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

Summary 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) [χ² = 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.     

Binge eating disorder and depression: A systematic review

The purpose of this systematic literature review is to examine previous studies that investigated the relation between depression and binge eating disorder (BED). Medline/PubMed published data from 1980 through 2006 was tracked using the following keywords: “binge eating disorder and depression”, “periodic binge eating and depression”, “binge eating disorder” and “periodic binge eating”. The findings of 14 studies were successfully highlighted: one cohort, four cross-sectional and nine case–control studies. Most studies (7/14) were conducted in the United States, with missing data varying between 2.3 and 44.32%, and seven studies emphasizing the most important variables. The majority of the studies (10/14) showed an association between depression and binge eating disorder, but carefully designed studies are required to minimize the limitations found in these studies.     

Sleep and eating in childhood: a potential behavioral mechanism underlying the relationship between poor sleep and obesity

ObjectiveThe goal of our study was to examine the associations between sleep and eating behaviors. Specifically, we examined associations between sleep duration and continuity with behaviors that promote eating regardless of true physiologic hunger state including emotional (food intake in response to emotional distress) external (eating in response to the sight or smell of food), and restrained eating (a paradoxical behavior; food intake is initially reduced to lose or maintain body weight, but followed by increased consumption and binge eating).ParticipantsFifty-six children (29 boys; 27 girls) ages 5 to 12 years participated in the study. Mean age was 7.7 ± 1.9 years, and average body mass index (BMI) was within the healthy range (17.8 ± 4.3 kg/m²).MethodsSleep duration, continuity and schedule were assessed using actigraphy and self-reports. The Child Dutch Eating Behavior Questionnaire-modified version (DEBQ-M) was used to examine levels of emotional, external and restrained eating in the children.ResultsAssociations between the sleep and eating behaviors were examined using partial correlations and multiple regression analyses. External eating score was negatively associated with sleep duration; emotional eating score was associated with lower levels of sleep continuity; and restrained eating score were associated with a later sleep start and later bedtime.ConclusionsShort sleep duration and poor sleep continuity were associated with higher levels of eating behaviors shown to be associated with increased food intake. Therefore, sleep loss may be associated with diminished self-regulation of appetite in children, increasing the risk for overeating and obesity.     

The dual-pathway and cognitive-behavioural models of binge eating: prospective evaluation and comparison

To evaluate and compare the dual-pathway, original cognitive-behavioural, and enhanced “transdiagnostic” cognitive-behavioural models of binge eating, using prospective data from a pre-adolescent sample. Models were tested using multilevel longitudinal structural equation modelling. Participants were 236 children (48% male) aged between 8 and 13 years at baseline, who were interviewed annually over a 2-year period. Binge eating was assessed using the Child Eating Disorder Examination. The dual-pathway and enhanced cognitive-behavioural models provided an acceptable fit to the data, whereas the original cognitive-behavioural model did not. Partial support is provided for the prospective validity of the dual-pathway and enhanced cognitive-behavioural models of binge eating in childhood. Results suggest that body dissatisfaction and weight and shape over-evaluation may both contribute to dieting behaviour in youth, and that dieting and affect-related difficulties both require consideration in theories of binge eating development.     

The influence of oxytocin on risk‐taking in the balloon analogue risk task among women with bulimia nervosa and binge eating disorder

Previous theoretical models of bulimia nervosa (BN) and binge eating disorder (BED) have implicated cross‐domain risk‐taking behaviour as a significant maintenance factor in both disorders. The present study aimed to test this hypothesis by administering the Balloon Analogue Risk Task (BART) to 25 women with BN or BED and 27 healthy comparison women without a history of an eating disorder. Furthermore, we tested the effect of a divided dose of 64 IU of oxytocin on risk‐taking behaviour in the BART. Contrary to our hypothesis, women with BN or BED did not exhibit baseline differences in performance on the BART in the placebo condition (t = 1.42, df = 50, P = 0.161, d = 0.39). Oxytocin did not have a main effect on performance in the BART (F = 0.01, df = 1, P = .907, η²_partial < 0.001); however, there was an interaction, such that participants in the BN/BED participant group, compared to the healthy comparison group, demonstrated safer behaviour on the BART in the oxytocin condition, but not in the placebo condition (F = 4.29, df = 1, P = 0.044, η²_partial = 0.082). These findings cast doubt on the common assumption that individuals with BN and BED exhibit greater risk‐taking behaviour in all domains and add to the evidence that oxytocin plays a functional role in modulating behaviours that entail trade‐offs between reward approach and risk in humans. We recommend that future dose‐response studies investigate the effect of oxytocin on reward approach behaviour further in women with recurrent binge eating behaviour, as well as the clinical significance of this effect.     

Further evidence for a low body weight in male children and adolescents with Asperger's disorder

The study explores the common clinical impression and previously reported finding by Hebebrand et al. (7) of reduced body weight in male children and adolescents with Asperger's disorder (AD). Body weight and height of 36 consecutively admitted male patients with AD were retrospectively assessed for the calculation of body mass indices (BMI, kg/m²). The BMIs were transformed to percentile ranks and plotted into BMI-centiles representative for the German population. In addition, comorbid psychopathology was assessed to explore a possible relationship between associated psychopathology and body weight. The mean BMI-centile of all patients was 34.7 ± 31.8 and, thus, differed significantly from the mean centile of an age- and gender-matched psychiatric control group, which was 52.7 ± 28.3. Thirteen patients had a BMI below the 10th centile and five even below the third. Three of the latter presented with disturbed eating behaviour. Altogether four patients showed disturbed eating behaviour. They had a significantly lower mean BMI-centile than the rest of the group. The BMI-centiles of patients with other additional psychopathology did not differ significantly from the mean percentile of the whole cohort. The results clearly show an increased risk for underweight and disturbed eating behaviour in patients with Asperger's disorder which should be evaluated in further studies. Accepted: 26 January 1999     

The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication.

BACKGROUND: Little population-based data exist on the prevalence or correlates of eating disorders. METHODS: Prevalence and correlates of eating disorders from the National Comorbidity Replication, a nationally representative face-to-face household survey (n = 9282), conducted in 2001-2003, were assessed using the WHO Composite International Diagnostic Interview. RESULTS: Lifetime prevalence estimates of DSM-IV anorexia nervosa, bulimia nervosa, and binge eating disorder are .9%, 1.5%, and 3.5% among women, and .3% .5%, and 2.0% among men. Survival analysis based on retrospective age-of-onset reports suggests that risk of bulimia nervosa and binge eating disorder increased with successive birth cohorts. All 3 disorders are significantly comorbid with many other DSM-IV disorders. Lifetime anorexia nervosa is significantly associated with low current weight (body-mass index <18.5), whereas lifetime binge eating disorder is associated with current severe obesity (body-mass index > or =40). Although most respondents with 12-month bulimia nervosa and binge eating disorder report some role impairment (data unavailable for anorexia nervosa since no respondents met criteria for 12-month prevalence), only a minority of cases ever sought treatment. CONCLUSIONS: Eating disorders, although relatively uncommon, represent a public health concern because they are frequently associated with other psychopathology and role impairment, and are frequently under-treated.     

Effects of milnacipran on binge eating - a pilot study

Selective serotonin reuptake inhibitors and selective norepinephrine reuptake inhibitors are effective in the treatment of bulimia nervosa. There have been relatively few studies of the efficacy of specific serotonin and norepinephrine reuptake inhibitors in the treatment of eating disorders. Twenty-five outpatients with binge eating episodes, diagnosed as anorexia nervosa, binge-eating/purging type, bulimia nervosa/purging type, or bulimia nervosa/non-purging type, were treated with milnacipran and 20 patients completed the 8-week study. Symptom severity was evaluated using the Bulimic Investigatory Test, Edinburgh (BITE) self-rating scale before administration of milnacipran and after 1, 4, and 8 weeks treatment. The scores improved after 8 weeks, especially drive to, and regret for, binge eating. Milnacipran was more effective in patients without purging and in younger patients, while there was no difference in the efficacy of milnacipran among subtypes of eating disorders.     

Initial test of an emotional avoidance model of restriction in anorexia nervosa using ecological momentary assessment

It has been hypothesized that restrictive eating allows individuals with anorexia nervosa (AN) to avoid contact with negative emotions; however, this presumption has not been directly tested. In this study, we conducted an initial investigation examining whether restrictive eating serves an emotional avoidance function among individuals with AN. Females with AN (n = 118) reported on negative and positive affect, anxiety/tension, and eating behaviors at multiple time points daily over a 2-week period using ecological momentary assessment methodology. Affective patterns were compared using generalized estimating equation models between days in which participants reported either: (1) relatively high restriction (without binge eating); (2) relatively low restriction (without binge eating); (3) binge eating; or (4) no restriction or binge eating. We hypothesized that, if restriction were functioning to avoid negative affect, average negative affect and anxiety/tension, as well as average negative and positive affect lability, would be lower and average positive affect would be higher on days characterized by high levels of restriction compared to other eating patterns. Contrary to hypotheses: (1) average negative affect, anxiety/tension, and positive affect were not significantly different between days characterized by high restriction and those characterized by low or no restriction; (2) Negative affect and anxiety/tension lability were higher on days characterized by high restriction compared to no restriction or binge eating days; (3) Anxiety/tension lability was higher on days characterized by high versus low levels of restriction. This patterns of findings does not support an avoidance model of restrictive eating for individuals with AN.     

Neuroendocrine responsivities of the pituitary dopamine system in male schizophrenic patients during treatment with clozapine, olanzapine, risperidone, sulpiride, or haloperidol

Background Atypical antipsychotic drugs, in clinical doses, occupy 5-HT2 receptors near saturation, while D2 dopamine receptors, assessed usually in striatum by SPECT or PET methods, are occupied to different degrees. We hypothesized that these differences in D2 receptor occupancies may also be evaluated by a neuroendocrine approach, namely by measuring the plasma prolactin responses to i. m. administered haloperidol, since the expected elevations depend mainly on the free remaining D2 receptors in the tuberoinfundibular tract. Methods We measured the plasma prolactin levels at 0, 30, 60, 90, and 120 minutes after administration of 5 mg haloperidol i. m. in six groups of male patients with schizophrenia: a) 33 patients in a drug-free state, b) 15 patients on treatment with clozapine (range 200–600 mg/day), c) 15 patients on olanzapine (10–30 mg/day), d) 14 patients on risperidone (8–16 mg/day), e) 23 patients on haloperidol (10–40 mg/day), f) 14 patients on sulpiride (600–1600 mg/day). Data were also obtained from a group of 14 healthy male control subjects. The differences in baseline prolactin levels and in the responses to acute haloperidol of the seven groups were compared. Results The baseline prolactin levels did not differ significantly in the groups of controls (8.3±3.8 ng/ml), drug-free patients (8.0±3.6) and patients treated with clozapine (7.7±3.8), they were moderately elevated in patients treated with olanzapine (16.8±8.9), elevated in patients on haloperidol (34.4±17.3), and they were even higher in the groups of patients treated with risperidone (54.9±22.4) or sulpiride (58.8±27.0). All groups of patients gave attenuated prolactin responses to i. m. haloperidol compared to healthy controls. During treatment with haloperidol, risperidone, or sulpiride, no significant prolactin increases after i. m. haloperidol were observed. The group treated with olanzapine gave significant prolactin increases, which were lower than those obtained in the group of patients treated with clozapine, who gave responses similar to that of the drug-free patients. Conclusions Plasma prolactin levels and responses to i. m. haloperidol of patients on treatment with antipsychotic drugs, reflect the prolactin release potencies of the drugs, which are related, but not restricted, to their affinities to D2 dopamine receptors. According to the prolactin baseline levels and responses to i. m. haloperidol, the drugs of this study can be categorized for their potency to the pituitary dopamine system that controls prolactin release, as follows: sulpiride > risperidone > haloperidol > olanzapine > clozapine. This categorization is similar to that obtained by binding studies in striatal D2 dopamine receptors using brain imaging techniques. Received: 26 March 2001 / Accepted: 21 June 2001