Transmission from vaccinated individuals in a large SARS-CoV-2 Delta variant outbreak.

An outbreak of over 1,000 COVID-19 cases in Provincetown, Massachusetts (MA), in July 2021-the first large outbreak mostly in vaccinated individuals in the US-prompted a comprehensive public health response, motivating changes to national masking recommendations and raising questions about infection and transmission among vaccinated individuals. To address these questions, we combined viral genomic and epidemiological data from 467 individuals, including 40% of outbreak-associated cases. The Delta variant accounted for 99% of cases in this dataset; it was introduced from at least 40 sources, but 83% of cases derived from a single source, likely through transmission across multiple settings over a short time rather than a single event. Genomic and epidemiological data supported multiple transmissions of Delta from and between fully vaccinated individuals. However, despite its magnitude, the outbreak had limited onward impact in MA and the US overall, likely due to high vaccination rates and a robust public health response.

Behaviourally assessed negative urgency is uniquely associated with binge-eating frequency.

OBJECTIVE: Binge eating appears to be associated with impulsivity, especially in response to negative affect (i.e., negative urgency). However, negative urgency is typically assessed via self-report, which captures only some aspects of urgency and may be subject to bias. Few studies have examined impulsivity following experimental manipulations of affect in binge-eating samples. METHOD: In the present study, individuals who engage in regular binge eating completed a behavioural impulsivity (go/no-go) task with high- and low-calorie food stimuli, once following negative affect induction and once following neutral affect induction. RESULTS: Greater behavioural impulsivity to high-calorie food cues while in a negative (and not a neutral) affective state was associated with more frequent binge-eating behaviour. Further, this behavioural measure of negative urgency uniquely accounted for variance in binge-eating frequency when controlling for self-reported negative urgency, suggesting that behavioural measures may be a useful complement to self-report measures. DISCUSSION: These findings provide novel and compelling evidence for the relationship between negative urgency and binge eating, highlighting negative urgency as a potentially important target for intervention.

A randomized, controlled pilot study of positive affect treatment adapted for anorexia nervosa.

OBJECTIVE: Novel treatments for adults with anorexia nervosa (AN) are sorely needed. Although psychological interventions have been developed for AN, none have been identified as superior to one another or nonspecific treatments. Common comorbidities (e.g., mood and anxiety disorders) are rarely targeted in AN treatments, possibly impairing long-term clinical improvement. AN is associated with reward processing dysfunctions paralleling those identified in affective disorders; however, few treatments directly target these processes. METHOD: We adapted Positive Affect Treatment, a neuroscience-informed behavioral treatment developed for affective disorders, to the treatment of AN (PAT-AN). Adults with AN (N = 20) were randomized to 20 weeks of PAT-AN or waitlist to investigate the feasibility, acceptability, preliminary efficacy, and target engagement (on reward mechanisms) of PAT-AN. RESULTS: PAT-AN demonstrated strong retention (100%) and acceptability ratings (M = 5.67-5.95 on a 7-point scale). BMI (p = .006) and eating disorder symptoms (p < .001) improved over PAT-AN sessions. The PAT-AN group showed medium to large pre-to-post-treatment improvements in BMI, eating disorder symptoms and impairment, depressive and anxiety symptoms, and some reward indices (ds = .56-.87); changes were largely sustained at 3-month follow-up. Waitlist showed negligible changes (ds < .20) on nearly all measures. DISCUSSION: PAT-AN holds promise as an innovative treatment with capability to simultaneously improve eating disorder symptoms, affective symptoms, and underlying reward mechanisms. Findings should be interpreted cautiously due to small sample size and permitted concurrent enrollment in other treatments. Future, larger-scale research is warranted to establish the efficacy of PAT-AN. PUBLIC SIGNIFICANCE: This study provided a preliminary evaluation of Positive Affect Treatment for anorexia nervosa (PAT-AN), a novel, neuroscience-informed treatment aimed at increasing rewarding life experiences outside of one's eating disorder. Initial results suggest that PAT-AN is considered acceptable and may alleviate eating disorder, depressive, and anxiety symptoms. Therefore, this study presents promising data on a treatment that may hold potential for improving the lives of individuals with this disorder.

Causal discovery analysis: A promising tool in advancing precision medicine for eating disorders.

OBJECTIVE: Precision medicine (i.e., individually tailored treatments) represents an optimal goal for treating complex psychiatric disorders, including eating disorders. Within the eating disorders field, most treatment development efforts have been limited in their ability to identify individual-level models of eating disorder psychopathology and to develop and apply an individually tailored treatment for a given individual's personalized model of psychopathology. In addition, research is still needed to identify causal relationships within a given individual's model of eating disorder psychopathology. Addressing this limitation of the current state of precision medicine-related research in the field will allow us to progress toward advancing research and practice for eating disorders treatment. METHOD: We present a novel set of analytic tools, causal discovery analysis (CDA) methods, which can facilitate increasingly fine-grained, person-specific models of causal relations among cognitive, behavioral, and affective symptoms. RESULTS: CDA can advance the identification of an individual's causal model that maintains that individuals' eating disorder psychopathology. DISCUSSION: In the current article, we (1) introduce CDA methods as a set of promising analytic tools for developing precision medicine methods for eating disorders including the potential strengths and weaknesses of CDA, (2) provide recommendations for future studies utilizing this approach, and (3) outline the potential clinical implications of using CDA to generate personalized models of eating disorder psychopathology. PUBLIC SIGNIFICANCE STATEMENT: CDA provides a novel statistical approach for identifying causal relationships among variables of interest for a given individual. Person-specific causal models may offer a promising approach to individualized treatment planning and inform future personalized treatment development efforts for eating disorders.

Urine Residual Volume in Normal Dogs Determined by Direct Measurement and Comparison to Two-Dimensional Ultrasonographic Measurement.

Normal urine residual volume (URV) in dogs has not previously been established by direct measurement. Twenty-two client-owned normal healthy dogs (8 female spayed, 12 male castrated, 2 male intact) without history of urinary abnormalities were included. Dogs were walked outside for 5 min to allow for natural voiding, immediately followed by urinary bladder ultrasound and urinary catheterization. The URV was recorded, and the ultrasound images were used to estimate URV for each dog. There was no significant difference between male and female URV; therefore, all data were pooled. With a 90% confidence interval, URV was 0-0.47 mL/kg with a mean URV of 0.21 mL/kg and a median value of 0.175 mL/kg. There was no significant difference between the measured URV and the ultrasound-determined URV. This case series supports previously established normal URV in the dog; however, a reference interval based on a larger population of dogs with further evaluation of body size/weight, sex, and neuter status is recommended to be established for use in clinical setting to differentiate normal urination from urinary retention in patients.

Cerebrospinal fluid mutant huntingtin is a biomarker for huntingtin lowering in the striatum of Huntington disease mice.

Huntington disease (HD) is a neurodegenerative disease caused by a trinucleotide repeat expansion in the HTT gene encoding an elongated polyglutamine tract in the huntingtin (HTT) protein. Expanded mutant HTT (mHTT) is toxic and leads to regional atrophy and neuronal cell loss in the brain, which occurs earliest in the striatum. Therapeutic lowering of mHTT in the central nervous system (CNS) has shown promise in preclinical studies, with multiple approaches currently in clinical development for HD. Quantitation of mHTT in the cerebrospinal fluid (CSF) is being used as a clinical pharmacodynamic biomarker of target engagement in the CNS. We have previously shown that the CNS is a major source of mHTT in the CSF. However, little is known about the specific brain regions and cell types that contribute to CSF mHTT. Therefore, a better understanding of the origins of CSF mHTT and whether therapies targeting mHTT in the striatum would be expected to be associated with significant lowering of mHTT in the CSF is needed. Here, we use complementary pharmacological and genetic-based approaches to either restrict expression of mHTT to the striatum or selectively deplete mHTT in the striatum to evaluate the contribution of this brain region to mHTT in the CSF. We show that viral expression of a mHTT fragment restricted to the striatum leads to detectable mHTT in the CSF. We demonstrate that targeted lowering of mHTT selectively in the striatum using an antisense oligonucleotide leads to a significant reduction of mHTT in the CSF of HD mice. Furthermore, using a transgenic mouse model of HD that expresses full length human mHTT and wild type HTT, we show that genetic inactivation of mHTT selectively in the striatum results in a significant reduction of mHTT in the CSF. Taken together, our data supports the conclusion that the striatum contributes sufficiently to the pool of mHTT in the CSF that therapeutic levels of mHTT lowering in the striatum can be detected by this measure in HD mice. This suggests that CSF mHTT may represent a pharmacodynamic biomarker for therapies that lower mHTT in the striatum.

Micro-level de-coupling of negative affect and binge eating in relationship to macro-level outcomes in binge eating disorder treatment.

BACKGROUND: While negative affect reliably predicts binge eating, it is unknown how this association may decrease or 'de-couple' during treatment for binge eating disorder (BED), whether such change is greater in treatments targeting emotion regulation, or how such change predicts outcome. This study utilized multi-wave ecological momentary assessment (EMA) to assess changes in the momentary association between negative affect and subsequent binge-eating symptoms during Integrative Cognitive Affective Therapy (ICAT-BED) and Cognitive Behavior Therapy Guided Self-Help (CBTgsh). It was predicted that there would be stronger de-coupling effects in ICAT-BED compared to CBTgsh given the focus on emotion regulation skills in ICAT-BED and that greater de-coupling would predict outcomes. METHODS: Adults with BED were randomized to ICAT-BED or CBTgsh and completed 1-week EMA protocols and the Eating Disorder Examination (EDE) at pre-treatment, end-of-treatment, and 6-month follow-up (final N = 78). De-coupling was operationalized as a change in momentary associations between negative affect and binge-eating symptoms from pre-treatment to end-of-treatment. RESULTS: There was a significant de-coupling effect at follow-up but not end-of-treatment, and de-coupling did not differ between ICAT-BED and CBTgsh. Less de-coupling was associated with higher end-of-treatment EDE global scores at end-of-treatment and higher binge frequency at follow-up. CONCLUSIONS: Both ICAT-BED and CBTgsh were associated with de-coupling of momentary negative affect and binge-eating symptoms, which in turn relate to cognitive and behavioral treatment outcomes. Future research is warranted to identify differential mechanisms of change across ICAT-BED and CBTgsh. Results also highlight the importance of developing momentary interventions to more effectively de-couple negative affect and binge eating.

Gastrointestinal Interoception in Eating Disorders: Charting a New Path.

PURPOSE OF REVIEW: Abnormal interoception has been consistently observed across eating disorders despite limited inclusion in diagnostic conceptualization. Using the alimentary tract as well as recent developments in interoceptive neuroscience and predictive processing as a guide, the current review summarizes evidence of gastrointestinal interoceptive dysfunction in eating disorders. RECENT FINDINGS: Eating is a complex process that begins well before and ends well after food consumption. Abnormal prediction and prediction-error signals may occur at any stage, resulting in aberrant gastrointestinal interoception and dysregulated gut sensations in eating disorders. Several interoceptive technologies have recently become available that can be paired with computational modeling and clinical interventions to yield new insights into eating disorder pathophysiology. Illuminating the neurobiology of gastrointestinal interoception in eating disorders requires a new generation of studies combining experimental probes of gut physiology with computational modeling. The application of such techniques within clinical trials frameworks may yield new tools and treatments with transdiagnostic relevance.

Beyond Description and Deficits: How Computational Psychiatry Can Enhance an Understanding of Decision-Making in Anorexia Nervosa.

PURPOSE OF REVIEW: Despite decades of research, knowledge of the mechanisms maintaining anorexia nervosa (AN) remains incomplete and clearly effective treatments elusive. Novel theoretical frameworks are needed to advance mechanistic and treatment research for this disorder. Here, we argue the utility of engaging a novel lens that differs from existing perspectives in psychiatry. Specifically, we argue the necessity of expanding beyond two historically common perspectives: (1) the descriptive perspective: the tendency to define mechanisms on the basis of surface characteristics and (2) the deficit perspective: the tendency to search for mechanisms associated with under-functioning of decision-making abilities and related circuity, rather than problems of over-functioning, in psychiatric disorders. RECENT FINDINGS: Computational psychiatry can provide a novel framework for understanding AN because this approach emphasizes the role of computational misalignments (rather than absolute deficits or excesses) between decision-making strategies and environmental demands as the key factors promoting psychiatric illnesses. Informed by this approach, we argue that AN can be understood as a disorder of excess goal pursuit, maintained by over-engagement, rather than disengagement, of executive functioning strategies and circuits. Emerging evidence suggests that this same computational imbalance may constitute an under-investigated phenotype presenting transdiagnostically across psychiatric disorders. A variety of computational models can be used to further elucidate excess goal pursuit in AN. Most traditional psychiatric treatments do not target excess goal pursuit or associated neurocognitive mechanisms. Thus, targeting at the level of computational dysfunction may provide a new avenue for enhancing treatment for AN and related disorders.

Eating Disorder Examination-Questionnaire and Clinical Impairment Assessment norms for intersectional identities using an MTurk sample.

OBJECTIVE: There are limited data to guide the interpretation of scores on measures of eating-disorder psychopathology among underrepresented individuals. We aimed to provide norms for the Eating Disorder Examination-Questionnaire (EDE-Q) and Clinical Impairment Assessment (CIA) across racial/ethnic, gender, and sexual identities, and sexual orientations and their intersections by recruiting a diverse sample of Amazon MTurk workers (MTurkers; N = 1782). METHOD: We created a comprehensive, quantitative assessment of racial/ethnic identification, gender identification, sex assigned at birth, current sexual identification, and sexual orientation called the Demographic Assessment of Racial, Sexual, and Gender Identities (DARSGI). We calculated normative data for each demographic category response option. RESULTS: Our sample was comprised of 68% underrepresented racial/ethnic identities, 42% underrepresented gender identities, 13% underrepresented sexes, and 49% underrepresented sexual orientations. We reported means and standard deviations for each demographic category response option and, where possible, mean estimates by percentile across intersectional groups. EDE-Q Global Score for a subset of identities and intersections in the current study were higher than previously reported norms for those identities/intersections. DISCUSSION: This is the most thorough reporting of norms for the EDE-Q and CIA among racial/ethnic, sexual, and gender identities, and sexual orientations and the first reporting on multiple intersections, filling some of the gaps for commonly used measures of eating-disorder psychopathology. These norms may be used to contextualize eating-disorder psychopathology reported by underrepresented individuals. The data from the current study may help inform research on the prevention and treatment of eating-disorder psychopathology in underrepresented groups. PUBLIC SIGNIFICANCE: We provide the most thorough reporting on racial/ethnic, sexual, and gender identities, and sexual orientations for the Eating Disorder Examination - Questionnaire and Clinical Impairment Assessment, and the first reporting on intersections, which fills some of the gaps for commonly used measures of eating-disorder psychopathology. These norms help inform research on the prevention and treatment of eating-disorder psychopathology in underrepresented groups.

Potent and sustained huntingtin lowering via AAV5 encoding miRNA preserves striatal volume and cognitive function in a humanized mouse model of Huntington disease.

Huntington disease (HD) is a fatal neurodegenerative disease caused by a pathogenic expansion of a CAG repeat in the huntingtin (HTT) gene. There are no disease-modifying therapies for HD. Artificial microRNAs targeting HTT transcripts for degradation have shown preclinical promise and will soon enter human clinical trials. Here, we examine the tolerability and efficacy of non-selective HTT lowering with an AAV5 encoded miRNA targeting human HTT (AAV5-miHTT) in the humanized Hu128/21 mouse model of HD. We show that intrastriatal administration of AAV5-miHTT results in potent and sustained HTT suppression for at least 7 months post-injection. Importantly, non-selective suppression of huntingtin was generally tolerated, however high dose AAV5-miHTT did induce astrogliosis. We observed an improvement of select behavioural and modest neuropathological HD-like phenotypes in Hu128/21 mice, suggesting a potential therapeutic benefit of miRNA-mediated non-selective HTT lowering. Finally, we also observed that potent reduction of wild type HTT (wtHTT) in Hu21 control mice was tolerated up to 7 months post-injection but may induce impairment of motor coordination and striatal atrophy. Taken together, our data suggests that in the context of HD, the therapeutic benefits of mHTT reduction may outweigh the potentially detrimental effects of wtHTT loss following non-selective HTT lowering.

Intrinsic mutant HTT-mediated defects in oligodendroglia cause myelination deficits and behavioral abnormalities in Huntington disease.

White matter abnormalities are a nearly universal pathological feature of neurodegenerative disorders including Huntington disease (HD). A long-held assumption is that this white matter pathology is simply a secondary outcome of the progressive neuronal loss that manifests with advancing disease. Using a mouse model of HD, here we show that white matter and myelination abnormalities are an early disease feature appearing before the manifestation of any behavioral abnormalities or neuronal loss. We further show that selective inactivation of mutant huntingtin (mHTT) in the NG2+ oligodendrocyte progenitor cell population prevented myelin abnormalities and certain behavioral deficits in HD mice. Strikingly, the improvements in behavioral outcomes were seen despite the continued expression of mHTT in nonoligodendroglial cells including neurons, astrocytes, and microglia. Using RNA-seq and ChIP-seq analyses, we implicate a pathogenic mechanism that involves enhancement of polycomb repressive complex 2 (PRC2) activity by mHTT in the intrinsic oligodendroglial dysfunction and myelination deficits observed in HD. Our findings challenge the long-held dogma regarding the etiology of white matter pathology in HD and highlight the contribution of epigenetic mechanisms to the observed intrinsic oligodendroglial dysfunction. Our results further suggest that ameliorating white matter pathology and oligodendroglial dysfunction may be beneficial for HD.

The role of rumination and positive beliefs about rumination in eating pathology.

PURPOSE: General and eating disorder (ED)-specific ruminations have been identified as key factors that may contribute to eating pathology. Positive beliefs about rumination (e.g., "Ruminating helps me to prevent future mistakes") may impact this association. However, the effect of positive beliefs about rumination on the links between rumination and ED symptom severity has not been investigated. This study sought to clarify relations between rumination and ED symptom severity and to evaluate the potential moderating effect of positive beliefs about rumination on these associations. METHODS: During a laboratory visit, undergraduate participants (N = 473, MAge = 18.90 ± 2.27, MBMI = 23.45 kg/m2 ± 4.31, 54.8% female) completed an online battery of questionnaires assessing general and ED-specific ruminative processes (e.g., brooding, reflection), positive beliefs about rumination, and global ED symptoms. Hierarchical multiple regression analyses assessed the unique contributions of specific ruminative processes, and the moderating effect of positive beliefs on associations between ruminative processes and ED symptom severity. RESULTS: Hierarchical multiple regression results suggest that, after controlling for gender and BMI, ED-specific brooding, b = 1.32, SE = 0.13, ß = 0.46, p < 0.0001, and reflection, b = 1.44, SE = 0.33, ß = 0.19, p < 0.0001, accounted for unique variance in ED symptom severity. Moderation model results indicate that, at low levels of general reflection, b = - 0.06, SE = 0.02, ß = - 0.51, p = 0.003, and ED-specific reflection, b = - 0.15, SE = 0.03, ß = - 0.59, p < 0.0001, increased positive beliefs about rumination were associated with greater ED symptom severity. CONCLUSION: Findings suggest ED-specific rumination accounts for ED symptom severity above and beyond general rumination, and that rumination-related expectancies influence the association between reflection and ED symptom severity. LEVEL OF EVIDENCE: Level III, evidence obtained from a well-designed cohort study.

Exploring the contributions of affective constructs and interoceptive awareness to feeling fat.

PURPOSE: Feeling fat, a subjective feeling of being overweight that does not always correspond to actual body weight, is commonly reported in patients with an eating disorder. Research suggests that feeling fat relates to deficits in interoceptive awareness, the perception and integration of signals related to body states. Relatedly, recent work has linked feeling fat to affective constructs, such as depressive symptoms and guilt. The current study explores the unique relationships between feeling fat, self-reported, and objective IA, guilt, alexithymia, and depressive symptoms. METHOD: Female undergraduates (N = 128) completed the 11th item of the Eating Disorder Examination Questionnaire, the Toronto Alexithymia Scale, the Guilt subscale of the Positive and Negative Affect Schedule, and the Beck Depression Inventory-II. Participants also completed two IA measures: a heartbeat perception task and the Multidimensional Assessment of Interoceptive Awareness. RESULTS: All collected measures explained 56% of the variability in feeling fat. Depressive symptoms, self-reported IA, and BMI accounted for significant variability in feeling fat. Relative weights analyses revealed that depressive symptoms accounted for the most variability in feeling fat (19%). This finding remained significant after controlling for BMI, which also accounted for significant variability in feeling fat (25%). CONCLUSIONS: Our results replicate previous findings that depressive symptoms relate significantly to feeling fat and extend this work by incorporating the role of interoceptive awareness, guilt, and alexithymia. Endorsement of feeling fat during an intake assessment may alert clinicians to assess for depressive symptoms, and focusing on depressive symptoms in treatment may improve feeling fat. LEVEL OF EVIDENCE: Level I Evidence obtained from an experimental study.

Eating disorders during the COVID-19 pandemic and quarantine: an overview of risks and recommendations for treatment and early intervention.

Individuals with eating disorders (EDs) are at significant risk for increases in symptomatology and diminished treatment access during the COVID-19 pandemic. Environmental precautions to limit coronavirus spread have affected food availability and access to healthy coping mechanisms, and have contributed to weight-stigmatizing social media messages that may be uniquely harmful to those experiencing EDs. Additionally, changes in socialization and routine, stress, and experiences of trauma that are being experienced globally may be particularly deleterious to ED risk and recovery. This paper presents a brief review of the pertinent literature related to the risk of EDs in the context of COVID-19 and offers suggestions for modifying intervention efforts to accommodate the unique challenges individuals with EDs and providers may be experiencing in light of the ongoing public health crisis.

Naturalistically assessed associations between physical activity, affective functioning, and binge eating among adults with binge-eating disorder.

Binge-eating disorder (BED) is associated with overweight/obesity, physical inactivity, and disturbances in affective functioning. While research suggests that physical activity (PA) may have beneficial effects on BED symptoms, little is known about the daily correlates of PA. As a first step in understanding the processes linking PA and binge eating, this study examined associations between PA (i.e., self-reported time engaged in moderate-to-vigorous PA), affective functioning (i.e., positive and negative affect, body satisfaction, emotion regulation), and eating-related cognitions and behaviors (i.e., craving, overeating, loss of control eating) measured via ecological momentary assessment (EMA). Adults with BED (N = 91) completed a seven-day EMA protocol during which they completed repeated measures of these variables. Results indicated individuals who reported greater time engaged in PA over the EMA protocol evidenced higher positive affect and body satisfaction, and lower overeating (between-subjects effects). No significant within-subjects effects were observed. Findings demonstrate that individual differences in PA levels were related to more adaptive affective functioning and eating regulation in daily life. Results highlight the relevance of PA in BED, and the need for future studies to identify the timescale of these relationships using objective measurements of PA.

Dynamic Stress Responses and Real-Time Symptoms in Binge-Eating Disorder.

BACKGROUND: Stress is a dynamic construct that predicts a range of health behaviors and conditions, including binge eating and excess weight. Thus far, there have been limited and inconsistent findings regarding stress responses in binge-eating disorder (BED) and insufficient consideration of temporal patterns of stress responses across the weight spectrum. PURPOSE: The present study used ecological momentary assessment (EMA) to examine stress reactivity (i.e., the magnitude of the initial stress response), recovery (i.e., how long the stress response lasts before returning to baseline), and pileup (i.e., accumulation of repeated experiences of stressors and responses over time) as predictors of binge-eating symptoms (BES) and food craving in BED. METHODS: Adults with BED (N = 115) completed a 7 day EMA protocol assessing stressful events, perceived stress, binge eating, and food craving prior to being randomized to a behavioral intervention. RESULTS: Generalized estimating equations indicated that moments of greater stress pileup predicted greater subsequent BES (within-person effect). Participants with higher perceived stress and pileup reported greater overall BES and craving, and those with better recovery reported higher overall craving (between-person effects). CONCLUSIONS: Findings highlight the importance of considering the dynamic nature of stress responses and, particularly, that the accumulation of stress over the day is an important trigger for BES.

The Role of Disgust in Eating Disorders.

PURPOSE OF REVIEW: In current review, we evaluate the current literature examining the role of disgust in eating disorders (EDs), and provide a theoretical model designed to inform the study and treatment of disgust-based symptoms in EDs. RECENT FINDINGS: Findings from this review suggest that aberrant disgust-conditioning processes represent promising but understudied mechanisms that may contribute to the risk and maintenance of core eating disorder (ED) psychopathology. In addition, preliminary evidence supports the use of interventions designed to target aversive disgust cues and disrupt maladaptive disgust-based conditioning that may maintain eating pathology. However, experimental studies designed to elucidate the role of disgust and aversive learning processes remain limited. Disgust is a promising risk and maintenance factor in EDs. Future systematic investigation is needed to examine disgust-based processes at a mechanistic level in order to better understand the links between disgust, avoidance behaviors, and EDs. Further investigation of the mechanistic role of disgust in EDs is warranted.

Anhedonia, positive affect dysregulation, and risk and maintenance of binge-eating disorder.

Low positive affect has been identified as an antecedent of binge-eating episodes among individuals with binge-eating disorder (BED), yet positive affect has received far less attention in eating disorders research than its counterpart, negative affect. In this article, we argue that the low levels of positive affect which occur with anhedonia (i.e., loss of interest or pleasure in activities) may contribute to the onset and maintenance of BED. We introduce a theoretical model in which anhedonia increases the risk for BED through its interrelationships with dysregulated eating and weight gain, and we describe potential direct (e.g., reward-related processes) as well as indirect (e.g., influences on depressive symptoms and physical activity) pathways by which anhedonia may lead to adverse eating- and weight-related outcomes. We also propose a momentary maintenance model in which low positive affect and positive affect dysregulation occurring with anhedonia maintain binge eating directly and indirectly through maladaptive health behaviors, such as decreased physical activity, less healthy eating, and fewer social interactions, which in turn maintain anhedonia. We draw upon outside literature to present evidence that aligns with the proposed risk and maintenance models and conclude by outlining avenues for future research-including methodological/measurement, theoretical, and clinical research directions.

Registered report: Initial development and validation of the eating disorders safety behavior scale.

Anxiety and eating disorders (EDs) often co-occur, prompting calls to explore anxiety-related maintenance processes in ED samples. Safety behaviors, which function to prevent a feared outcome from occurring or to reduce anxiety associated with a feared stimulus, are observed across anxiety disorders and, along with overt avoidance behaviors, are an important target in treatment. Data suggest that individuals with EDs also engage in safety behaviors. However, no existing assessments provide a comprehensive measure of eating-disorder-specific overt avoidance and safety behaviors. The goal of this Stage 1 Registered Report is to develop a comprehensive self-report measure of ED-specific safety behaviors. In Study 1, we will recruit 50 women with EDs to complete the scale and provide feedback on the response scale. Feedback from these participants will be used to refine the measure. In Study 2, we will evaluate the psychometric properties of the measure in a large sample of women with EDs (n dependent on the size of measurement) and a community sample without current or a history of ED symptoms. We will explore the measure factor structure, known-groups validity by comparing scores from women with EDs to healthy controls, internal consistency, and convergent and divergent validity with other psychological instruments.