Binge Eating Disorder Diagnosis and Treatment Options

Transcription

1 DISEASE MANAGEMENT CNS Drugs 1999 May; 11 (5): /99/ /$05.50/0 Adis International Limited. All rights reserved. Binge Eating Disorder Diagnosis and Treatment Options Timothy D. Brewerton Eating Disorders Program, Department of Psychiatry and Behavioural Sciences, Medical University of South Carolina, Charleston, South Carolina, USA Contents Abstract History and Diagnostic Classification Epidemiology Medical Comorbidity Psychiatric Comorbidity Treatment Psychotherapeutic Strategies Psychopharmacological Strategies Conclusion Abstract Binge eating disorder (BED) is a newly proposed eating disorder diagnosis that appears in the appendix of DSM-IV. BED describes a syndrome of recurrent binge eating in the absence of any maladaptive compensatory behaviours. Individuals with BED appear to demonstrate a primary disturbance of eating behaviour, which in some people may be secondary to affective and/or anxiety disorders. The chronic, recurrent bingeing associated with BED is thought to typically lead to obesity and its accompanying morbidity and mortality. BED is also associated with significant psychiatric comorbidity, including affective, anxiety and personality disorders, although the degree of psychopathology is usually not as severe as that of bulimia nervosa. In this paper, the history, diagnosis, epidemiology, associated psychiatric comorbidity and treatment approaches of BED are reviewed. Generally, cognitive-behavioural therapy and/or antidepressant medications are key treatment approaches. 1. History and Diagnostic Classification A new diagnostic category called binge eating disorder (BED) has been proposed in the appendix of DSM-IV. [1-6] BED is characterised by recurrent episodes of binge eating at least 2 days a week for at least 6 months, which is longer than the 3 months duration of bingeing required for a DSM-IV diagnosis of bulimia nervosa. BED also requires a subjective sense of a loss of control over the binge eating, as well as the presence of at least 3 of 5 specific criteria, including eating more rapidly than usual, eating large quantities of food when not physically hungry, eating alone due to embarrassment, eating until uncomfortably full and feeling selfdisgust, guilt or depression after bingeing. [1] Aspecific syndrome of overeating in the context of obesity was first described by Stunkard, who de-

2 352 Brewerton lineated the night eating syndrome in the 1950s. [7,8] Night eating syndrome is similar to, but distinct from, BED, which does not have the nocturnal component as a diagnostic requirement. In night eating syndrome, overeating episodes are not necessarily true binges; the episodes only occur at night, and the subsequent anorexia and food restriction occur in the morning. This pattern of restrained eating during the day is thought to contribute to the next cycle of overeating or bingeing at night for both night eating syndrome and BED. Other terms have appeared over the years to describe the phenomenon of severe, recurrent overeating or binge eating not complicated by purging, including obese bingeeaters, compulsive overeaters [9-11] and the stuffing syndrome. [12] Since DSM-III was first published in 1980, such patients have been classified as eating disorder not otherwise classified, but this is a nonspecific term and includes a number of subsyndromal features. [13] The discipline of psychiatry in the US first acknowledged binge eating in DSM-III (1980) in the classification of bulimia, a diagnosis that encompassed not only bingeing, but also purging and preoccupation with body shape and weight. [13] DSM-III-R, the revised edition of DSM-III published in 1987, adopted the term bulimia nervosa, which was originally coined in 1979 by Russell, [14] who conceptualised bulimia nervosa as an ominous variant of anorexia nervosa. [15] Binge eating per se without compensatory anti-obesity behaviours, was not identified as a specific psychiatric syndrome or problem until DSM-IV included BED in the Appendix as a diagnosis to be considered. [1] As psychiatric knowledge has accumulated and evolved over time, so our diagnostic nomenclature has evolved to reflect this knowledge and to more precisely describe psychiatric disease states. As part of this process, the eating disorders have only recently received serious research attention compared with other disorders. The inclusion of binge eating without compensatory behaviours as an illness is a natural extension of this evolving process of understanding the bulimic disorders spectrum. BED is in fact a serious behavioural health problem that appears to have been underrecognised and undertreated. In my opinion, the diagnostic recognition of BED will allow this group of patients to be further studied from a clinical research perspective, and it will also allow them to get more accessible and appropriate treatment. However, the exact boundaries of the disorder remain to be further delineated, and it is likely that eating disorder diagnostic criteria in general will continue to evolve as our knowledge base expands, particularly in the area of genetics of psychiatric disorders and obesity. One of the existing problems regarding the diagnosis of BED includes differentiating it from bulimia nervosa, nonpurging type, as currently defined by DSM-IV. [16] The nonpurging type of bulimia nervosa involves fasting and excessive exercise as compensatory behaviours, as well as binge eating and preoccupation with body weight and shape. [1] However, it is arguable to what extent the similarities between the nonpurging type of bulimia nervosa and BED appear to outweigh their differences. In clinical practice, these disorders tend not to be distinct entities, but rather exist on a continuum. Patients may move in and out of specific eating disorder diagnostic criteria over time. Sometimes it is also quite difficult clinically to distinguish between what are appropriate versus inappropriate bodyweight loss measures, such as to what extent exercising is excessive or compulsive. It is notable to this discussion that patients with obesity and bingeing behaviour [17,18] and patients with BED have been reported to have similar attitudes about body shape and weight compared with patients with both nonpurging [19] and purging bulimia nervosa. [20] However, regardless of what label the syndrome carries, it is clear from epidemiological studies that a significant number of people experience clinically significant binge eating not complicated by compensatory measures. Taken together, this condition, now called BED, certainly warrants further recognition, treatment and research. One laboratory study of patients with obesity and BED compared with patients with obesity but without BED confirmed that BED patients eat significantly more calories during a binge meal than

3 Binge Eating Disorders: Diagnosis and Treatment 353 non-bed patients. [21,22] Dietary restraint and/or disinhibition appear to play major roles in triggering binge episodes. [23-25] 2. Epidemiology As discussed in section 1, investigators have noted for several decades that clinically significant recurrent binge eating occurs in a significant subset of obese individuals. As a logical progression of this inquiry, the prevalence rates of BED were initially reported in samples of obese patients attending weightloss programmes or clinics. [3-5] In these cohorts, 20 to 46% of patients were said to endorse BED criteria using self-report questionnaires. [3,5,10,11] However, an important finding has been that patients tend to over-endorse BED symptoms on selfreport measures when compared with structured interviews using standardised criteria. [8,26,27] Spitzer and associates reported that the prevalence of BED in cross-sections of weight control patients as assessed by questionnaire was approximately 30%, with the rate being slightly higher in females than males. [3] These same authors went on to complete 2 field studies of nonpatient community samples and reported a BED prevalence of 3.3 and 4.6%, with overall rates again being comparable in women and men (5.3 and 3.1%, respectively). [5] In a sample of college students, the BED prevalence rate was 2.6%, and likewise there was no significant gender difference, which is an important difference between BED and bulimia nervosa patient groups. The validity of the diagnosis of BED has been strengthened by links with impaired functioning in occupational and social areas, overconcern with body shape and weight, degree of general psychopathology and amount of time dieting. Interestingly, there were no significant racial differences found in BED prevalence rates in any of these studies. Our group surveyed a representative sample of over 3000 adult women in the US (the National Women s Study) using a structured, computerised telephone interview based directly on proposed DSM-IV criteria for BED and DSM-III-R criteria for bulimia nervosa. [28-30] Our results indicated that 1.0% of women over the age of 18 years met full lifetime criteria for BED over and above another 2.4% of women who met lifetime bulimia nervosa criteria. Approximately two-thirds of both diagnostic groups met current diagnostic criteria, which was defined as the 12-month prevalence rate. Significant differences were not found for age, bodyweight or race between respondents with BED and those with bulimia nervosa, although both the BED and the bulimia nervosa respondents were significantly younger and heavier than the non-bed/nonbulimia nervosa respondents. Interestingly, when we relaxed the binge duration criterion to 3 months (from 6 months), the BED prevalence rate increased to 1.6% (from 1.0%). [28] Because these results were acquired from a meticulously controlled, representative sample, they substantiate that a sizeable group of adult women in the US have clinically significant bingeing without purging. These results contribute to the credibility of BED. Results from a structured telephone interview completed in a community-based Californian, US sample indicated that 1.8% of 455 adult women met DSM-IV BED criteria. [31] In addition, another 3.8% of these women met all BED criteria except that of frequency. Results from a questionnaire-based community studyinnorwayof1849womenindicatedthatthe lifetime prevalence of BED was 3.2%. [32] In a similar study based on a self-report questionnaire completed in France, the rate of BED was 9 to 15% in bodyweight control samples and 0.7% in a community sample of 447 nontreatment-seeking women. [33] A very low BED prevalence in the UK was also recently reported. [34] Despite the major methodological differences among these studies, the results indicate that the prevalence of BED, like that of other eating disorders, may indicate some degree of cultural variability. 3. Medical Comorbidity Medical conditions associated with BED are essentially the same medical conditions that are associated with obesity, including higher mortality and morbidity from adult-onset (type 2) diabetes

4 354 Brewerton mellitus, hyperlipidaemias, cardiovascular diseases, several cancers and sleep apnoea. In general, disease prevalence increases as bodymass index [bodyweight (kg)/height (m) 2 ]increases. As the increasingly apparent interrelationships between psychiatric disorders and obesity are recognised, and as the pervasive stigmatisation of both the mentally ill and the obese in Western culture continues, a comprehensive psychiatric perspective is going to be needed for optimal evaluation and treatment of patients with BED. This is especially true given the fact that many medications, both psychotropic and nonpsychotropic, are associated with bodyweight gain and subsequent obesity. Hence, clinicians are often faced with the proverbial rock and a hard place. Obese patients with BED appear to have higher degrees of both eating- and bodyweight-related pathology, body image distortion and body preoccupation when compared with obese patients without BED. [11,35,36] It also appears that obese patients who binge eat find it more difficult to lose bodyweight and remain in weightloss programmes, [10,37] although in one well controlled study the presence of BED did not affect outcome of bodyweight loss, nor was there a higher withdrawal rate when compared with the non-bed obese patients. [38] On the contrary, in the community study by Ferguson and Spitzer, successful dieters were less likely to meet BED criteria than unsuccessful dieters. [39] No differences have been found in serum lipid levels, thyroid hormone levels or resting metabolic rate between obese binge eaters and nonbinge eaters. [40,41] The degree of bodyweight cycling or yo-yo dieting has been reported to be higher in obese patients with binge eating compared with those without bingeing in one, [42] but not in another, study. [41] 4. Psychiatric Comorbidity The relationship between eating disorders, including BED, and other psychiatric disorders has been a significant area of interest to clinicians and researchers alike. Several investigators have noted that binge eating occurs in a subset of obese patients in response to emotional stress, a phenomena which has been termed emotional eating. [43,44] In one study, BED patients were more likely to overeat in response to negative emotional states. [19] Diagnostic studies of obese patients with BED indicate higher than expected rates of affective, anxiety and personality disorders, as well as emotional problems in general. [40,42,44-50] In a study of 107 obese women meeting BED criteria who completed several psychometric instruments, there was a significant positive relationship between binge eating severity and degree of psychiatric symptomatology. [44] DeZwaan and colleagues also found a relationship between binge eating and a number of measures of psychopathology. [42] In a structured telephone interview of a large, nonclinical sample of US women (n = 3006) [the National Women s Study], the lifetime prevalence of major depression was 31% in respondents meeting BED criteria and 36% in respondents meeting bulimia nervosa criteria; rates which were significantly higher than the nonbingeing group (15%). [28] It is important to note that major depression was not present in the majority of respondents, since some BED opponents argue that binge eating is merely a symptom, albeit atypical, of depression. Although these results do not support this hypothesis, BED may be associated with subclinical affective and perhaps anxiety disorders. A recent study confirmed that dysphoric mood states often trigger binge eating episodes accompanied by a subjective sense of being out of control. [44] However, these patients do not necessarily meet the criteria for major depression at the time of bingeing, or ever. In a study of the chronological relationship between the times of onset of bingeing, dieting and depression, it was found that BED patients on average tended to begin bingeing during adolescence before the onset of dieting, obesity or depression. [51] At any rate, the higher rates of depression associated with BED are compatible with an affect dysregulation hypothesis for binge eating. In the National Women s Study, Dansky and colleagues also discovered that the lifetime prevalence of post-traumatic stress disorder was 21% in BED

5 Binge Eating Disorders: Diagnosis and Treatment 355 respondents compared with 9% in the nonbingeing respondents. [28] In contrast with bulimia nervosa, the rates of crime victimisation experiences, including rape, molestation, attempted sexual assault and aggravated assault, were comparable with the non- BED/non-bulimia nervosa group. Nevertheless, the higher rate of lifetime post-traumatic stress disorder in the patients with BED imply that they may have been exposed to other types of traumatic events or experiences more frequently in comparison with the people without BED or bulimia nervosa. In a study of a clinical sample, there was no significant difference in reported rates of sexual abuse in BED versus non-bed obese patients, but BED patients did have significantly higher rates of panic disorder and personality disorders than the non-bed obese patients. [47] In clinical practice, patients with BED often report histories of significant family dysfunction associated with emotional abuse and/or neglect, if not overt childhood physical and/or sexual abuse. Hodges and colleagues reported results from the Family Environment Scale in 131 patients with an eating disorder presenting for evaluation and treatment, including 43 with BED. [52] Significantly lower scores were found on the activity-recreation subscale for the BED group compared with the anorexia nervosa, bulimia nervosa and anorexia nervosa plus bulimia nervosa groups. Results also indicated that the patients with BED perceived their families to be less cohesive compared with the anorexia nervosa patients, but not the bulimia nervosa patients. In addition, the patients with BED had higher control and conflict subscale scores, and lower cohesiveness, expressiveness, independence, intellectualcultural and activity-recreation subscale scores, when compared with 2 healthy control samples previously published. Impulsive behaviours, such as compulsive buying and kleptomania, have been reported in patients with BED. [53] In addition, higher rates of cluster B and C personality disorders, but not substance abuse disorders, have been reported in patients with BED. [47,49] Furthermore, the rates of alcoholism in the family members of patients with BED were significantly higher. [47] Given these data, researchers have placed BED within the continuum of compulsive-impulsive disorders [53] as well as the affective spectrum disorders. [54] 5. Treatment 5.1 Psychotherapeutic Strategies Studies indicate that behavioural treatments for obesity tend to only work in the short term for the vast majority of patients attempting to lose bodyweight. [37] However, patients with BED seem to be relatively less responsive to these commonly employed treatment strategies. Even if bodyweight is successfully reduced in the short term, BED patients may be more apt to relapse in the long term. Converging evidence suggests that dietary restraint or overt dieting has a disinhibiting effect on overeating or bingeing and consequently contributes to the marked bodyweight fluctuations that are typical of these patients histories. Importantly, the psychiatric comorbidity and/or emotional issues are not addressed in strictly behavioural forms of treatment and may therefore contribute to refractoriness and/or relapse. Patients with BED usually have a variety of needs that are best approached from the perspective of the biopsychosocial model. A multidisciplinary approach is therefore usually required for optimal evaluation and treatment, including networking among all professionals involved, e.g. the patient s primary care provider, psychiatrist, psychotherapist, dietician, physical therapist, etc. Most clinicians who work with BED patients share the common treatment philosophy of initially making the goal of bodyweight loss secondary to the primary goal of decreasing or eliminating binge eating and normalising eating behaviour. In addition, addressing associated psychiatric disorders and/or emotional symptoms often must take precedence in order for successful treatment to occur. Guided by the successes in treating bulimia nervosa, [55,56] major depression and most anxiety disorders, recent well controlled studies [57-61] using manual-driven cognitive-behavioural therapy have shown great promise in the treatment of BED. In

6 356 Brewerton cognitive-behavioural therapy, specific attention is directed toward the patient s behaviour and thought patterns instead of the traditional focus on associated feelings, intrapsychic conflicts and other psychodynamic issues, such as transference. In addition, cognitive-behavioural therapy places a strong emphasis on education, monitoring of food intake, identifying cognitive distortions (or false beliefs) and replacing them with rational or reality-based thoughts. So far, there has been one uncontrolled trial [62] and a few controlled trials of cognitivebehavioural therapy in BED [57-61] (table I). Even less well studied is the effect of interpersonal psychotherapy on BED (table I), which has also been found to be helpful in both patients with major depression and those with bulimia nervosa. [56,58,59] Taken together, the preponderance of evidence supports the premise that effective treatment for patients with BED, at least in the short term, should focus first on reducing binge eating per se as well as on establishing a regular meal pattern with little or no snacking, particularly before bedtime. In addition, identifying and challenging distorted thoughts associated with this eating disorder is warranted. If bingeing and its associated dietary restraint and disinhibition are controlled, then some degree of bodyweight loss is often a natural outcome. As a result, patients may also have more energy to begin a reasonable exercise programme, starting off and progressing very slowly, and consequently becoming less depressed and anxious. In patients with significant concomitant psychiatric comorbidity (usually mood and/or anxiety disorders) psychotherapeutic strategies will of course need to address these disorders as well. Furthermore, when patients are unresponsive to reasonable trials of psychotherapeutic and/or behavioural approaches, then psychopharmacological interventions should be considered as adjunctive treatment. 5.2 Psychopharmacological Strategies Because of the convincing links between serotonin (5-hydroxytryptamine; 5-HT) dysregulation and affective, anxiety and eating disorders, [63] clinical researchers have speculated that the selective serotonin reuptake inhibitors (SSRIs) could possibly be effective treatments for obesity as well as BED. The published results from controlled studies aresummarisedintableii. [64-67] Preliminary results from open-label drug studies in patients with BED using SSRIs other than fluoxetine and fluvoxamine, e.g. paroxetine, have Table I. Psychotherapy studies in binge eating disorder (BED) and related conditions Reference Patients Treatment Duration Results (weeks) Telch et al. [57] 44 women with nonpurging bulimia nervosa CBT vs wait list 10 94% decrease in binge eating with CBT (79% abstinent) vs 9% decrease with no Tx Wilfrey et al. [58] Smith et al. [59] Eldredge et al. [60] Agras et al. [61] Agras et al. [62] 55 women with nonpurging bulimia nervosa 8 obese women with binge eating 44 women and 2 men with BED not responsive to CBT and bodyweight loss Tx 93 obese women with BED not responsive to 12 weeks of CBT 43 women and 7 men with BED not responsive to CBT CBT vs IPT vs wait list 16 Both CBT (48%) and IPT (71%) significantly reduced binge eating compared with no Tx (10%). Good follow-up data at 6 and 12 months Open CBT 16 81% decrease in binge eating Extended CBT vs wait list following CBT and bodyweight loss Tx CBT followed by bodyweight loss Tx IPT added to CBT (12 weeks) 36 (total) Extending CBT led to improvement in 67% of patients previously unresponsive 52 week follow-up CBT = cognitive-behavioural therapy; IPT = interpersonal psychotherapy; Tx = treatment. Reductions in binge eating and abstinence rates were mostly maintained. Successful bodyweight loss linked to binge abstinence 24 (total) No added benefit of IPT to CBT nonresponders

7 Binge Eating Disorders: Diagnosis and Treatment 357 Table II. Psychopharmacological studies in binge eating disorder (BED) and related conditions Reference Patients Treatment Duration Results Marcus et al. [45] 45 obese women with and without binge eating Greeno & Wing [64] 50 overweight women with and without BED Fluoxetine + behaviour modification vs placebo + behaviour modification 52 weeks Presence of binge eating did not predict bodyweight loss, which was greater with drug Fluoxetine vs placebo 4-6 days Fluoxetine significantly reduced binge frequency vs placebo irrespective of BED status Darga et al. [65] 45 women with obesity Fluoxetine vs placebo 52 weeks Significant early bodyweight loss with fluoxetine, but effect disappeared by end of 1 year because of regain Hudson et al. [67] 85 patients with BED (77 women and 8 men) McCann & Agras [68] 23 women with nonpurging bulimia nervosa Alger et al. [69] 22 patients with bulimia and 33 with obesity and bingeing Guy-Grand et al. [70] 822 obese patients (662 women and 160 men) Fluvoxamine vs placebo Desipramine vs placebo Imipramine vs naltrexone vs placebo Dexfenfluramine vs placebo Stunkard et al. [71] 28 women with BED Dexfenfluramine vs placebo Marrazzi et al. [72] 36-year-old woman with BED Naltrexone vs placebo (single case, crossover design) Drewnowski et al. [73] 41 women (16 with obesity and binge eating and 25 with normal bodyweight) BMI = bodymass index; IV = intravenous. Naloxone vs butorphanol vs placebo 9 weeks Fluvoxamine significantly reduced binge frequency and increased rate of BMI reduction 12 weeks 63% decrease and 60% abstinence with desipramine vs 16 and 15%, respectively, with placebo 8 weeks Imipramine and naltrexone significantly reduced duration of binge episodes in patients with obesity and bingeing and bulimia, respectively 52 weeks Dexfenfluramine significantly reduced bodyweight vs placebo 8 weeks Dexfenfluramine significantly reduced binge frequency vs placebo 18 weeks Naltrexone reduced binge eating vs placebo, especially at high dosage (400 mg/day) Single dose (acute IV bolus) Naloxone reduced intake of sweet and high fat foods in patients with obesity and bingeing vs butorphanol and placebo demonstrated notable reductions in binge frequency (see McElroy et al. [53] for review). More controlled studies in patients with BED using new generation antidepressants are definitely required, but agents which inhibit serotonin reuptake show some promise. Reports of studies involving tricyclic antidepressants (TCAs) indicate their possible usefulness in binge eaters, despite their relative lack of neurotransmitter specificity and more numerous adverse effects and complications compared with newer antidepressants (table II). [68,69] TCAs, especially desipramine, may hence offer some relief as pharmacological treatments for BED, as well as for bulimia nervosa. In clinical practice, however, it is generally advised that the initial psychopharmacological treatment strategy involves an SSRI. [54] The TCAs are commonly associated with bodyweight gain, probably resulting from a combination of induced hyperphagia via stimulation of hypothalamic noradrenergic pathways as well as a decrease in metabolic rate. However, among the TCAs, desipramine is probably the least likely to cause these adverse effects. Treatment of BED with monoamine oxidase inhibitors (MAOIs) is of dubious value in patients who by definition are out of control of their eating and who would have difficulty maintaining the required restriction of tyramine-rich foods. However, MAOIs should be a consideration in distinct cases of atypical depression (characterised by hyperphagia, hypersomnia and anxiety) that have not

8 358 Brewerton responded to SSRIs (e.g. fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram), other agents that inhibit serotonin reuptake (e.g. venlafaxine), serotonin antagonist/reuptake inhibitors [SARIs] (e.g. nefazodone) and TCAs (e.g. desipramine). Table III provides recommended initial starting and maintenance dosages for the treatment of BED. It should be noted that it may take several weeks for the full effect of the medicine to occur. Dexfenfluramine, a pre-synaptic agonist of serotonin and a mild reuptake inhibitor, is no longer an option for patients with obesity, bulimia nervosa or BED, but its efficacy indicates a specific mechanism of action that is likely to be considered in the process of future drug development. [70,71,74-76] In each of the studies on patients with binge eating, binge frequency almost invariably returned to baseline levels after discontinuing the drug, much like the bodyweight regain that commonly occurs when any type of anorexiant is stopped. Its potential to produce life-threatening primary pulmonary hypertension was of great concern to researchers, clinicians and patients alike. [77] When it was discovered that it also induced valvular heart disease it was taken off the international market. [78] No reports were found in the literature on the effects of psychostimulants in the treatment of BED. Although stimulants have been shown to suppress binge eating in the short term, [79] the risks of dependence and the possible aggravation or induction of affective and psychotic symptoms make this class of drugs undesirable as therapeutic tools. The opioid receptor antagonists, naltrexone and naloxone, have been reported to exhibit therapeutic effects in patients with BED and binge eating (table II). [69,72,73] These studies may be relevant to the report that obese BED patients have significantly higher pain detection thresholds when compared with both non-bed obese patients and healthy controls. [80] Finally, sibutramine, a serotonin and noradrenaline (norepinephrine) reuptake inhibitor without apparent antidepressant properties, has just been released in the US for the adjunctive treatment of obesity (along with behaviour therapy). Results from a number of double-blind, placebo-controlled studies have demonstrated that this new agent is effective in patients with obesity. [81,82] However, its usefulness in the treatment of BED per se has not yet been reported, even in open studies, but it nevertheless holds promise on theoretical grounds. Even though sibutramine is not an antidepressant, antidepressant response has generally not been found to be associated with anti-bulimic response in studies of bulimia nervosa or BED. In the only published study reporting on the combination of psychotherapy with medication, the addition of desipramine did not increase the anti-binge effect of cognitive-behavioural therapy. However, Table III. Recommended daily initiation doses (mg) and maintenance dosages (mg/day) of psychopharmacological agents for the treatment of binge eating disorder Drug Initiation dose a Initiation dose b Maintenance dosage Fluoxetine Sertraline Paroxetine Fluvoxamine Citalopram Venlafaxine Nefazodone Desipramine Imipramine Clomipramine Naltrexone a Patients with panic attacks/disorder typically require lower initiation doses of antidepressants than those without the disorder since these agents may exacerbate anxiety acutely before they eventually attenuate or alleviate it. b Patients without panic attacks/disorder.

9 Binge Eating Disorders: Diagnosis and Treatment 359 bodyweight loss per se was facilitated by the combination. [83] More time and knowledge will be required to determine how similar the pharmacological mechanisms underlying binge eating reduction are to those underlying bodyweight reduction per se.however, whether the addition of cognitive-behavioural therapy to antidepressants enhances response has not yet been determined, but my clinical impression is that it does help. Future avenues to more effective pharmacological treatments for BED will most likely follow obesity research studies, as well as new developments in the treatment of bulimia nervosa. Under current investigation are agents that enhance energy expenditure and which target leptin and its receptors, neuropeptide satiety agents, e.g. neuropeptide Y, cholecystokinin and obesity genes. [84] 6. Conclusion In summary, the proposed diagnostic entity in DSM-IV of BED appears to be a well validated condition characterised by recurrent binge eating without compensatory behaviours of any type. BED differs from bulimia nervosa, nonpurging type, by the absence of fasting or excessive exercise as a way of counteracting the inevitable bodyweight gain effects of binge eating. However, in the clinical setting these conditions may be difficult to distinguish from each other given their overlap in symptoms as well as inconsistencies in self-report. The lifetime prevalence of BED in US women is approximately 1%, and a sizeable proportion (up to 30%) of those seeking bodyweight loss treatment in bariatric programmes will also meet the criteria. It is essential that the diagnosis of BED not be based on self-report alone, since over reporting is possible. Although a self-report instrument may serve as a useful screening tool, actual diagnoses should be based on structured clinical interviews. BED is often associated with specific medical and psychiatric comorbidities, especially obesity and its complications, affective disorders and anxiety disorders, particularly panic disorder and posttraumatic stress disorder. Both psychotherapeutic and psychopharmacological treatment strategies show efficacy in the studies done so far, but the field is young. Current data suggest starting with cognitive-behavioural therapy and aggressively treating associated psychiatric comorbidity, perhaps with an SSRI such as fluoxetine or fluvoxamine. If this fails, a trial of desipramine, nefazodone, venlafaxine or naltrexone/naloxone should be a consideration. In all cases a comprehensive risk-benefit analysis (of both treatment and nontreatment) must be conducted before treatment is initiated. References 1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Press, Spitzer RL, Devlin MJ, Walsh BT, et al. Binge eating disorder: to be or not to be in DSM-IV. Int J Eat Dis 1991; 10: Spitzer RL, Yanovski S, Wadden T, et al. Binge eating disorder: its further validation in a multisite study. Int J Eat Dis 1993; 13: Spitzer RL, Stunkard A, Yanovski S, et al. Binge eating disorder should be included in DSM-IV: a reply to Fairburn et al. s The classification of recurrent overeating: the binge eating disorder proposal. Int J Eat Dis 1993; 13: Spitzer RL, Yanovski S, Wadden T, et al. Binge eating disorder: its further validation in a multisite study. Int J Eat Dis 1993; 13: Brody ML, Walsh BT, Devlin MJ. Binge eating disorder: reliability and validity of a new diagnostic category. J Consult Clin Psychol 1994; 62: Stunkard AJ. Eating patterns and obesity. Psychiatr Q 1959; 33: Stunkard AJ, Berkowitz R, Wadden T, et al. Binge eating disorder and the night-eating syndrome. Int J Obesity 1996; 20: Loro AD Jr, Orleans CS. Binge eating in obesity: preliminary findings and guidelines for behavioral analysis and treatment. Addict Behav 1981; 6: Marcus MD, Wing RR. Binge eating among the obese. Ann Behav Med 1987; 9: de Zwaan MD, Mitchell JE. Binge eating in the obese. Ann Med 1992; 24: Kornhaber A. The stuffing syndrome. Psychosomatics 1970; 11 (6): American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 3rd ed. Washington, DC: American Psychiatric Press, American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Press, Russell GFM. Bulimia nervosa, an ominous variant of anorexia nervosa. Psychol Med 1979; 9: Spitzer RL. Nonpurging bulimia nervosa and binge eating disorder. Am J Psychiatry 1991; 148: Cash TF. Binge-eating and body images among the obese: a further evaluation. J Soc Behav Personal 1991; 6: Wilson GT, Nonas CA, Rosenblum GD. Assessment of binge eating in obese patients. Int J Eat Dis 1993; 13: 25-33

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