Resurgence of Eating Disorders with Olanzapine.

BACKGROUND: Olanzapine is commonly utilized in palliative care for the treatment of nausea, and a known side effect of olanzapine is increased appetite. Olanzapine is also known to cause re-emergence of eating disorders (EDs) in patients utilizing olanzapine for its antipsychotic effects. It is unclear to what extent this may also occur in patients with serious/life-limiting illness. METHODS AND RESULTS: We present a case of a 70-year-old female with recurrent ovarian cancer and a history of bulimia nervosa (BN) that developed resurgence of her BN after initiation of olanzapine for cancer-associated nausea. Her BN resolved with reducing the dose of olanzapine. CONCLUSION: It is important to recognize that recurrence of EDs can occur when using olanzapine in the palliative care setting.

Reactivity to 35% carbon dioxide in bulimia nervosa and panic disorder.

The inhalation of 35% carbon dioxide (CO2) induces panic and anxiety in people with panic disorder (PD) and in people with various other psychiatric disorders. The anxiogenic effect of CO2 in people with eating disorders has received sparse attention despite the fact that PD and bulimia nervosa (BN) have several common psychological and neurobiological features. This study compared CO2-reactivity across three groups of participants: females with BN, females with PD, and female controls without known risk factors for enhanced CO2-reactivity (e.g., social anxiety disorder, first degree relatives with PD). Reactivity was measured by self-reported ratings of panic symptomatology and subjective anxiety, analyzed as both continuous variables (change from room-air to CO2) and dichotomous variables (positive versus negative responses to CO2). Analyses of each outcome measure demonstrated that CO2-reactivity was similar across the BN and PD groups, and reactivity within each of these two groups was significantly stronger than that in the control group. This is the first study to demonstrate CO2-hyperreactivity in individuals with BN, supporting the hypothesis that reactivity to this biological paradigm is not specific to PD. Further research would benefit from examining transdiagnostic mechanisms in CO2-hyperreactivity, such as anxiety sensitivity, which may account for this study's results.

High-dose escitalopram in the treatment of binge-eating disorder with obesity: a placebo-controlled monotherapy trial.

OBJECTIVE: The purpose of this study was to evaluate the efficacy and safety of high-dose escitalopram in the treatment of binge-eating disorder (BED) associated with obesity. METHOD: Forty-four outpatients with BED by DSM-IV criteria and obesity were randomized to receive either escitalopram (N = 21) or placebo (N = 23) in a 12-week, double-blind, flexible dose (10-30 mg/day) study. RESULTS: In the primary analysis, escitalopram (mean dose 26.5 mg/day) and placebo had similar rates of reduction of binge episodes, binge days and obsessive-compulsive symptoms of BED. However, escitalopram was associated with statistically significant reductions in weight, body mass index (BMI), and global severity of illness scores. In a secondary analysis, escitalopram was associated with statistically significant reductions in frequency of binge episodes and binge days, weight, BMI and severity of illness, but not in obsessive-compulsive symptoms of BED. No changes in metabolic variables, including measures of ghrelin and leptin, were observed. High-dose escitalopram was well tolerated. CONCLUSION: High-dose escitalopram was not efficacious in reducing obsessive-compulsive symptoms of BED, but was efficacious in reducing weight and global severity of illness. No definitive conclusions about its efficacy in reducing binge-eating frequency could be drawn due to limitations related to statistical power.

Paraventricular opioids alter intake of high-fat but not high-sucrose diet depending on diet preference in a binge model of feeding.

Previous work from our laboratory indicates that when rats are given a choice between a high-fat and a high-sucrose diet, opioid blockade with naltrexone (NTX) in a reward-related site (central amygdala) inhibits intake of the preferred diet only, whereas NTX injected into a homeostasis-related site, such as the hypothalamic paraventricular nucleus (PVN), inhibits intake of both diets. However, other work suggests that opioids increase intake of fat specifically. The present study further investigates the role of PVN opioids in food choices made by calorically-replete animals. We used a binge model with chow-maintained rats given 3-h access to a choice of a high-fat or high-sucrose diet 3 days a week. We hypothesized that intra-PVN injection of the mu-opioid agonist, DAMGO (0, 0.025, 0.25, and 2.5 nmol) would enhance, and NTX (0, 10, 30, and 100 nmol) would inhibit intake of both diets to an equal extent. We found that when animals were divided into groups according to sucrose or fat preference, DAMGO increased fat intake in fat-consuming animals, while having no effect on intake of either diet in sucrose-consuming animals. NTX, however, inhibited fat intake in both groups. Intra-PVN NTX did not inhibit intake of sucrose when presented in the absence of a fat choice, but did so when injected peripherally. Furthermore, intra-PVN and systemic NTX inhibited intake of chow by 24-h-food-deprived animals. These results indicate a complex role for PVN opioids in food intake with preference, nutrient type, and energy state affecting the ability of these compounds to change behavior.

Clozapine/olanzapine-induced recurrence or deterioration of binge eating-related eating disorders.

OBJECTIVE: To explore the association between eating disorders (EDs) prior to the use of clozapine/olanzapine (pre-clozapine/olanzapine EDs) and after initiation of these antipsychotics (post-clozapine/olanzapine EDs). METHOD: Sixty-four consecutively admitted patients receiving clozapine/olanzapine were screened using the M-Composite International Diagnostic Interview (M-CIDI) to identify subjects with pre-clozapine/olanzapine EDs (DSM-IV criteria). We investigated post-clozapine/olanzapine EDs and binge eating behavior using the Questionnaire on Eating and Weight Patterns (QEWP) and used the Naranjo probability scale as objective causality assessment. RESULTS: Post-clozapine/olanzapine EDs were significantly more frequent in patients with pre-clozapine/olanzapine EDs (5 of 6) when compared to patients without pre-clozapine/olanzapine EDs (4 of 58) [chi(2) = 26.29; df = 1; p < 0.001] [odds ratio (OR) 67.5; 95% CI: 6.3-725.8]. According to the Naranjo probability scale, recurrence or deterioration of EDs in patients with prior EDs was definitely (n = 1) or probably (n = 4) related to the intake of clozapine/olanzapine. CONCLUSION: Clozapine/olanzapine may induce recurrence or deterioration of binge eating symptomatology or full-blown EDs in patients with prior EDs.