Jacqueline C. Carter

Compulsive overeating as an addiction disorder. A review of theory and evidence.

In this paper we argue that compulsive overeating has compelling similarities to conventional drug addiction. Our case is based on their comparable clinical features, the biological mechanisms they have in common, and on evidence that the two disorders have a shared diathesis. In making the argument for overeating as an addictive behaviour, it is clearly not appropriate to include all cases of excessive food consumption in this taxon. Nor are we claiming that obesity and addiction are one and the same. However, it is proposed that Binge Eating Disorder (BED) is a phenotype particularly well-suited to such a conceptualization, and that sound clinical and scientific evidence exists to support this viewpoint. We have provided some recommendations for treatment modifications that recognize the similarities between treating drug dependence and compulsive overeating.

Relapse in anorexia nervosa: a survival analysis.

BACKGROUND Knowledge about factors that predict relapse in anorexia nervosa (AN) is needed for the development of effective relapse prevention treatments and may also advance understanding of the psychopathology of AN. The aim of the present study was to examine the rate, timing and prediction of relapse in AN following weight restoration in a specialized in-patient treatment programme. METHOD Fifty-one consecutive first-admission AN patients who were weight-restored following in-patient treatment participated in the study. Follow-up assessments were conducted a median of 15 months post-discharge. Relapse of AN was defined as a body mass index <17.5 for 3 consecutive months. Data were analysed using Kaplan-Meier survival analysis and Cox regression. RESULTS The overall rate of relapse was 35% and the mean survival time was 18 months. The highest risk period was from 6 to 17 months after discharge. Several significant predictors of relapse were identified: a history of suicide attempt; previous specialized treatment for an eating disorder; severity of obsessive-compulsive symptoms at presentation; excessive exercise immediately after discharge; and residual concern about shape and weight at discharge. CONCLUSIONS There continues to be a significant risk of relapse among AN patients who remain well for the first year post-discharge. Several variables were shown to be associated with an elevated risk of relapse. These findings have implications for the development of initial treatments and relapse prevention strategies for AN.

Eating disorder examination questionnaire: norms for young adolescent girls

This paper reports young adolescent female norms for the Eating Disorder Examination Questionnaire (EDE-Q). The standardization sample was comprised of 808 girls aged between 12 and 14 years from three single-sex schools (one private and two state schools). Means, standard deviations and percentile ranks for raw EDE-Q subscale scores are presented. Prevalence figures for key eating disorder behaviors over the previous two weeks were as follows: 4% self-induced vomiting; 1% laxative misuse; 0.4% diuretic misuse; and 8% regular binge eating.

Cognitive-behavioral self-help for binge eating disorder: a controlled effectiveness study.

The aim of this study was to evaluate the effectiveness of 2 methods of administering a cognitive-behavioral self-help program for binge eating disorder. The study was designed to reproduce many of the conditions that apply in settings in which self-help interventions are most relevant. Seventy-two women with binge eating disorder were randomly assigned to 1 of 3 conditions for 12 weeks: pure self-help (PSH), guided self-help (GSH), or a waiting list (WL) control condition (followed by PSH or GSH). They were then followed up for 6 months. Both PSH and GSH had a substantial and sustained impact with almost half the participants ceasing to binge eat. There was little change in the WL condition. Cognitive-behavioral self-help may be of value both as an initial treatment for binge eating disorder and as a form of secondary prevention.

Dopamine for "wanting" and opioids for "liking": a comparison of obese adults with and without binge eating.

Obesity research suffers from an overinclusion paradigm whereby all participants with a BMI beyond a certain cutoff value (e.g., 30) are typically combined in a single group and compared to those of normal weight. There has been little attempt to identify meaningful subgroups defined by their salient biobehavioral differences. In order to address this limitation, we examined genetic and psychological indicators of hedonic eating in obese adults with (n = 66) and without (n = 70) binge eating disorder (BED). Our analyses focused on dopamine (DA) and opioid genetic markers because of their conjoint association with the functioning of brain reward mechanisms. We targeted three functional polymorphisms related to the D2 receptor (DRD2) gene, as well as the functional A118G polymorphism of the mu‐opioid receptor (OPRM1) gene. We found that significantly more obese controls had the “loss‐of‐function” A1 allele of Taq1A compared to their BED counterparts, whereas the “gain‐of‐function” G allele of A118G occurred with greater frequency in the BED group. A significant gene–gene combination χ2 analysis also indicated that of those participants with the gain‐gain genotype (G+ and A1), 80% were in the BED group whereas only 35% with the loss‐loss genotype (G− and A1+) were in this group. Finally, BED subjects had significantly higher scores on a self‐report measure of hedonic eating. Our findings suggest that BED is a biologically based subtype of obesity and that the proneness to binge eating may be influenced by a hyper‐reactivity to the hedonic properties of food—a predisposition that is easily exploited in our current environment with its highly visible and easily accessible surfeit of sweet and fatty foods.

Subcallosal cingulate deep brain stimulation for treatment-refractory anorexia nervosa: a phase 1 pilot trial

BACKGROUND Anorexia nervosa is characterised by a chronic course that is refractory to treatment in many patients and has one of the highest mortality rates of any psychiatric disorder. Deep brain stimulation (DBS) has been applied to circuit-based neuropsychiatric diseases, such as Parkinsons disease and major depression, with promising results. We aimed to assess the safety of DBS to modulate the activity of limbic circuits and to examine how this might affect the clinical features of anorexia nervosa. METHODS We did a phase 1, prospective trial of subcallosal cingulate DBS in six patients with chronic, severe, and treatment-refractory anorexia nervosa. Eligible patients were aged 20-60 years, had been diagnosed with restricting or binge-purging anorexia nervosa, and showed evidence of chronicity or treatment resistance. Patients underwent medical optimisation preoperatively and had baseline body-mass index (BMI), psychometric, and neuroimaging investigations, followed by implantation of electrodes and pulse generators for continuous delivery of electrical stimulation. Patients were followed up for 9 months after DBS activation, and the primary outcome of adverse events associated with surgery or stimulation was monitored at every follow-up visit. Repeat psychometric assessments, BMI measurements, and neuroimaging investigations were also done at various intervals. This trial is registered with ClinicalTrials.gov, number NCT01476540. FINDINGS DBS was associated with several adverse events, only one of which (seizure during programming, roughly 2 weeks after surgery) was serious. Other related adverse events were panic attack during surgery, nausea, air embolus, and pain. After 9 months, three of the six patients had achieved and maintained a BMI greater than their historical baselines. DBS was associated with improvements in mood, anxiety, affective regulation, and anorexia nervosa-related obsessions and compulsions in four patients and with improvements in quality of life in three patients after 6 months of stimulation. These clinical benefits were accompanied by changes in cerebral glucose metabolism (seen in a comparison of composite PET scans at baseline and 6 months) that were consistent with a reversal of the abnormalities seen in the anterior cingulate, insula, and parietal lobe in the disorder. INTERPRETATION Subcallosal cingulate DBS seems to be generally safe in this sample of patients with chronic and treatment-refractory anorexia nervosa. FUNDING Klarman Family Foundation Grants Program in Eating Disorders Research and Canadian Institutes of Health Research.

Reward sensitivity and the D2 dopamine receptor gene: A case-control study of binge eating disorder

OBJECTIVE The sensitivity of dopamine reward pathways has been implicated in the risk for various psychiatric disorders including compulsive overeating. The evidence is divided, however, about the direction of causal association. One argument is that a Reward Deficiency Syndrome is the risk factor, while others contend that hyper-sensitivity to reward enhances the motivation for pleasurable activities like eating. Unfortunately, little human research has bridged the gap between psychological and neurobiological approaches to brain reward functioning and disorder. The present study addressed this issue by implementing psychological and biological markers of reward sensitivity in the assessment protocol. METHODS Adults with binge eating disorder (BED) were compared to samples of normal-weight and obese controls on two personality measures of reward sensitivity and were genotyped for six markers of the DRD2 dopamine receptor gene. RESULTS Genotype x Group ANOVAs revealed significant main effects and an interaction on the personality measures for Taq1A. BED and obese subjects reported greater reward sensitivity than normal-weight controls, but only among those carrying the A1 allele. We also found that normal-weight controls with at least one copy of the T allele of the C957T marker had significantly lower reward sensitivity scores than any of the other groups who did not differ from each other. CONCLUSIONS Given evidence linking the A1 allele with reduced receptor density, an inverse relationship was expected between psychological measures of reward sensitivity and presence of the A1 allele. One explanation for our findings could be that the BED and obese participants possess another genetic variant that interacts with the A1 allele to produce higher dopamine activity. These findings have implications for future studies of the molecular genetics of BED and obesity, and for behavioural and pharmacologic therapies targeting these conditions.

Food addiction: its prevalence and significant association with obesity in the general population.

Background ‘Food addiction’ shares a similar neurobiological and behavioral framework with substance addiction. However whether, and to what degree, ‘food addiction’ contributes to obesity in the general population is unknown. Objectives to assess 1) the prevalence of ‘food addiction’ in the Newfoundland population; 2) if clinical symptom counts of ‘food addiction’ were significantly correlated with the body composition measurements; 3) if food addicts were significantly more obese than controls, and 4) if macronutrient intakes are associated with ‘food addiction’. Design A total of 652 adults (415 women, 237 men) recruited from the general population participated in this study. Obesity was evaluated by Body Mass Index (BMI) and Body Fat percentage measured by dual-energy X-ray absorptiometry. ‘Food addiction’ was assessed using the Yale Food Addiction Scale and macronutrient intake was determined from the Willet Food Frequency Questionnaire. Results The prevalence of ‘food addiction’ was 5.4% (6.7% in females and 3.0% in males) and increased with obesity status. The clinical symptom counts of ‘food addiction’ were positively correlated with all body composition measurements across the entire sample (p<0.001). Obesity measurements were significantly higher in food addicts than controls; Food addicts were 11.7 (kg) heavier, 4.6 BMI units higher, and had 8.2% more body fat and 8.5% more trunk fat. Furthermore, food addicts consumed more calories from fat and protein compared with controls. Conclusion Our results demonstrated that ‘food addiction’ contributes to severity of obesity and body composition measurements from normal weight to obese individuals in the general population with higher rate in women as compared to men.

'Food addiction' and its association with a dopaminergic multilocus genetic profile

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.

The slippery slope: prediction of successful weight maintenance in anorexia nervosa

BACKGROUND Previous research has found that many patients with anorexia nervosa (AN) are unable to maintain normal weight after weight restoration. The objective of this study was to identify variables that predicted successful weight maintenance among weight-restored AN patients. METHOD Ninety-three patients with AN treated at two sites (Toronto and New York) through in-patient or partial hospitalization achieved a minimally normal weight and were then randomly assigned to receive fluoxetine or placebo along with cognitive behavioral therapy (CBT) for 1 year. Clinical, demographic and psychometric variables were assessed after weight restoration prior to randomization and putative predictors of successful weight maintenance at 6 and 12 months were examined. RESULTS The most powerful predictors of weight maintenance at 6 and 12 months following weight restoration were pre-randomization body mass index (BMI) and the rate of weight loss in the first 28 days following randomization. Higher BMI and lower rate of weight loss were associated with greater likelihood of maintaining a normal BMI at 6 and 12 months. An additional predictor of weight maintenance was site; patients in Toronto fared better than those in New York. CONCLUSIONS This study found that the best predictors of weight maintenance in weight-restored AN patients over 6 and 12 months were the level of weight restoration at the conclusion of acute treatment and the avoidance of weight loss immediately following intensive treatment. These results suggest that outcome might be improved by achieving a higher BMI during structured treatment programs and on preventing weight loss immediately following discharge from such programs.