Objective:There is long-standing interest in how best to define stages of illness for anorexia nervosa, including remission and recovery. The authors used data from a previously published study to ...examine the time course of relapse over the year following full weight restoration.Methods:Following weight restoration in an acute care setting, 93 women with anorexia nervosa were randomly assigned to receive fluoxetine or placebo and were discharged to outpatient care, where they also received cognitive-behavioral therapy for up to 1 year. Relapse was defined on the basis of a priori clinical criteria. Fluoxetine had no impact on the time to relapse. In the present analysis, for each day after entry into the study, the risk of relapse over the following 60 days and the following 90 days was calculated and a parametric function was fitted to approximate the Kaplan-Meier estimator.Results:The risk of relapse rose immediately after entry into the study, reached a peak after approximately 60 days, and then gradually declined. There was no indication of an inflection point at which the risk of relapse fell precipitously after the initial peak.Conclusions:This analysis highlights the fact that adult patients with anorexia nervosa are at increased risk of relapse in the first months following discharge from acute care, suggesting a need for frequent follow-up and relapse prevention–focused treatment during this period. After approximately 2 months, the risk of relapse progressively decreases over time.
Objective
Long‐term outcome studies of anorexia nervosa (AN) have demonstrated that up to 20% of cases will follow an unremitting course despite many attempts at symptom‐based treatments. The ...objectives of this study are to identify in a younger age group with AN whether persistent illness can be identified early and prevented.
Methods
An extensive literature review of such studies published in Pubmed was conducted.
Results
This review revealed that these studies have generally been conducted in adult patients who have been chronically ill over many years.
Discussion
Despite that fact that there is little published evidence on severe and persistent illness in a younger rage group, there are important clinical questions to consider in such a group of AN individuals. This commentary attempts to answer these questions, often in the absence of research evidence. These questions include whether it is possible to identify those who will go on to develop a severe, enduring course; whether early intervention can prevent the development of a such a course; and whether a focus on quality of life rather symptom alleviation is appropriate for a younger age group of unremitted sufferers. In the absence of research that that clearly informs these questions, the authors are left to recommend answers to these question based on a case by case interrogation of relevant factors, including the presence of the risk architecture to which AN has been strongly linked, the age of the patient, the wishes of the family and importantly, the opinions of expert bioethicists and clinicians sufficiently knowledgeable about the psychopathology, natural history, and treatment of AN to be able to render an informed decision.
► Validation for the
Yale Food Addiction Scale to identify those with addictive tendencies to food. ► Obese food addicts show higher comorbidity with binge eating, depression and ADHD than controls. ...► Food addicts are more impulsive and show more addictive personality traits than controls. ► Our findings have demonstrated strong parallels between food and substance abuse.
There is growing evidence of ‘food addiction’ (FA) in sugar- and fat-bingeing animals. The purpose of this study was to investigate the legitimacy of this disorder in the human condition. It was also our intention to extend the validation of the
Yale Food Addiction Scale (YFAS) – the first tool developed to identify individuals with addictive tendencies towards food. Using a sample of obese adults (aged 25–45 years), and a case–control methodology, we focused our assessments on three domains relevant to the characterization of conventional substance-dependence disorders: clinical co-morbidities, psychological risk factors, and abnormal motivation for the addictive substance. Results were strongly supportive of the FA construct and validation of the YFAS. Those who met the diagnostic criteria for FA had a significantly greater co-morbidity with Binge Eating Disorder, depression, and attention-deficit/hyperactivity disorder compared to their age- and weight-equivalent counterparts. Those with FA were also more impulsive and displayed greater emotional reactivity than obese controls. They also displayed greater food cravings and the tendency to ‘self-soothe’ with food. These findings advance the quest to identify clinically relevant subtypes of obesity that may possess different vulnerabilities to environmental risk factors, and thereby could inform more personalized treatment approaches for those who struggle with overeating and weight gain.
Objective:This study evaluated the benefits of olanzapine compared with placebo for adult outpatients with anorexia nervosa.Methods:This randomized double-blind placebo-controlled trial of adult ...outpatients with anorexia nervosa (N=152, 96% of whom were women; the sample’s mean body mass index BMI was 16.7) was conducted at five sites in North America. Participants were randomly assigned in a 1:1 ratio to receive olanzapine or placebo and were seen weekly for 16 weeks. The primary outcome measures were rate of change in body weight and rate of change in obsessionality, assessed with the Yale-Brown Obsessive Compulsive Scale (YBOCS).Results:Seventy-five participants were assigned to receive olanzapine and 77 to receive placebo. A statistically significant treatment-by-time interaction was observed, indicating that the increase in BMI over time was greater in the olanzapine group (0.259 SD=0.051 compared with 0.095 SD=0.053 per month). There was no significant difference between treatment groups in change in the YBOCS obsessions subscale score over time (−0.325 compared with −0.017 points per month) and there were no significant differences between groups in the frequency of abnormalities on blood tests assessing potential metabolic disturbances.Conclusions:This study documented a modest therapeutic effect of olanzapine compared with placebo on weight in adult outpatients with anorexia nervosa, but no significant benefit for psychological symptoms. Nevertheless, the finding on weight is notable, as achieving change in weight is notoriously challenging in this disorder.
Anorexia nervosa (AN) is a highly heritable psychiatric disorder characterized by starvation and emaciation and associated with changes in brain structure. The precise nature of these changes remains ...unclear, as does their developmental time course and capacity for reversal with weight-restoration. In this comprehensive neuroimaging study, we sought to characterize these changes by measuring subcortical volume and cortical surface architecture in women with acute and remitted AN.
Structural magnetic resonance imaging data was acquired from underweight women with a current diagnosis of AN (acAN: n = 23), weight-recovered women with a past diagnosis of AN (recAN: n = 24), and female controls (HC: n = 24). Subcortical segmentation and cortical surface reconstruction were performed with FreeSurfer 6.0.0, and group differences in regional volume and vertex-wise, cortex-wide thickness, surface area, and local gyrification index (LGI), a measure of folding, were tested with separate univariate analyses of covariance.
Mean hippocampal and thalamic volumes were significantly reduced in acAN participants, as was mean cortical thickness in four frontal and temporal clusters. Mean LGI was significantly reduced in acAN and recAN participants in five frontal and parietal clusters. No significant group differences in cortical surface area were detected.
Reductions in subcortical volume, cortical thickness, and right postcentral LGI were unique to women with acute AN, indicating state-dependence and pointing towards cellular remodeling and sulcal widening as consequences of disease manifestation. Reductions in bilateral frontal LGI were observed in women with acute and remitted AN, suggesting a role of atypical neurodevelopment in disease vulnerability.
Abstract Background Our objective was to employ a novel genetic methodology – whereby functional variants of the dopamine pathway were aggregated to reflect a polygenic liability – in the study of ...food addiction . We anticipated that the composite index of elevated dopamine signaling (a multilocus genetic profile score MLGP) would distinguish those with a designation of food addiction (according to the Yale Food Addiction Scale YFAS criteria), and age and weight equivalent controls. Our second aim was to assess whether this index was positively associated with eating-related sub-phenotypes of food addiction (e.g. binge eating and food cravings). Methods Adults ( n = 120) recruited from the community were solicited for an overeating/overweight study. Eating-behavior questionnaires were completed and a blood sample was taken for genotyping. Results and conclusions The YFAS identified 21 participants with food addiction. As predicted, the MLGP score was higher in those with YFAS-diagnosed food addiction, and it correlated positively with binge eating, food cravings, and emotional overeating. We then tested a multiple-mediation model proposing that reward-driven overeating facilitates the relationship between the MLGP score and food addiction. The model was statistically significant, supporting the view that the relationship between a composite genetic index of dopamine signaling and food addiction is mediated by certain aspects of reward-responsive overeating.
•Both long acting methylphenidate and cognitive behavioral therapy were associated with significant improvement in clinical outcomes in adult women with binge eating disorder.•Methylphenidate was ...associated with greater decrease in body mass index over treatment than CBT; however, the durability of these effects is unknown.•Two traits of impulsivity were predictive of clinical outcomes.
Cognitive behavioral therapy (CBT) is a well-established treatment for binge eating disorder (BED); however, this treatment is underutilized, highlighting the need for additional treatment alternatives. Dopamine neurotransmission has been associated with dysregulated eating, and pharmaceutical agents targeting the dopamine system are associated with decreased binge eating and weight. The primary objective of the current investigation was to evaluate the efficacy of psychostimulant medication versus current best practices in the treatment of BED symptoms, in a randomized trial of methylphenidate versus CBT for BED. The secondary objective was to evaluate the ability of impulsivity to predict treatment outcomes. Female outpatients with BED were randomized to receive methylphenidate (n = 22) or CBT (n = 27) for 12 weeks. The primary outcome was objective binge episode frequency; secondary outcomes included subjective binge episode frequency, body mass index (BMI), BED symptoms, and quality of life. Results showed that both treatments had a significant impact on primary and secondary outcomes. Methylphenidate and CBT were associated with decreases in subjective and objective binge episodes; methylphenidate was associated with greater decreases in BMI. Two impulsivity traits predicted clinical outcomes. Results provide preliminary support for the therapeutic benefit of methylphenidate in BED treatment, and prognostic utility of impulsivity in this context.
While the study of binge eating disorder (BED) has burgeoned in the past decade, an understanding of its neurobiological underpinnings is still in the early stages. Previous research suggests that ...BED may be an overeating syndrome characterized by a hyper-responsiveness to reward, and a strong dopamine signaling in the neuro-circuitry that regulates pleasure and appetitive behaviors. We investigated the D2 receptors genes (DRD2/ANKK1) and their relation to the BED phenotype and four sub-phenotypes of BED that reflect an enhanced response to positive food stimuli.
In a sample of 230 obese adults with and without BED, we genotyped five functional markers of the D2 receptor: rs1800497, rs1799732, rs2283265, rs12364283, and rs6277, and assessed binge eating, emotional eating, hedonic eating, and food craving from dimensionally-scored, self-report questionnaires.
Compared to weight-matched controls, BED was significantly related to the rs1800497 and rs6277 genotypes that reflect enhanced dopamine neurotransmission. BED participants were also less likely to carry the minor T allele of rs2283265. The same markers related to the sub-phenotypes of BED with rs1800497 showing the strongest effects in the predicted direction.
This study supports the view that BED may be a condition that has its causal origins in a hypersensitivity to reward — a predisposition that is likely to foster overeating in our current environment with abundant availability of highly palatable and calorically-dense processed foods.
► Three functional D2 markers indicate enhanced dopamine signaling in binge eating disorder. ► BED sub-phenotypes also linked to reward sensitivity. ► Binge eating, hedonic eating, emotional eating, and food cravings linked to dopamine regulation.
Objective: The ADHD–obesity link has been suggested to result from a shared underlying basis of suboptimal dopamine (DA); however, this theory conflicts evidence that an amplified DA signal increases ...the risk for overeating and weight gain. A model was tested in which ADHD symptoms, predicted by hypodopaminergic functioning in the prefrontal cortex, in combination with an enhanced appetitive drive, predict hedonic eating and, in turn, higher body mass index (BMI). Method: DRD2 and DRD4 markers were genotyped. The model was tested using structural equation modeling in a nonclinical sample (N = 421 adults). Results: The model was a good fit to the data. Controlling for education, all parameter estimates were significant, except for the DRD4-ADHD symptom pathway. The significant indirect effect indicates that overeating mediated the ADHD symptoms–BMI association. Conclusion: Results support the hypothesis that overeating and elevated DA in the ventral striatum—representative of a greater reward response—contribute to the ADHD symptom–obesity relationship.
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