slower to achieve its effects. By using CBT patients record how much food they eat and periods of vomiting with the purpose of identifying and avoiding emotional fluctuations that bring on episodes of bulimia on a regular basis. Barker (2003) states that research has found 40–60% of patients using cognitive behaviour therapy to become symptom free. He states in order for the therapy to work, all parties must work together to discuss, record and develop coping strategies. Barker (2003) claims by making people aware of their actions they will think of alternatives. Patients undergoing CBT who exhibit early behavioral changes are most likely to achieve the best treatment outcomes in the long run. Researchers have also reported some positive outcomes for interpersonal psychotherapy and dialectical behavior therapy.
Maudsley Family Therapy a.k.a. Family Based Treatment (FBT), developed at the Maudsley Hospital in London for the treatment of anorexia nervosa (AN) has been shown to have positive results for the treatment of bulimia nervosa. FBT has been shown through empirical research to be the most effective treatment of AN for patients under the age of eighteen and within three years of onset of illness. The studies to date using FBT to treat BN have been promising.
The use of Cognitive Behavioral Therapy (CBT) has been shown to be quite effective for treating bulimia nervosa (BN) in adults, but little research has been done on effective treatments of BN for adolescents. Although CBT is seen as more cost efficient and helps individuals with BN in self-guided care, Family Based Treatment (FBT) might be more helpful to younger adolescents who need more support and guidance from their families. Adolescents are at the stage where their brains are still quite malleable and developing gradually. Therefore, young adolescents with BN are less likely to realize the detrimental consequences of becoming bulimic and have less motivation to change, which is why FBT would be useful to have families intervene and support the teens. Working with BN patients and their families in FBT can empower the families by having them involved in their adolescent's food choices and behaviors, taking more control of the situation in the beginning and gradually letting the adolescent become more autonomous when they have learned healthier eating habits.
Adolescents with BN whom are either resistant to change or have not been successful with treatments such as CBT (Cognitive Behavioral Therapy) or IPT (Interpersonal Psychotherapy) could get recommended to try Cue Exposure (CE) by therapists. In this type of therapy, a patient is presented in the beginning of each session with a "forbidden food", allowing the individual to pick up the item to feel and smell it, but they are not allowed to eat it. This will usually provoke a lot of stress and anxiety in the adolescent with BN, which ultimately leads them to have a feeling of intense hunger and wish to partake in binge eating. To help control their eating behaviors, the therapist attempts with CE to expose the adolescent to the food and condition them in order to not feel as much anxiety when presented with the food. If they do not feel as much stress or anxiety when the food is right in front of them, then they will be less likely to feel the need to binge and then purge.
Some researchers have also claimed positive outcomes in hypnotherapy treatment. The twelve-step model, used for chemically dependent individuals, was applied to bulimic patients with good results. Researchers at Ohio State University, in a preliminary study, incorporated the twelve-step model in their treatment of bulimic women in an inpatient unit. They reported positive outcomes.
Some researchers have hypothesized a relationship to mood disorders and clinical trials have been conducted with tricyclic antidepressants, MAO inhibitors, mianserin, fluoxetine, lithium carbonate, nomifensine, trazodone, and bupropion.
Research groups who have seen a relationship to seizure disorders have attempted treatment with phenytoin, carbamazepine, and valproic acid. Opiate antagonists naloxone and naltrexone, which block cravings for gambling, have also been used.
|Country||Year||Sample size and type||Incidence|
|Australia||2008||1,943 adolescents (ages 15–17)||1.0% male||6.4% female|
|Portugal||2006||2,028 high school students||0.3% female|
|Brazil||2004||1,807 students (ages 7–19)||0.8% male||1.3% female|
|Spain||2004||2,509 female adolescents (ages 13–22)||1.4% female|
|Hungary||2003||580 Budapest residents||0.4% male||3.6% female|
|Australia||1998||4,200 high school students||0.3% combined|
|USA||1996||1,152 college students||0.2% male||1.3% female|
|Norway||1995||19,067 psychiatric patients||0.7% male||7.3% female|
|Canada||1995||8,116 (random sample)||0.1% male||1.1% female|
|Japan||1995||2,597 high school students||0.7% male||1.9% female|
|USA||1992||799 college students||0.4% male||5.1% female|
It is not known if combining pharmacotherapy with psychotherapy will improve the outcome of the treatments. Any trials which originally suggested that such combinations should improve the outcome, have not proven to be exceptionally powerful. Some positive outcomes of treatments can include: abstinence from binge eating, a decrease in obsessive behaviours to lose weight and in shape preoccupation, less severe psychiatric symptoms, a desire to counter the effects of binge eating, as well as an improvement in social functioning and relapse rates.
Evidence of binging and purging before the 20th century
Although diagnostic criteria for bulimia nervosa did not appear until 1979, evidence suggests that binging and purging were popular in certain ancient cultures. The first documented account of behavior resembling bulimia nervosa was recorded in Xenophon’s Anabasis around 370 B.C, in which Greek soldiers purged themselves in the mountains of Asia Minor. It is unclear whether this purging was preceded by binging. In ancient Egypt, physicians recommended purging once a month for three days in order to preserve health. This practice stemmed from the belief that human diseases were caused by food itself. In ancient Rome, elite society members would vomit in order to “make room” in their stomachs for more food at all day banquets. Emperors Claudius and Vitellius both were gluttonous and obese, and they often resorted to habitual purging.
Historical records also suggest that some saints who developed anorexia (as a result of a life of asceticism) may also have displayed Bulimic behaviors. Saint Mary Magdalen de Pazzi (1566–1607) and Saint Veronica Giuliani (1660–1727) were both observed binge eating—giving in, as they believed, to the temptations of the devil. Saint Catherine of Siena (1347–1380) is known to have supplemented her strict abstinence from food by purging as reparation for her sins. Catherine died from starvation at age thirty-three.
While the psychological disorder “bulimia nervosa” is relatively new, the word “bulimia,” signifying overeating, has been present for centuries. The Babylon Talmud referenced practices of “bulimia,” yet scholars believe that this simply referred to overeating without the purging or the psychological implications bulimia nervosa. In fact, a search for evidence of bulimia nervosa from the 17th to late 19th century revealed that only a quarter of the overeating cases they examined actually vomited after the binges. There was no evidence of deliberate vomiting or an attempt to control weight.
In the 20th century
At the turn of the century, bulimia (overeating) was described as a clinical symptom, but rarely in the context of weight control. Purging, however, was seen in anorexic patients and attributed to gastric pain rather than another method of weight control.
In 1930, admissions of anorexia nervosa patients to the Mayo Clinic from 1917 to 1929 were compiled. Fifty-five to sixty-five percent of these patients were reported to be voluntarily vomiting in order to relieve weight anxiety. Records show that purging for weight control continued throughout the mid-1900s. Several case studies from this era reveal patients suffering from the modern description of bulimia nervosa. In 1939, Rahman and Richardson reported that out of their six anorexic patients, one had periods of overeating and another practiced self-induced vomiting. Wulff, in 1932, treated “Patient D,” who would have periods of intense cravings for food and overeat for weeks, which often resulted in frequent vomiting. Patient D, who grew up with a tyrannical father, was repulsed by her weight and would fast for a few days, rapidly losing weight. Ellen West, a patient described by Ludwig Binswanger in 1958, was teased by friends for being fat and excessively took thyroid pills to lose weight, later using laxatives and vomiting. She reportedly consumed dozens of oranges and several pounds of tomatoes each day, yet would skip meals. After being admitted to a psychiatric facility for depression, Ellen ate ravenously yet lost weight, presumably due to self-induced vomiting. However, while these patients may have met modern criteria for bulimia nervosa, they cannot technically be diagnosed with the disorder, as it had not yet appeared in the Diagnostic and Statistical Manual of Mental Disorders at the time of their treatment.
An explanation for the increased instances of bulimic symptoms may be due to the 20th century’s new ideals of thinness. The shame of being fat emerged in the 1940s, when teasing remarks about weight became more common. The 1950s, however, truly introduced the trend of an aspiration for thinness.
In 1979, Gerald Russell first published a description of bulimia nervosa, in which he studied patients with a “morbid fear of becoming fat” who overate and purged afterwards. He specified treatment options and indicated the seriousness of the disease, which can be accompanied by depression and suicide. In 1980, bulimia nervosa first appeared in the DSM-III.
After its appearance in the DSM-III, there was a sudden rise in the documented incidences of bulimia nervosa. In the early 1980s, incidences of the disorder rose to about 40 in every 100,000 people. This decreased to about 27 in every 100,000 people at the end of the 1980s/early 1990s. However, bulimia nervosa’s prevalence was still much higher than anorexia nervosa’s, which at the time occurred in about 14 people per 100,000.
In 1991, Kendler et al. documented the cumulative risk for bulimia nervosa for those born before 1950, from 1950 to 1959, and after 1959. The risk for those born after 1959 is much higher than those in either of the other cohorts.
|Wikimedia Commons has media related to Bulimia nervosa.|
- Hay PJ, Claudino AM (2010). "Bulimia nervosa". Clinical Evidence 2010: 1009. PMC 3275326. PMID 21418667.
- Douglas Harper (November 2001). "Online Etymology Dictionary: bulimia". Online Etymology Dictionary. Retrieved 2008-04-06.
- "Teen Bulimia Statistics". Retrieved 3 April 2013.
- Russell G (1979). "Bulimia nervosa: An ominous variant of anorexia nervosa". Psychological Medicine 9 (3): 429–48. doi:10.1017/S0033291700031974. PMID 482466.
- Palmer R (2004). "Bulimia nervosa: 25 years on". The British Journal of Psychiatry : The Journal of Mental Science 185 (6): 447–8. doi:10.1192/bjp.185.6.447. PMID 15572732.
- Barker, P (2003). Psychiatric and Mental Health Nursing: The Craft of Caring. Great Britain: Arnold. ISBN 0340810262.[page needed]
- Fairburn, Christopher G. (1995). Overcoming binge eating. New York: Guilford Press. ISBN 0-89862-179-8.[page needed]
- Murphy B, Manning Y (2003). "An introduction to anorexia nervosa and bulimia nervosa". Nursing Standard (Royal College of Nursing (Great Britain) : 1987) 18 (14–16): 45–52; quiz 54–5. doi:10.7748/ns2003.12.18.14.45.c3520. PMID 14705352.
- Yager J (1991). "Bulimia nervosa". The Western Journal of Medicine 155 (5): 523–4. PMC 1003077. PMID 1815403.
- Newell, Robert; Gournay, Kevin, eds. (2000). Mental Health Nursing: An Evidence-based Approach. ISBN 978-0-443-05873-8.[page needed]
- Kendler KS, MacLean C, Neale M, Kessler R, Heath A, Eaves L (1991). "The genetic epidemiology of bulimia nervosa". The American Journal of Psychiatry 148 (12): 1627–37. PMID 1842216.
- Bulik CM, Sullivan PF, Kendler KS (1998). "Heritability of binge-eating and broadly defined bulimia nervosa". Biological Psychiatry 44 (12): 1210–8. doi:10.1016/S0006-3223(98)00280-7. PMID 9861464.
- "Bulimia Nervosa". National Eating Disorders Association. Retrieved 18 April 2014.
- American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. p. 347. ISBN 978-0-89042-555-8.
- Barlow, D. H.; Durand, V. M. (2011). Abnormal psychology: An integrative approach (6th ed.). Belmont, CA: Wadsworth, Cengage Learning.[page needed]
- "Bulimia Nervosa". Let's Talk Facts (American Psychiatric Association): 1. 2005. Retrieved 13 September 2013.
- Joseph AB, Herr B (1985). "Finger calluses in bulimia". The American Journal of Psychiatry 142 (5): 655. PMID 3857013.
- Wynn DR, Martin MJ (1984). "A physical sign of bulimia". Mayo Clinic Proceedings 59 (10): 722. doi:10.1016/s0025-6196(12)62063-1. PMID 6592415.
- Dorfman J, The Center for Special Dentistry.
- "Eating Disorders". Oral Health Topics A–Z. American Dental Association. Archived from the original on Feb 3, 2009.
- Mcgilley BM, Pryor TL (June 1998). "Assessment and Treatment of Bulimia Nervosa". American Family Physician 57 (11): 2743–50. PMID 9636337.
- Mehler PS (2003). "Bulimia Nervosa". The New England Journal of Medicine 349 (9): 875–81. doi:10.1056/NEJMcp022813. PMID 12944574.
- "Symptoms Of Bulimia Nervosa". Illawarra Mercury. February 23, 2001.[unreliable source?]
- Walsh BT, Roose SP, Glassman AH, Gladis M, Sadik C (1985). "Bulimia and depression". Psychosomatic Medicine 47 (2): 123–31. doi:10.1097/00006842-198503000-00003. PMID 3863157.
- Patton GC, Coffey C, Carlin JB, Sanci L, Sawyer S (2008). "Prognosis of adolescent partial syndromes of eating disorder". The British Journal of Psychiatry : The Journal of Mental Science 192 (4): 294–9. doi:10.1192/bjp.bp.106.031112. PMID 18378993.
- Carlson, N.R., et al. (2007). Psychology: The Science of Behaviour – 4th Canadian ed.. Toronto, ON: Pearson Education Canada.[page needed]
- Shader, Richard I. (2004). Manual of Psychiatric Therapeutics. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-4459-8.[page needed]
- Castro-Fornieles J, Gual P, Lahortiga F, Gila A, Casulà V, Fuhrmann C, Imirizaldu M, Saura B, Martínez E, Toro J (September 2007). "Self-oriented perfectionism in eating disorders". The International Journal of Eating Disorders 40 (6): 562–568. doi:10.1002/eat.20393. PMID 17510925.
- Walsh JM, Wheat ME, Freund K (2000). "Detection, evaluation, and treatment of eating disorders". Journal of General Internal Medicine 15 (8): 577–90. doi:10.1046/j.1525-1497.2000.02439.x. PMC 1495575. PMID 10940151.
- American Psychiatric Association (2000). "Diagnostic criteria for 307.51 Bulimia Nervosa". Diagnostic and Statistical Manual of Mental Disorders (4th, text revision (DSM-IV-TR) ed.). ISBN 0-89042-025-4. Retrieved 2010-03-14.
- Barlow, David H.; Durand, Vincent Mark (2002). Abnormal psychology: an integrative approach. Belmont, CA: Wadsworth/Thomson Learning. ISBN 0-534-63362-5.[page needed]
- "Biological Causes of Anorexia Nervosa and Bulimia Nervosa". Retrieved 3 April.
- Ribasés M, Gratacòs M, Fernández-Aranda F, Bellodi L, Boni C, Anderluh M, Cavallini MC, Cellini E, Di Bella D, Erzegovesi S, Foulon C, Gabrovsek M, Gorwood P, Hebebrand J, Hinney A, Holliday J, Hu X, Karwautz A, Kipman A, Komel R, Nacmias B, Remschmidt H, Ricca V, Sorbi S, Wagner G, Treasure J, Collier DA, Estivill X (2004). "Association of BDNF with anorexia, bulimia and age of onset of weight loss in six European populations". Human Molecular Genetics 13 (12): 1205–1212. doi:10.1093/hmg/ddh137. PMID 15115760.
- Wonderlich, Stephen; Mitchell, James E.; de Zwaan, Martina; Steiger, Howard, eds. (2008). "1". Annual Review of Eating Disorders – part 2. Radcliffe Publishing. pp. 14–15. ISBN 978-1-84619-244-9.
- Hirschberg AL (2012). "Sex hormones, appetite and eating behaviour in women". Maturitas 71 (3): 248–56. doi:10.1016/j.maturitas.2011.12.016. PMID 22281161.
- Broft A, Shingleton R, Kaufman J, Liu F, Kumar D, Slifstein M, Abi-Dargham A, Schebendach J, Van Heertum R, Attia E, Martinez D, Walsh BT (July 2012). "Striatal dopamine in bulimia nervosa: A pet imaging study". The International Journal of Eating Disorders 45 (5): 648–656. doi:10.1002/eat.20984. PMC 3640453. PMID 22331810.
- Kaye WH, Wierenga CE, Bailer UF, Simmons AN, Wagner A, Bischoff-Grethe A (2013). "Does a Shared Neurobiology for Foods and Drugs of Abuse Contribute to Extremes of Food Ingestion in Anorexia and Bulimia Nervosa?". Biological Psychiatry 73 (9): 836–42. doi:10.1016/j.biopsych.2013.01.002. PMID 23380716.
- Smith KA, Fairburn CG, Cowen PJ (1999). "Symptomatic Relapse in Bulimia Nervosa Following Acute Tryptophan Depletion". Archives of General Psychiatry 56 (2): 171–6. doi:10.1001/archpsyc.56.2.171. PMID 10025442.
- Weltzin TE, Fernstrom MH, Fernstrom JD, Neuberger SK, Kaye WH (1995). "Acute tryptophan depletion and increased food intake and irritability in bulimia nervosa". The American Journal of Psychiatry 152 (11): 1668–71. PMID 7485633.
- Carlson, Neil R.; Buskist, William; Heth, C. Donald; Schmaltz, Rod (2010). Psychology: the science of behaviour (4th Canadian ed.). Toronto: Pearson Education Canada. p. 415. ISBN 978-0-205-70286-2.
- Becker AE, Burwell RA, Gilman SE, Herzog DB, Hamburg P (2002). "Eating behaviours and attitudes following prolonged exposure to television among ethnic Fijian adolescent girls". The British Journal of Psychiatry : The Journal of Mental Science 180 (6): 509–14. doi:10.1192/bjp.180.6.509. PMID 12042229.
- Trull, Thimothy (2010-10-08). Abnormal Psychology and Life: A Dimensional Approach. Belmont CA: Wadsworth, Cengage Learning. pp. 236–8. ISBN 978-1-111-34376-7.
- Byrne SM, McLean NJ (2002). "The cognitive-behavioral model of bulimia nervosa: A direct evaluation". The International Journal of Eating Disorders 31 (1): 17–31. doi:10.1002/eat.10002. PMID 11835294.
- Nolen-Hoeksema, Susan (2013). (Ab)normal Psychology. McGraw Hill. p. 338. ISBN 0078035384.
- Zieve, David. "Bulimia". PubMed Health. Retrieved April 18, 2011.
- Thompson, J. Kevin; Stice, Eric (2001). "Thin-Ideal Internalization: Mounting Evidence for a New Risk Factor for Body-Image Disturbance and Eating Pathology". Current Directions in Psychological Science 10 (5): 181–3. doi:10.1111/1467-8721.00144. JSTOR 20182734.
- Papies EK, Nicolaije KA (2012). "Inspiration or deflation? Feeling similar or dissimilar to slim and plus-size models affects self-evaluation of restrained eaters". Body Image 9 (1): 76–85. doi:10.1016/j.bodyim.2011.08.004. PMID 21962524.
- Makino M, Tsuboi K, Dennerstein L (2004). "Prevalence of eating disorders: a comparison of Western and non-Western countries". MedGenMed : Medscape General Medicine 6 (3): 49. PMC 1435625. PMID 15520673.
- Hay PJ, Mond J, Buttner P, Darby A (2008). "Eating Disorder Behaviors Are Increasing: Findings from Two Sequential Community Surveys in South Australia". In Murthy, R. Srinivasa. PloS One 3 (2): e1541. doi:10.1371/journal.pone.0001541. PMC 2212110. PMID 18253489.
- Gelder, Michael Graham; Mayou, Richard; Geddes, John (2005). Psychiatry. ISBN 978-0-19-852863-0.[page needed]
- van Son GE, van Hoeken D, Bartelds AI, van Furth EF, Hoek HW (2006). "Urbanisation and the incidence of eating disorders". The British Journal of Psychiatry : The Journal of Mental Science 189 (6): 562–3. doi:10.1192/bjp.bp.106.021378. PMID 17139044.
- "Bulimia". finddoctorsonline.com.
- Grohol, John (March 19, 2009). "Black Girls At Risk for Bulimia".
- Tölgyes T, Nemessury J (2004). "Epidemiological studies on adverse dieting behaviours and eating disorders among young people in Hungary". Social Psychiatry and Psychiatric Epidemiology 39 (8): 647–54. doi:10.1007/s00127-004-0783-z. PMID 15300375.
- Franko DL, Becker AE, Thomas JJ, Herzog DB (2007). "Cross-ethnic differences in eating disorder symptoms and related distress". The International Journal of Eating Disorders 40 (2): 156–64. doi:10.1002/eat.20341. PMID 17080449.
- McBride, Hugh. "Study Reveals Stunning Prevalence of Bulimia Among African-American Girls". Archived from the original on Feb 10, 2012.
- Hoste RR, Labuschagne Z, Le Grange D (2012). "Adolescent Bulimia Nervosa". Current Psychiatry Reports 14 (4): 391–7. doi:10.1007/s11920-012-0280-0. PMID 22614677.
- Agras WS, Walsh T, Fairburn CG, Wilson GT, Kraemer HC (2000). "A Multicenter Comparison of Cognitive-Behavioral Therapy and Interpersonal Psychotherapy for Bulimia Nervosa". Archives of General Psychiatry 57 (5): 459–66. doi:10.1001/archpsyc.57.5.459. PMID 10807486.
- Agras WS, Crow SJ, Halmi KA, Mitchell JE, Wilson GT, Kraemer HC (2000). "Outcome Predictors for the Cognitive Behavior Treatment of Bulimia Nervosa: Data from a Multisite Study". The American Journal of Psychiatry 157 (8): 1302–8. doi:10.1176/appi.ajp.157.8.1302. PMID 10910795.
- Wilson GT, Loeb KL, Walsh BT, Labouvie E, Petkova E, Liu X, Waternaux C (1999). "Psychological versus pharmacological treatments of bulimia nervosa: Predictors and processes of change". Journal of Consulting and Clinical Psychology 67 (4): 451–9. doi:10.1037/0022-006X.67.4.451. PMID 10450615.
- Trunko ME, Rockwell RE, Curry E, Runfola C, Kaye WH (2007). "Management of bulimia nervosa". Women's Health (London, England) 3 (2): 255–65. doi:10.2217/17455057.3.2.255. PMID 19803857.
- Fairburn CG, Agras WS, Walsh BT, Wilson GT, Stice E (2004). "Prediction of Outcome in Bulimia Nervosa by Early Change in Treatment". The American Journal of Psychiatry 161 (12): 2322–4. doi:10.1176/appi.ajp.161.12.2322. PMID 15569910.
- Safer DL, Telch CF, Agras WS (2001). "Dialectical Behavior Therapy for Bulimia Nervosa". The American Journal of Psychiatry 158 (4): 632–4. doi:10.1176/appi.ajp.158.4.632. PMID 11282700.
- Lock J, le Grange D (2005). "Family-based treatment of eating disorders". The International Journal of Eating Disorders 37: S64–7; discussion S87–9. doi:10.1002/eat.20122. PMID 15852323.
- Keel PK, Haedt A (2008). "Evidence-Based Psychosocial Treatments for Eating Problems and Eating Disorders". Journal of Clinical Child and Adolescent Psychology : The Official Journal for the Society of Clinical Child and Adolescent Psychology, American Psychological Association, Division 53 37 (1): 39–61. doi:10.1080/15374410701817832. PMID 18444053.
- Le Grange D, Lock J, Dymek M (2003). "Family-based therapy for adolescents with bulimia nervosa". American Journal of Psychotherapy 57 (2): 237–51. PMID 12817553.
- Castro-Fornieles J, Bigorra A, Martinez-Mallen E, Gonzalez L, Moreno E, Font E, Toro J (2011). "Motivation to change in adolescents with bulimia nervosa mediates clinical change after treatment". European Eating Disorders Review : The Journal of the Eating Disorders Association 19 (1): 46–54. doi:10.1002/erv.1045. PMID 20872926.
- Martinez-Mallén E, Castro-Fornieles J, Lázaro L, Moreno E, Morer A, Font E, Julien J, Vila M, Toro J (November 2007). "Cue exposure in the treatment of resistant adolescent bulimia nervosa". The International Journal of Eating Disorders 40 (7): 596–601. doi:10.1002/eat.20423. PMID 17607695.
- Barabasz M (1990). "Treatment of bulimia with hypnosis involving awareness and control in clients with high dissociative capacity". International Journal of Psychosomatics : Official Publication of the International Psychosomatics Institute 37 (1–4): 53–6. PMID 2246105.
- Barabasz M (2007). "Efficacy of Hypnotherapy in the Treatment of Eating Disorders". The International Journal of Clinical and Experimental Hypnosis 55 (3): 318–35. doi:10.1080/00207140701338688. PMID 17558721.
- Griffiths, Rosalyn A. (1995). "Two-Year Follow-Up Findings of Hypnobehavioural Treatment for Bulimia Nervosa". Australian Journal of Clinical and Experimental Hypnosis 23 (2): 135–44.[unreliable source?]
- Kraft T, Kraft D (2009). "The Place of Hypnosis in Psychiatry, Part 3: the Application to the Treatment of Eating Disorders" (PDF). Australian Journal of Clinical and Experimental Hypnosis 37 (1): 1–20.
- Giannini AJ, Keller M, Colapietro G, Melemis SM, Leskovac N, Timcisko T (1998). "Comparison of Alternative Treatment Techniques in Bulimia: The Chemical Dependency Approach". Psychological Reports 82 (2): 451–8. doi:10.2466/pr0.19220.127.116.111. PMID 9621718.
- Mitchell JE, Raymond N, Specker S (1993). "A review of the controlled trials of pharmacotherapy and psychotherapy in the treatment of bulimia nervosa". The International Journal of Eating Disorders 14 (3): 229–47. doi:10.1002/1098-108X(199311)14:3<229::AID-EAT2260140302>3.0.CO;2-X. PMID 8275060.
- Walsh, B T (1995). "Pharmacotherapy of eating disorders". In Brownell, K D. Eating Disorders and Obesity: A Comprehensive Handbook. New York: Guilford. pp. 329–40. ISBN 978-0-89862-850-0.
- Mitchell JE, Christenson G, Jennings J, Huber M, Thomas B, Pomeroy C, Morley J (1989). "A Placebo-Controlled, Double-Blind Crossover Study of Naltrexone Hydrochloride in Outpatients with Normal Weight Bulimia". Journal of Clinical Psychopharmacology 9 (2): 94–7. doi:10.1097/00004714-198904000-00004. PMID 2656781.
- Slaby, Andrew Edmund (1993). The eating disorders. Berlin: Springer-Verlag. ISBN 0-387-94002-2.[page needed]
- Machado PP, Machado BC, Gonçalves S, Hoek HW (2007). "The prevalence of eating disorders not otherwise specified". The International Journal of Eating Disorders 40 (3): 212–7. doi:10.1002/eat.20358. PMID 17173324.
- Vilela JE, Lamounier JA, Dellaretti Filho MA, Barros Neto JR, Horta GM (2004). "Transtornos alimentares em escolares" [Eating disorders in school children]. Jornal De Pediatria (in Portuguese) 80 (1): 49–54. doi:10.1590/S0021-75572004000100010. PMID 14978549.
- Lahortiga-Ramos F, De Irala-Estévez J, Cano-Prous A, Gual-García P, Martínez-González MA, Cervera-Enguix S (2005). "Incidence of eating disorders in Navarra (Spain)". European Psychiatry : The Journal of the Association of European Psychiatrists 20 (2): 179–85. doi:10.1016/j.eurpsy.2004.07.008. PMID 15797704.
- Hay P (1998). "The epidemiology of eating disorder behaviors: An Australian community-based survey". The International Journal of Eating Disorders 23 (4): 371–82. doi:10.1002/(SICI)1098-108X(199805)23:4<371::AID-EAT4>3.0.CO;2-F. PMID 9561427.
- Pemberton AR, Vernon SW, Lee ES (1996). "Prevalence and Correlates of Bulimia Nervosa and Bulimic Behaviors in a Racially Diverse Sample of Undergraduate Students in Two Universities in Southeast Texas". American Journal of Epidemiology 144 (5): 450–5. doi:10.1093/oxfordjournals.aje.a008950. PMID 8781459.
- Götestam KG, Eriksen L, Hagen H (1995). "An epidemiological study of eating disorders in Norwegian psychiatric institutions". The International Journal of Eating Disorders 18 (3): 263–8. doi:10.1002/1098-108X(199511)18:3<263::AID-EAT2260180308>3.0.CO;2-O. PMID 8556022.
- Garfinkel PE, Lin E, Goering P, Spegg C, Goldbloom DS, Kennedy S, Kaplan AS, Woodside DB (July 1995). "Bulimia nervosa in a Canadian community sample: prevalence and comparison of subgroups". The American Journal of Psychiatry 152 (7): 1052–8. PMID 7793442.[dead link]
- Suzuki K, Takeda A, Matsushita S (1995). "Coprevalence of bulimia with alcohol abuse and smoking among Japanese male and female high school students". Addiction (Abingdon, England) 90 (7): 971–5. doi:10.1111/j.1360-0443.1995.tb03506.x. PMID 7663319.
- Heatherton TF, Nichols P, Mahamedi F, Keel P (November 1995). "Body weight, dieting, and eating disorder symptoms among college students, 1982 to 1992". The American Journal of Psychiatry 152 (11): 1623–9. PMID 7485625.[dead link]
- Giannini, A. J. (1993). "A history of bulimia". In The Eating disorders (pp. 18–21). Springer New York.
- Russell, G. (1997). The history of bulimia nervosa. D. Garner & P. Garfinkel (Eds.), Handbook of Treatment for Eating Disorders (2nd ed., pp. 11–24). New York, NY: The Guilford Press.
- Casper, Regina C. (1983). "On the emergence of bulimia nervosa as a syndrome a historical view". International Journal of Eating Disorders 2 (3): 3. doi:10.1002/1098-108X(198321)2:3<3::AID-EAT2260020302>3.0.CO;2-D.
- Kendler KS, MacLean C, Neale M, Kessler R, Heath A, Eaves L (1991). "The genetic epidemiology of bulimia nervosa". The American Journal of Psychiatry 148 (12): 1627–37. PMID 1842216.