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Bulimia nervosa

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Bulimia nervosa
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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 or diuretic, and/or excessive exercise. Some individuals may tend to alternate between bulimia nervosa and anorexia nervosa. These acts are also commonly accompanied with fasting over an extended period of time.[1][2] It is often associated with negative emotions such as guilt and self-loathing. Bulimia nervosa is considered to be less life threatening than anorexia; however, the occurrence of bulimia nervosa is higher.[3] Bulimia nervosa is nine times more likely to occur in women than men (Barker 2003). The vast majority of those with bulimia nervosa are at normal weight.[4] Antidepressants, especially SSRIs, are widely used in the treatment of bulimia nervosa (Newell and Gournay 2000).

The term bulimia comes from Greek βουλιμία (boulīmia; ravenous hunger), a compound of βους (bous), ox + λιμός (līmos), hunger.[5] Bulimia nervosa was named and first described by the British psychiatrist Gerald Russell in 1979.[6][7] Bulimia is strongly familial. Twin studies estimate the heritability of syndromic bulimia to be 54-83%.[8][9]

Nearly all individuals with bulimia nervosa also have an additional psychiatric disorder.[10] Common comorbidities are mood disorders, anxiety, impulse control, and substance-misuse disorders.[10] 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.[11]

The overwhelming majority (90-95 percent) of individuals with bulimia are women.[12] Males do develop the disorder. However, they 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, are another large group of males with eating disorders. 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. Over the years the size and weight of the average woman has increased with improved nutrition. Over the years 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:

The erosion on the lower teeth was caused by Bulimia. For comparison, the upper teeth were restored with porcelain veneers.[17]

The frequent contact between teeth and gastric acid, in particular, may cause:

Signs

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
  • depression

[21] 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.[22]

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.[22]

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.[23] Another study by the Royal Children's Hospital in Melbourne on a cohort of 2000 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.[24] 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.[25] 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.[26] Bulimia nervosa may affect up to 1% of young woman and after 10 years of diagnosis, half will recover fully, a third will recover partially, and 10-20% will still have symptoms.[27]

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.[28]

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.[29] 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.[30] 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.[31]

Causes

Biological

Like with anorexia nervosa, there is evidence of genetic predispositions contributing to the onset of this eating disorder.[32] 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.[33][34]

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.[35]

Social

Media portrayals of an 'ideal' body shape are widely considered to be a contributing factor to bulimia[1] (Barker 2003). 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.[36] 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.[37]

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 and 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.[38][39]

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.[40]

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.[41]

Superscript text==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.[42] Studies on time trends in the prevalence of bulimia nervosa have also yielded inconsistent results.[43] 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 (Gelder, Mayou and Geddes 2005). There is a perception that bulimia is most prevalent amongst girls from middle-class families,[44] 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.[45]

Treatment

The treatment of this complex disorder is very critical, and thus the treatment providers should have expertise in eating disorders and adolescence health. There are two main types of treatment given to those suffering with bulimia nervosa; psychopharmacological and psychosocial treatments.[46]

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.[47] 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 (Gelder, Mayou and Geddes 2005). 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.[48][49] Patients undergoing CBT who exhibit early behavioral changes are most likely to achieve the best treatment outcomes in the long run.[50] Researchers have also reported some positive outcomes for interpersonal psychotherapy and dialectical behavior therapy.[51][52]

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.[53]

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.[54] 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.[55] Therefore, young adolescents with BN are less likely to realize the detrimental consequences of becoming bulimic and have less motivation to change,[56] which is why FBT would be useful to have families intervene and support the teens.[54] 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.[54]

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.[57] 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.[58][59][60] [61] 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.[62]

Pharmacological treatment

Some researchers have hypothesized a relationship to mood disorders and clinical trials have been conducted with tricyclic antidepressants,[63] MAO inhibitors, mianserin, fluoxetine,[64] 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.[65]

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.[66]

Country Year Sample size and type Incidence
Australia 2008 1,943 adolescents (ages 15–17) 1.0% male 6.4% female[24]
Portugal 2006 2,028 high school students 0.3% female[67]
Brazil 2004 1,807 students (ages 7–19) 0.8% male 1.3% female[68]
Spain 2004 2,509 female adolescents (ages 13–22) 1.4% female[69]
Hungary 2003 580 Budapest residents 0.4% male 3.6% female[70]
Australia 1998 4,200 high school students 0.3% combined[71]
USA 1996 1,152 college students 0.2% male 1.3% female[72]
Norway 1995 19,067 psychiatric patients 0.7% male 7.3% female[73]
Canada 1995 8,116 (random sample) 0.1% male 1.1% female[74]
Japan 1995 2,597 high school students 0.7% male 1.9% female[75]
USA 1992 799 college students 0.4% male 5.1% female[76]

There are higher rates of eating disorders in groups involved in activities which idealize a slim physique, such as dance,[70] gymnastics, modeling, cheerleading, running, acting, swimming, diving, rowing and figure skating. Bulimia is thought to be more prevalent among Caucasians.,[77] 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.[78]

Further reading

For individuals and families being affected by bulimia nervosa, the following resources might be very helpful: http://www.nationaleatingdisorders.org/ http://www.eatingdisorders.org.au/ http://www.oa.org/ http://helpguide.org/mental/bulimia_signs_symptoms_causes_treatment.htm

See also

Wikimedia Commons has media related to Bulimia nervosa.

Notes

  1. ^ a b Barker, P (2003) Psychiatric and Mental Health Nursing: The Craft of Caring Arnold, Great Britain.
  2. ^ Fairburn, Christopher G. (1995). Overcoming binge eating. New York: Guilford Press. ISBN 0-89862-179-8.[page needed]
  3. ^ Manning, Y., & Murphy, B. (2003). An introduction to anorexia nervosa and bulimia nervosa.Nursing Standard, 18.14-16, 45. Academic OneFile Retrieved April 9, 2012,from http://go.galegroup.com.myaccess.library.utoronto.ca/ps/i.do?id=GALE%7CA112313754&v=2.1&u=utoronto_main&it=r&p=AONE&sw=w
  4. ^ "Bulimia nervosa". Yager,J. 2012. {{cite web}}: Unknown parameter |month= ignored (help)
  5. ^ Douglas Harper (2001). "Online Etymology Dictionary: bulimia". Online Etymology Dictionary. Retrieved 2008-04-06. {{cite web}}: Unknown parameter |month= ignored (help)
  6. ^ Russell G (1979). "Bulimia nervosa: an ominous variant of anorexia nervosa". Psychological Medicine. 9 (3): 429–48. doi:10.1017/S0033291700031974. PMID 482466. {{cite journal}}: Unknown parameter |month= ignored (help)
  7. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)
  8. ^ Kendler KS; MacLean, C; Neale, M; Kessler, R; Heath, A; Eaves, L (1991). "The genetic epidemiology of bulimia nervosa". American Journal of Psychiatry. 148 (8): 1627–37. PMID 1842216. {{cite journal}}: Unknown parameter |month= ignored (help)
  9. ^ Bulik CM; Sullivan, PF; Kendler, KS (1998). "Heritability of binge-eating and broadly defined bulimia nervosa". The Biological Psychiatry. 44 (12): 1210–8. doi:10.1016/S0006-3223(98)00280-7. PMID 9861464. {{cite journal}}: Unknown parameter |month= ignored (help)
  10. ^ a b Phillipa J Hay, Angélica Medeiros Claudino (2010). "Bulimia nervosa". Clin Evid (Online). PMCID: PMC3275326. {{cite journal}}: Unknown parameter |month= ignored (help)
  11. ^ Yager, J. (1991). Bulimia Nervosa. The Western Journal of Medicine, 155(5), 523. Retrieved March 17, 2012, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1003077/
  12. ^ David Barlow and Mark Durand: Abnormal Psychology: An Integrative Approach
  13. ^ Barlow, D. H., and V. M. Durand. Abnormal psychology: An integrative approach. 6th. Belmont, CA: Wadsworth, Cengage Learning, 2011. Print.
  14. ^ Eating Disorders. Let's Talk About. American Psychiatric Association. 2005. ISBN 0-89042-352-0.
  15. ^ Joseph AB, Herr B (1985). "Finger calluses in bulimia". The American Journal of Psychiatry. 142 (5): 655. PMID 3857013. {{cite journal}}: Unknown parameter |month= ignored (help)
  16. ^ Wynn DR, Martin MJ (1984). "A physical sign of bulimia". Mayo Clinic Proceedings. Mayo Clinic. 59 (10): 722. PMID 6592415. {{cite journal}}: Unknown parameter |month= ignored (help)
  17. ^ Dorfman J, The Center for Special Dentistry.
  18. ^ a b "Eating Disorders". Oral Health Topics A–Z. American Dental Association.
  19. ^ Mcgilley BM, Pryor TL (1998). "Assessment and treatment of bulimia nervosa". American Family Physician. 57 (11): 2743–50. PMID 9636337. {{cite journal}}: Unknown parameter |month= ignored (help)
  20. ^ Mehler, Philip S. . "Bulimia Nervosa." The New England Journal of Medicine. N.p., 28 Aug. 2003. Web. 1 Dec. 2012. <http://bf4dv7zn3u.search.serialssolutions.com.myaccess.library.utoronto.ca/?ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info:sid/summon.serialssolutions.com&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Clinical+practice.+Bulimia+nervosa&rft.jtitle=The+New+England+journal+of+medicine&rft.au=Mehler%2C+Philip+S&rft.date=2003-08-28&rft.issn=1533-4406&rft.volume=349&rft.issue=9&rft.spage
  21. ^ Mercury, Illawarra. "Symptoms Of Bulimia Nervousa". Retrieved Aug 20 2012. {{cite web}}: Check date values in: |accessdate= (help)
  22. ^ a b Barker, P (2003) Psychiatric and Mental Health Nursing: The Craft of Caring, Arnold, Great Britain.
  23. ^ Walsh BT, Roose SP, Glassman AH, Gladis M, Sadik C (1985). "Bulimia and depression". Psychosomatic Medicine. 47 (2): 123–31. PMID 3863157.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ a b Patton GC, Coffey C, Carlin JB, 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  25. ^ Carlson, N.R., et al. (2007). Psychology: The Science of Behaviour - 4th Canadian ed.. Toronto, ON: Pearson Education Canada.
  26. ^ Shader, Richard I. (2004). Manual of Psychiatric Therapeutics. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-4459-8.[page needed]
  27. ^ Hay PJ, Bacaltchuk J. "Bulimia nervosa" (PDF). {{cite journal}}: Cite journal requires |journal= (help)
  28. ^ "Self-Oriented Perfectionism in Eating Disorders". International Journal of Eating Disorders. 40 (6): 562–568. 2. doi:10.1002/eat.20393. Retrieved 12 February 2012. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  29. ^ Walsh JM, Wheat ME, Freund K (2000). "Detection, evaluation, and treatment of [[eating disorder]]s the role of the primary care physician". Journal of General Internal Medicine. 15 (8): 577–90. doi:10.1046/j.1525-1497.2000.02439.x. PMC 1495575. PMID 10940151. {{cite journal}}: URL–wikilink conflict (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  30. ^ 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 |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)
  31. ^ Barlow, David H.; Durand, Vincent Mark (2002). Abnormal psychology: an integrative approach. Belmont, CA: Wadsworth/Thomson Learning. ISBN 0-534-63362-5.[page needed]
  32. ^ "Biological Causes of Anorexia Nervosa and Bulimia Nervosa". Retrieved 3 April. {{cite web}}: Check date values in: |accessdate= (help)
  33. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1093/hmg/ddh137, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1093/hmg/ddh137 instead.
  34. ^ "1". Annual Review of Eating Disorders – part 2 (PDF). 2008. pp. 14–15. ISBN 978-1-84619-244-9.
  35. ^ Hirschberg, Angelica L. (2011). "Sex hormones, appetite and eating behaviour in women". Elsevier. 71 (1): 248–256. doi:10.1016/j.maturitas.2011.12.016. {{cite journal}}: Unknown parameter |month= ignored (help)
  36. ^ Carlson, N. (2007). Psychology: the science of behaviour-4th Canadian ed. Toronto, ON: Pearson Education Canada. p. 415. ISBN 978-0-205-64524-4. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  37. ^ 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. 180 (6): 509–14. doi:10.1192/bjp.180.6.509. PMID 12042229. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  38. ^ Trull, Thimothy. Abnormal Psychology and Life: A Dimensional Approach. 20 Davis Drive Belmont, CA: Wadsworth, Cengage Learning. pp. 236–238. ISBN ISBN 978-1-111-34376-7. {{cite book}}: Check |isbn= value: invalid character (help)CS1 maint: location (link)
  39. ^ Byrne, S. M., & McLean, N. J. (2002). The cognitive-behavioral model of bulimia nervosa: A direct evaluation. International Journal of Eating Disorders, 31, 17-31.
  40. ^ Zieve, David. "Bulimia". PubMed Health. Retrieved April 18, 2011.
  41. ^ Thompson, Kevin (2001). "Eating Pathology Thin-Ideal Internalization: Mounting Evidence for a New Risk Factor for Body-Image Disturbance and". Current Directions in Psychological Science. 10: 181–183. doi:10.1111/1467-8721.00144. Retrieved October 3, 2011. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  42. ^ 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)
  43. ^ Hay PJ, Mond J, Buttner P, Darby A (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: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  44. ^ "Bulimia".
  45. ^ Grohol, John (March 19, 2009). "Black Girls At Risk for Bulimia".
  46. ^ "Adolescent Bulimia Nervosa". Curr Psychiatry Rep. 14: 391–397. 2012. doi:10.1007/s11920-012-0280-0. {{cite journal}}: Unknown parameter |authors= ignored (help)
  47. ^ Agras, MD, W. Stewart (2005). "A Multicenter Comparison of Cognitive-Behavioral Therapy and Interpersonal Psychotherapy for Bulimia Nervosa". Arch Gen Psychiatry. 57. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  48. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  49. ^ Wilson GT, Loeb KL, Walsh BT; et al. (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. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  50. ^ Curry E, Kaye WH, Rockwell RE, Runfola C, Trunko ME. "Management of bulimia nervosa". Women's Health London. 3 (2).{{cite journal}}: CS1 maint: multiple names: authors list (link)
  51. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  52. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  53. ^ Lock J, le Grange D (2005). "Family-based treatment of eating disorders". The International Journal of Eating Disorders. 37. Suppl (S1): S64–7, discussion S87–9. doi:10.1002/eat.20122. PMID 15852323.
  54. ^ a b c "Evidence-Based Psychosocial Treatments for Eating Problems and Eating Disorders". Journal of Clinical Child & Adolescent Psychology. 37 (1): 39–61. 2008. doi:10.1080/15374410701817832. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  55. ^ Le Grange, Daniel (2010). "Family-Based Treatment for Adolescents with Bulimia Nervosa". The Australian and New Zealand Journal of Family Therapy. 31 (2): 165–175. {{cite journal}}: |access-date= requires |url= (help)
  56. ^ "Motivation to change in adolescents with bulimia nervosa mediates clinical change after treatment". European Eating Disorders Review. 19: 46–54. 27. doi:10.1002/erv.1045. Retrieved 12 February 2012. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  57. ^ "Cue Exposure in the Treatment of Resistant Adolescent Bulimia Nervosa". International Journal of Eating Disorders. 40 (7): 596–601. 2. doi:10.1002/eat.20423. Retrieved 20 February 2012. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  58. ^ 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.
  59. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)
  60. ^ Griffiths RA (1995). "Two-Year Follow-Up Findings of Hypnobehavioural Treatment for Bulimia Nervosa". Australian Journal of Clinical and Experimental Hypnosis. 23 (2): 135–44.
  61. ^ Kraft T, Kraft D (2009). The Place of Hypnosis in Psychiatry, Part 3: the Application to the Treatment of Eating Disorders' Australian Journal of Clinical and Experimental Hypnosis, 37, (1): 1-20.
  62. ^ AJ Giannini,M Keller,G Colapietro, SM Melemis, N Leskovak, T Timcisko. (1998) Comparison of alternative treatment techniques in bulimia; the chemical dependency approach. Psychological Reports. 82(2):451-8.PMID 9621718
  63. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  64. ^ 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)
  65. ^ Mitchell JE, Christenson G, Jennings J; et al. (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. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  66. ^ Slaby, Andrew Edmund (1993). The eating disorders. Berlin: Springer-Verlag. ISBN 0-387-94002-2.[page needed]
  67. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  68. ^ Vilela JE, Lamounier JA, Dellaretti Filho MA, Barros Neto JR, Horta GM (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)CS1 maint: multiple names: authors list (link)
  69. ^ 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. 20 (2): 179–85. doi:10.1016/j.eurpsy.2004.07.008. PMID 15797704. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  70. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)
  71. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)
  72. ^ 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. PMID 8781459. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  73. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  74. ^ 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)
  75. ^ Suzuki K, Takeda A, Matsushita S (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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  76. ^ 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)
  77. ^ 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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  78. ^ McBride, Hugh. "Study Reveals Stunning Prevalence of Bulimia Among African-American Girls".
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