Neural Correlates of Failed Inhibitory Control as an Early Marker of Disordered Eating in Adolescents

BackgroundBinge eating and other forms of disordered eating behavior (DEB) are associated with failed inhibitory control. This study investigated the neural correlates of failed inhibitory control as a potential biomarker for DEB.MethodsThe study used prospective longitudinal data from the European IMAGEN study adolescent cohort. Participants completed baseline assessments (questionnaires and a brain scan [functional magnetic resonance imaging]) at 14 years of age and a follow-up assessment (questionnaires) at 16 years of age. Self-reported binge eating and/or purging were used to indicate presence of DEB. Neural correlates of failed inhibition were assessed using the stop signal task. Participants were categorized as healthy control subjects (reported no DEB at both time points), maintainers (reported DEB at both time points), recoverers (reported DEB at baseline only), and developers (reported DEB at follow-up only). Forty-three individuals per group with complete scanning data were matched on gender, age, puberty, and intelligence (N = 172).ResultsAt baseline, despite similar task performance, incorrectly responding to stop signals (failed inhibitory control) was associated with greater recruitment of the medial prefrontal cortex and anterior cingulate cortex in the developers compared with healthy control subjects and recoverers.ConclusionsGreater recruitment of the medial prefrontal and anterior cingulate regions during failed inhibition accords with abnormal evaluation of errors contributing to DEB development. As this precedes symptom onset and is evident despite normal task performance, neural responses during failed inhibition may be a useful biomarker of vulnerability for DEB. This study highlights the potential value of prospective neuroimaging studies for identifying markers of illness before the emergence of behavior changes.     

The Course of Eating Disorders Involving Bingeing and Purging Among Adolescent Girls: Prevalence,Stability, and Transitions

Purpose

To quantify eating disorder (ED) stability and diagnostic transition among a community-based sample of adolescents and young adult females in the United States.

A new animal model of binge eating: key synergistic role of past caloric restriction and stress

Dieting and stress are important in the etiology and maintenance of eating disorders, and dieting strongly predicts stress-induced overeating in humans. We hypothesized that caloric restriction and stress interact in a unique manner to promote binge eating. To test this hypothesis, a group of young female rats were cycled through a restriction period (4 days of 66% of control food intake) followed by 6 days of free feeding prior to being stressed by acute foot shock. After three of these cycles, the food intake of rats exposed only to restriction (R), or only to stress (S), did not differ from controls. However, R+S rats that were restricted and refed, despite normal body weight and food intake after free feeding, engaged in a powerful bout of hyperphagia when stressed (Experiment 1). The R + S effect was replicated in an older group of rats (Experiment 2). The hyperphagia was characteristically binge-like, it constituted a 40% selective increase in highly palatable (HP) food (P < .001) over a discrete period of time (within 24 h post-stress), and reflected feeding for reward (higher HP:chow ratio) over metabolic need as occurred after restriction (higher chow:HP ratio). Subsequent experiments revealed that binge eating did not occur if only chow was available (Experiment 3) or if restriction-refeeding (R-R) did not proximally precede stress (Experiment 4). Experiment 5 revealed that a history of R-R cycles followed by only one stress episode was sufficient to increase intake to 53% above controls as early as 2 h after stress (P < .001). This animal model of binge eating should facilitate investigations into the neurochemical changes induced by dieting and environmental stress to produce disordered eating and provide a preclinical tool to test preventive strategies and treatments more relevant to bulimia nervosa, multiple cases of binge eating disorder (BED) and binge-purge type anorexia nervosa.     

Association between A218C polymorphism of the tryptophan-hydroxylase-1 gene,harm avoidance and binge eating behavior in bulimia nervosa

Genes involved in serotonin transmission are likely involved in the biological predisposition to bulimia nervosa. We investigated whether the A218C polymorphism of the tryptophan-hydroxylase-1 gene was associated to bulimia nervosa and/or to some phenotypic aspects of the disorder. One hundred eighty Caucasian women (91 patients with bulimia nervosa and 89 healthy controls) were enrolled into the study. They underwent a blood sample collection for A218C polymorphism of the tryptophan-hydroxylase-1 genotyping and a clinical evaluation assessing comorbidity for Axis I and II psychiatric disorders, harm avoidance personality dimension and bulimic symptoms. The distribution of both tryptophan-hydroxylase-1 A218C genotypes and alleles did not significantly differ between patients and controls. Bulimic women with the AA genotype exhibited a more severe binge eating behavior and higher harm avoidance scores than those with CC genotype. These findings support the idea that tryptophan-hydroxylase-1 A218C polymorphism does not play a part in the genetic susceptibility to bulimia nervosa, but it seems to be involved in predisposing bulimic patients to a more disturbed eating behavior and higher harm avoidance.     

Associations of social capital with binge drinking in a national sample of adults: The importance of neighborhoods and networks

BackgroundWhile considerable research on adult binge drinking has focused on social influences, the potential role of social capital has been largely overlooked. This study examines the role of social capital, assessed in terms of both neighborhood and social network characteristics, in understanding adult binge drinking.MethodsAdults ages 30–80 were randomly drawn from the RAND American Life Panel and completed an online survey (analytic sample n = 1383). The main predictor variables were neighborhood cohesion, neighborhood order, and social network density. Associations of social capital with past month binge drinking (any, number of days) were examined, controlling for demographic characteristics.ResultsZero-inflated negative binominal regression analysis indicated that any binge drinking was more likely among adults who lived in highly ordered neighborhoods and who had denser social networks but was negatively associated with neighborhood cohesion. However, binge drinking was more frequent among those who lived in neighborhoods lacking order and who had sparser social networks, but had no association with neighborhood cohesion. Age was not found to moderate associations of social capital with binge drinking.ConclusionsGiven that the associations of social capital with adult binge drinking behavior appear to differ by level of influence and type of drinking behavior, there is a need to gain a more nuanced understanding of these complex associations, including the mechanisms through which they operate.     

Binge Eating Disorder: A Psychiatrist's Commentary on Clinical Considerations

PurposeOf the 3 major eating disorders, anorexia nervosa, bulimia nervosa, and binge eating disorder (BED), BED is the most common and exists in the practices of most primary care and psychiatric clinicians. However, BED often goes unrecognized and thus untreated.MethodsReviewed in this commentary are the basic elements in the diagnosis of BED, demographic and clinical characteristics, screening options, the importance of comorbidities, pathophysiology, and available treatments.FindingsPsychological treatments, including cognitive-behavioral therapy, interpersonal therapy, and behavioral weight loss, have been recommended as first-line options and are supported by several different meta-analytic reviews. Lisdexamfetamine is currently the only medication approved by the US Food and Drug Administration for the treatment of BED. Effect sizes for lisdexamfetamine versus placebo for response, remission, and avoidance of relapse in BED are robust, but its use may be limited by tolerability. This is also the case for topiramate, an anticonvulsant that has been used “off-label” to treat BED.ImplicationsAdditional medication choices approved by the US Food and Drug Administration for the treatment of BED are needed. Moving forward, opportunities to leverage modern technology to broaden access to treatment are highly desirable.     

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.     

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Adolescent alcohol use may interfere with neurodevelopment, increasing the likelihood of adult alcohol use disorders (AUDs). We investigated whether adolescent intermittent ethanol (AIE) exposure alters the adult reward response to ethanol. Adolescent rats were administered ethanol once (moderate exposure; Cohort 1) or three times per day (severe exposure; Cohort 2) in a 2 days on/2 days off pattern. In adulthood, subjects responded for electrical stimulation directed at the posterior lateral hypothalamus in a discrete-trial intracranial self-stimulation (ICSS) procedure that provides current-intensity thresholds as a measure of brain reward function. The effects of ethanol administration and withdrawal were assessed. Control rats showed dose-dependent threshold elevations after acute ethanol, indicating reward deficits. A majority of moderately AIE-exposed rats (Cohort 1) showed threshold lowering after ethanol, suggesting ethanol-induced reward enhancement in this sub-set of rats. Rats exposed to severe AIE (Cohort 2) showed no threshold elevation or lowering, suggesting a blunted affective ethanol response. Daily ethanol induced threshold elevations 24 h after administration in control rats but not in either group of AIE-exposed rats, suggesting decreased sensitivity to the negative affective state of ethanol withdrawal. Withdrawal from a 4-day ethanol binge produced robust and enduring threshold elevations in all rats, although threshold elevations were diminished in rats exposed to severe AIE. These results indicate that AIE exposure diminished reward deficits associated with ethanol intoxication and withdrawal and may have increased ethanol-induced reward enhancement in a sub-set of rats. In humans, enhanced ethanol reward accompanied by reduced withdrawal severity may contribute to the development of AUDs.