Management of Psychiatric Comorbidity in Anorexia ... - Springer Link

CNS Drugs 2006; 20 (8): 655-663 1172-7047/06/0008-0655/$39.95/0

THERAPY IN PRACTICE

© 2006 Adis Data Information BV. All rights reserved.

Management of Psychiatric Comorbidity in Anorexia Nervosa and Bulimia Nervosa Blake D. Woodside and Randolf Staab Program for Eating Disorders and the Department of Psychiatry, Toronto General Hospital, Toronto, Ontario, Canada

Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 655 1. General Approaches to Treating Comorbidity in Eating Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 656 2. Disorders of Mood . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 656 2.1 Depression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 656 2.2 Bipolar Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 658 3. Anxiety Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 658 3.1 Obsessive-Compulsive Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 659 3.2 Panic Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 659 3.3 Social Anxiety Disorder/Social Phobia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 660 3.4 Specific Phobias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 660 3.5 Post-traumatic Stress Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 660 4. Substance Abuse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 662 5. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 662

Abstract

The eating disorders anorexia nervosa and bulimia nervosa present with comorbidity in a number of important areas, including depression, bipolar disorder, anxiety disorders (obsessive-compulsive disorder, panic disorder, social anxiety disorder and other phobias, and post-traumatic stress disorder) and substance abuse. The most important principle of treating comorbidity in these conditions is the recognition of the effect of starvation and unstable eating on both the diagnosis and response to treatment of the comorbidity. This article reviews the identification of the most common areas of comorbidity and describes treatment approaches for these conditions. When it occurs, clinicians should treat comorbidity in patients with eating disorders in the usual fashion, but must remain aware that the disturbed eating itself will negatively affect response to treatment.

656

Woodside & Staab

Treating the eating disorders anorexia nervosa and bulimia nervosa is a relatively complex procedure at the best of times. The addition of significant psychiatric comorbidity, an all too common occurrence, adds yet more complexity to this situation. This article describes the common areas of comorbidity in these conditions that might present to the average clinician and lays out the useful approaches to treatment. The article does not attempt to address all possible areas of comorbidity. 1. General Approaches to Treating Comorbidity in Eating Disorders There are a few basic premises that must be considered when attempting to treat comorbidity in anorexia nervosa and bulimia nervosa. The first is the profound effect of starvation on mood and cognition. Most of our understanding of the effects of starvation and hunger on mental state comes from the seminal study of Keys and colleagues.[1] This study, conducted at the University of Minnesota, USA, at the end of World War II, subjected 36 conscientious objectors to a period of 6 months of semi-starvation, during which time the participants’ physical and psychological responses to starvation were monitored. Somewhat surprisingly to the investigators, the psychological effects of starvation were found to be just as important as the physical effects. Subjects in the experiment described a wide range of alterations in their mood, cognition and general intellectual functioning. While the study may seem to be relevant only to anorexia nervosa, individuals with bulimia nervosa experience many of the same effects, although to a diluted extent. At present, the dominant theory of the underlying causes of binge eating suggests that bingeing is largely a release phenomenon, an adverse effect of underlying hunger and starvation. It is of course thought that additional cues can be added to hunger, i.e. loneliness, boredom, anger, etc., but that these are less likely to cause binge © 2006 Adis Data Information BV. All rights reserved.

eating in an individual who is not nutritionally deprived to begin with. Individuals who binge-eat in response to hunger or dieting are thought to be genetically predisposed to such behaviour. Such individuals are continuously hungry and thus experience attenuated starvation effects. The main principle of treating comorbidity in these eating disorders is that minimal change can be expected in a comorbid condition if the patient is still starved. Without concurrent interventions to alter nutritional status, very little, if any, improvement can be expected in virtually any comorbid condition. As the specific approaches to treatment of the underlying eating disturbance are somewhat specialised, most clinicians gravitate to what they know how to treat, specifically the common types of comorbid illnesses that these individuals experience. Clinicians who are asked to treat comorbid conditions need to be reasonably convinced that some intervention focused on the core eating disorder symptoms is being provided if the expectation is for significant change to occur in the area of comorbidity. If no such intervention is being provided, then the clinician needs to be very realistic about the likelihood of a successful treatment. 2. Disorders of Mood Disorders of mood are extremely common comorbid conditions in individuals with eating disorders. The lifetime prevalence of comorbid depression in those with eating disorders approaches 75% in some studies.[2,3] Bipolar disorder occurs in a minority of those with either anorexia nervosa or bulimia nervosa. Perhaps 10% of patients with a severe eating disorder will also experience a comorbid bipolar illness at some point in their lifetime.[4] 2.1 Depression

The first problem in treating depression in patients with eating disorders is accurate diagnosis. It CNS Drugs 2006; 20 (8)

Treating Comorbidity in Eating Disorders

is extremely difficult to make an accurate diagnosis of depression in either anorexia nervosa or bulimia nervosa as a result of the confounding effects of starvation. In anorexia nervosa, most patients will identify that their mood is abnormal and usually will use the word ‘depressed’. A more careful investigation will usually reveal that what is happening is that the patient is experiencing flat or empty mood, or extreme lability of mood. The assessment of vegetative symptoms is not very helpful – energy, libido, appetite and sleep are all disrupted on account of starvation. Cognitively, the patient may experience significant helplessness or hopelessness, but this is often due to the chronic nature of their condition or is a consequence of some adverse effects of being ill on their lives or general functioning. For bulimia nervosa, the most common presentation is labile mood, often with suicidality. A careful history will usually identify this pattern and allow for it to be distinguished from the more typical picture of relentless depressed mood that is the hallmark of a genuine depression. As is the case with anorexia nervosa, an assessment of vegetative and cognitive features may be of little help in making the diagnosis.

657

necessary to reduce the dosage of the antidepressant on the basis of a patient’s weight, some patients of very low weight may need to be given lower dosages than normal if they experience very significant adverse effects. However, it is very important to provide an adequate dosage of the drug in question. In the clinical experience of the authors, it is important to make the patient aware that if his or her eating does not improve substantially then he or she should expect only limited benefits from the antidepressant treatment (in the order of a 25% improvement in mood). There are no specific trials examining this issue. Such a patient should be informed that complete resolution of mood symptoms is extremely unlikely without a concurrent resolution of the underlying eating disturbance, and that the antidepressant is not likely to have much of an effect on underlying anorexic symptomatology. These issues are commonly misunderstood by individuals with eating disorders.

If the clinician is convinced that a genuine depressive illness accompanies either anorexia nervosa or bulimia nervosa, then it is appropriate to initiate treatment. In such a case, any modern antidepressant is acceptable, with the exception of bupropion, which can be associated with seizures in those with binge eating and/or purging. The benefits of older antidepressants, such as TCAs and MAOIs, need to be carefully weighed against their less favourable adverse effect profiles and risk when taken in overdose.

If the patient is also making improvements in his or her eating, it is our experience that a period of approximately 6 weeks of normal eating is usually enough to ‘clear the field’ and allow for a more typical assessment of mood. This is true both for those with bulimia nervosa and anorexia nervosa. It is commonly believed that those with anorexia nervosa will not respond to antidepressants until they are fully weight-restored. This is not actually the case; individuals who are in treatment that allows for steady improvements in nutritional status and weight gain will look much more ‘normal’ after 1–2 months of such treatment, and will achieve much more typical responses to antidepressant therapy as long as they continue to eat normally.

Dosages used should be those for depression in any other setting. Therefore, for example, fluoxetine, paroxetine and citalopram should be started at 20 mg/day, sertraline at 100 mg/day, venlafaxine at 75 mg/day, and so forth. Although it is not generally

Another significant issue is absorption of medication, especially among those patients with purging behaviours such as vomiting or laxative abuse. It is always worth asking about the timing of medication administration for such patients, just to make sure


CNS Drugs 2006; 20 (8)

658

Woodside & Staab

that they are being taken at a time when purging will not occur. There is a significant role for cognitive therapies for depression in these patients, especially as most of the psychotherapeutic treatments for both anorexia and bulimia nervosa do involve a cognitive component. There is, however, no evidence to suggest that cognitive therapy is a superior modality of treatment compared with pharmacological treatments, and very underweight patients may be too starved to participate effectively in cognitive therapy. Decisions regarding more aggressive treatment for depression accompanying significant eating disorder symptoms need to be made on a case-by-case basis. Augmentation strategies are useful at times but do not generally lead to a complete resolution of symptoms. There is probably no role for electroconvulsive therapy in depression accompanied by significant eating symptoms. 2.2 Bipolar Disorder

Diagnostically, the labile mood experienced by some patients, especially those with bulimia nervosa, may be confused with or obscure the signs of bipolar disorder. For those with anorexia nervosa, the affect-flattening effects of starvation may mask episodes of mildly elevated mood. Various treatments for the underlying eating disturbance may also have some impact on making an accurate diagnosis of bipolar disorder. For example, the administration of antipsychotics, either as a primary or secondary treatment for the eating disorder, may mask symptoms of mania. Treatment of bipolar disorder is as complex as that of depression in these patients. For individuals with bulimia nervosa, their unstable eating tends to make it difficult for them to experience normal mood. Purging behaviours can also pose a significant problem for these patients, not only because of drug absorption issues but because of fluid and © 2006 Adis Data Information BV. All rights reserved.

electrolyte disturbances. The latter issue is especially important if lithium is being used to treat the bipolar disorder, as low serum potassium levels can start to interfere with the renal control of lithium excretion, occasionally causing lithium toxicity. Careful monitoring of both serum electrolyte levels and lithium concentration is important in such patients. It is likely that the most vexing problem in the treatment of bipolar disorder in eating disorders is the patients’ extreme awareness and concerns about the common adverse effects of agents typically used to treat bipolar disorder. Being weight, shape and appearance conscious as a group, such individuals are very reluctant to consider taking any medication that might cause weight gain, such as lithium or atypical antipsychotics. Antiepileptic drugs (AEDs), such as valproic acid (sodium valproate), may be less prone to cause weight gain and can thus be attractive options. However, some AEDs can cause hair loss, which is often an issue for underweight patients with anorexia nervosa and which may cause such patients to refuse treatment. The authors favour a careful approach to patients with comorbid bipolar disorder – one that includes a long period of education about the various medications involved in treatment, their adverse effects and their likely beneficial effects. In our experience, no one medication is acceptable to all patients. Compliance with treatment is more of a challenge than with typical bipolar patients – already a challenging group to treat on their own. 3. Anxiety Disorders Anxiety disorders are fairly common areas of comorbidity in both anorexia nervosa and bulimia nervosa. Lifetime prevalences of obsessive-compulsive disorder (OCD) run at around 40% in patients with eating disorders. Panic disorder (11%), social phobia/social anxiety disorder (20%), specific phobias (15%), generalised anxiety disorder (10%) and CNS Drugs 2006; 20 (8)


post-traumatic stress disorder (PTSD) [13%] are all significant contributors to comorbidity in these patients.[5-7] 3.1 Obsessive-Compulsive Disorder

OCD represents a complex challenge, particularly in those with anorexia nervosa. Diagnostically, the main issues surround two factors. First, ritualistic activities that involve food should not be counted when attempting to make a diagnosis of OCD, as these behaviours are more properly part of the eating disorder. These activities include excessive exercise and behaviours such as repetitive weighing. The second area of confusion is slightly more subtle and relates to the personality of the majority of those with anorexia nervosa. Such individuals are generally very perfectionistic, a character trait that persists even after weight restoration.[8] Many have obsessive-compulsive personality disorder (OCPD). It is important to avoid mistaking a precise and rigid personality as OCD. Clinicians will recall that while the symptoms of OCD are ego-dystonic and troubling to the patient, the rigidity and precision of OCPD and its less severe counterparts are not particularly viewed by these patients as a problem. As is the case with disorders of mood, the treatment of OCD is generally not very effective in those who are nutritionally compromised. Very few receive any significant benefit from either pharmacological or psychotherapeutic treatments until changes have begun to occur in the core symptoms of the eating disorder. Once such changes have started, treatment with modern antidepressants is the first line of attack. There is controversy as to whether higher dosages produce either greater or more rapid improvement. Most experts expect that improvement will be slow and continue for up to 2 years after the initiation of treatment. Thus, the usual recommendation is to start with a typical dosage of antidepressant, for example fluoxetine, paroxetine or citalopram 20 mg/ © 2006 Adis Data Information BV. All rights reserved.

659

day. As is the case with depression, it is not generally necessary to reduce the dosage on account of the patient’s weight in anorexia nervosa. If a decision is made to increase the dosage of the antidepressant then it should be raised to the highest dosage that the patient can tolerate. Dosages of fluoxetine 80–100 mg/day, for example, are not uncommon in patients with treatment-resistant symptoms. Clinicians should resist the urge to increase the dosage of the antidepressant to these levels in patients whose eating is not improving. An additional strategy is to add a very small dose of an antipsychotic as an augmentation agent. Some experts believe that this produces a more intense and more rapid response than an antidepressant alone. The authors favour small dosages of risperidone, in the 0.5–2 mg/day range. As is the case with depression, the best results are achieved using a combination of pharmacotherapeutic and psychotherapeutic treatments. Cognitive therapeutic approaches, along with response prevention, are the treatment of choice for OCD; however, as with depression, these are unlikely to have much of an effect on individuals who are nutritionally compromised. Clinicians should note that the assessment of response will be complicated by the presence of the perfectionistic personality usually seen in patients with eating disorders; however, OCD symptoms are generally ego-dystonic and troubling to the patient, while perfectionism is not. Thus, the patient will be able to inform the clinician of whether his/her OCD has improved. 3.2 Panic Disorder

The symptoms of panic disorder are as troubling to the patient with an eating disorder as to any other patients, and such patients will generally readily accept treatment for panic disorder. The treatment of choice is the combination of an antidepressant and cognitive therapy; each of the two components alone CNS Drugs 2006; 20 (8)

660

Woodside & Staab

is about equally efficacious. As most medical practitioners do not have training in cognitive therapy, pharmacological agents become the treatment of choice for physicians. An antidepressant in a usual therapeutic dosage is the standard pharmacological treatment for panic disorder, with or without agoraphobia. Full response is typically seen after approximately 6 weeks of treatment. As is the case for most of the comorbid conditions discussed in this article, the treatment is much less likely to be successful if the patient has active eating symptoms, and a total resolution of symptoms will be uncommon in such patients.

latter fears are more properly treated as part of the eating disorder and should not be approached in isolation from the eating disturbance. Therefore, for example, it is uniformly unhelpful to try to treat the body image concerns of a woman with anorexia nervosa without attending to her nutritional status. Other phobias should be approached with systematic desensitisation. Flooding, a rapid form of desensitisation, should not be attempted unless the clinician has specific training in this technique and adequate resources to carry the treatment out properly. 3.5 Post-traumatic Stress Disorder

3.3 Social Anxiety Disorder/Social Phobia

Most patients with eating disorders who experience significant social anxiety disorder are also troubled by this condition and wish to have treatment. As is the case for most of the comorbidities discussed in this article, such treatment is most likely to be successful when significant change is occurring or has occurred in the patient’s eating. The only relevant diagnostic issues are that fear of eating in public should be viewed as a symptom of the underlying eating disturbance and that the social isolation caused by the underlying eating disorder should not be confused with a social phobia. Pharmacological treatments have only a minor role in the treatment of social anxiety disorder, with cognitive therapy providing the most relief. The typical time course of response is many months to 1 year or more. Some patients presenting with comorbid social anxiety disorder will also have depression, and if this is the case the disorder should be treated. 3.4 Specific Phobias

Specific phobias do not generally present in patients with eating disorders, apart from those fears that are core to the illness, such as the fear of fatness in anorexia nervosa or fears of specific foods. These © 2006 Adis Data Information BV. All rights reserved.

PTSD is fairly common as a comorbid condition with an eating disturbance. Rates of PTSD tend to increase with increasing severity of the eating disorder. For example, in the authors’ clinical programme (serving the most severe forms of anorexia nervosa) combined rates of physical and sexual abuse, which frequently lead to PTSD, are approximately 50% for the restricting forms of anorexia nervosa and over 80% for the binge-purging form of the illness.[9] There is considerable controversy surrounding the presence of a trauma history and its effect on other comorbid diagnoses. For example, an individual who has experienced severe and prolonged sexual abuse is likely to experience unstable mood, labile relationships and self-harm, all of which are diagnostic criteria for borderline personality disorder.[10,11] The effects of trauma are complex and the treatment of trauma is beyond the scope of this article. Suffice it to say that treatment is complex, lengthy and requires significant training, supervision and experience to undertake. For a good general reference to the nature and effects of trauma, readers are referred to Herman.[12] Clinicians should be aware that there are few or no published guidelines for the pharmacological treatment of PTSD in patients with eating disorders and that most of the comments that follow relate to the clinical experiCNS Drugs 2006; 20 (8)


ence of the authors. One useful reference is included in the reference list.[13] Clinicians are most likely to become involved in the treatment of comorbid PTSD via requests for medication to treat the anxiety that is so common in traumatised individuals. Such individuals tend to oscillate from being de-stimulated, where they feel very little and will describe themselves as ‘numb’, to hyper-stimulated, where they feel totally overwhelmed and out of control. It is during these latter times when such individuals will engage in selfharm or will seek medication to try to alleviate their anxiety. A period of hyper-stimulation is a common occurrence when a patient with an eating disorder first attempts to make changes to his/her eating. Both the nature of the food and the subsequent increased access to feelings once some nutritional improvement has occurred are common reasons for such patients to become activated. If such an individual does approach a clinician, the first thing to do is to establish whether the patient is being treated by another physician or therapist. If this is the case, the responsible clinician will first contact the primary therapist (with the permission of the patient) and indicate that a request for medication has been made. Medication should not be provided without the agreement of all those participating in the treatment of the patient, and ongoing communication about what is happening with medication is essential. It is also a good idea to make sure that one physician is responsible for prescribing all psychotropics to such a patient because of the risks of dependence outlined below. Once a decision to prescribe has been made, a series of complicated choices present themselves to the clinician. The patient will present with a confusing set of symptoms, usually including severe mood swings, intense anxiety and a mixture of phobic-like reactions. The usual temptation is to provide both an antidepressant and a benzodiazepine. This is almost © 2006 Adis Data Information BV. All rights reserved.

661

always the wrong choice, at least in terms of the use of a benzodiazepine. The patient will report a dramatic (although transient) decrease in his or her anxiety, and immediately begin to escalate the dosage. It is not uncommon to see such patients taking 10–12 mg of lorazepam or clonazepam a day, often obtained from multiple clinicians. This tends to lead such patients to periodically run out of their medications and abruptly withdraw themselves, often leading to seizures. A different approach, once the clinician has some basic knowledge about the nature of trauma, is to downplay the utility of anxiolytics to treat the hyperstimulation of PTSD and explain carefully that it is generally neither possible nor desirable to try to totally suppress this anxiety. The authors explain to such patients that the anxiety is there as a psychological response, usually to an environmental variable, and that the most effective way to deal with it is for the patient and his or her therapist to identify the stimulus for the anxiety and plan as to how to deal with the stimulus. The authors frame anxiolysis as a minor part of the solution, one to be used sparingly. To this end, the authors find the use of atypical antipsychotics in low dosages to be preferable to benzodiazepines. For example, quetiapine 12.5mg three times daily or risperidone 0.5 mg/day might be prescribed. In our experience, patients are less likely to massively escalate the dosage of these drugs. This is, at least in part, due to the slightly slower onset of action (the patient does not get a ‘rush’ as is the case with benzodiazepines) and because of the lack of severe withdrawal symptoms (as is found with short-acting benzodiazepines). Some patients will want or require higher dosages, for example up to 150–200mg of quetiapine per day. Clinicians should always try to manage with the lowest possible dosage of such medications and repeatedly stress to the patient the limited role they have to play in the treatment of PTSD. CNS Drugs 2006; 20 (8)

662

Woodside & Staab

Table I. Common areas of comorbidity in eating disorders, and their treatment Condition

Lifetime prevalence estimate as a comorbid condition[2-7,14]

Treatment approach and cautions

Depression

Up to 75%

Antidepressants; cognitive therapy

Bipolar disorder

10%

Anti-manic agents – be aware of effect of purging behaviours

Obsessive-compulsive disorder

40%

Antidepressants plus atypical antipsychotics as augmentation agents; cognitive therapy

Panic disorder

11%

Antidepressants; cognitive therapy

Social anxiety disorder/social phobia

15–20%

Cognitive therapy

Post-traumatic stress disorder

Prevalence varies with severity of eating disorder

Specialised trauma treatment – beware of excessive use of anxiolytics

Substance use disorders

15–40%, highest in bulimia nervosa

Concurrent treatment for eating disorder and substance use disorder most effective

Antidepressants are tempting to prescribe and most patients with PTSD are taking these drugs. This is most often a benign intervention that may or may not affect the course of recovery from PTSD. Antidepressants are very unlikely to produce a full remission if used alone. 4. Substance Abuse Substance abuse of various types is a common and very difficult area of comorbidity. Lifetime prevalence of alcohol abuse and dependence ranges from 17% in the restricting form of anorexia nervosa to 46% in bulimia nervosa.[14] Little data are available on the precise rates of abuse of prescription drugs such as benzodiazepines or other street drugs in patients with eating disorders, but dependence and abuse rates are thought to be significant. When substance use comorbidity occurs, it demands treatment as an urgent priority. For very underweight patients with anorexia nervosa, it may be that if such patients are admitted to a residential treatment facility then concurrent treatment for the substance dependence will be available. If this is not the case, or if the treatment for the eating disorder does not include a substance use component, it is usually advisable to try to ‘dry out’ the patient before attempting any significant treatment for the eating disorder. The most common way to do this is © 2006 Adis Data Information BV. All rights reserved.

30-day residential treatment facilities attached to ongoing follow-up. Pharmacological treatments for substance dependence are not prominent parts of the approach to these areas of comorbidity. It is likely that the best course of action for the average clinician is to make a referral for such a patient to a reputable treatment centre for substance use, ensuring that the centre in question is aware of the patient’s eating disorder. 5. Conclusion This article has provided a brief summary of the common forms of comorbidity with eating disorders that might present to the average clinician. For all of these areas of comorbidity, clinicians must be aware of the confounding effects of starvation and chaotic eating on their ability to diagnose, and on the adverse effects of the same on the response to treatment. For most areas of comorbidity, both pharmacological and psychotherapeutic approaches have a valuable role to play. Table I provides a summary of the prevalence and treatment of these comorbid conditions. Acknowledgements No sources of funding were used to assist in the preparation of this review. The authors have no conflicts of interest that are directly relevant to the content of this review.

CNS Drugs 2006; 20 (8)


References 1. Keys A, Brozek J, Henschel A, et al. The biology of human starvation. Minneapolis (MN): University of Minnesota Press, 1950 2. Piran N, Kennedy S, Garfinkel PE, et al. Affective disturbance in eating disorders. J Nerv Ment Dis 1985; 173: 395-400 3. Strober M, Katz J. Depression in the eating disorders: a review and analysis of descriptive, family and biological factors. In: Garner DM, Garfinkel PE, editors. Diagnostic issues in anorexia nervosa and bulimia nervosa. New York: Brunner/ Mazel, 1988: 80-111 4. Woodside DB, Garfinkel PE, Lin E, et al. Men with full and partial syndrome eating disorders: community comparisons with non-eating disordered men and eating disordered women. Am J Psychiatry 2001; 158: 570-4 5. Kaye WH, Bulik CM, Thornton L, et al. Comorbidity of anxiety disorders with anorexia and bulimia nervosa. Am J Psychiatry 2004; 161: 2215-21 6. Godart NT, Flament MF, Perdereau F, et al. Comorbidity between eating disorders and anxiety disorders: a review. Int J Eat Disord 2002; 32 (3): 253-70 7. Bulik CM. Anxiety, depression, and eating disorders. In: Fairburn CG, Brownell KD, editors. Eating disorders and obesity. New York: Guilford Press, 2002 8. Sutandar-Pinnock K, Woodside DB, Carter J, et al. Perfectionism in anorexia nervosa: a 6-24 month follow-up study. Int J Eat Disord 2002; 31: 290-9


663

9. Carter JC, Bewell C, Blackmore E, et al. The impact of childhood sexual abuse in anorexia nervosa. Child Abuse Negl 2006 Mar; 30: 257-69 10. Wonderlich SA, Brewerton TD, Jocic Z, et al. Relationship of childhood sexual abuse and eating disorders. J Am Acad Child Adolesc Psychiatry 1997; 36: 1107-15 11. Thompson KM, Wonderlich SA. Child sexual abuse and eating disorders. In: Thompson JK, editor. Handbook of eating disorders and obesity. Hoboken (NJ): John Wiley & Sons, 2004: 679-94 12. Herman JL. Trauma and recovery. New York: Basic Books, 1997 13. Schwarz MF, Cohn L, editors. Sexual abuse and eating disorders. New York: Brunner/Routledge, 1996 14. Bulik CM, Klump KL, Thornton L, et al. Alcohol use disorder comorbidity in eating disorders: a multicenter study. J Clin Psychiatry 2004; 65: 1000-6

Correspondence and offprints: Dr Blake D. Woodside, Department of Psychiatry, Toronto General Hospital, 200 Elizabeth St, Toronto, ON M5G 2C4, Canada. E-mail: [email protected]

CNS Drugs 2006; 20 (8)