Bulimia nervosa
Hi
Bulimia nervosa | |
---|---|
Specialty | Psychiatry ![]() |
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.[1]
The term bulimia comes from Greek βουλιμία (boulīmia; ravenous hunger), a compound of βους (bous), ox + λιμός (līmos), hunger;[2] literally, bulimia nervosa means disease of hunger affecting the nervous system.[3] Bulimia nervosa was named and first described by the British psychiatrist Gerald Russell in 1979.[4][5]
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.[6][7] 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.[4] Bulimia nervosa is considered to be less life threatening than anorexia; however, the occurrence of bulimia nervosa is higher.[8] Bulimia nervosa is nine times more likely to occur in women than men.[6] Up to 1% of women have bulimia nervosa.[1]
The majority of those with bulimia nervosa are at normal weight.[9] Antidepressants, especially SSRIs, are widely used in the treatment of bulimia nervosa.[10]
Bulimia is strongly familial. Twin studies estimate the heritability of syndromic bulimia to be 54–83%.[11][12]
Many individuals with bulimia nervosa also have an additional psychiatric disorder.[1] Common comorbidities are mood disorders, anxiety, impulse control, and substance-misuse disorders.[1] 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.[9]
The overwhelming majority (90–95 percent) of individuals with bulimia are women.[13] However, males do develop the disorder and some studies suggest that the prevalence among males is higher than previously believed. In general, males have a slightly later age of onset, and males with bulimia are more likely to have disturbances in the development of their identity with a greater tendency towards sexual inhibition in the context of heterosexuality, apparent asexuality, manifest homosexuality, or bisexuality. Males that participate in sports that require weight regulation, such as wrestling and horse racing, comprise another large group of males with eating disorders.[citation needed]
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. Anorexia and bulimia are the most culturally specific psychological disorders yet identified, and for many young women, looking good for their social life is much more important than being healthy. Self-worth, happiness, and success are largely determined by body measurements and percentage of body fat for young women.[citation needed]
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.[13]
Symptoms
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[14] 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
- Constipation
- Mallory-Weiss tears
- Infertility
- Enlarged glands in the neck, under the jaw line
- Peptic ulcers
- Calluses or scars on back of hands due to repeated trauma from incisors[15][16]
- Constant weight fluctuations are common
![](http://upload.wikimedia.org/wikipedia/commons/thumb/a/aa/Oral_Manifestation_of_Bulimia..jpg/220px-Oral_Manifestation_of_Bulimia..jpg)
The frequent contact between teeth and gastric acid, in particular, may cause:
- Severe dental erosion
- Perimolysis, or the erosion of tooth enamel[18]
- Swollen salivary glands[18][19]
- Constant vomiting can lead to gastroesophageal reflux[20]
Signs
These are some of the many signs that may indicate whether someone has bulimia nervosa:[21]
- 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
- depression
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.[6]
The person may also suffer physical complications such as tetany, epileptic seizures, cardiac arrhythmias and muscle weakness.(ICD-10).[citation needed]
People with bulimia nervosa may also exercise to a point that excludes other activities.[6]
Related disorders
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.[22] 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.[23] 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.[24] 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.
Diagnosis
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.[25] 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.[1]
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.[26]
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.[27] 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.[28] 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.[29]
Causes
Biological
Like with anorexia nervosa, there is evidence of genetic predispositions contributing to the onset of this eating disorder.[30] 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.[31][32]
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.[33]
Bulimia has been compared to drug addiction, though the empirical support for this characterization is limited.[34] However, people with bulimia nervosa may share dopamine D2 receptor-related vulnerabilities with those with substance abuse disorders.[35]
Dieting, a common behaviour in bulimics, is associated with lower plasma tryptophan levels.[citation needed] Decreased tryptophan levels in the brain, and thus the synthesis of serotonin, increases bulimic urges in currently and formerly bulimic individuals within hours.[36][37]
Social
Media portrayals of an 'ideal' body shape are widely considered to be a contributing factor to bulimia.[6] 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.[38] A survey of 15–18 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.[39]
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.[citation needed]
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.[citation needed]
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.[40][41]
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. 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.[42]
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.[43] 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.[44]
Epidemiology
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.[45] Studies on time trends in the prevalence of bulimia nervosa have also yielded inconsistent results.[46] 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[47] and in cities, with study finding that bulimia is five times more prevalent in cities than in rural areas.[48] There is a perception that bulimia is most prevalent amongst girls from middle-class families,[49] 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.[50]
There are higher rates of eating disorders in groups involved in activities which idealize a slim physique, such as dance,[51] gymnastics, modeling, cheerleading, running, acting, swimming, diving, rowing and figure skating. Bulimia is thought to be more prevalent among Caucasians,[52] 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.[53]
Treatment
There are two main types of treatment given to those suffering with bulimia nervosa; psychopharmacological and psychosocial treatments.[54]
Psychotherapy
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.[55] 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.[56] 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.[57][58] Patients undergoing CBT who exhibit early behavioral changes are most likely to achieve the best treatment outcomes in the long run.[59] Researchers have also reported some positive outcomes for interpersonal psychotherapy and dialectical behavior therapy.[60][61]
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 efficacious 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.[62]
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.[63] 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.[64] Therefore, young adolescents with BN are less likely to realize the detrimental consequences of becoming bulimic and have less motivation to change,[65] which is why FBT would be useful to have families intervene and support the teens.[63] 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.[63]
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.[66] 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.[67][68][69][70] 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.[71]
Pharmacological treatment
Some researchers have hypothesized a relationship to mood disorders and clinical trials have been conducted with tricyclic antidepressants,[72] MAO inhibitors, mianserin, fluoxetine,[73] 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.[74]
There has also been some research characterizing bulimia nervosa as an addiction disorder, and limited clinical use of topiramate, which blocks cravings for opiates, cocaine, alcohol and food.[75]
Country | Year | Sample size and type | Incidence | |
---|---|---|---|---|
Australia | 2008 | 1,943 adolescents (ages 15–17) | 1.0% male | 6.4% female[23] |
Portugal | 2006 | 2,028 high school students | 0.3% female[76] | |
Brazil | 2004 | 1,807 students (ages 7–19) | 0.8% male | 1.3% female[77] |
Spain | 2004 | 2,509 female adolescents (ages 13–22) | 1.4% female[78] | |
Hungary | 2003 | 580 Budapest residents | 0.4% male | 3.6% female[51] |
Australia | 1998 | 4,200 high school students | 0.3% combined[79] | |
USA | 1996 | 1,152 college students | 0.2% male | 1.3% female[80] |
Norway | 1995 | 19,067 psychiatric patients | 0.7% male | 7.3% female[81] |
Canada | 1995 | 8,116 (random sample) | 0.1% male | 1.1% female[82] |
Japan | 1995 | 2,597 high school students | 0.7% male | 1.9% female[83] |
USA | 1992 | 799 college students | 0.4% male | 5.1% female[84] |
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.[1]
See also
![](http://upload.wikimedia.org/wikipedia/en/thumb/4/4a/Commons-logo.svg/30px-Commons-logo.svg.png)
Notes
- ^ a b c d e f Hay, Phillipa J; Claudino, Angélica Medeiros (2010). "Bulimia nervosa". Clinical Evidence. 2010: 1009. PMC 3275326. PMID 21418667.
- ^ Douglas Harper (2001). "Online Etymology Dictionary: bulimia". Online Etymology Dictionary. Retrieved 2008-04-06.
{{cite web}}
: Unknown parameter|month=
ignored (help) - ^ "Teen Bulimia Statistics". Retrieved 3 April 2013.
- ^ a b Russell, Gerald (2009). "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. 185 (6): 447–8. doi:10.1192/bjp.185.6.447. PMID 15572732.
- ^ a b c d e 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. 18 (14–16): 45–52, quiz 54–5. PMID 14705352.
- ^ a b 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, Cynthia M; Sullivan, Patrick F; Kendler, Kenneth S (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.
- ^ a b Barlow, D. H.; Durand, V. M. (2011). Abnormal psychology: An integrative approach (6th ed.). Belmont, CA: Wadsworth, Cengage Learning.[page needed]
- ^ Eating Disorders. Let's Talk About. American Psychiatric Association. 2005. ISBN 0-89042-352-0.[dead link][page needed]
- ^ 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. Mayo Clinic. 59 (10): 722. PMID 6592415.
- ^ Dorfman J, The Center for Special Dentistry.
- ^ a b "Eating Disorders". Oral Health Topics A–Z. American Dental Association.
- ^ Mcgilley, Beth M; Pryor, Tamara L (1998). "Assessment and Treatment of Bulimia Nervosa". American Family Physician. 57 (11): 2743–50. PMID 9636337.
{{cite journal}}
: Unknown parameter|month=
ignored (help) - ^ Mehler, Philip S. (2003). "Bulimia Nervosa". 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, B. Timothy; Roose, Steven P.; Glassman, Alexander H.; Gladis, Madeline; Sadik, Carla (1985). "Bulimia and depression". Psychosomatic Medicine. 47 (2): 123–31. PMID 3863157.
- ^ a b Patton, G. C.; Coffey, C.; Carlin, J. B.; Sanci, L.; Sawyer, S. (2008). "Prognosis of adolescent partial syndromes of eating disorder". The British Journal of Psychiatry. 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, Josefina; Gual, Pilar; Lahortiga, Francisca; Gila, Araceli; Casulà, Vanesa; Fuhrmann, Cynthia; Imirizaldu, Milagros; Saura, Begoña; Martínez, Esteve; Toro, Josep (2007). "Self-oriented perfectionism in eating disorders". International Journal of Eating Disorders. 40 (6): 562–568. doi:10.1002/eat.20393. PMID 17510925.
{{cite journal}}
: Unknown parameter|displayauthors=
ignored (|display-authors=
suggested) (help); Unknown parameter|month=
ignored (help) - ^ Walsh, Judith M. E.; Wheat, Mary E.; Freund, Karen (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.
{{cite book}}
:|access-date=
requires|url=
(help); External link in
(help); Unknown parameter|chapterurl=
|chapterurl=
ignored (|chapter-url=
suggested) (help) - ^ 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.
{{cite web}}
: Check date values in:|accessdate=
(help) - ^ Ribasés, Marta; Gratacòs, Mònica; Fernández-Aranda, Fernando; Bellodi, Laura; Boni, Claudette; Anderluh, Marija; Cavallini, Maria Cristina; Cellini, Elena; Di Bella, Daniela; Erzegovesi, Stefano; Foulon, Christine; Gabrovsek, Mojca; Gorwood, Philip; Hebebrand, Johannes; Hinney, Anke; Holliday, Jo; Hu, Xun; Karwautz, Andreas; Kipman, Amélie; Komel, Radovan; Nacmias, Benedetta; Remschmidt, Helmut; Ricca, Valdo; Sorbi, Sandro; Wagner, Gudrun; Treasure, Janet; Collier, David A.; Estivill, Xavier (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.
{{cite journal}}
: Unknown parameter|displayauthors=
ignored (|display-authors=
suggested) (help) - ^ 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.
{{cite book}}
: Unknown parameter|displayeditors=
ignored (|display-editors=
suggested) (help) - ^ Hirschberg, Angelica Lindén (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, Allegra; Shingleton, Rebecca; Kaufman, Jenna; Liu, Fei; Kumar, Dileep; Slifstein, Mark; Abi-Dargham, Anissa; Schebendach, Janet; Van Heertum, Ronald; Attia, Evelyn; Martinez, Diana; Walsh, B. Timothy (2012). "Striatal dopamine in bulimia nervosa: A pet imaging study". International Journal of Eating Disorders. 45 (5): 648–656. doi:10.1002/eat.20984. PMC 3640453. PMID 22331810.
{{cite journal}}
: Unknown parameter|displayauthors=
ignored (|display-authors=
suggested) (help); Unknown parameter|month=
ignored (help) - ^ Kaye, Walter H.; Wierenga, Christina E.; Bailer, Ursula F.; Simmons, Alan N.; Wagner, Angela; Bischoff-Grethe, Amanda (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, Katharine A.; 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, A. E.; 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. 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, Susan M.; McLean, Neil J. (2002). "The cognitive-behavioral model of bulimia nervosa: A direct evaluation". International Journal of Eating Disorders. 31 (1): 17–31. doi:10.1002/eat.10002. PMID 11835294.
- ^ 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, Esther K.; Nicolaije, Kim A.H. (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. 6 (3): 49. PMC 1435625. PMID 15520673.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ Hay, Phillipa J.; Mond, Jonathan; Buttner, Petra; Darby, Anita (2008). Murthy, R. Srinivasa (ed.). "Eating Disorder Behaviors Are Increasing: Findings from Two Sequential Community Surveys in South Australia". PLoS ONE. 3 (2): e1541. doi:10.1371/journal.pone.0001541. PMC 2212110. PMID 18253489.
{{cite journal}}
: CS1 maint: unflagged free DOI (link) - ^ Gelder, Michael Graham; Mayou, Richard; Geddes, John (2005). Psychiatry. ISBN 978-0-19-852863-0.[page needed]
- ^ Van Son, G. E.; Van Hoeken, D.; Bartelds, A. I. M.; Van Furth, E. F.; Hoek, H. W. (2006). "Urbanisation and the incidence of eating disorders". The British Journal of Psychiatry. 189 (6): 562–3. doi:10.1192/bjp.bp.106.021378. PMID 17139044.
- ^ "Bulimia".
- ^ Grohol, John (March 19, 2009). "Black Girls At Risk for Bulimia".
- ^ a b 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, Debra L.; Becker, Anne E.; Thomas, Jennifer J.; Herzog, David B. (2007). "Cross-ethnic differences in eating disorder symptoms and related distress". 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".
- ^ Hoste, Renee Rienecke; Labuschagne, Zandre; Grange, Daniel (2012). "Adolescent Bulimia Nervosa". Current Psychiatry Reports. 14 (4): 391–7. doi:10.1007/s11920-012-0280-0. PMID 22614677.
- ^ Agras, W. Stewart; 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.
- ^ Gelder, Michael Graham; Mayou, Richard; Geddes, John (2005). Psychiatry. ISBN 978-0-19-852863-0.[page needed]
- ^ Agras, W. S.; 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". American Journal of Psychiatry. 157 (8): 1302–8. doi:10.1176/appi.ajp.157.8.1302. PMID 10910795.
- ^ Wilson, G. Terence; Loeb, Katharine L.; Walsh, B. Timothy; Labouvie, Erich; Petkova, Eva; Liu, Xinhua; Waternaux, Christine (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, Mary Ellen; Rockwell, Roxanne E; Curry, Elise; Runfola, Cristin; Kaye, Walter H (2007). "Management of bulimia nervosa". Women's Health. 3 (2): 255–65. doi:10.2217/17455057.3.2.255. PMID 19803857.
- ^ Fairburn, C. G.; Agras, WS; Walsh, BT; Wilson, GT; Stice, E (2004). "Prediction of Outcome in Bulimia Nervosa by Early Change in Treatment". American Journal of Psychiatry. 161 (12): 2322–4. doi:10.1176/appi.ajp.161.12.2322. PMID 15569910.
- ^ Safer, D. L.; Telch, CF; Agras, WS (2001). "Dialectical Behavior Therapy for Bulimia Nervosa". American Journal of Psychiatry. 158 (4): 632–4. doi:10.1176/appi.ajp.158.4.632. PMID 11282700.
- ^ Lock, James; Le Grange, Daniel (2005). "Family-based treatment of eating disorders". International Journal of Eating Disorders. 37: S64–7, discussion S87–9. doi:10.1002/eat.20122. PMID 15852323.
- ^ a b c Keel, Pamela K.; Haedt, Alissa (2008). "Evidence-Based Psychosocial Treatments for Eating Problems and Eating Disorders". Journal of Clinical Child & Adolescent Psychology. 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, Josefina; Bigorra, Aitana; Martinez-Mallen, Esteve; Gonzalez, Laura; Moreno, Elena; Font, Elena; Toro, Josep (2011). "Motivation to change in adolescents with bulimia nervosa mediates clinical change after treatment". European Eating Disorders Review. 19 (1): 46–54. doi:10.1002/erv.1045. PMID 20872926.
- ^ Martinez-Mallén, Esteban; Castro-Fornieles, Josefina; Lázaro, Luisa; Moreno, Elena; Morer, Astrid; Font, Elena; Julien, Joana; Vila, Montserrat; Toro, Josep (2007). "Cue exposure in the treatment of resistant adolescent bulimia nervosa". 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. 37 (1–4): 53–6. PMID 2246105.
- ^ Barabasz, Marianne (2007). "Efficacy of Hypnotherapy in the Treatment of Eating Disorders". 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, A. James; Colapietro, Gale; Leskovac, Nancy; Keller, Michelle; Melemis, Steven M.; Timcisko, Terri (1998). "Comparison of Alternative Treatment Techniques in Bulimia: The Chemical Dependency Approach". Psychological Reports. 82 (2): 451–8. doi:10.2466/pr0.1998.82.2.451. PMID 9621718.
- ^ Mitchell, James E.; Raymond, Nancy; Specker, Sheila (1993). "A review of the controlled trials of pharmacotherapy and psychotherapy in the treatment of bulimia nervosa". 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; Fairburn (eds.). Eating Disorders and Obesity: A Comprehensive Handbook. New York: Guilford. pp. 329–40. ISBN 978-0-89862-850-0.
{{cite book}}
:|editor2-first=
missing|editor2-last=
(help) - ^ Mitchell, James E.; Christenson, Gary; Jennings, Jeffrey; Huber, Marguerite; Thomas, Brenda; Pomeroy, Claire; Morley, John (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, Paulo P.P.; Machado, Barbara C.; Gonçalves, Sónia; Hoek, Hans W. (2007). "The prevalence of eating disorders not otherwise specified". International Journal of Eating Disorders. 40 (3): 212–7. doi:10.1002/eat.20358. PMID 17173324.
- ^ Vilela, João E. M; Lamounier, Joel A; Dellaretti Filho, Marcos A; Barros Neto, José R; Horta, Gustavo M (2004). "Transtornos alimentares em escolares". Jornal de Pediatria (in Portuguese). 80 (1): 49–54. doi:10.1590/S0021-75572004000100010. PMID 14978549.
{{cite journal}}
: Unknown parameter|trans_title=
ignored (|trans-title=
suggested) (help) - ^ Lahortiga-Ramos, Francisca; De Irala-Estévez, Jokin; Cano-Prous, Adrián; Gual-García, Pilar; Martínez-González, Miguel Ángel; Cervera-Enguix, Salvador (2005). "Incidence of eating disorders in Navarra (Spain)". European Psychiatry. 20 (2): 179–85. doi:10.1016/j.eurpsy.2004.07.008. PMID 15797704.
- ^ Hay, Phillipa (1998). "The epidemiology of eating disorder behaviors: An Australian community-based survey". 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, A. R.; Vernon, S. W.; Lee, E. S. (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, K. Gunnar; Eriksen, Lasse; Hagen, Helge (1995). "An epidemiological study of eating disorders in Norwegian psychiatric institutions". 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; et al. (1995). "Bulimia nervosa in a Canadian community sample: prevalence and comparison of subgroups". The American Journal of Psychiatry. 152 (7): 1052–8. PMID 7793442.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Suzuki, Kenji; Takeda, AYA; Matsushita, Sachio (1995). "Coprevalence of bulimia with alcohol abuse and smoking among Japanese male and female high school students". Addiction. 90 (7): 971–5. doi:10.1111/j.1360-0443.1995.tb03506.x. PMID 7663319.
- ^ Heatherton TF, Nichols P, Mahamedi F, Keel P (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.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link)