Study Of Binge Eating Disorder Research Articles

SAT-119 Effect of Binge Eating Diagnosed Prior to Bariatric Surgery on Weight Loss up to 2 Years after Surgery

Screening for binge eating (BE) is a component of the preoperative evaluation for bariatric surgery. As eating behavior affects directly any treatment for obesity and may be related to the response to surgery, the study of binge eating disorder (BED) and loss of control has been gaining more attention in recent years. After bariatric surgery, the acute ingestion of large volumes of food is difficult or impossible. In patients in whom BED is the most important factor for weight gain, this restriction could be a determinant feature of the success of the surgical treatment. However, there is no clear understanding of how BE courses over longer periods of time, and if (and how) it changes during the post-operative period. In this way, we aimed to evaluate the effect of BE presenting pre-bariatric surgery on weight loss up to 2 years after surgery. This is a prospective observational study involving 106 Brazilian patients submitted to Roux-en-Y gastric bypass (between March 2010 and December 2014) in a University hospital. In the preoperative period, patients were clinically and nutritionally (anthropometry and food records) evaluated. For the screening of BED, a Portuguese, validated version of the Binge Eating Scale was administered. Follow-up weight loss was obtained (3, 6, 12, 24 months) from the patients’ electronic medical records. The percentage of excess weight loss (%EWL) was examined by pairwise comparison of estimated marginal means (P < 0.050). Of the patients, 40.6% were classified as having BE at baseline. The mean BMI was 48.21 (S.D. 7.25) kg/m². Weight loss was significant between follow-up times, with the exception of the period between 12 and 24 months. Patients with BED had a more marked %EWL at 24 months post-operatively than did patients without BE (76.8 +/- 3.0% vs. 67.3 +/- 2.5%, p = 0.030). For patients being referred for Roux-en-Y bypass, the presence of BED at baseline may indicate higher weight loss at 24 months.

449. Preclinical Models for the Study of Binge Eating Disorder

449. Preclinical Models for the Study of Binge Eating Disorder

Overview of the treatment of binge eating disorder.

We performed a qualitative review of treatment studies of binge eating disorder (BED), focusing on randomized clinical trials (RCTs). Limited effectiveness has been demonstrated for self-help strategies, and substantial effectiveness has been shown for cognitive behavioral therapy (CBT) and interpersonal therapy (IPT). CBT and IPT may each be more effective than behavior weight loss therapy (BWLT) for reducing binge eating over the long term. The stimulant pro-drug lisdexamfetamine dimesylate (LDX) is the only drug approved by the FDA for the treatment of BED in adults based on 2 pivotal RCTs. Topiramate also decreases binge eating behavior, but its use is limited by its adverse event profile. Antidepressants may be modestly effective over the short term for reducing binge eating behavior and comorbid depressive symptoms, but are not associated with clinically significant weight loss. A RCT presented in abstract form suggests that intranasal naloxone may decrease time spent binge eating. There is no RCT of obesity surgery in BED, but many patients with BED seek and receive such surgery. While some studies suggest patients with BED and obesity do just as well as patients with obesity alone, other studies suggest that patients with BED have more post-operative complications, less weight loss, and more weight regain. This evidence suggests that patients with BED would benefit from receiving highly individualized treatment.

Mindfulness trait, eating behaviours and body uneasiness: a case-control study of binge eating disorder.

Binge eating disorder (BED) is a complex and multifaceted eating disorder, and the literature indicates that BED patients show greater difficulty in identifying and making sense of emotional states, and that they have limited access to emotion regulation strategies. Findings show many links between mindfulness and emotional regulation, however there has been no previous research on mindfulness traits in BED patients. One hundred fifty BED patients (N=150: women=98, men=52; age 49.3±4.1) were matched for gender, age, marital status and educational level with 150 non-bingeing obese and 150 normal-weight subjects. All were assessed with the Five Facet Mindfulness Questionnaire (FFMQ), Binge Eating Scale (BES), Objective bulimic episodes (EDE-OBEs) and Body Uneasiness Test (BUT). For all the participants past or current meditation experience was an exclusion criteria. Findings showed that Mindfulness-global, Non reactivity to experience, Acting with awareness, Describing with words and Observation of experience scores were significantly lower in BED than control groups (p<0.05). However, on the mindfulness measures, the obese control group did not differ from the normal weight control group. Moreover, correlations showed that mindfulness was more widely negatively correlated with the BED's OBEs, BES and BUT-GSI scores. Meanwhile, binge eating behaviours, frequency and severity (OBEs and BES) were more negatively correlated with action (Nonreactivity- to-experience and Acting-with-awareness scores). Body Uneasiness was more negatively correlated with mental processes (Describing-with-words and Observation-ofexperience) and mindfulness features. Implications on understanding of the mechanisms underlying the development and maintenance of problematic eating in BED were considered. Moreover, clinical considerations on treatment targets of mindfulnessbased eating awareness training were discussed.

Binge eating disorder and the dopamine D2 receptor: Genotypes and sub-phenotypes

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.

By how much will the proposed new DSM‐5 criteria increase the prevalence of binge eating disorder?

To estimate how much the prevalence of binge eating disorder will increase under the new proposed DSM-5 criteria, which relax the requirements for the frequency and duration of eating binges. Interview data from a nonclinical sample of 888 first-degree relatives who had participated in a family study of binge eating disorder were analyzed. The probands in this study (not included in this analysis) had been selected to either have binge eating disorder or no history of eating binges. The increase in the prevalence of binge eating disorder using the proposed DSM-5 criteria relative to the DSM-IV criteria was 2.9% in women and 3.0% men for lifetime prevalence, and 7.7% in women and 0% in men for the point prevalence. Changes in frequency and duration of binge episodes proposed for DSM-5 will likely have only a minimal effect on the prevalence of binge eating disorder.

A Structural Approach to the Familial Coaggregation of Disorders

The demonstration that 2 disorders coaggregate in families is often the first step in the exploration of genetic factors common to the 2 disorders. Previous methods of analyzing familial coaggregation have used either (1) a typical measure of association (eg, the odds ratio) between a disorder in an individual and another disorder in family members, or (2) a linear structural equation model (SEM). The association method accommodates case-control sampling of families, but may not assess the causal effect of interest because it is not based on an underlying causal model. The SEM method is based on a causal model, but cannot easily accommodate case-control sampling or direct effects of 1 disorder on the other within individuals. We develop a new method of analyzing coaggregation based on directed acyclic graphs. Because this method is a generalization of structural equation models and uses measures of association that accommodate case-control sampling and direct effects, it combines the strengths of both previous methods. In the absence of direct effects between disorders, our approach provides a valid estimate of the causal coaggregation effect. In the presence of direct effects, our approach provides an upper-bound estimate and (assuming additive linear effects of latent familial and nonfamilial factors) a lower-bound estimate of the causal coaggregation effect. For illustration, we applied our method to a family study of binge eating disorder and bipolar disorder.

Personality and eating behaviors: A case–control study of binge eating disorder

Questions have been raised about the validity of binge eating disorder (BED) as psycho-pathologically distinct from other forms of overeating. Our purpose was to ascertain whether BED individuals differed in important ways from nonbinging obese adults. BED adults were recruited from the community as were weight-matched (obese) and normal-weight control (NWC) groups. All groups were equivalent for age and gender distribution, and were assessed on several personality traits and eating behaviors. BED individuals and obese controls did not differ on the personality traits. Both were more reward sensitive, and had greater anxiousness, impulsivity, and addictive personality traits than NWC. However, BED individuals reported significantly greater hedonic eating compared with the obese, who had higher levels than NWC. Our findings provided no evidence of a psychological identity unique to obese adults with BED although their eating behaviors are markedly hedonically driven-i.e., more responsive to factors external to physiological needs.

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 × 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.

Large Study of Binge-Eating Disorder Is a First

Large Study of Binge-Eating Disorder Is a First

Dopamine Transporter Gene (DAT1) Associated with Appetite Suppression to Methylphenidate in a Case–Control Study of Binge Eating Disorder

Response to psychomotor stimulants is highly variable across individuals. Such inconsistencies are influenced by many factors including drug dose and polymorphic differences in genes that encode proteins, such as the dopamine transporter (DAT1), which are relevant to the site of action of these substances. The current study used a double blind, crossover (methylphenidate vs placebo) design to assess DAT1 genotype differences on appetite ratings to a snack-food cue in subjects with binge eating disorder (BED) (n=32) and healthy age-matched controls (n=46). ANOVA results indicated a significant genotype x diagnostic group interaction whereby BED subjects with at least one copy of the 9-repeat allele showed a significant suppression of appetite in response to methylphenidate compared with controls with this allele, or to subjects with the 10/10 genotype (irrespective of diagnosis) whose drug response was indistinguishable from placebo. The most probable explanation for these findings is that some, currently unknown, genetic variant, which is overrepresented in those with BED, interacts with DAT1 to suppress appetite in response to stimulant administration. The current findings have implications for treatment response to drugs currently in use (or being developed) for the treatment of overeating and overweight.

Placebo response in binge eating disorder

Objective:Placebo response in studies of binge eating disorder (BED) has raised concern about its diagnostic stability. The aims of this study were (1) to compare placebo responders (PRs) with nonresponders (NRs); (2) to investigate the course of BED following placebo response; and (3) to examine attributions regarding placebo response.Method:The baseline placebo run-in phase (BL) was part of a RCT investigating sibutramine hydrochloride for BED; it included 451 participants, ages 19–63, diagnosed with BED. Follow-up (FU) included 33 PRs.Results:In this study, 32.6% of participants responded to placebo (PRs = 147; NRs = 304). PRs exhibited significantly less symptom severity. At FU (n = 33), many PRs reported continued symptoms.Conclusion:PRs exhibited significantly less severe pathology than NRs. Placebo response in BED may transitory or incomplete. The results of this study suggest variable stability in the BED diagnosis. © 2006 by Wiley Periodicals, Inc. Int J Eat Disord 2007

Laboratory studies of binge eating disorder.

Because of questions about the accuracy of reported food intake, and in order to study psychological and environmental factors which might affect eating, a number of investigators have examined the eating behavior of individuals with binge eating disorder (BED) under controlled conditions that permit food consumption to be measured. Published studies that evaluated the eating behavior of individuals with BED in a laboratory were reviewed. In laboratory meals, individuals with BED consumed more kilocalories than individuals of similar weight who did not meet criteria for BED. These differences are observed consistently when subjects are asked to binge eat and when they are not. In a laboratory setting, individuals with BED exhibit objectively abnormal eating behavior. These data support, but do not prove, the validity of BED as a diagnostic entity.