Surgery for Obesity and Impact on Disordered · Eating ... Bariatric surgery has been effective for treatment of severe obesity ..... As guiding principles for the revision .... Statistical Manual of Mental Disorders (4th Ed.). ...... concerns (e.g., facial features) to assist the diag- nosis. ...... Set Your Body Free, a CBT intervention eval-.
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Bariatric surgery includes a number of different procedures to help individuals with severe obesity lose weight. The most common procedures in use include gastric bypass, sleeve gastrectomy, and adjustable gastric banding.
and motivated patients with a BMI>40 kg/m2 or for individuals with a BMI of 35–40 kg/m2 and significant obesity-related comorbidities like type 2 diabetes mellitus, obstructive sleep apnea, or hypertension. Patient selection involves a multidisciplinary screening process including medical, nutritional, and psychological evaluations. Many patients are also required to document completion of a physician-supervised diet and lifestyle modification program. Bariatric surgery includes a range of different procedures. All procedures restrict gastric capacity to reduce food intake (e.g., gastric sleeve, adjustable gastric banding). Some procedures also alter the digestive tract to cause malabsorption (e.g., Rouxen-Y gastric bypass). In the general adult population, outcomes vary across patients and procedures. Patients who undergo bariatric surgery with an experienced surgeon in a high-volume hospital have lower mortality and fewer complications. Most individuals experience maximum weight loss within the first year post-surgery. In the longer term, many regain some of the weight that they initially lost. Post-surgery weight and maintenance are best when accompanied by healthy lifestyle changes and lifelong follow-up.
Context
Screening and Approval for Surgery
Bariatric surgery has been effective for treatment of severe obesity after nonsurgical approaches have failed. It is considered for well-informed
The routine screening and approval process includes a psychological evaluation and clearance by a licensed mental health professional. The
Bariatric (Weight Loss) Surgery ▶ Surgery for Obesity and Impact on Disordered Eating
Bariatric Surgery Melissa Kalarchian School of Nursing, Duquesne University, Pittsburgh, PA, USA
Synonyms Weight loss surgery
Definition
# Springer Nature Singapore Pte Ltd. 2017 T. Wade (ed.), Encyclopedia of Feeding and Eating Disorders, DOI 10.1007/978-981-287-104-6
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psychological evaluation is not standardized, and providers vary in how they assess candidates for bariatric surgery. Typical evaluations address weight and dieting history; psychopathology, including eating disorders; social supports; and knowledge about surgery. In addition to a clinical interview, some providers utilize psychological testing. Testing may include measures of eating pathology, mood, substance use, personality, and/or cognitive functioning. However, many tests lack well-established psychometrics or norms specifically for this patient population. The vast majority of candidates are cleared for bariatric surgery on the basis of the psychological evaluation. For a relatively small proportion of individuals, bariatric surgery is denied or delayed on the basis of the psychological evaluation. Typical reasons for denial included severe, uncontrolled psychiatric disorders (e.g., bipolar disorder) or a lack of understanding of the surgery (e.g., inability to provide informed consent). With respect to eating disorders, it should be noted that binge eating is relatively common among individuals seeking treatment of obesity. Presurgery binge eating disorder tends to improve after surgery and does not attenuate post-surgery weight loss. Thus, binge eating disorder is not considered a contraindication to bariatric surgery per se. Providers who screen and approve candidates for bariatric surgery should keep abreast of best practices in an evolving field. The American Society for Metabolic and Bariatric Surgery (ASMBS), the largest national society for this specialty, issues guidelines and recommendations, as well as position and consensus statements, relevant to all aspects of bariatric surgery (asmbs. org). In 2015, the ASMBS Integrated Health Clinical Issues and Guidelines Committee is currently updating its recommendations for the presurgery psychosocial evaluation.
Changes in Eating, Body Weight, and Nutrition Patients are placed on a liquid diet immediately following bariatric surgery. As solid foods are gradually reintroduced, patients are instructed to
Bariatric Surgery
limit portions, chew well, and stop as soon as they feel full. Eventually most individuals are able to consume small quantities of a range of healthy foods. Eating too much at one time or too quickly can lead to gastrointestinal symptoms like nausea and vomiting. For some, severe and persistent vomiting may contribute to the development of nutritional complications like low iron, B12, or folic acid. Eating patterns such as frequent snacking on high-calorie foods can contribute to inadequate initial weight loss or significant regain. Technical problems with the surgical procedure can also lead to complications. Patients presenting with poor weight outcomes following bariatric surgery should undergo medical, nutritional, and psychological evaluations. This includes anatomic evaluation of the gastrointestinal tract using upper gastrointestinal endoscopy and radiology. Depending on the results, some patients may be deemed candidates for a subsequent surgical procedure, known as revisional or reoperative bariatric surgery. It should be noted that revisional bariatric surgery has been associated with lesser weight loss and greater complications than initial procedures. Other patients may be referred for behavioral treatment of obesity or eating disorders.
Post-surgery Eating Disorders Providers who assess and treat problems with eating and weight following bariatric surgery should have accurate knowledge about bariatric surgery and experience with this patient population. However, even among experts, there has not been consensus as to how to conceptualize and assess eating disorders after bariatric surgery. The development of full-syndrome eating disorders like anorexia nervosa, bulimia nervosa, or binge eating disorder is uncommon after bariatric surgery. With respect to binge eating episodes, patients are generally unable to consume objectively large amounts of food at one time due to a reduced gastric capacity. Nonetheless, some individuals report the onset or persistence of episodes of loss of control over eating. (Loss of control is the subjective experience that an individual
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cannot control what or how much one is eating, independent of the amount consumed.) A relatively large body of evidence now suggests that patients who experience recurrent loss of control over eating post-surgery have poorer weight outcomes. Thus, post-surgery loss of control over eating may warrant clinical intervention. Apart from loss of control over eating, there is a dearth of information on other types of disordered eating that may occur following bariatric surgery. One example is grazing, which is generally characterized by a repetitive eating pattern of smaller amounts throughout the day. Another example is night eating, which is marked by evening hyperphasia and/or nocturnal awakening to eat. Definitions and terminology have varied, and standardized instruments designed specifically for the assessment of bariatric surgery patients are lacking.
Future Directions
Current Controversies
Cross-References
There has been debate about whether or not the psychological evaluation or physician-supervised diet should serve a gatekeeping function to determine who can or cannot proceed to surgery. It is important to keep in mind that no robust presurgery predictors of post-surgery outcomes have emerged from the literature. Moreover, there is a lack of effective nonsurgical treatments for severe obesity. Ultimately, candidates and their health-care providers must weigh the potential benefits and risks of bariatric surgery. Another controversy has been the use of bariatric surgery in patients with a BMI below 35 kg/m2 for treatment of type 2 diabetes. Increasingly, studies show that bariatric surgery can be an effective treatment for type 2 diabetes in carefully screened patients for whom nonsurgical management has not been effective. Finally, some have expressed concern about the increasing use of bariatric surgery in youth. Current evidence suggests that extremely obese teens who have achieved their adult stature can experience weight loss and improvements in health following surgery. Nonetheless, questions and concerns persist about the potential long-term impact on growth and development.
▶ Obesity ▶ Obesity and Eating Disorders ▶ Purpose of Assessment
Bariatric surgery is a rapidly changing field. Emerging research suggests that post-surgery weight loss is related to a complex interplay of neuronal, hormonal, cognitive, and behavioral factors. In the future, a more complete understanding of mechanisms underlying changes in eating and body weight following the different procedures will improve our ability to optimize patient outcomes. More research is needed on how to define and treat eating disorders in bariatric surgery patients. Assessments should include not only loss of control over eating but also a broad range of eating behaviors and other factors considered important by patients and providers. Hypothesis-driven, prospective studies of large, diverse samples of bariatric surgery patients will help move the field forward.
References and Further Reading Conceição, E. M., Mitchell, J. E., Engel, S. G., Machado, P. P. P., Lancaster, K., & Wonderlich, S. A. (2014). What is “grazing”? Reviewing its definition, frequency, clinical characteristics, and impact on bariatric surgery outcomes, and proposing a standardized definition. Surgery for Obesity and Related Diseases, 10(5), 973–982. Greenberg, I., Sogg, S., & M Perna, F. (2009). Behavioral and psychological care in weight loss surgery: Best practice update. Obesity, 17(5), 880–884. Kalarchian, M. A., Marcus, M. D., Courcoulas, A. P., Cheng, Y., & Levine, M. D. (2014). Self-report of gastrointestinal side effects after bariatric surgery. Surgery for Obesity and Related Diseases, 10(6), 1202–1207. Meany, G., Conceição, E., & Mitchell, J. E. (2014). Binge eating, Binge eating disorder and loss of control eating: Effects on weight outcomes after bariatric surgery. European Eating Disorders Review, 22(2), 87–91. Mitchell, J. E., King, W. C., Courcoulas, A., Dakin, G., Elder, K., Engel, S., . . . Wolfe, B. (2015). Eating behavior and eating disorders in adults before bariatric surgery. International Journal of Eating Disorders, 48(2), 215–222.
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52 Parker, K., O’Brien, P., & Brennan, L. (2014). Measurement of disordered eating following bariatric surgery: A systematic review of the literature. Obesity Surgery, 24(6), 945–953. Wadden, T. A., Faulconbridge, L. F., Jones-Corneile, L. R., Sarwer, D. B., Fabricatore, A. N., Thomas, J. G., . . . Williams, N. N. (2011). Binge eating disorder and the outcome of bariatric surgery at one year: A prospective, observational study. Obesity, 19(6), 1220–1228.
Behavioral Affective Response ▶ Emotion Expression in Individuals with Feeding and Eating Disorders
Binge Eating Disorder ▶ Bipolar Disorder and Eating Disorders ▶ Eating Disorder Questionnaire (EDQ) ▶ Impact of Psychiatric Comorbidity on Eating Disorder Outcomes ▶ Starvation in Children, Adolescents, and Young Adults: Relevance to Eating Disorders ▶ Substance-Related Disorders in Eating Disorders
Binge Eating Scale (BES) Elizabeth W. Cotter1 and Nichole R. Kelly2,3 1 Department of Health Studies, American University, Washington, DC, USA 2 Department of Human Development and Family Studies, Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development Colorado State University, Bethesda, MD, USA 3 Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
Synonyms Loss of control eating; Objective binge eating
Behavioral Affective Response
Definition The binge eating scale (BES) is a 16-item selfreport questionnaire designed to capture the behavioral (eight items, e.g., large amount of food consumed), as well as the cognitive and emotional (eight items, e.g., feeling out of control while eating, preoccupation with food and eating), features of objective binge eating (OBE) in overweight and obese adults (Gormally et al. 1982). For each item, respondents are asked to select one of three or four response options, coded zero to two or three, respectively. Individuals’ scores are summed and range from 0 to 46, with higher scores indicating more severe binge eating problems. Marcus et al. (1988) created clinical cutoff scores for the BES representing none-to-minimal (27) binge eating problems. Importantly, the BES was created before binge eating disorder (BED) was officially recognized as a psychiatric diagnosis (American Psychiatric Association 2013) and thus is not intended to detect the presence of this disorder. Rather, it has been suggested that this measure be used as a brief screening tool to identify the severity of binge eating behavior in overweight and obese adults, to tailor obesity interventions, and to track treatment outcomes (Gormally et al. 1982; Marcus et al. 1988). Although the BES has been used with children and adolescents sparingly, we only present data from adults in this chapter, as this measure was created specifically for this age group.
Reliability Estimated internal consistency of the measure is generally acceptable (Cronbach’s alphas were reported above .8) across samples, including men and women from the community, college students, treatment-seeking adults, racially/ethnically diverse groups, and adults from the United States and abroad (e.g., Celio et al. 2004; Freitas et al. 2006; Kelly et al. 2012; Minnich et al. 2014; Ricca et al. 2000; Timmerman 1999). Adequate test-retest reliability has also been reported among adult females’ samples over a ~2-week interval (e.g., Timmerman 1999).
Binge Eating Scale (BES)
Validity
Factor Structure The initial development of the scale (Gormally et al. 1982) yielded two eightitem factors representing the behavioral and cognitive/emotional aspects of binge eating. More recent examinations of the scale (e.g., Kelly et al. 2012) further support this two-factor solution, suggesting that the existing subscales remain appropriate across a range of samples. Of interest, Kelly et al. reported measurement invariance between White/Caucasian and Black/African American female college samples, suggesting that, while the same two-factor solution may be adequate for both racial/ethnic groups, the items might be assessing different constructs (see Race/ Ethnicity subsection for further discussion). Concurrent Validity In support of the validity of the BES, numerous studies have identified significant associations with other questionnaires assessing related attitudes, behavior, and mood symptoms. For instance, Mitchell and Mazzeo (2004) examined the BES in a sample of 259 undergraduates, including 73 Black/African American women and 131 White/Caucasian women, and found that BES scores in both groups of women were moderately to strongly correlated with a measure of general eating disorder symptomatology (r = 0.80 and 0.52, respectively). In Ricca et al.’s (2000) research involving 344 outpatient men and women with obesity, BES scores were significantly associated with state (r = 0.25) and trait anxiety (r = 0.32), depressive symptoms (r = 0.30), and BMI (r = 0.13) providing further evidence of concurrent validity. Gender Although the BES has primarily been studied in women, researchers have specifically examined the BES in men. For example, Minnich et al. (2014) examined the BES in a sample of 302 primarily White/Caucasian (88.8%) undergraduate men. Concurrent validity was established with significant correlations in the expected directions at two separate time points with measures of body dissatisfaction (r = 0.52, 0.31), drive for muscularity (r = 0.19, 0.15), self-esteem
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(r = 0.39, 0.25), depressive symptoms (r = 0.54, 0.50), anxiety symptomatology (r = 0.33, 0.27), and BMI (r = 0.27, 0.32). BES scores also appear consistent with established gender differences in BED prevalence, such that women endorse significantly higher average BES scores than men (e.g., Ricca et al. 2000). Race/Ethnicity The BES has been used among diverse adult samples in both the United States and abroad and has been translated into several different languages (e.g., Freitas et al. 2006; Ricca et al. 2000). Because the BES was originally developed and normed in a primarily White/Caucasian sample, research has since investigated whether racial/ethnic variations in this measure exist. Data from Kelly et al. (2012) indicate that White/Caucasian college women (n = 1467) reported a significantly stronger association between body dissatisfaction and BES scores than Black/African American college women (n = 741). White/Caucasian women also endorsed higher scores on the BES than their Black/African American peers (M = 11.42, SD = 8.16 and M = 8.69, SD = 6.80, respectively). Taken together, data indicate that, on average, binge eating behavior among Black/African American men and women may occur less frequently, may be less emotionally distressing, and may be less associated with body image concerns compared to their White/Caucasian peers. Qualitative data are needed to further clarify whether binge eating behavior manifests differently among various racial/ethnic groups.
Clinical Usefulness to Assess Binge Eating Episode Size A core feature of BED according to DSM-5 criteria (American Psychiatric Association 2013) is the presence of recurrent objective bulimic episodes (OBEs), which involves the consumption of unambiguously large amounts of food, in addition to a sense of loss of control (LOC) while eating. However, subjective bulimic episodes (SBEs), the consumption of smaller amounts of food with LOC, are also associated with significant eating
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disorder symptomatology and general psychopathology. While the BES was only designed to capture OBEs, research has examined whether this measure adequately captures both types of binge eating episodes. Timmerman (1999) compared BES scores to data from 28-day food records in a sample of 56 healthy, primarily White/Caucasian (91%) women who engaged in OBEs at least twice per month in the absence of regular compensatory behaviors. Participants received training in measuring and recording food intake accurately prior to beginning the study. The BES demonstrated significant, moderate associations (r = 0.39–0.40) with several indicators of SBEs, including calories consumed during SBEs, number of SBEs, and number of SBE days. Small-tomoderate, significant correlations (r = 0.29–0.32) were also noted between the BES and similar indicators of OBEs. Importantly, BES scores were not correlated with overall caloric intake. Timmerman (1999) also divided participants into groups based on BES clinical cutoffs. Significant differences emerged between the mild (17) and severe (27) groups, such that the severe group endorsed higher levels of the following: number of calories consumed during SBEs, number of calories consumed during SBEs and OBEs combined, number of total SBEs, number of OBE days, number of SBE days, and number of combined OBE and SBE days. In Celio et al.’s (2004) research, the BES was also correlated with frequency of OBEs and number of days, but no other form of overeating, including SBEs or objective overeating without LOC. Taken together, existing research indicates that the BES does not successfully discriminate between SBEs and OBEs, but appears to be a good indicator of severity of LOC eating.
Comparisons to Diagnostic Interviews Although the BES was not developed with the intention of diagnosing BED, some researchers have examined the potential utility of this measure as a replacement for more costly, time-consuming diagnostic clinical interviews that require trained mental health staff. Therefore, it is important to
Binge Eating Scale (BES)
consider the concordance between the BES and standard diagnostic clinical interviews. Eating Disorder Examination (EDE, Fairburn and Cooper 1993) Celio et al. (2004) compared the BES with the gold standard interview for eating disorder symptom assessment, the EDE, in a sample of 157 primarily White/Caucasian (70.3%) women seeking treatment for BED. Results suggested that the BES (using a severe cutoff score of 27) was reasonably sensitive in detecting individuals with BED (85.1%), but demonstrated low specificity (20%), such that many women without BED obtained BES scores above the severe cutoff. Structured Clinical Interview for DSM Disorders (SCID; First et al. 2007) Freitas and colleagues (2006) examined the clinical utility of the Portuguese version of the BES as a measure of BED in a sample of 178 Brazilian women with obesity. Comparisons were made between the SCID, a semi-structured psychiatric interview, and a BES cutoff score of 17. Again, the BES demonstrated higher sensitivity (97.8%) than specificity (47.7%); over half of the participants who were not diagnosed with BED according to the SCID scored above the clinical cutoff on the BES, while only ~2% of those diagnosed with BED scored below the cutoff. A large sample of outpatient men and women with obesity (N = 344; Ricca et al. 2000) completed the SCID and the BES; their data yielded a sensitivity of 84.8% and a specificity of 74.6%. Based on the existing research, it appears that the BES may demonstrate slightly stronger concordance with clinical interviews in community samples compared to clinical samples, although the potential for false positives remains a concern in the majority of studies. As such, it is recommended that the BES not be used independently to diagnose BED, but may be a useful initial screening tool (as originally suggested by Gormally et al. (1982)).
Summary and Future Directions Overall, scores on the BES (Gormally et al. 1982) have demonstrated good reliability, and the
Binge-Eating Disorder
measure appears to be valid for the assessment of binge eating severity for clinical, community, and college samples in the United States and abroad. Given discordance between the BES and clinical interviews, particularly the tendency to overdiagnose BED when using the BES clinical cutoffs, it is suggested that the BES be used as a brief screening device rather than a diagnostic indicator. The BES may also be more useful in terms of capturing general LOC eating patterns rather than identifying specific binge episodes. Although the BES may be used with diverse patient and community samples, there remains a need to further examine the validity of this measure, particularly among Asian and Hispanic/Latino groups. Additional research is also needed with men outside of college samples, including community and clinical settings. Longitudinal studies are also needed to evaluate whether the BES is a prospective indicator of disordered eating pathology as the majority of research cited herein reported cross-sectional data.
Cross-References ▶ Binge Eating Disorder ▶ Choosing an Assessment Instrument/Method ▶ Eating Disorder Examination (EDE)/(EDE-Q) ▶ Obesity and Eating Disorders ▶ Severity Dimensions ▶ Structured Clinical Interview for DSM-IV (SCID)
References and Further Reading American Psychiatric Association. (2013). The diagnostic and statistical manual of mental disorders: DSM 5. Washington, DC: American Psychiatric Association. bookpointUS. Celio, A. A., Wilfley, D. E., Crow, S. J., Mitchell, J., & Walsh, B. T. (2004). A comparison of the binge eating scale, questionnaire for eating and weight patternsrevised, and eating disorder examination questionnaire with instructions with the eating disorder examination in the assessment of binge eating disorder and its symptoms. International Journal of Eating Disorders, 36(4), 434–444. Fairburn, C., & Cooper, Z. (1993). The eating disorder examination. In C. Fairburn & G. Wilson (Eds.), Binge eating: Nature, assessment and treatment (12th ed., New York, NY : Guilford, pp. 317–360).
55 Freitas, S. R., Lopes, C. S., Appolinario, J. C., & Coutinho, W. (2006). The assessment of binge eating disorder in obese women: A comparison of the binge eating scale with the structured clinical interview for the DSM-IV. Eating Behaviors, 7(3), 282–289. First, M. B., Spitzer, R. L., Gibbon, M., & Williams, J. B. (2007). SCID-I/P. Gormally, J., Black, S., Daston, S., & Rardin, D. (1982). The assessment of binge eating severity among obese persons. Addictive Behaviors, 7(1), 47–55. Kelly, N. R., Mitchell, K. S., Gow, R. W., Trace, S. E., Lydecker, J. A., Bair, C. E., & Mazzeo, S. (2012). An evaluation of the reliability and construct validity of eating disorder measures in white and black women. Psychological Assessment, 24(3), 608. Marcus, M. D., Wing, R. R., & Hopkins, J. (1988). Obese binge eaters: Affect, cognitions, and response to behavioral weight control. Journal of Consulting and Clinical Psychology, 56(3), 433. Minnich, A. M., Gordon, K. H., Holm-Denoma, J. M., & Troop-Gordon, W. (2014). A test of an interactive model of binge eating among undergraduate men. Eating Behaviors, 15(4), 625–631. Mitchell, K. S., & Mazzeo, S. E. (2004). Binge eating and psychological distress in ethnically diverse undergraduate men and women. Eating Behaviors, 5(2), 157–169. Ricca, V., Mannucci, E., Moretti, S., Di Bernardo, M., Zucchi, T., Cabras, P., & Rotella, C. (2000). Screening for binge eating disorder in obese outpatients. Comprehensive Psychiatry, 41(2), 111–115. Timmerman, G. M. (1999). Binge eating scale: Further assessment of validity and reliability1. Journal of Applied Biobehavioral Research, 4(1), 1–12.
Binge-Eating Disorder Anja Hilbert Behavioral Medicine, Integrated Research and Treatment Center Adiposity Diseases, University of Leipzig Medical Center, Leipzig, Saxony, Germany
Definition Binge-eating disorder (BED) was first included as its own diagnostic entity in the Fifth Edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; American Psychiatric Association [APA], 2013). Listed as a Feeding and Eating Disorder, the main characteristic of BED
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Binge-Eating Disorder
Binge-Eating Disorder, Table 1 Diagnostic criteria of binge-eating disorder according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5; APA 2013) Binge-eating disorder A. Recurrent episodes of binge eating 1. Definitely large amount of food 2. Sense of lack of control over eating B. At least 3 of the following: Eating rapidly, eating until uncomfortably full, eating without hunger, eating alone, disgust after eating C. Marked distress D. At least 1 episode of binge eating per week for 3 months E. No recurrent compensatory behavior, not exclusively during bulimia nervosa or anorexia nervosa
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is recurrent binge eating (A.): During binge-eating episodes an amount of food is consumed that is unambiguously larger than what others would eat under comparable circumstances within a certain time, coupled with a subjective sense of loss of control over eating (objective binge eating). As opposed to binge eating in bulimia nervosa, binge eating in BED occurs in the absence of regular inappropriate compensatory behaviors, such as self-induced vomiting, fasting, or laxative misuse, aimed at preventing weight gain (E.). For diagnosis of BED, binge eating is required to occur at least once per week over 3 months (D.) and in association with behavioral abnormalities (B.) and marked distress (C.) (Table 1). DSM-5 offers two specifications for the diagnosis of BED: (a) current severity according to the frequency of binge-eating per week (mild, 1–3 episodes; moderate, 4–7 episodes; severe, 8–13 episodes; extreme, 14 or more episodes); and (b) remission status after full criteria have been met (partial remission, less than one binge-eating episode per week; full remission, no diagnostic criterion met). In addition, within the Other Specified Feeding or Eating Disorder section of DSM-5 (OSFED; 307.59), a lower-threshold form of BED was newly defined, also associated with significant distress or impairment in life functioning: Objective binge eating can be classified as BED of low
frequency and/or limited duration if occurring less than once per week and/or for less than 3 months, the time criterion of BED (D.). For this diagnosis, all other DSM-5 criteria of BED are required to be met. According to the International Classification of Diseases and Related Health Problems Tenth Edition (ICD-10; World Health Organization 1992), BED is subsumed under the Other Eating Disorders (F50.8), without any further specification of diagnostic criteria or guidelines. For the Eleventh Edition of ICD (ICD-11), scheduled for 2017, BED was designated as its own eating disorder (Uher and Rutter 2012). However, deviating from the DSM-5, the ICD-11 diagnosis of BED was proposed to be broadened and based on objective or subjective binge eating. Thus, in addition to objective binge eating, as defined in the DSM-5, subjective binge eating, involving the consumption of an amount of food that is subjectively larger than what others would eat under comparable circumstances, combined with a subjective sense of loss of control over eating, could be used for diagnosis of BED, making the loss of control over eating the decisive criterion of binge eating. Proposed for the other eating disorders as well, the diagnostic time frame for BED was shortened to 1 month, during which binge eating is required to occur regularly and in the absence of regular inappropriate compensatory behavior.
Historical Background Stunkard first described the symptoms of BED in 1959 in obese men and women who presented with recurrent episodes of binge eating but did not purge. It was, however, only four decades later that BED was introduced in the DSM. In the Fourth Edition of the DSM (DSM-IV; APA 1994), BED was included as a provisional eating disorder diagnosis in need of further study and subsumed under the Eating Disorders Not Otherwise Specified. Even as a provisional diagnosis, the introduction of BED in the DSM was controversial, related to concerns about proliferation of diagnoses, lack of evidence on the specific diagnostic criteria of BED, and potential overlap with
Binge-Eating Disorder
bulimia nervosa. A major problem with DSM-IV was that most cases in clinical settings were diagnosed with the residual category Eating Disorders Not Otherwise Specified, leading to uncertainties in classification and treatment, and making a revision of the DSM diagnostic system for eating disorders necessary. As guiding principles for the revision, the DSM-5 Eating Disorders Task Force aimed for maximum clinical utility, solid empirical evidence, and high continuity with the DSM-IV. The revision was based on a large body of empirical research, published since 1994 and compiled in state-of-the-art reviews (e.g., Striegel-Moore and Franko 2008; Wonderlich et al. 2009; Keel et al. 2012). Herein, it was demonstrated that BED has validity (i.e., demonstrable boundaries towards normality and neighboring syndromes) and clinical utility (i.e., nontrivial information about psychobiological correlates, prognosis, and/or treatment outcome; see Current Knowledge). Consequently, the DSM-5 adopted the DSM-IV diagnostic criteria in a virtually identical form, with one exception: In order to match the thresholds proposed for bulimia nervosa, the diagnostic time frame was shortened from 6 to 3 months, and the frequency threshold of objective binge-eating episodes required for diagnosis of BED was decreased from at least 2 per week to at least 1 per week. Indeed, emerging evidence indicates that the use of DSM-5 diagnostic criteria reduced the number of cases with EDNOS, and led to an increase in the prevalence rate of BED, similar to that of the other defined eating disorders.
Current Knowledge Extant literature shows that individuals with BED suffer from increased eating disorder (e.g., shape or weight concern) and general psychopathology (e.g., depressiveness, anxiety), high comorbidity with Axis I (e.g., mood disorders, anxiety disorders, substance use disorders) and Axis II disorders (e.g., avoidant, borderline personality disorder), overweight and obesity, and impaired mental and physical quality of life, when compared to normal weight or overweight/obese
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individuals without BED (Kessler et al. 2013). When compared to the other eating disorders anorexia nervosa and bulimia nervosa, BED displayed a roughly similar psychological impairment. Empirical classification studies (e.g., latent structure analyses) have shown that the clinical profile of BED is distinct from that of the other eating disorders, although a clear delineation from obesity is still outstanding (Wonderlich et al. 2009). Laboratory test meal studies objectively demonstrated greater abnormalities in food intake (e.g., greater consumption of calories in test meal paradigms) in BED than in weight-matched controls without BED, further speaking to the validity of this disorder. BED, with a lifetime prevalence rate of 1.9% is the most prevalent eating disorder (DSM-IV) and presents with a distinct sociodemographic profile (e.g., later age of onset, lower preponderance of female gender, higher rates of obesity), when compared to anorexia nervosa and bulimia nervosa. Regarding etiology, BED seems to be preceded by multiple mental, physical, and social correlates of risk, most of which are shared with the other eating disorders. However, longitudinal evidence on the development of BED is limited. A few prospective studies indicated that childhood loss of control eating including both objective and subjective binge eating, predicts a later development of full- or partial-syndrome BED and may, in vulnerable youth, precede excess weight gain and metabolic dysfunction (Hilbert et al. 2013). Formal genetic studies suggested the role of familial and genetic risk factors of binge eating. However, molecular genetic studies have not confirmed the contribution of any specific gene or genetic pathway to the development of BED. BED has been theorized to be maintained through emotional, social, and cognitive dysfunctions. Emotional dysfunctions were found to be similar to those in anorexia nervosa and bulimia nervosa. Binge eating in BED has been found to be preceded by negative affect in descriptive, laboratory, and ecological momentary assessment studies. However, no clear evidence exists that binge eating reduces negative affect, as stipulated by the prominent affect regulation model. Negative affect frequently arises from interpersonal
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problems (e.g., social anxiety, poor social support), characteristic of BED and similar to those of the other eating disorders, supporting the validity of the interpersonal model of binge eating. This model posits that interpersonal problems adversely impact affect, resulting in binge eating. Further, individuals with BED, as did individuals with anorexia nervosa and bulimia nervosa, displayed deficits in executive functioning when compared to weight-matched controls, especially for disorder-relevant cues (e.g., set-shifting difficulties with food stimuli; Kittel et al. 2015), likely increasing the probability of binge eating. Likewise, preliminary studies of brain function in BED suggested a diminished activity in brain areas related to inhibitory control (e.g., ventromedial prefrontal cortex, inferior frontal gyrus, insula) compared to obese and normal weight controls. A greater striatocortical pathway dysfunction in reward processing, analogous to substance use disorders, was suggested for BED; however, the food addiction or eating addiction hypothesis in BED is awaiting definitive evidence. Among evidence-based treatment approaches, cognitive-behavioral therapy and interpersonal psychotherapy are standard specialty treatments for BED, leading to large and long-lasting improvements of binge eating and associated psychopathology (Hay 2013). Manualized self-help approaches, based on cognitive-behavioral principles and guided by a coach, have further proven to be efficacious, especially with lower levels of psychopathology. Overall, response to psychological treatment seems to be higher in BED than in anorexia nervosa and bulimia nervosa. In contrast to standard specialty treatments for BED, behavioral weight loss treatment for obesity yielded only moderate effects when treating obese individuals with BED, lending clinical utility to the diagnosis of BED. In addition, the symptomatology of BED seems to impair long-term efficacy of conservative and surgical approaches to weight loss treatment. It is of note that the rates of individuals with BED receiving treatment for the eating disorder are low, speaking for a necessary improvement in the provision of care. Consistent with the substantial disease-related burden associated with BED, health care utilization and health
Binge-Eating Disorder
care costs are generally increased in individuals with BED. Recently, the first medication for BED was approved in the US (lisdexamfetamine dimesylate); however, the evidence on pharmacotherapy for BED, especially regarding long-term outcomes, remains limited. Regarding long-term outcome, when compared to anorexia nervosa or bulimia nervosa, the natural course of BED seems to be more variable, with tendencies towards recovery and relapse likely embedded in a chronic course. BED seems to be less prone than anorexia nervosa or bulimia nervosa to migrate to another eating disorder. The evidence is insufficient on the predictive value of BED or binge eating for weight gain, or adverse medical outcomes including mortality, although BED may precede these outcomes.
Current Controversies Currently, it remains unresolved, and this concerns other eating disorders as well, how to best operationalize binge eating – the core diagnostic criterion of BED (A.) – and more specifically, how to define loss of control and demarcate an unusually large amount of food. Concerns persist on the lack of evidence base for the behavioral indicators of binge eating (B.) and marked distress (C.). It has been noted that no parallel of these criteria exists in the diagnostic criteria of other eating disorders with binge eating, especially bulimia nervosa. The determination of illness severity is another difficulty that is beginning to be addressed empirically. The evidence is accruing that body image disturbance, expressed as Undue influence of weight or shape on self-evaluation, is associated with greater illness severity, while being unrelated to body mass index, and has potential relevance in the prediction of treatment outcome (Grilo 2013). Undue influence of weight or shape on self-evaluation is required to diagnose both anorexia nervosa and bulimia nervosa according to the DSM and has been recommended as a diagnostic specifier or criterion of BED for forthcoming editions of diagnostic systems. Further difficulties exist in the differentiation from other eating disorders such as bulimia nervosa, especially in case of nonpurging
Bipolar Affective Disorder (BAD)
compensatory behaviors (e.g., Other Specified Feeding or Eating Disorder Obesity, excessive exercising) and in case of dietary restriction (e.g., weight loss diets). In addition, symptom overlap exists with night eating syndrome, newly included as an Other Specified Feeding or Eating Disorder in the DSM-5, which should not be diagnosed if symptoms can be better explained by BED.
Future Directions Further evidence is needed on the reliability and validity of BED, taking into account the changes to diagnostic criteria in DSM-5 and ICD-11. A promising research avenue is the simplification of diagnostic criteria for BED and other eating disorders, for example, as detailed in the Broad Categories for the Diagnosis of Eating Disorders (BCD-ED) approach (Walsh and Sysko 2009). The definition of binge eating also warrants further consideration. Further evidence is warranted on the specification of restrictive eating in relation to the maintenance of binge-eating episodes in BED. Future treatments should be closely informed by current research on the maintenance of this disorder (e.g., cognitive dysfunction). Another major challenge for research lies in the dissemination and implementation of evidence-based approaches to treatment. More evidence is needed on the etiology and long-term outcome of BED.
Cross-References ▶ Future Directions in Classification ▶ Loss of Control (LOC) Eating in Children ▶ Obesity ▶ Obesity and Eating Disorders ▶ Other Specified Feeding or Eating Disorder (OSFED)
59 Hay, P. (2013). A systematic review of evidence for psychological treatments in eating disorders: 2005–2012. International Journal of Eating Disorders, 46, 462–469. Hilbert, A., Hartmann, A. S., Czaja, J., & Schoebi, D. (2013). Natural course of preadolescent loss of control eating. Journal of Abnormal Psychology, 122, 684–693. Keel, P. K., Brown, T. A., Holland, L. A., et al. (2012). Empirical classification of eating disorders. Annual Review of Clinical Psychology, 8, 381–404. Kessler, R. C., Berglund, P. A., Chiu, W. T., Deitz, A. C., Hudson, J. I., Shahly, V., Aguilar-Gaxiola, S., Alonso, J., Angermeyer, M. C., Benjet, C., Bruffaerts, R., de Girolamo, G., de Graaf, R., Maria Haro, J., Kovess-Masfety, V., O’Neill, S., Posada-Villa, J., Sasu, C., Scott, K., Viana, M. C., & Xavier, M. (2013). The prevalence and correlates of binge eating disorder in the World Health Organization World Mental Health Surveys. Biological Psychiatry, 73, 904–914. Kittel, R., Brauhardt, A., & Hilbert, A. (2015). Cognitive and emotional functioning in binge-eating disorder: A systematic review. International Journal of Eating Disorders, 48, 535–554. Striegel-Moore, R. H., & Franko, D. L. (2008). Should binge eating disorder be included in the DSM-V? A critical review of the state of the evidence. Annual Review of Clinical Psychology, 4, 305–324. Uher, R., & Rutter, M. (2012). Classification of feeding and eating disorders: Review of evidence and proposals for ICD-11. World Psychiatry, 11, 80–92. Walsh, B. T., & Sysko, R. (2009). Broad categories for the diagnosis of eating disorders (BCD-ED): An alternative system for classification. International Journal of Eating Disorders, 42, 754–764. Wonderlich, S. A., Gordon, K. H., Mitchell, J. E., et al. (2009). The validity and clinical utility of binge eating disorder. International Journal of Eating Disorders, 42, 687–705.
General References American Psychiatric Association. (1994). Diagnostic and Statistical Manual of Mental Disorders (4th Ed.). Arlington: American Psychiatric Association. American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th Ed.). Arlington: American Psychiatric Association. World Health Organization. (1992). International Classification of Diseases and Related Health Problems Tenth Edition (ICD-10). Geneva: World Health Organization.
References and Further Reading Grilo, C. M. (2013). Why no cognitive body image feature such as overvaluation of shape/weight in the binge eating disorder diagnosis? International Journal of Eating Disorders, 46, 208–211.
Bipolar Affective Disorder (BAD) ▶ Bipolar Disorder and Eating Disorders
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Bipolar Disorder and Eating Disorders Anna I. Guerdjikova1,2 and Susan L. McElroy1,2 1 Lindner Center of HOPE, Mason, OH, USA 2 Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati, OH, USA
Synonyms Anorexia nervosa; Binge eating disorder; Bipolar affective disorder (BAD); Bulimia nervosa; Eating disorder not otherwise Specified; Manicdepressive illness (MAD)
Definitions Bipolar disorder is also known as “manic-depressive illness” is defined by the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM) 5 (A.P.A. 2013) as a brain illness, characterized by periods of elevated mood and periods of depression. The elevated mood is significant; it impairs daily functioning and is known as mania or hypomania, depending on the severity of the episode or presence of psychosis. During a manic episode, the individual feels and/or acts abnormally and persistently elated, energetic, goal oriented, or irritable and might make poorly thought out decisions with little regard to the consequences. The need for sleep is usually reduced, individuals are more talkative than usual, and the disturbance in mood is observable by others. Periods of depression are characterized by low moods, pessimistic outlook for the future, decreased energy, motivation, and interest in hobbies and usual activities. Some individuals cycle from low mood to elevated mood without periods of normalized stable mood, while others experience periods of stable mood in between manic and depressive episodes. Depending on the severity of the mood dysregulation, bipolar disorder is classified as bipolar I disorder (most severe mania,
Bipolar Disorder and Eating Disorders
characterized by the presence of manic episodes and depressive episodes), bipolar II disorder (less severe mania, characterized by the presence of hypomanic episodes and depressive episodes) and bipolar disorder not otherwise specified. DSM-5 outlines three types of eating disorders – anorexia nervosa, bulimia nervosa, and binge eating disorder. Anorexia nervosa is characterized with persistent restriction of food intake leading to significantly low body weight along with intense fear of gaining weight or becoming fat. Individuals with bulimia nervosa engage in repetitive overeating (binge eating) followed by purging episodes (by vomiting or abusing laxative or diuretics), and their selfevaluation is unduly influenced by body shape and weight. Binge eating disorder is characterized with at least weekly episodes of eating unusually large amounts of food in a short period of time accompanied by the feeling of out of control during the binges and without engagement in any compensatory behaviors.
Historical Overview As early as fifth century BC, the Hippocratic School used the terms “melancholia” and “mania” to define abnormal behavioral states different from febrile illness. Early description of mania as “yellow bile on the frontal portions of the brain, which alters the imagination and as a consequence, reason” was provided by Posidonius (c. 135–51 BC). In the late seventeenth century, Theophilus Bonet published “Sepuchretum,” a text that drew from his experience performing 3000 autopsies, in which he connected mania and melancholy in a condition called “manico-melancolicus.” This was a substantial step in defining bipolar illness because until then, mania and depression were usually considered separate states. However, it was not until the late eighteenth century when the Spanish physician Andres Piquet wrote that “melancholia and mania are terms denoting a single disease accompanied by several disorders of mood.” Later in the nineteenth century, Esquirol commented on the probable genetics of bipolar
Bipolar Disorder and Eating Disorders
disorder by stating that “It would be difficult not to concede a hereditary transmission of mania, when one recalls that everywhere some members of certain families are struck in several successive generations.” In 1854, the French psychiatrist Jean-Pierre Falret published an article describing what he called “la folie circulaire” (circular insanity). His article detailed patients switching through severe depression and manic states, and is considered the first documented diagnosis of bipolar disorder (Yildiz et al. 2015). The term “bipolar,” meaning “two poles,” and signifying the polar opposites of mania and depression, first appeared in the third revision of American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1980. Similarly, various presentations of eating dysregulations, including historical notes on religious fasting dating as far as BC, have been described. The first anorexia nervosa cases appeared in medical literature in the early seventeenth century with the work of the English physician Dr. Morton. A century later, Sir W. Gull, the prominent physician to Queen Victoria published “Anorexia Hysterica,” and coined the term anorexia nervosa to distinguish the disorder from the umbrella term “hysteria.” While binging and purging were both known through ancient history with the Hebrew Talmud (A.D. 400–500) referring to a ravenous hunger that should be treated with sweet foods (boolmot), and the Romans using the word “vomitorium” (a special room where the wealthy Romans would go to purge after a large meal), the term bulimia nervosa was not uniformly used until 1979 when it was introduced by Gerald Russel and then included as a formal diagnosis in DSM-III in 1987 (Gordon 2000). Binge eating disorder was first formally described in 1959 by Albert Stunkard as a form of abnormal eating among obese people. Overall, eating disorders received little systematic attention until the middle of the twentieth century when they were conceptualized as mental illness and further included in formal disease classifications. As recently as 2013, binge eating disorder was added to DSM-5 as a standalone eating disorder. The anecdotal clinical observations on the overlap between mood and eating dysregulations and its
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treatment implications sparked scientific interest and lead to systematic research starting in the early 1990s. Epidemiology and Course of Bipolar and Eating Disorders The estimated worldwide prevalence of bipolar disorder is up to 2.4% (0.0% in Nigeria and 3.3% in the Unites States) and it is considered to be among the top 20 causes of disability. While bipolar illness is known to have a strong genetic component with estimated heritability between 60% and 85%, its complex genetic etiology remains largely unknown. Like bipolar disorder, eating disorders are highly heritable illnesses associated with decreased quality of life, increased disability, morbidity, and mortality. Both bipolar disorders and eating disorders start most commonly in adolescence and the course of illness can be acute, intermittent, or chronic. Comorbidity of Bipolar Disorder and Eating Disorders Patients with bipolar disorder have been shown to have elevated rates of co-occurring anorexia nervosa, bulimia nervosa, and binge eating disorder and conversely, patients with eating disorders are reported to have elevated rates of comorbid bipolar disorder (McElroy et al. 2011). Controlled family history studies have found elevated rates of bipolar disorders in the first-degree relatives of individuals with anorexia nervosa, bulimia nervosa, and binge eating disorder. Moreover, community studies found hypomania to be associated with binge eating behaviors. The National Comorbidity Survey Replication found that bipolar I and II disorders were associated with bulimia nervosa and binge eating disorder, but not anorexia nervosa (Hudsonet al. 2007). Bipolar patients with eating disorders are shown to have more weight disturbance, more depressive episodes or recurrences, and greater psychiatric comorbidity than bipolar patients without eating disorders. The precise pathophysiology of the overlap between eating disorders and bipolar disorders remains unknown. Growing research demonstrates that eating disorders are associated with
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elevated familial rates of bipolar disorder suggesting certain genetic overlap. Moreover, dysregulation in some neurotransmitter and neurotrophin systems may play a role in the pathophysiology of both illnesses. For example, abnormalities in brain-derived neurotrophic factor, a protein involved in the regulation of mood and appetite, are found in individuals with bipolar disorder and those with eating disorders. Similarly, variants of the neurotrophic tyrosine kinase receptor 3 gene are associated with early-onset bipolar disorder and eating disorders. Of interest, in both bipolar and eating disorders, similarly elevated comorbidity with anxiety, alcohol, and drug use disorders are observed, suggesting that bipolar disorders and eating disorders may be related by sharing a neurobiological dysregulation of mood, eating behavior, and impulse control. Indeed, is has been hypothesized that certain impulsive behaviors, including binge eating, may have mood stabilizing effects and that some patients with bipolar disorder might selfmedicate their mood dysregulation with impulsive overeating (e.g., binge eating). In this context of shared neurobiology, it is not surprising that eating disorders respond to treatments with moodimproving properties (e.g., antidepressants and/or cognitive-behavioral therapy). For example, the binge eating of bulimia nervosa and binge eating disorder responds to antidepressants and conversely, interventions related to regulating food intake and decreasing dysfunctional eating behaviors can stabilize mood.
Treatment Psychological Treatments There have been no randomized, controlled trials of any psychotherapy methods in the treatment of patients with bipolar disorder and a co-occurring eating disorder. Certain psychological interventions, briefly described below, hold promise when addressing mood and comorbid eating dysregulations because they are effective in bipolar disorder alone or in eating disorders treatment alone. In general, psychological treatments are not
Bipolar Disorder and Eating Disorders
recommended as a monotherapy when treating bipolar disorder with a comorbid eating disorder and in most cases should be considered as an adjunct to pharmacotherapy. Psychoeducation Psychoeducation is a behavioral training aimed at adjusting lifestyle to cope with mental and /or physical illness by enhancement of illness awareness, early detection of relapse, and treatment adherence. Psychoeducation empowers patients with various tools, allowing them to be more active in their treatment, and is a widely used method in addressing both mood and eating disorders. Cognitive-Behavior Therapy (CBT) Cognitive-behavior therapy is considered the “gold standard” in the treatment of bulimia nervosa and binge eating disorder. CBT has also shown promise in the treatment of acute bipolar depression and for relapse prevention when given to euthymic bipolar patients for up to 2 years. The main goals in CBT when used for targeting both mood and eating dysregulations is to enhance medication adherence, to improve self-esteem and self-image, and to reduce maladaptive and high-risk behaviors associated with the comorbidity (Hofmannet al. 2012). Dialectical-Behavior Therapy (DBT) In dialectical-behavior therapy (DBT), the main treatment target is emotional dysregulation, which is a core symptom in both bipolar and eating disorders. Skillful responses based on mindfulness, distress tolerance, emotional regulation, and interpersonal effectiveness are used to replace ineffective and maladaptive behaviors, with particular focus on managing impulsivity and interpersonal difficulties. Family-Focused Therapy (FFT) Family-focused therapy is the “gold standard” in the treatment of eating disorders, particularly anorexia nervosa, in adolescents and young adults. Several randomized controlled trials support the effectiveness of FFT for adults with bipolar disorder
Bipolar Disorder and Eating Disorders
(Milkowitz 2008). FFT is heavily focused on providing solid psychoeducation about the eating or mood disorder for the whole family. Strategies for problem solving and coping with interfamilial stress are often learned through role-playing. Pharmacological Treatments As with psychological treatments, there have been no randomized, controlled trials of a pharmacologic agent specifically in the treatment of patients with bipolar disorder and a co-occurring eating disorder. When treating such patients, there are several therapeutic goals, including (ideally) selecting an agent effective in treating both syndromes, or at the minimum, selecting an agent that treats one syndrome without exacerbating the other, either by therapeutic action or side effects (McElroy et al. 2006). For example, comorbid binge eating disorder might be an important reason for weight gain and obesity in patients with bipolar illness and certain mood stabilizing and antimanic agents (e.g., clozapine, olanzepine, and valproate) may further exacerbate comorbid binge eating behavior and weight gain. Moreover, unrecognized bipolar disorder in patients with eating disorders could lead to development of manic symptoms if antidepressants are used for bulimia nervosa or binge eating disorder. Thus, careful diagnosis of presenting and comorbid conditions is the first step in successful pharmacological management of bipolar disorder when co-occurring with an eating disorder. Clinically, when treating bipolar illness comorbid with anorexia nervosa, addressing the malnutrition along with mood stabilization is the primary treatment goal. When treating bipolar illness associated with bulimia nervosa or binge eating disorder, targeting mood dysregulation and achieving euthymia is often the first step in addressing the eating symptomatology as well. Indeed, there are mostly case reports of successful pharmacotherapy of bipolar patients with a co-occurring eating disorder. Of note, the specificities of the eating disorder, namely the need for weight restoration in anorexia nervosa or need for weight loss in binge eating disorder, should guide therapeutic decisions, as detailed below.
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Lithium Lithium, the oldest and best researched agent in bipolar disorder, has been tested in placebocontrolled trials in the treatment of anorexia nervosa and bulimia nervosa. While patients with anorexia receiving lithium achieved significantly greater weight gain and displayed significantly greater improvement on a measure of insight compared to placebo, lithium was not efficacious in decreasing purging episodes in bulimia nervosa patients. However, there are case reports of bipolar patients with anorexia nervosa or bulimia nervosa responding well to lithium. There have been no randomized, controlled trials of mood-stabilizing agents in the treatment of binge eating disorder. Antipsychotic Medication Antipsychotic medication is generally not recommended when treating bipolar illness comorbid with bulimia nervosa or binge eating disorder because of the side effect of weight gain associated with some of those agents. Sparse data suggests, however, that second generation antipsychotics might attenuate preoccupation with food and weight of anorexia nervosa. Olanzepine was superior to placebo and resulted in rapid weight gain and reduction in obsessive symptoms in a small controlled study. Quetiapine and aripiprazole have been investigated in open-label trials only but might hold promise for weight restoration and reduction of obsessivecompulsive symptoms in a carefully selected group of patients with anorexia nervosa. Antiepileptic Medication Topiramate and zonisamide, two novel antiepileptic agents, have demonstrated efficacy in the treatment of bulimia nervosa, binge eating disorder, and obesity. Topiramate was, however, not superior to placebo in the treatment of acute bipolar mania in a number of randomized, controlled trials and its efficacy in treating bipolar depression has been only partially supported. There have been no randomized, controlled trials of zonisamide in the treatment of bipolar disorder, although some anecdotal data suggest
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that this agent may have thymoleptic properties. Topiramate and zonisamide might thus offer promise as adjunctive treatments along with mood-stabilizing agents for patients with bipolar disorder and comorbid bulimia nervosa or binge eating disorder. Antidepressants Though commonly used in bipolar disorder, antidepressant medication in bipolar illness treatment is controversial (Kendall et al. 2014). Antidepressant monotherapy is contraindicated in bipolar I depression, but may be used in bipolar II depression. Antidepressants from various classes have proven efficacious in bulimia nervosa and binge eating disorder in randomized, placebo-controlled trials and could be used along with mood stabilizers with a low risk of weight gain, appetite stimulation, or binge eating exacerbation in patients with bipolar II disorder and comorbid bulimia nervosa or binge eating disorder. In contrast, trials of antidepressants in anorexia nervosa have been almost uniformly negative and antidepressants should not be considered the first line of treatment when addressing bipolar disorder comorbid with anorexia nervosa (Flament et al. 2012). In summary, in regards to pharmacotherapy, mania and anorexia nervosa might improve on lithium and certain atypical antipsychotic medication; if lithium is used, regular renal and thyroid function monitoring is mandated. Bipolar depression and binge eating or bulimia nervosa might improve on antidepressants along with a moodstabilizing agent. Stabilization of affective symptoms in patients with bipolar disorder and a co-occurring eating disorder with a moodstabilizing agent with a low risk of exacerbating the eating disorder is often the important first step when treating this comorbidity.
Conclusion and Future Directions Recognition of comorbid eating disorders in patients with bipolar disorder and vice versa has important implications for treatment. In routine clinical practice, if comorbidity is suspected, the administration of a brief self-report measure like
Bipolar Disorder and Eating Disorders
the Eating Attitudes Test and Mood Disorder Questionnaire (Rush et al. 2008) might assist the diagnostic process. Comprehensive evaluation of patients with bipolar disorder should include a systematic assessment for eating disorders and conversely, patients with eating disorder should be questioned about mood instability to further inform treatment selection toward agents parsimoniously addressing both syndromes, if present. Of note, in patients with history of mood dysregulation presenting for obesity management a thorough psychiatric assessment might help uncover mood and eating disorder comorbidity and further guide treatment decisions. Patients with bipolar disorder and a co-occurring eating disorder present with multidimensional problems that most commonly cannot be treated with a single intervention and benefit from a team approach to management to optimize outcomes. Ideally, a team of professionals, including a psychiatrist, a dietician, a social worker, and a therapist would be available to provide support for the patient and their family. Despite significant scientific progress that was made in the last 30 years, future research into the epidemiology, psychology, neurobiology, and treatment of co-occurring bipolar disorder and eating disorders is greatly needed.
Cross-References ▶ Anorexia Nervosa ▶ Binge Eating Scale (BES) ▶ Binge Eating Disorder ▶ Bulimia Nervosa ▶ Cognitive Behavioral Therapy ▶ Eating Disorder Examination (EDE)/(EDE-Q) ▶ Maudsley Model of Anorexia Nervosa Treatment for Adults (MANTRA) ▶ Structured Clinical Interview for DSM-IV (SCID)
References and Further Reading A.P.A. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: A.P.A. Flament, M. F., Bissada, H., & Spettigue, W. (2012). Evidence-based pharmacotherapy of eating disorders.
Body Checking Questionnaire (BCQ) International Journal of Neuropsychopharmacology, 15(2), 189–207. Gordon, R. A. (2000). Eating disorders: Anatomy of a social epidemic. Malden: Blackwell Publishers. Hofmann, S. G., Asnaani, A., Vonk, I. J., Sawyer, A. T., & Fang, A. (2012). The efficacy of cognitive behavioral therapy: A review of meta-analyses. Cognitive Therapy and Research, 36(5), 427–440. Hudson, J. I., Hiripi, E., Pope, H. G., Jr., & Kessler, R. C. (2007). The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biological Psychiatry, 61(3), 348–358. Kendall, T., Morriss, R., Mayo-Wilson, E., Marcus, E., & Guideline Development Group of the National Institute for Health Care and Excellence. (2014). Assessment and management of bipolar disorder: summary of updated NICE guidance. BMJ, 349, g5673. McElroy, S. L., Frye, M. A., Hellemann, G., Altshuler, L., Leverich, G. S., Suppes, T., et al. (2011). Prevalence and correlates of eating disorders in 875 patients with bipolar disorder. Journal of Affective Disorders, 128(3), 191–198. McElroy, S. L., Kotwal, R., & Keck, P. E., Jr. (2006). Comorbidity of eating disorders with bipolar disorder and treatment implications. Bipolar Disorders, 8(6), 686–695. Milkowitz, D. J. (2008). Bipolar disorder: A family-focused treatment approach. New York: Guilford Press. Rush, A. J., First, M. B., & Blacker, D. (2008). Handbook of psychiatric measures. Arlington: American Psychiatric Association. Yildiz, A., Ruiz, P., & Nemeroff, C. (2015). The bipolar book. History, neurobiology, and treatment. New York: Oxford University Press.
Body Checking Questionnaire (BCQ) Deborah Lynn Reas Regional Department of Eating Disorders (RASP), Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway
Definition The Body Checking Questionnaire (BCQ) (Reas et al. 2002) is a 23-item self-report inventory designed to assess the frequency of body checking behaviors. Body checking refers to the checking of one’s body shape, weight, or size. The BCQ items measure the frequency of body checking
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behaviors, such as measuring or pinching specific body parts (e.g., thighs, waist, upper arms, etc.), using mirrors to monitor one’s shape, wearing special clothes or jewelry to gauge fit, or feeling for bone protrusion. Each BCQ item is scored on a 5-point Likert-type scale ranging from 1 (never) to 5 (very often); thus, higher scores indicate higher frequency of checking (total scores range from 23 to 115). The BCQ is the first instrument developed specifically to assess body checking behaviors and has been translated into several languages, including Norwegian, Italian, German, and Portuguese. Prior to its development in 2002, assessment options for body checking were scant, limited to few behavioral items on broader measures of body image or eating disorders. The emphasis on repeated body checking as a behavioral manifestation of the “core psychopathology” of eating disorders (i.e., the overevaluation of weight and shape and their control) (Fairburn 2008) within cognitivebehavioral models of eating disorders has greatly stimulated clinical and research attention to this construct over the past decade.
Background and Development The initial item pool of the BCQ consisted of 38 items selected based on a literature review and clinical observations (Reas et al. 2002). Content validity was assessed using patient feedback and expert panel ratings for item relevance and representativeness. To examine the factor structure of the original 38 items, an exploratory factor analysis (EFA) was run using 244 female undergraduates and 15 female outpatients with DSM-IV eating disorders being treated at a university clinic, with a total sample mean age of 21.8 years (15–51 years). Based on a principal component analysis using oblique rotation, 10 items were removed due to cross loadings or low loadings on a factor (1 were retained. An overall appearance factor comprised of 13 items (e.g., checking reflection in mirror, using clothes to gauge fit, eliciting appearance-related judgments from others) accounted for 20.6% of the total variance, a factor comprised of 9 items linked to specific body parts
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(e.g., pinching stomach, checking for cellulite on thighs) accounted for 15.5% of the variance, and an idiosyncratic checking factor consisting of 6 items (e.g., feeling for bone protrusion, checking diameter of wrist, using jewelry) accounted for 15.2% of the total variance. A higher-order factor structure was tenable based upon correlations ranging from r = 0.56 to r = 0.85. In a second study, a confirmatory factor analysis (CFA) using maximum likelihood factor analysis was run for the 28-item version of the BCQ. The second sample was comprised of 149 female college students and 16 female outpatients diagnosed with a DSM-IV eating disorder (ED) recruited from a university clinic. Results showed strong and significant individual item loadings as well as loadings of subfactors to the higher-order factor, but the model showed marginal fit due to within-factor correlated measurement error. Five items were deleted due to redundancy, and the resulting model showed good fit (CFI = 0.90, IFI = 0.90, RMSEA = 0.076), with three subfactors that are highly correlated. A cross-validation of the 23-item BCQ was performed in the original sample of 259 study participants, and fit indices confirmed the adequacy of the model. The final 23-item BCQ was found to have satisfactory reliability and validity. Internal consistency was 0.88, 0.92, and 0.83 for the overall appearance, specific body parts, and idiosyncratic checking subscales, respectively. Test-retest reliability was 0.94, indicating good temporal stability. The total BCQ score was found to correlate significantly with measures of similar constructs, including the Body Shape Questionnaire (BSQ; r = 0.86), the Body Image Avoidance Questionnaire (BIAQ; r = 0.66), and the Eating Attitudes Test-26 (EAT-26; r = 0.70). Additionally, a higher frequency of body checking was associated with negative attitudes toward weight and shape, as well as eating disorder pathology. The BCQ score also differed significantly between nonclinical, female college students (M = 56.0, SD = 16.0) and patients (M = 82.1, SD = 18.0). College females with elevated body shape concerns as determined by the Body Shape Questionnaire scored significantly higher than women with fewer concerns, and
Body Checking Questionnaire (BCQ)
similarly, dieters (M = 71.1, SD = 17.0) scored higher than non-dieters among nonclinical women (M = 54.2, SD = 16.0).
Current Knowledge Since its publication, the BCQ has been studied increasingly in diverse clinical and nonclinical populations worldwide. Despite long-standing clinical observations of checking behavior, body checking received scant research attention prior to its inclusion in cognitive-behavioral models of eating disorders in the late 1990s. Body checking behaviors have been described as distressing, time-consuming, “noxious” behaviors (Shafran et al. 2004), which magnify perceived imperfections, serving to worsen and maintain body size preoccupation. A landmark experimental study using manipulation trials in healthy controls has since established a causal link between the level of body checking and body dissatisfaction, feelings of fatness, and body-related self-critical thinking (Shafran et al. 2007). More recent research has provided additional support for the reliability and validity of the BCQ as a measure of body checking behavior. Table 1 summarizes normative data and sample characteristics from a selection of larger normative studies conducted in nonclinical, female populations. Internal consistency data is also provided where available. Consistent with the study describing the initial development of the BCQ (Reas et al. 2002), research has consistently found the BCQ to distinguish between women with high versus low weight and shape concerns, dieters versus non-dieters, and ED patients versus controls. For example, Calugi et al. (2006) investigated psychometric properties of the Italian version of the BCQ using a larger population (N = 422), including 151 patients diagnosed with a clinical ED. Significant differences were observed between controls and patients (M = 62.6, SD = 24.1 vs M = 44.2, SD = 14.7). Additional analyses across diagnostic subgroups revealed that patients with BN scored significantly higher than patients with AN, with the lowest scores for EDNOS (M = 71.8, SD = 23.9; M = 58.3, SD = 23.9;
Body Checking Questionnaire (BCQ)
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Body Checking Questionnaire (BCQ), Table 1 Selected larger normative studies of the Body Checking Questionnaire (BCQ) in university women
Country N Setting Gender Age (M, SD, range) BMI (M, SD, range) Total BCQ (M, SD) Cronbach’s alpha Total Overall appearance Specific body parts Idiosyncratic
Reas et al. (2002) USA 149a University Female 20.8 (16–56)
Calugi et al. (2006) Italy 422 University Female 24.1 (5.9)
22.1 (16.3–37.7)
20.4 (2.2)
56.0 (16.0)
44.2 (14.7)
N/A 80.3% in normal BMI range 48.8 (14.9)
N/A 0.88
N/A 0.89
N/A 0.83
0.92
0.83
0.87
0.83
0.86
0.70
Campana et al. (2013) Brazil 546b University Female 18–55 years
Lydecker et al. (2014) USA 1,011 University Female 18–25
White et al. (2015) USA 650 University Female 19.64 (2.23)
N/A
22.41 (4.13)
52.1 (17.9)
47.6 (15.8)
0.94
0.96
BCQ Body Checking Questionnaire, BMI Body Mass Index, N/A not available a Please see Reas et al. (2002) for Study 1 which provided test development data for an additional N = 244 college females b Please see Campana et al. (2013) for Study 2 which provided data for an additional N = 404 women recruited from weight-loss centers/gyms
M = 64.4, SD = 23.3). A Brazilian study of 546 nonclinical college women scored significantly higher than ED patients (M = 48.28, SD = 13.68 vs M = 77.75, SD = 20.33) (Campana et al. 2013). This study also showed an inverse association between age and BCQ, such that younger age was associated with more frequent checking. In a large and ethnically diverse nonclinical sample by Lydecker et al. (2014) of 1,011 university women, the average total score was 52.14 (17.95). Additional analyses of racial influences on the BCQ revealed lower scores for black women (N = 260; 25.7%) compared to white participants or Asian participants (Ms = 47.04, 53.59, and 55.69, p 6 months in one study) and later menarchal age are determinants of bone density impairment. Growth Hormone (GH) - Insulin-like growth factor I (IGF-I) axis: Hepatic IGF-I secretion decreases as body mass index (BMI) and body fat decline. IGF-I enhances bone formation through its action on mature osteoblasts, and circulating IGF-I is important for preservation of cortical bone mass. IGF-I levels in patients with AN are positively correlated with BMD, irrespective of BMI levels. Adolescents with AN have low IGF-I levels despite high GH levels, reflecting an acquired GH resistance. As such, bone formation rates are decreased, associated with decreased bone turnover. In one study, the administration of supraphysiologic GH doses to adult women with AN was not shown to increase levels of IGF-I or bone formation markers (Fazeli et al. 2010). This observation reinforces the role that GH resistance and low IGF-I levels play in impaired bone metabolism in AN. Hypothalamic–pituitary–thyroid axis: Thyroid function may also be altered, with low T3 and low or low normal thyroxine which is thought to be related to diminished peripheral conversion. In addition, thyroid-stimulating hormone is typically low or low normal. These findings are consistent with a “sick euthyroid” state. The contribution of thyroid axis alterations to bone loss in AN is currently unclear. Hypothalamic–pituitary–adrenal axis: Individuals with AN have higher serum and urinary cortisol levels than controls. Hypercortisolemia has deleterious effects on bone strength and is detrimental to the bone through enhanced osteoblast and osteocyte apoptosis and reduced osteoblast and osteoclast formation. Cortisol is also known to increase the life span of osteoclasts
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leading to a temporary increase in bone resorption. Psychotropic medications: A common medication used in individuals with AN is a selective serotonin reuptake inhibitor (SSRI). One study reported that adolescents and young adults with AN taking SSRIs for more than 6 months had lower BMD (Misra et al. 2010). In addition, SSRIs have been associated with accelerated hip bone loss in postmenopausal women, lower hip BMD in aged men, and increased risk for fragility fractures in men and women over 50 years old. There is concern that SSRIs may have a harmful effect on bone mineral accrual if taken during childhood, a concerning finding as these agents are prescribed for young adolescents with AN. Measurement of Bone Health The most widely used imaging tool for the assessment of bone health is dual-energy x-ray absorptiometry (DXA), a measure of bone mineral content in a projected bone area (Gordon et al. 2014; Lewiecki et al. 2008). A BMD T-score (for adults) or Z-score (for adolescents) is generated by the scanner, which is then adjusted for age, gender, and often ethnicity. The interpretation of DXA Z-scores, which provide a two-dimensional assessment of bone density, can be challenging due to potential confounding by bone size. In an adolescent with growth deficits and short stature due to chronic AN, DXA results may overestimate skeletal losses. Therefore, bone mineral content and BMD should be adjusted for height in those with delayed growth or puberty, a serious complication of AN. Despite these limitations, DXA is a widely used densitometric technique that is safe, rapid, and reproducible and has low-radiation exposure. Individuals with AN should have DXA scans obtained annually during the period of restrictive eating due to a known high risk for low BMD and ongoing skeletal losses. Different groups of investigators use varying criteria to define skeletal losses and states of bone health, and preferred terminology also varies between children/adolescents and adults. The International Society for Clinical Densitometry (ISCD) recommends the term “osteopenia” not
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be used in pediatrics and should be reserved to describe deficits in bone mass in adults. ISCD has identified “low bone mass or BMD” (defined as BMD Z-score < 2.0 SD) as the preferred term for identifying children and adolescents with compromised skeletal health. According to recent ISCD guidelines, a diagnosis of osteoporosis must include both a documented low bone mass by DXA and evidence of skeletal fragility (Gordon et al. 2014; Lewiecki et al. 2008). Recent technology has improved a clinician’s ability to evaluate bone health with greater accuracy in the form of axial and peripheral quantitative computed tomography (QCT). These assessment tools provide a measurement of volumetric BMD and are more accurate than DXA, particularly in growing adolescent patients whose bone size changes over time and for individuals with chronic illness. However, the high radiation dose associated with axial QCT has limited its utility in general clinical practice. In contrast, peripheral QCT, and especially high-resolution peripheral QCT, examines bone microarchitecture with increased precision. Although these technologies are often available only at academic centers, ongoing research continues to consider whether computed tomography should be used as part of routine clinical practice. Management of Low Bone Density in Anorexia Nervosa Weight Gain and Resumption of Menstrual Function
In patients with AN, the best approach to managing bone health is treatment of the eating disorder, including normalization of weight and resumption of menstrual function (Misra and Klibanski 2014a, b). Studies in adolescents with AN have shown that weight gain and menstrual restoration halt skeletal losses. On the other hand, studies in adults have shown that while there is some improvement in bone accrual with weight gain, BMD remains lower than in healthy controls and catch-up does not occur. Weight restoration can be difficult to achieve and sustain in patients with AN. Therefore, it is critical to identify effective therapies to counter low bone density in this population.
Bone Health
Calcium
Sufficient calcium intake during adolescence is needed to maximize skeletal growth during the pubertal growth spurt. Given the known beneficial effects of calcium on bone mineralization among healthy youth, it is important to optimize intake of this micronutrient in patients with AN. Calcium requirements are ideally achieved through the diet. The Institute of Medicine recommends 1,000 mg/day of calcium for 4–8-year-olds and 1,300 mg for those aged 9–18 years. In adolescents with AN, reaching these nutritional goals can be challenging, and supplementation may be needed. Vitamin D
Vitamin D is necessary for efficient intestinal calcium absorption. Higher intake of vitamin D is associated with lower risk for stress fractures among healthy adolescent girls (Sonneville et al. 2012). There are no randomized controlled trials (RCTs) examining the use of vitamin D supplementation on bone density in AN. However, at least 600 IU of vitamin D per day is recommended to optimize bone health. Physical Activity
Among healthy children, engaging in physical activity early in life improves bone mass. Further, regularly menstruating adolescents are known to have a higher bone mass than sedentary controls. However, once young women become amenorrheic, the protective effect of exercise is lost. There are also data to suggest that physical activity may be detrimental in severely ill subjects with AN. Physical activity needs to be carefully weighed against delayed weight gain, prolonged amenorrhea, and the risk of fractures in young women with AN. Estrogen Replacement Therapy
The hypoestrogenic state in adolescents with AN is a risk factor for reduced BMD. Studies suggest that the use of oral contraceptives in these patients is not beneficial for bone health. Klibanski et al. conducted a randomized placebo-controlled trial testing skeletal effects of estrogen replacement therapy in 48 adults with AN. Patients were
Bone Health
followed for a mean of 1.5 years. The trial found no significant difference in lumbar spine BMD between the two groups. Only the most severely malnourished subjects (104 can be used as a cutoff to indicate caseness.
I have absolutely no control No, probably not
Most or all of the time
Okay about how my body looks/ never binge eat A great deal less
Historical Background The BULIT was first developed in 1984 to assess bulimia nervosa based on the DSM-III criteria. In 1991, an evaluation of the BULIT-R appeared, with the self-report items updated to assess DSM-III-R criteria for bulimia nervosa. It was developed over four stages with a number of
Bulimia Test-Revised (BULIT-R)
different groups of women, including women being treated for bulimia nervosa and healthy controls (Thelen et al. 1991). Further investigation suggests that it appears to be a valid instrument with which to identify individuals who meet DSM-IV criteria for bulimia nervosa (Thelen et al. 1996). The original factor structure of the BULIT-R revealed five similar, yet inconsistent factors, at two different stages of scale development. At the first stage of data analysis, the five factors identified for females were (1) binging and control, (2) radical weight loss and body image, (3) laxative and diuretic use, (4) self-induced vomiting, and (5) exercise. A similar five-factor structure was evident in the second study, with the exception of body image which loaded on the binging and control factor. Additionally, laxative use factored with vomiting rather than diuretic use.
Current Knowledge Two examinations of the BULIT-R in community adolescent populations have been conducted. In the first study (Vincent et al. 1999), 603 secondary school students participated, which included 306 girls aged between 11 and 17 years (M = 13.66, S.D. = 1.12) and 297 boys aged between 11 and 18 years (M = 13.89, S.D. = 1.13). In the second study (McCarthy et al. 2002), data were collected annually on three occasions from two samples of 12–18year-old females, one recruited from three public middle schools (n = 239; mean age 12.8 years) and one from two public high schools (n = 119; mean age 15.9 years). A factor analysis in the first study identified four similar factors for adolescent boys and girls: binging, control, normative weight loss (dieting and exercise), and extreme weight loss behaviors (vomiting, diuretics, and laxatives). The fourfactor structure extracted for girls accounted for 61.4% of the total variance, and for boys, the fourfactor structure accounted for 54.4% of the total variance. In this sample, the BULIT-R also demonstrated good reliability and adequate concurrent
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validity with five questions measuring binge eating as defined by the DSM-IV criteria for binge eating. The second study also gave results that provided strong evidence for the reliability and stability of the BULIT-R. Mean levels of the BULITR were remarkably consistent over 3 years, and this lack of change raised questions about the developmental trajectory of bulimic behaviors through adolescence. Given that larger epidemiological studies show that binge eating and purging are more likely to emerge in later adolescence, through to early adulthood, it may be that these findings simply reflect the lack of growth in these behaviors over that developmental period.
Current Controversies There has been some difficulty experienced in obtaining a stable factor structure of the BULITR across different groups. A review of factor analyses of the BULIT-R (Berrios-Hernandez et al. 2007) concluded that a number of solutions had been identified, the four- and five-factor structure previously outlined, as well as a one- and six-factor structure. The authors conducted a confirmatory factor analysis of the BULIT-R between 200 European-American women from a southwestern public university in the United States and 204 Spanish white women attending college at the University of Granada, Spain. They tested the different BULIT-R models reported previously by various investigators: a one-factor model, a four-factor model, a five-factor model, and a six-factor model. All the models fit poorly, and therefore an exploratory factor analysis was used to examine the structure in the cross-cultural sample. In the American sample, six factors were identified, but only four in the Spanish sample. Only two factors were the same between the two samples and also were consistent with previous results from other studies: binge eating and body concerns. An investigation of a subset of the 23 BULITR items which assess the binge eating, loss of control, and body image factors identified by
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Thelen et al. (1991) has shown it to be an excellent overall measure of binge eating disorder in obese populations (Vander Wal et al. 2011). This measure, called the Binge Eating Disorder Test (BEDT), does not include items loading on factors associated with purging behaviors, including radical weight loss measures, laxative/diuretic abuse, self-induced vomiting, and inappropriate/excessive exercise. The only exception was the addition of the item that assesses how the person feels right after binge eating, designed to measure disgust with oneself after binge eating, one of the features of binge eating disorder. The sensitivity, specificity, and positive and negative predictive values of the BULIT-R, BEDT, and the subscales of the Eating Disorder Examination-Questionnaire (EDE-Q) have been compared with respect to the BEDT diagnosis (Vander Wal et al. 2011). Results indicated that the BEDT performed best across all these indices, achieving 100%.
Future Directions The usefulness of the BULIT-R with adolescent and young adult community samples requires further investigation. Therefore, it may be that its use is best limited to clinical populations at this time, but further work is required to ascertain its unique contribution compared to other self-report instruments which assess diagnostic criteria, such as the Eating Disorder Examination.
Burnout
Cross-References ▶ Eating Disorder Questionnaire (EDQ)
References and Further Reading Berrios-Hernandez, M. N., Rodriguez-Ruiz, S., Perez, M., Gleaves, D. H., Maysonet, M., & Cepeda-Benito, A. (2007). Cross-cultural assessment of eating disorders: Psychometric properties of a Spanish version of the Bulimia Test-Revised. European Eating Disorders Review, 15(6), 418–424. McCarthy, D. M., Simmons, J. R., Smith, G. T., Tomlinson, K. L., & Hill, K. K. (2002). Reliability, stability, and factor structure of the Bulimia Test-Revised and eating disorder inventory-2 scales in adolescence. Assessment, 9(4), 382–389. Thelen, M. H., Farmer, J., Wonderlich, S., & Smith, M. (1991). A revision of the bulimia test: The BULITR. Psychological Assessment, 3, 119–124. Thelen, M. H., Mintz, L. B., Vander, W., & Jillon, S. (1996). The Bulimia Test-Revised: Validation with DSM-IV criteria for bulimia nervosa. Psychological Assessment, 8(2), 219–221. Vander Wal, J. S., Stein, R. I., & Blashill, A. J. (2011). The EDE-Q, BULIT-R, and BEDT as self-report measures of binge eating disorder. Eating Behaviours, 12(4), 267–271. Vincent, M. A., McCabe, M. P., & Ricciardelli, L. A. (1999). Factorial validity of the Bulimia Test-Revised in adolescent boys and girls. Behaviour Research & Therapy, 37(11), 1129–1140.
Burnout ▶ Assessment Burden
