From gut microbiota to brain: implications on binge eating disorders.

The prevalence of eating disorders has been increasing over the last 50 years. Binge eating disorder (BED) and bulimia nervosa (BN) are two typical disabling, costly and life-threatening eating disorders that substantially compromise the physical well-being of individuals while undermining their psychological functioning. The distressing and recurrent episodes of binge eating are commonly observed in both BED and BN; however, they diverge as BN often involves the adoption of inappropriate compensatory behaviors aimed at averting weight gain. Normal eating behavior is coordinated by a well-regulated trade-off between intestinal and central ingestive mechanism. Conversely, despite the fact that the etiology of BED and BN remains incompletely resolved, emerging evidence corroborates the notion that dysbiosis of gastrointestinal microbiome and its metabolites, alteration of gut-brain axis, as well as malfunctioning central circuitry regulating motivation, execution and reward all contribute to the pathology of binge eating. In this review, we aim to outline the current state of knowledge pertaining to the potential mechanisms through which each component of the gut-brain axis participates in binge eating behaviors, and provide insight for the development of microbiome-based therapeutic interventions that hold promise in ameliorating patients afflicted with binge eating disorders.

Facial femininity and perceptions of eating disorders: A reverse-correlation study.

Eating disorders are prevalent in college students but college students are not accurate in identifying the presence of eating disorders (ED) especially when race is involved. Much has been researched about diagnostic ability in vignette form, but little outside of this. For example, it is not known how facial features, such as perceived femininity, may affect observers' beliefs about the likelihood of disordered eating depending on race. In the present study, we examined how biases regarding facial appearance and disordered eating may differ depending on the race of face images. Using a technique called reverse correlation, we estimated the image templates associated with perceived likelihood of disordered eating using both White and Black Faces. Specifically, we recruited 28 college students who categorized White and Black faces according to perceived likelihood of an eating disorder diagnosis in the presence of image noise. Subsequently, we asked Amazon Mechanical Turk participants to categorize the resulting race-specific face templates according to perceived ED likelihood and femininity. The templates corresponding to a high likelihood of an ED diagnosis were distinguished from low-likelihood images by this second independent participant sample at above-chance levels. For Black faces, the templates corresponding to a high likelihood of an ED diagnosis were also selected as more feminine than low-likelihood templates at an above-chance level, whereas there was no such effect found for White faces. These results suggest that stereotyped beliefs about both femininity and the likelihood of disordered eating may interact with perceptual processes.

Converging vulnerability factors for compulsive food and drug use.

Highly palatable foods and substance of abuse have intersecting neurobiological, metabolic and behavioral effects relevant for understanding vulnerability to conditions related to food (e.g., obesity, binge eating disorder) and drug (e.g., substance use disorder) misuse. Here, we review data from animal models, clinical populations and epidemiological evidence in behavioral, genetic, pathophysiologic and therapeutic domains. Results suggest that consumption of highly palatable food and drugs of abuse both impact and conversely are regulated by metabolic hormones and metabolic status. Palatable foods high in fat and/or sugar can elicit adaptation in brain reward and withdrawal circuitry akin to substances of abuse. Intake of or withdrawal from palatable food can impact behavioral sensitivity to drugs of abuse and vice versa. A robust literature suggests common substrates and roles for negative reinforcement, negative affect, negative urgency, and impulse control deficits, with both highly palatable foods and substances of abuse. Candidate genetic risk loci shared by obesity and alcohol use disorders have been identified in molecules classically associated with both metabolic and motivational functions. Finally, certain drugs may have overlapping therapeutic potential to treat obesity, diabetes, binge-related eating disorders and substance use disorders. Taken together, data are consistent with the hypotheses that compulsive food and substance use share overlapping, interacting substrates at neurobiological and metabolic levels and that motivated behavior associated with feeding or substance use might constitute vulnerability factors for one another. This article is part of the special issue on 'Vulnerabilities to Substance Abuse'.

Food-related impulsivity assessed by longitudinal laboratory tasks is reduced in patients with binge eating disorder in a randomized controlled trial.

Food-related impulsivity, i.e. a food-related attentional bias proposed to be due to increased reward sensitivity and diminished inhibitory control, has been cross-sectionally associated with binge eating disorder. To analyze changes in food-related impulsivity, we implemented longitudinal analyses of objective laboratory tasks in a randomized controlled trial called IMPULS. Patients who attended an impulsivity-focused group intervention (IG N = 31) and control patients who did not take part in the intervention (CG N = 25) were compared before (T0) and after the intervention period (T1) and at three months follow-up (T2). Patients' impulsive gaze behavior towards food vs. neutral stimuli was measured in two eye tracking paradigms, one addressing reward sensitivity and another addressing inhibitory control. Initial fixations of food vs. neutral stimuli were increased at T0 (IG: p = .014, CG: p = .001), but not at T1 and T2 in IG (T1: p = .178, T2: p = .203) and in CG after Bonferroni correction only at T2 (T1: p = .031, T2: p = .002). Patients from IG increased dwell time on neutral stimuli at T1 contrary to patients from CG (p = .016) and rated the presented food stimuli as less positive (e.g. pleasantness p < .001 at T1 and T2). A possible explanation for this observation is reduced reward sensitivity, which implies a short-term treatment effect. Both groups showed improvement in inhibiting eye movements towards food and neutral stimuli over time (i.e. first saccade errors overall p < .001, second saccade errors overall p < .003). This could indicate increased inhibitory control due to training effects from the study paradigm. The results suggest that food-related impulsivity represents an underlying mechanism of BED and that it is modifiable by cognitive behavioral interventions.

Resting State Hypoconnectivity of Reward Networks in Binge Eating Disorder.

The clinical presentation of binge eating disorder (BED) and data emerging from task-based functional neuroimaging research suggests that this disorder may be associated with alterations in reward processing. However, there is a dearth of research investigating the functional organization of brain networks that mediate reward in BED. To address this gap, 27 adults with BED and 21 weight-matched healthy controls (WMC) completed a multimodel assessment consisting of a resting functional magnetic resonance imaging scan, behavioral tasks measuring reward-based decision-making (i.e., delay discounting and reversal learning), and self-report assessing clinical symptoms. A seed-based approach was employed to examine the resting state functional connectivity (rsFC) of the striatum (nucleus accumbens [NAcc] and ventral and dorsal caudate), a collection of regions implicated in reward processing. Compared with WMC, the BED group exhibited lower rsFC of striatal seeds, with frontal regions mediating executive functioning (e.g., superior frontal gyrus [SFG]) and posterior, parietal, and temporal regions implicated in emotional processing. Lower NAcc-SFG rsFC was associated with more difficulties with reversal learning and binge eating frequency in the BED group. Results suggest that hypoconnectivity of striatal networks that integrate self-regulation and reward processing may promote the clinical phenomenology of BED. Interventions for BED may benefit from targeting these circuit-based disturbances.

The Neurobiology of Binge-eating Disorder Compared with Obesity: Implications for Differential Therapeutics.

PURPOSE: Emerging work indicates divergence in the neurobiologies of binge-eating disorder (BED) and obesity despite their frequent co-occurrence. This review highlights specific distinguishing aspects of BED, including elevated impulsivity and compulsivity possibly involving the mesocorticolimbic dopamine system, and discusses implications for differential therapeutics for BED. METHODS: This narrative review describes epidemiologic, clinical, genetic, and preclinical differences between BED and obesity. Subsequently, this review discusses human neuroimaging work reporting differences in executive functioning, reward processing, and emotion reactivity in BED compared with obesity. Finally, on the basis of the neurobiology of BED, this review identifies existing and new therapeutic agents that may be most promising given their specific targets based on putative mechanisms of action relevant specifically to BED. FINDINGS: BED is characterized by elevated impulsivity and compulsivity compared with obesity, which is reflected in divergent neurobiological characteristics and effective pharmacotherapies. Therapeutic agents that influence both reward and executive function systems may be especially effective for BED. IMPLICATIONS: Greater attention to impulsivity/compulsivity-related, reward-related, and emotion reactivity-related processes may enhance conceptualization and treatment approaches for patients with BED. Consideration of these distinguishing characteristics and processes could have implications for more targeted pharmacologic treatment research and interventions.

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

PURPOSE: Of 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. METHODS: Reviewed 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. FINDINGS: Psychological 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. IMPLICATIONS: Additional 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.

Assessing for Eating Disorders: A Primer for Gastroenterologists.

Eating disorders involve irregularities in eating behavior that may cause gastrointestinal (GI) symptoms. Consequently, many patients with eating disorders seek gastroenterological healthcare at some point in their illness, with many seeking this care even before they seek treatment for and/or diagnosed with their eating disorder. As such, the gastroenterology provider is in a unique position to identify, manage, and facilitate treatment for an eating disorder early in the course of the illness. Although assessing eating disorders is already a difficult task, the identification of eating disorders in patients with GI disease represents an even greater challenge. In particular, common GI symptoms, such as nausea, vomiting, and bloating, may disguise an eating disorder because these symptoms are often viewed as a sufficient impetus for dietary restriction and subsequent weight loss. In addition, the focus on identifying an organic etiology for the GI symptoms can distract providers from considering an eating disorder. During this prolonged diagnostic evaluation, the eating disorder can progress in severity and become more difficult to treat. Unfortunately, a misconception that hinders eating disorder detection is the notion that the rate or method of weight loss is associated with an eating disorder. Regardless of whether weight loss is slow or rapid, purposeful or accidental, eating disorder behaviors and thought patterns may be present. Unidentified eating disorders are not only dangerous in their own right but also can interfere with effective management of GI disease and its symptoms. As such, it is imperative for the GI provider to remain well versed in the identification of these diseases.

Specific gut microbial, biological, and psychiatric profiling related to binge eating disorders: A cross-sectional study in obese patients.

BACKGROUND & AIMS: Binge eating disorder (BED) is a frequent eating disorder associated with obesity and co-morbidities including psychiatric pathologies, which represent a big health burden on the society. The biological processes related to BED remain unknown. Based on psychological testing, anthropometry, clinical biology, gut microbiota analysis and metabolomic assessment, we aimed to examine the complex biological and psychiatric profile of obese patients with and without BED. METHODS: Psychological and biological characteristics (anthropometry, plasma biology, gut microbiota, blood pressure) of 101 obese subjects from the Food4Gut cohort were analysed to decipher the differences between BED and Non BED patients, classified based on the Questionnaire for Eating Disorder Diagnosis (Q-EDD). Microbial 16S rDNA sequencing and plasma non-targeted metabolomics (liquid chromatography-mass spectrometry) were performed in a subcohort of 91 and 39 patients respectively. RESULTS: BED subjects exhibited an impaired affect balance, deficits in inhibition and self-regulation together with marked alterations of eating behaviour (increased emotional and external eating). BED subjects displayed a lower blood pressure and hip circumference. A decrease in Akkermansia and Intestimonas as well as an increase in Bifidobacterium and Anaerostipes characterized BED subjects. Interestingly, metabolomics analysis revealed that BED subjects displayed a higher level of one food contaminants, Bisphenol A bis(2,3-dihydroxypropyl) ether (BADGE.2H(2)O) and a food derived-metabolite the Isovalerylcarnitine. CONCLUSIONS: Non-targeted omics approaches allow to select specific microbial genera and two plasma metabolites that characterize BED obese patients. Further studies are needed to confirm their potential role as drivers or biomarkers of binge eating disorder. Food4gut, clinicaltrial.gov:NCT03852069, https://clinicaltrials.gov/ct2/show/NCT03852069.

Combined antisaccade task and transcranial direct current stimulation to increase response inhibition in binge eating disorder.

Binge eating disorder (BED) is associated with deficient response inhibition. Malfunctioning response inhibition is linked to hypoactivation of the dorsolateral prefrontal cortex (dlPFC), where excitability could be increased by anodal transcranial direct current stimulation (tDCS). Response inhibition can be assessed using an antisaccade task which requires supressing a dominant response (i.e. saccade) towards a newly appearing picture in the visual field. We performed a double-blind, randomised, placebo-controlled proof-of-concept-study in which we combined a food-modified antisaccade task with tDCS in people with BED. We expected task learning and modulatory tDCS effects. Sixteen people were allocated to a 1 mA condition, 15 people to a 2 mA condition. Each participant underwent the food-modified antisaccade task at three measurement points: baseline without stimulation, anodal verum and sham stimulation at the right dlPFC in a crossover design. The error rate and the latencies of correct antisaccades decreased over time. No tDCS effect on the error rate could be observed. Compared to sham stimulation, 2 mA tDCS decreased the latencies of correct antisaccades, whereas 1 mA tDCS increased it. Self-reported binge eating episodes were reduced in the 2 mA condition, while there was no change in the 1 mA condition. Participants demonstrated increased response inhibition capacities by a task learning effect concerning the error rate and latencies of correct antisaccades over time as well as a nonlinear tDCS effect represented by ameliorated latencies in the 2 mA and impaired latencies in the 1 mA condition. The reduction of binge eating episodes might indicate a transfer effect to everyday life. Given that the reduction in binge eating was observed before tDCS administration, this effect could not be the result of neuromodulation. Randomized clinical trials are needed to fully understand this reduction, and to explore the efficacy of a combined antisaccade and tDCS training for BED.

The Co-occurrence of Pediatric Obesity and ADHD: an Understanding of Shared Pathophysiology and Implications for Collaborative Management.

PURPOSE OF REVIEW: To describe what is known about the association between obesity and attention-deficit hyperactivity disorder (ADHD) in children along with the co-occurring conditions of sleep dysfunction, loss of control/binge eating disorder (LOC-ED/BED), and anxiety. RECENT FINDINGS: Obesity and ADHD share common brain pathways (hypothalamic, executive, and reward centers) with pathophysiology in these areas manifesting in partial or complete expression of these diseases. Sleep dysfunction, LOC-ED/BED, and anxiety share similar pathways and are associated with this disease dyad. The association of obesity and ADHD with sleep dysfunction, LOC-ED/BED, and anxiety is discussed. An algorithm outlining decision pathways for patients with obesity and with and without ADHD is presented. Future research exploring the complex pathophysiology of both obesity and ADHD as well as co-occurring conditions is needed to develop clinical guidelines and ultimately assist in providing the best evidence-based care.

Binge eating for sucrose is time of day dependent and independent of food restriction: Effects on mesolimbic structures.

Binge eating behavior (BEB) is the most common condition among eating disorders. In animal models, binge eating behavior is defined as overconsumption in a brief time interval and it develops as a progressive increase in food intake along time. It is triggered by restricting food access to regular chow or to palatable food and is associated with dopamine release from the ventral tegmental area to the nucleus accumbens. The dopamine system, exhibits day-night patterns, suggesting regulation by the circadian system. This study explored in rats the differential contribution of restricted food access to chow and sucrose for developing BEB, it explored whether BEB exhibits a day-night pattern, and whether behavioral changes are associated with the number of tyrosine hydroxylase (TH) positive cells in the ventral tegmental area, with the expression of dopamine 1 receptors (D1) and glutamate receptor subunit 1 receptors (GLUR1) in the nucleus accumbens. Present data indicate that under conditions of restricted access binge eating is developed for chow or sucrose. Both types of binge eating were independent of each other and exhibited a day-night pattern with increased intensity during the active phase (night). Binge eating was preceded by anticipatory activation, except when restricted food access was given during the day. Increased optical density for D1 receptors was found after exposure to the combination of restricted food access and sucrose. No association was observed between binge eating and the number of positive cells to TH in the ventral tegmental area, nor for GLUR1 in the nucleus accumbens. Present results point out the importance of time schedules to eat, highlighting an increased vulnerability to develop binge eating during the active phase. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Effects of naltrexone on alcohol, sucrose, and saccharin binge-like drinking in C57BL/6J mice: a study with a multiple bottle choice procedure.

Chronic alcohol (ethyl alcohol, EtOH) binging has been associated with long-term neural adaptations that lead to the development of addiction. Many of the neurobiological features of EtOH abuse are shared with other forms of binging, like pathological feeding. The drinking-in-the-dark (DID) paradigm has been used extensively to study the neurobiology of EtOH binge-like drinking due to its ability to promote high intakes relevant to human behavior. DID can also generate high consumption of other tastants, but this procedure has not been fully adapted to study forms of binging behavior that are not alcohol-driven. In the present study, we used a modified version of DID that uses multiple bottle availability to promote even higher levels of EtOH drinking in male C57BL/6J mice and allows a thorough investigation of tastant preferences. We assessed whether administration of systemic naltrexone could reduce binging on EtOH, sucrose, and saccharin separately as well as in combination. Our multiple bottle DID procedure resulted in heightened levels of consumption compared with previously reported data using this task. We found that administration of the opioid receptor antagonist naltrexone reduced intakes of preferred, highly concentrated EtOH, sucrose, and saccharin. We also report that naltrexone was able to reduce overall intakes when animals were allowed to self-administer EtOH, sucrose, or saccharin in combination. Our modified DID procedure provides a novel approach to study binging behavior that extends beyond EtOH to other tastants (i.e. sucrose and artificial sweeteners), and has implications for the study of the neuropharmacology of binge drinking.

Attention-deficit hyperactivity disorder symptomatology, binge eating disorder symptomatology, and body mass index among college students.

Objective: To explore the relationship between symptoms of attention-deficit hyperactivity disorder (ADHD), symptoms of binge eating disorder, and body mass index (BMI) among students at a southern university. Participants: Two hundred seventy-seven college students. Methods: Between January 31, 2013 and March 27, 2013, participants completed the Adult ADHD Self-Report Scale (ASRS) Screener and the Binge Eating Scale (BES) in addition to permitting researchers to measure their height and weight. Results: Higher ASRS scores, higher BMIs, and lower BES scores were observed among men. Among both men and women, BES scores were positively correlated with BMI and ASRS scores; however, the correlation between ASRS and BMI was not significant. Conclusion: Binge eating disorder symptomatology was associated with increased ADHD symptomatology and a higher BMI among both men and women. Among students presenting with obesity or ADHD, screening for binge eating may assist with the identification of problematic eating behaviors.

Weight and age do not account for a worse executive functioning among BED-obese patients.

PURPOSE: Research has demonstrated impaired executive functioning among Binge Eating Disorder (BED) patients that could be influenced by age and weight. We aim to compare decision-making, set-shifting and central coherence between BED-obese patients (BED-Ob), non-BED-obese patients (non-BED-Ob), and normal-weight healthy controls (NW-HC) without the influence of these variables. METHODS: Overall, 35 BED-Ob, 32 non-BED-Ob and 26 NW-HC participants completed the Iowa Gambling Task, the Trail Making Test and the Rey-Osterrieth Complex Figure Test. RESULTS: BED-Ob patients showed higher cognitive impairment compared to NW-HC on decision-making, set-shifting, visual attention and memory. CONCLUSIONS: BED-Ob patients have an impaired cognitive profile on decision-making, set-shifting, visual attention and memory but not impaired central coherence. As all groups were aged-matched and no significant differences between BED-Ob and non-BED-Ob participants were evident, our results demonstrate that this impairment is independent from weight/age, pointing out that it is BED itself to account for inefficiencies in cognitive functioning. LEVEL OF EVIDENCE: Level III, case-control study.

Dietary patterns of patients with binge eating disorders with and without night eating.

OBJECTIVE: This study aimed to compare dietary patterns (timing and frequency of binge episodes, caloric intake and macronutrient composition) of patients with binge eating disorders (BE) with and without night eating syndrome (NES). DESIGN: The study includes 59 women (18-60) who sought treatment for Eating Disorders (EDs) and were diagnosed with BED or BN (BE) with or without NES. They were divided into two groups: NES-BE and BE-only. The participants kept 7-day, 24-h food diaries and completed demographic and depression questionnaires. RESULTS: NES-BE reported significantly a higher frequency of binge days and binge episodes during the week, and more energy and fat consumption than BE-only. CONCLUSIONS: Individuals with NES-BE exhibit higher levels of eating pathology than individuals with BE-only. Thus, NES-BE may not be simply a variant of BED or BN but rather a separate entity that may lead to a more severe disorder and require early assessment and more intensive and suitable treatment. LEVEL OF EVIDENCE: Level V, cross-sectional descriptive study.

Neurocognitive findings in young adults with binge eating disorder.

Objectives: Binge-eating disorder (BED) has been associated with cognitive impairment, including on measures of impulsivity, but it is not clear in prior literature whether these deficits may have been associated with obesity, rather than BED per se. Impulsivity may play a role in predisposing people towards BED as well as in the chronicity of symptoms. The aim of this study was to examine cognitive functions between BED and healthy controls matched for age, gender, and body mass indices.Methods: Individuals with BED and healthy controls were recruited from the general community using media advertisements. After providing informed consent, study participants completed a clinical interview and computerised neuropsychological testing. Group differences were analysed.Results: Groups did not differ significantly on age, gender, education levels, or body mass indices. The BED group (N = 17) exhibited significantly impaired stop-signal response inhibition (Stop-Signal Task) and executive planning (Stockings of Cambridge Task) compared to healthy controls (N = 17). Spatial working memory and set-shifting were intact.Discussion: BED appears to be associated with motor disinhibition and impaired executive planning even controlling for obesity. Longitudinal work is needed to clarify whether motor impulsivity predisposes people to BED, and/or contributes to persistence of symptoms over time.Key pointsBinge-eating disorder is common, under-recognised, and associated with untoward physical and health sequelae.The neurobiological basis of binge-eating disorder is unclear; cognitive testing may offer insights.Many prior cognitive studies have not controlled for potential confounds, especially group differences in body mass indices (BMI). Obesity in itself has been linked with cognitive dysfunction.Here, we compared cognition between people with binge-eating disorder and controls, matched for BMI and other measures.Binge-eating disorder was associated with impaired response inhibition and executive planning.These results inform neurobiological models of binge-eating disorder and may suggest new treatment targets for this condition.

A Systematic Review of Taste Differences Among People With Eating Disorders.

BACKGROUND: Eating disorders are a significant cause of morbidity and mortality. The etiology and maintenance of eating-disorder symptoms are not well understood. Evidence suggests that there may be gustatory alterations in patients with eating disorders. OBJECTIVE: This article systematically reviews research assessing gustatory differences in patients with anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). METHOD: A systematic review was performed, following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, examining taste and eating disorders. We reviewed electronic databases and identified 1,490 peer-reviewed English-language studies. Of these, 49 met inclusion criteria. RESULTS: Studies employed psychophysical measures (n = 27), self-reported questionnaires (n = 5), and neuroimaging techniques (i.e., electroencephalography, functional magnetic resonance imaging; n = 17). Psychophysical studies showed that individuals with BN, in general, had greater preference for sweetness than healthy controls, and those with AN had a greater aversion for fat than controls. In neuroimaging studies, findings suggested that predictable administration of sweet-taste stimuli was associated with reduced activation in taste-reward regions of the brain among individuals with AN (e.g., insula, ventral, and dorsal striatum) but increased activation in BN and BED. DISCUSSION: To our knowledge, this systematic review is the first to synthesize literature on taste differences in AN, BN, and BED. The inconsistency and variability in methods used across studies increased difficulties in comparing studies and disease processes. Further studies with well-defined population parameters are warranted to better understand how taste varies in patients with eating disorders.

Physical activity levels and correlates in nationally representative sample of U.S. adults with healthy weight, obesity, and binge-eating disorder.

OBJECTIVES: This study compared the patterns of moderate and vigorous physical activity (PA) and health conditions in a nationally representative sample of adults categorized with healthy weight (HW) without eating disorder history, obesity without eating disorder history (OB), or current binge-eating disorder (BED) with obesity (BED+OB). METHOD: We used the third National Epidemiological Survey on Alcohol and Related Conditions to compare PA intensity, duration, and their relationships with health indicators in the three groups: HW (n = 11,635), OB (n = 11,056), and BED+OB (n = 110). RESULTS: Prevalence of physical inactivity was significantly greater in OB (38.1%) and BED (51.4%) than HW (30.3%). Prevalence of vigorous PA was significantly lower in OB (45.5%) and BED (31.7%) than HW (54.0%). Duration of moderate and vigorous activity per week was significantly shorter in BED+OB than HW and duration of vigorous activity was shorter in OB than HW. Regardless of PA intensity, BED+OB reported poorer physical and mental health than OB and HW. Greater PA intensity and duration were associated with better physical health, particularly in OB. DISCUSSION: In this nationally representative study of U.S. adults, obesity was associated with physical inactivity. Comorbid obesity and BED was associated with lower PA levels and poorer health. Particularly among adults with obesity, greater PA intensity was associated with better physical health, and greater duration of PA was associated with better physical and mental health. The findings highlight the importance of screening for BED in addition to obesity status and for promoting PA to improve health in U.S. adults.