The Interplay of Mood Disorders and Eating Disorders

TABLE. Lifetime prevalence of mood disorders in patients with eating disorders

Significance for the Practicing Psychiatrist

Disordered eating behaviors commonly co-occur with mood disorders, particularly in women. The following Case Vignette, in which an eating disorder diagnosis is established during treatment, is a common one in clinical practice. It raises many questions for the treating clinician about appropriate diagnosis and treatment, as well as how best to understand the etiology and interconnectedness of these difficulties.

CASE VIGNETTE

Becka is a 20-year-old college sophomore with a psychiatric history of “depression and anxiety,” who is referred for evaluation of persistent depressive symptoms with passive suicidal ideation. The initial evaluation reveals that over the past 7 months Becka has been restricting her caloric intake to barely 1200 calories a day, and she has started a stringent exercise regimen. These behaviors have led to a 15-lb weight loss. She admits she would like to lose more weight, despite her BMI of 17.8 kg/m2. She also reports several neurovegetative symptoms, including depressed mood, anhedonia, impaired sleep, low energy, and persistent thoughts of death.

Epidemiology and etiologic considerations

Data from epidemiologic research support the overlap between eating disorders (eg, anorexia nervosa, bulimia nervosa, binge eating disorder) and mood disorders. For example, approximately 5% of patients with MDD also have an eating disorder (all DSM-IV diagnoses)¹; for female patients with MDD, this rate has been reported to be as high as 33%.² Similarly, mood disorders are a common comorbidity among patients with eating disorders (Table).

Neurovegetative features (eg, decreased or increased appetite) are common in mood disorders such as MDD. The effects of mood and anxiety on appetite, as well as the epidemiology data that suggest high comorbidity between eating disorders and affective disorders, have led clinicians to ponder explanatory models. Although some lines of evidence suggest a shared etiology between the disorders (eg, serotonergic dysfunction), the manner and extent to which shared biological factors are at play is not clear. Overall, it is probably too simplistic to conceive of an eating disorder as simply a sequela of a mood or anxiety disorder-or a mood/anxiety problem as a sequela of an eating disorder. Most likely, these disparate conditions share some etiologic factors.

Diagnostic challenges

Axis I diagnosis of comorbid mood and eating disorders, and determination of which clinical problem is more “primary,” can present a challenge. For example, several neurovegetative symptoms of depression, including fatigue, insomnia, poor concentration, and dysphoria, may be the sequelae of malnutrition. Therefore, a diagnosis of a coexisting depressive disorder may be delayed or deferred if the clinical history suggests that the restrictive behavior predated the mood symptoms. As discussed by Israel and Steiger,³ the question of identifying “depression as a symptom” of an eating disorder, rather than an independent syndrome, is significant in terms of guiding treatment and expected clinical response. For example, mood symptoms secondary to malnutrition tend to improve with weight restoration.

Although patients with bulimia nervosa and binge eating disorder do not suffer from acute starvation, other features may serve to amplify and/or create mood symptoms. For example, some or even most symptoms in patients with comorbid MDD and bulimia nervosa or binge eating disorder may stem from dissatisfaction with shape and weight. Disruptions in energy, concentration, and sleep cycle, as well as the “increased or decreased appetite” typically observed in MDD, may result from the effects of food restriction, binge eating, and/or vomiting. Moreover, these behaviors can lead to medical problems (eg, anemia, electrolyte disturbance).

Recovered or long-term weight-restored individuals with anorexia nervosa experience significantly elevated rates of depression, anxiety, and obsessive behavior compared with healthy controls.^4,5 Therefore, careful evaluation for the possibility of a past eating disorder is important in any general psychiatric consultation. Eliciting a history of an eating disorder might heighten the clinician’s sensitivity to the potential presence of current mood symptoms. Conversely, given that fewer than half of individuals with bulimia nervosa or binge eating disorder have ever sought treatment specifically for their eating disorder but have at some point received care for an emotional problem, a thorough psychiatric review of symptoms may elicit a history of an eating disorder in a patient who presents with a different complaint.

Careful assessment of suicidality is critical in patients with eating disorders because suicide is a major cause of death in this population. Suicide has consistently been identified as the second most common cause of death after medical complications in patients with anorexia nervosa. Rates of suicide attempts range from 3.0% to 29.7% in patients with anorexia nervosa and from 10% to 40% in those with bulimia nervosa.^6-8 Research on suicidality in binge eating disorder is limited. One study found that 12.5% of individuals with binge eating disorder who presented for outpatient treatment had a lifetime history of attempted suicide.⁹ Notably, completed suicide is more common in individuals with anorexia nervosa. The rates (standardized mortality ratio) for completed suicide in persons with anorexia nervosa have been reported to be up to 5.2 to 30 times higher than those of the general population.^8,10

Psychotherapy

When therapeutic goals are established for patients with active mood and eating disorder symptoms, the selection of a treatment setting should be guided by a careful assessment of acute medical and psychiatric risks. Persons with a BMI of less than 16.0 kg/m² or frequent purging that leads to electrolyte abnormalities may require inpatient hospitalization for medical stabilization and early nutritional rehabilitation, even if they do not meet criteria for hospitalization on the basis of the severity of their mood symptoms alone. In the outpatient setting, routine monitoring of weight, vital signs, and (especially in those who purge) serum electrolytes should be incorporated into the treatment of patients with comorbid mood and eating disorders.

Treatment modalities for eating disorders and mood disorders often overlap. Cognitive-behavioral therapy (CBT), which addresses dysfunctional beliefs and maladaptive behaviors that perpetuate symptomatology, is a well-established evidence-based treatment for both disorders.¹¹ In addition to its efficacy for MDD, CBT monotherapy has been shown to achieve remission rates in nearly 50% of patients with bulimia nervosa.¹² Remission rates of about 50% to 60% were seen when individuals with binge eating disorder received CBT.^13,14 Unfortunately, while the evidence supporting the use of CBT for both binge eating disorder and bulimia nervosa is strong, CBT has not shown similar rates of efficacy with anorexia nervosa.

Initially developed for the treatment of depression, interpersonal psychotherapy is a time-limited intervention that has also shown efficacy for the treatment of bulimia nervosa and binge eating disorder.¹⁵

Pharmacotherapy

Pharmacotherapy remains an important treatment modality for comorbid mood and eating disorders. Given the improvement in mood symptoms with re-nourishment, weight restoration is recommended before evaluation for the need for medication.

SSRIs are effective for the treatment of bulimia nervosa. Fluoxetine was approved by the FDA for the treatment of bulimia nervosa after this agent showed significant efficacy in reducing binge eating and purging behaviors, even in the absence of comorbid depressive disorder.¹⁶ Interestingly, fluoxetine was more efficacious for symptoms of bulimia nervosa at a dosage of 60 mg daily than 20 mg daily (the typical dosage for treating depression). However, in a relapse-prevention study in which patients with anorexia nervosa had recently successfully completed full weight restoration through inpatient treatment, fluoxetine was no different than placebo in preventing relapse.¹⁷

Bupropion has an FDA “black box” warning for use in patients with bulimia nervosa and anorexia nervosa. It should be generally avoided for treatment of these eating disorders and comorbid depression because it has been linked to a possible increase in seizure risk. In a trial that compared bupropion with placebo for treatment of bulimia nervosa, 4 of 55 women experienced grand mal seizures.¹⁸

Other treatment options include lisdexamfetamine, which was approved for the treatment of binge eating disorder after showing efficacy in patients with moderate to severe illness.¹⁹ However, clinical trials to date have not compared CBT with lisdexamfetamine in patients with binge eating disorder, and this option may be considered a second- or third-line option after other, more established pharmacotherapies (eg, SSRIs, topiramate) have been ineffective or not tolerated.

Pharmacotherapy for anorexia nervosa and comorbid depression has yielded far less promising results-there is currently no FDA-approved medication for anorexia nervosa. There have been no statistically significant improvements in eating-related or depressive symptoms with antidepressant treatment among individuals with anorexia nervosa.¹⁷

In the acute setting, lack of efficacy with antidepressants may be secondary to neurobiological alterations that result from starvation.²⁰ Of mechanistic relevance to this finding may be tryptophan-depletion studies. Patients with depression who were previously in remission with fluoxetine treatment had mood symptom relapse with low tryptophan levels-a nutritional status that may also be caused by malnutrition.²¹

Disclosures:

Dr Uniacke is an upcoming Chief Resident in the department of psychiatry at the Columbia University Medical Center in New York City. Dr Broft is Assistant Professor of Psychiatry at the Columbia University Medical Center; she is also a psychiatrist in private practice in New York City. The authors report no conflicts of interest concerning the subject matter of this article.

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