Search Results (3,944)

Numerous types of environmental toxicants alter human metabolomics, directly or indirectly, through gut microbial dysbiosis, upsetting immune homeostasis. Environmental toxicants capable of these direct and indirect effects have included heavy metals, pesticides, herbicides, polychlorinated biphenyl (PCB) congeners, and endocrine-disrupting chemicals. The cell and molecular events induced by some diverse toxicants are reviewed, along with their potential additive, synergistic, and antagonistic effects on immune homeostasis (increasing proinflammatory immune cell activation and suppressing immunoregulation), which leads to systemic oxidative stress (OS). As people are exposed in varying degrees to countless chemicals and environmental factors over a lifetime, it is challenging to correlate specific diagnoses to any single toxicant or exposure, which is often a key challenge in linking environmental exposure to health outcomes. However, many toxicants have the common mechanistic effect of OS. The effects of toxicants are more pronounced with aging due to cumulative exposures and immunoaging (immunosenescence), with chronic low-grade inflammation referred to as “inflammaging”. The cell and molecular mechanisms of toxicants include altered calcium flux, mitochondrial dysfunction, and increased levels of damage-associated molecular patterns (alarmins) that trigger an inflammatory response and possibly promote autoimmune and neurological disorders. OS skews type-1 immunity for defenses against pathogens and cancers more toward type-2 immune responses to self-antigens (autoimmunity). The toxicants may directly affect the innate and adaptive immune cells inducing this skewing, or they may modify portions of gut microbial species and strains and their production of metabolites that indirectly affect systemic immunity. These latter toxicant influences require metabolomic analysis of the differential structures and activities of the microbial metabolites. The damaging effects of OS and inflammation disrupting immune homeostasis and leading to disorders are reviewed and discussed. The need for well-designed studies that allow for standardized comparison of exposures and related effects are emphasized, and their real-world limitations noted. Full article

Protein intrinsically disordered regions (IDRs) play important biological roles despite lacking stable structures. IDRs drive the formation of both biomolecular condensates via liquid–liquid phase separation (LLPS) and solid fibrous amyloid aggregates. Amyloids can be pathogenic and may exhibit self-perpetuating (prion) properties. Relationships between LLPS and the amyloid-forming and prion-propagating abilities of IDRs remain poorly understood. The N-proximal IDR of the yeast translation termination factor eRF3 (Sup35) can form both liquid condensates and heritable amyloid-based prions and serves as a powerful model for investigating these phenomena due to the availability of simple phenotypic, cytological and biochemical assays. Deletion analysis demonstrates that the N-proximal prion domain (Sup35N) of Sup35 is sufficient for chaperone-dependent prion propagation and that various regions of this domain show differential impacts on LLPS, amyloid aggregation, and prion inheritance. Specifically, the N-terminal NQ-rich stretch and the region of oligopeptide repeats are the most important contributors to the LLPS and formation of amyloid fibrils, while oligopeptide repeats and the C-terminal region of Sup35N are crucial for prion inheritance. Contrary to previous reports, the NQ-rich stretch is not required for prion formation and inheritance in yeast. Our data indicate that, in addition to amino acid composition, specific sequence motifs control reversible and heritable assemblies of Sup35. Full article

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interactions, communication deficits, and excessive repetitive behaviors. While ASD has a strong genetic basis, growing evidence suggests that epileptic seizures may serve as environmental risk factors for ASD development. The high comorbidity between epilepsy and ASD (20–30%) suggests potential shared neurobiological mechanisms, yet the causal relationship remains poorly understood. To investigate the causal role of seizures in the development of ASD-like pathology, we exposed adolescent mice (3 weeks old) to electroconvulsive seizures (ECS) for 10 consecutive days. This repeated ECS exposure led to the emergence of autistic-like behaviors including significantly decreased sociability, increased repetitive self-grooming, enhanced marble burying behavior, and anxiety-like behaviors, without affecting general locomotor activity. Additionally, repeated exposure to ECS induced significant changes in glutamatergic neurotransmission in the mice’s prefrontal cortex and hippocampus, brain regions critically involved in social cognition and behavioral regulation. Interestingly, these changes occurred without alterations in other excitatory/inhibitory neuronal markers, suggesting a specific impact on glutamate receptor expression rather than a general disruption of excitatory/inhibitory balance. These findings suggest that repeated seizures may contribute to ASD-like symptoms by specifically affecting key glutamatergic neurotransmitter systems, providing insights into the neurobiological mechanisms underlying the comorbidity between epilepsy and autism. In addition, repeated ECS differentially regulated histone deacetylase (HDAC) transcripts in a region-specific manner and produced seizure-intensity-dependent transcriptomic signatures. Full article

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and the dual GIP/GLP-1 co-agonist tirzepatide are increasingly prescribed for obesity and type 2 diabetes in populations enriched for binge-spectrum eating pathology. A recurring controversy asks whether these agents treat eating pathology or merely mask it. This critical narrative review argues that, posed as a simple binary, the question is under-specified, and reframes it around three problems. The central is a measurement problem: several intended effects of GLP-1 RAs are scored as improvement by eating-disorder instruments, creating a diagnostic blind spot. In the one disorder where a weight-acting drug has been tested against a placebo, efficacy on weight coincided with no effect on the psychological core—the dissociation that confounds measurement during GLP-1 RA therapy. The second is a phenotype problem: because BED subtypes already moderate response to drug versus psychological treatment, an agent acting on appetite and reward should not act uniformly, though this remains a hypothesis. The third concerns the post-discontinuation trajectory, and a therapy–harm asymmetry emerges across the spectrum. A factorial, phenotype-stratified trial with disorder-core endpoints and drug-free follow-up could resolve these questions; meanwhile, prudent practice combines uncontaminated pre-treatment screening, monitoring not reliant on confounded self-report, discontinuation planning, and integration with psychological care. Full article

Background/Objectives: The aim of the present study was to investigate the mechanisms in Parkinson’s disease (PD), a progressive neurodegenerative disorder characterized by loss of dopaminergic neurons, aggregation of α-synuclein, mitochondrial dysfunction, oxidative stress, neuroinflammation, gut dysbiosis, and blood–brain barrier (BBB) impairment. Although there are several approved therapies that have been developed, their aqueous solubility, oral bioavailability, first-pass metabolism, and inability to penetrate the BBB make them less effective over time. This review is intended to critically analyze the potential of self-nanoemulsifying drug delivery systems (SNEDDSs) as a pathogenesis-related approach to enhance the delivery and therapeutic activity of repurposed drugs and conventional drugs for PD. Methods: A comprehensive literature search was conducted to address the pathogenic mechanisms of PD, the deficiencies of current pharmacotherapy, recent developments in SNEDDS formulation strategies and their application in improving oral bioavailability, lymphatic transport, BBB penetration and targeted brain delivery. A special focus was dedicated to drug repurposing, functionalized SNEDDSs, PEGylation, and gut–brain axis modulation. Results: SNEDDSs significantly enhance the water solubility, stability, intestinal absorption and systemic exposure of poorly water-soluble therapeutic agents and, to a certain extent, lymphatic uptake to avoid first-pass metabolism. These systems include improved brain delivery, decreased pharmacokinetic variability, and prolonged drug levels within the therapeutic range. Moreover, SNEDDSs can be used to deliver multiple molecules that are found to be neuroprotective, antioxidant, anti-inflammatory and probiotic, all at once, which can act on multiple pathogenic mechanisms associated with PD. Functionalized and PEGylated SNEDDSs add further to formulation stability, extend systemic circulation and increase efficiency of brain targeting. Conclusions: SNEDDSs are a promising translational nanomedicine platform for enhancing the effectiveness of conventional and repurposed therapeutics in PD, which address key pharmacokinetic and biological challenges. The next generation of oral therapies with targeted surface engineering, precision drug repurposing and clinical validation will be expected to bring about a faster advancement of drugs that can alter the course of disease rather than giving only symptomatic relief. Full article

Self-determination is critical in promoting classroom engagement among students with autism spectrum disorder. The Self-Determined Learning Model of Instruction (SDLMI), an evidence-based practice for enhancing self-determination in students with disabilities, has gained increasing scholarly attention. However, empirical studies in Chinese contexts remain limited. This exploratory, descriptive implementation study used an A–B–M single-case approach with two individual cases to examine descriptive patterns in self-determination skills, perceived opportunities for self-determination, and classroom engagement before, during, and after the implementation of an SDLMI-based action-plan in Mandarin-speaking special education classrooms in Fujian Province, China. Preliminary findings indicated positive trends in students’ self-determination skills and classroom engagement after the implementation of the SDLMI, as well as increased perceived school-based opportunities for self-determination and mixed changes in perceived home-based opportunities. These findings are consistent with the existing international literature and provide preliminary case-level support for the cultural feasibility of adapting SDLMI practices within Chinese special education settings. Further research with larger samples and more rigorous experimental designs must fully assess its effectiveness and generalizability. Full article

Background: Recovering from COVID-19 does not always lead to complete recovery, and many patients report symptoms of anxiety and depression. One potential mechanism behind these disorders is dysbiosis. The aim of this study was to evaluate the impact of psychobiotic therapy on the effectiveness of treating anxiety and depressive symptoms in individuals who had previously experienced COVID-19. Methods: This study was designed as a randomized, double-blind, placebo-controlled trial. A total of 62 participants were randomly allocated to one of two groups: a psychobiotic group (PG; 23 women, 9 men) receiving 3 × 10⁹ CFU Lactobacillus helveticus and Bifidobacterium longum, or a control group (CG; 21 women, 9 men) receiving a placebo, for 6 weeks. Fifty-six participants finalized the study and were included in the analysis (28 per group). The severity of depressive and anxiety symptoms at baseline and after the intervention was assessed using validated self-assessment tools: the Hospital Anxiety and Depression Scale (HADS), the Generalized Anxiety Disorder 7-item scale (GAD-7), the Beck Depression Inventory (BDI), and the Hopkins Symptom Checklist (SCL-90). Additionally, the profile of selected short-chain fatty acids (SCFAs) in the stool was assessed. Results: Following the supplementation period, the PG showed significantly lower median levels of depression and anxiety compared to the CG, corresponding to a 57.2% reduction in anxiety severity (GAD-7) and a 50.9% reduction in depressive symptoms (BDI) (HADS—Depression and Anxiety, and GAD-7: p = 0.0001; BDI: p = 0.0003). Additionally, the prevalence of anxiety and depressive symptoms significantly decreased in the PG compared to the CG based on the HADS-A (p = 0.0044), GAD-7 (p = 0.0219), and BDI (p = 0.0011) scores. Among the measured SCFAs, only the butyric acid concentration in PG increased significantly during supplementation (baseline vs. follow-up—p = 0.0338) and was higher in PG than in CG at the study’s end (p = 0.0248). However, in the PG, changes in the concentrations of all analyzed acids correlated with a reduction in the severity of anxiety symptoms measured using the HADS-A. Conclusions: Psychobiotic supplementation in individuals recovering from COVID-19 who exhibit anxiety and/or depressive symptoms led to mood improvement and a reduction in symptom severity, and it may serve as a supportive treatment. Full article

The cohesin complex is a highly conserved, ring-shaped protein assembly that plays fundamental roles in chromosome biology. Originally identified as the molecular glue that holds sister chromatids together from DNA replication until cell division, cohesin has since been recognized as a pleiotropic regulator of genome organization, gene expression, DNA repair, and cell fate determination. In embryonic stem cells (ESCs), cohesin’s functions extend beyond canonical sister chromatid cohesion to include the maintenance of three-dimensional (3D) chromatin architecture through DNA loop extrusion, regulation of pluripotency-associated transcriptional programs, and facilitation of homologous recombination-mediated DNA repair during the prolonged S phase. Recent discoveries have revealed that meiosis-specific cohesin components, particularly the α-kleisin subunit REC8 and its interacting partner STAG3, are expressed and functionally active in mitotic ESC chromosomes, where they contribute to chromosomal organization and sister chromatid cohesion in concert with mitotic RAD21-containing cohesin. Furthermore, the interplay between cohesin and condensin complexes at shared genomic binding sites has emerged as a critical determinant of chromosome topology, with cohesin depletion leading to aberrant condensin accumulation and chromosome hypercompaction. Importantly, perturbations in cohesin function not only impair ESC self-renewal but also direct lineage-specific differentiation, linking cohesin to stem cell fate determination. Germline mutations in cohesin and its regulators underlie a spectrum of developmental disorders termed cohesinopathies, while somatic mutations are frequently observed in various cancers. This review provides a comprehensive overview of the diverse roles of cohesin in chromosome structure, cell cycle regulation, and stem cell biology, with particular emphasis on recent findings in ESCs that illuminate the complex interplay between mitotic and meiotic cohesin complexes. Full article

Background/Objectives: Depression and anxiety disorders exhibit significant clinical heterogeneity, which complicates diagnosis and treatment. This study investigated whether tripartite interactions between biological sex, the serotonin transporter gene promoter region (5-HTTLPR), and brain-derived neurotrophic factor (BDNF) G196A polymorphisms explain specific symptom-level variations. Methods: A community sample of 271 Australian adults was genotyped for common 5-HTTLPR (short/long) and BDNF (G/A) variants. Participants completed self-reported measures of anxiety (SAS), depression subtypes (SDS; clinical content scales), and psychological resilience (CDRISC). Morning salivary cortisol, BMI, and substance use were assessed as potential confounds. Statistical analyses utilised a three-way factorial ANCOVA to test for interactions on raw scores, controlling for age. Significant omnibus interactions were decomposed via planned stratified ANCOVAs within each 5-HTTLPR stratum. Results: The BDNF GA genotype exerted opposite effects on anxiety and anhedonia depending on sex and 5-HTTLPR background. In females, GA was associated with increased symptoms on an ss background, whereas in males, GA was associated with increased symptoms on an ll background. These effects were highly specific to anxiety and anhedonic depression, while depressed mood, cognitive, and somatic subtypes remained unaffected. Findings were independent of cortisol, BMI, smoking, alcohol use, and psychological resilience. Conclusions: The findings reveal a complex, sex-dependent genetic interaction that selectively influences anhedonia and anxiety. They should be interpreted in the context of modest subgroup sizes following genotype stratification and require replication in larger independent cohorts. Nonetheless, this study highlights the value of considering sex-stratified genetic backgrounds and symptom specificity to advance personalised precision medicine in psychiatry. Full article

Prenatal alcohol exposure (PAE) leads to fetal alcohol spectrum disorder (FASD), the most common preventable cause of neurodevelopmental impairment. The classical narrative attributes the clinical picture of FASD exclusively to direct ethanol-induced brain injury. In the present review, we argue that this perspective is incomplete and leads to diagnostic errors, most often to the misdiagnosis of ADHD in children who in fact have FASD. We propose that, alongside the direct neurotoxicity of ethanol, an important and clinically under-recognized complementary mechanism is gut–brain axis dysfunction: alcohol damages the enteric nervous system and enteric glial cells, induces dysbiosis with deep deficits of butyrate and other short-chain fatty acids (SCFAs), damages the enterochromaffin cells responsible for 90% of peripheral serotonin production, and—through translocation of lipopolysaccharide (LPS) and activation of the Toll-like receptor 4 (TLR4)—sustains a neuroinflammatory brain signature. This cascade—superimposed on direct ethanol neurotoxicity—may account for the high rates of depression, anxiety, self-injurious behavior, and suicide attempts observed in individuals with FASD and for the limited efficacy of traditional interventions focused solely on the central nervous system. The 2024 Polish Institute of Mother and Child (Okulicz-Kozaryn et al.) study showed that 50.3% of pregnant women consumed alcohol, and 11% did so regularly, against only 7% who admitted so in questionnaires. The real clinical picture of children with FASD is further complicated by three factors to which we devote separate sections in this paper: prenatal co-exposure to nicotine, cannabinoids, and opioids; the loss of vertical microbiota transmission and breastfeeding in children transferred to foster care (where the prevalence of FASD is 18.8% and in children’s homes in some regions reaches up to 80%); and the substantial over-representation of preterm and small-for-gestational-age (SGA) infants (in the Hasken et al. cohort, 18.4% of children with FASD were born preterm and 51.4% were born SGA). In the final section, we present a structured, staged protocol for nutritional and microbiological intervention grounded in a hierarchy of evidence: from interventions supported by randomized controlled trials (RCT-level; choline) through interventions supported by strong mechanistic rationale and RCTs in related populations (sodium butyrate, Lactobacillus rhamnosus GG, GOS/FOS prebiotics—galacto-oligosaccharides and fructo-oligosaccharides, and omega-3 fatty acids) to experimental interventions. The protocol also covers the window before 2 years of age: we argue that, given the over-representation of preterm and SGA infants among children with FASD, the analogy to preterm infants on parenteral nutrition and to post-institutional infants applies in substantial part to the same patients, which justifies extending the indications for choline and other nutritional interventions. The paper includes a compact table of dosing proposals for each age window (from pregnancy to school-age child) and provides clinicians with concrete answers: where to start, what to avoid, and what to monitor, with explicit signposting of regulatory limitations for individual substances in Poland and the European Union. Full article

Dementia with Lewy bodies (DLB) is increasingly conceptualised not merely as a disorder of neuronal death but as a primary synaptopathy in which the functional collapse of synaptic transmission and plasticity precedes, and predicts, neurodegeneration and clinical decline. Two genetic determinants dominate the heritable risk architecture of DLB: the α-synuclein gene SNCA, in which both copy-number variation and missense mutations exert dose- and conformation-dependent effects, and GBA1, encoding the lysosomal hydrolase glucocerebrosidase (GCase), the single most influential genetic risk factor for the disease. Here we synthesise evidence that these loci converge on a shared pathogenic endpoint—the impairment of activity-dependent synaptic plasticity. We argue that GBA1 loss-of-function and the resulting accumulation of glucosylceramide stabilise specific neurotoxic α-synuclein proteoforms, including soluble oligomers and self-templating conformational strains bearing defined post-translational modifications. These proteoforms are trafficked to, and enriched within, presynaptic terminals, where they disrupt SNARE-complex assembly and synaptic-vesicle dynamics, while postsynaptically they perturb NMDA and AMPA receptor trafficking, dysregulate dendritic calcium, and compromise synaptic mitochondrial bioenergetics. The net consequence is a metaplastic shift away from long-term potentiation (LTP) and toward aberrant long-term depression (LTD), a signature of synaptic failure detectable before frank pathology. We map these molecular events onto disease-relevant circuits—particularly the cholinergic basal forebrain and hippocampal–cortical and thalamocortical networks—and relate them to the defining neuropsychiatric features of DLB, including cognitive fluctuations and recurrent visual hallucinations. Finally, we evaluate emerging therapeutic strategies that target the GBA1–α-synuclein axis and that aim to restore synaptic plasticity directly. Positioning DLB within the framework of genetically determined plasticity deficits clarifies its kinship with other neuropsychiatric disorders and identifies the synapse as the most tractable node for early, disease-modifying intervention. We further examine how GBA1 allele severity and zygosity grade the phenotype, which genetic and environmental factors modify penetrance in carriers, and what distinguishes this synaptopathy from those driven by PSEN1/PSEN2, MAPT, or HTT, and we summarise the therapeutic pipeline—including enzyme augmentation and adeno-associated viral GBA1 gene therapy—that targets it. Full article

Background: Attention-deficit/hyperactivity disorder (ADHD) is frequently associated with emotional dysregulation, socio-emotional difficulties, and low self-esteem. Narrative-based approaches, including therapeutic writing, may support identity development and promote adaptive self-representations. However, there is limited evidence regarding structured, group-based therapeutic writing interventions for this population, particularly for female subjects. This case series provides preliminary and exploratory evidence regarding the feasibility of and potential changes associated with this approach in female adolescents with ADHD. Methods: This case series included four adolescents (aged 11–14 years) with a clinical diagnosis of ADHD and presenting with emotional and socio-emotional difficulties. Participants underwent a structured group intervention consisting of seven sessions integrating therapeutic writing techniques and cognitive–behavioral principles, supervised by a specialized psychotherapist. The following outcome measures were collected at baseline (t0) and post-intervention (t1): Difficulties in Emotion Regulation Scale (DERS-SF), Difficulties in Emotion Regulation Scale (SSIS-SEL), and Rosenberg Self-Esteem Scale (RSE_TOT). Data were analyzed using linear mixed-effects models, with results interpreted as exploratory estimates of pre–post changes. Results: Following the intervention, positive pre–post changes were observed in socio-emotional competencies and self-esteem. Statistically significant pre–post changes were observed in self-esteem and in socio-emotional competencies, particularly in self-awareness and self-regulation. Reductions were observed in emotional regulation difficulties, although these changes did not reach statistical significance. Conclusions: This case series suggests that a structured group-based therapeutic writing intervention may be associated with improvements in self-esteem and selected aspects of socio-emotional functioning in adolescents with ADHD. Given the small sample size and exploratory design, findings should be interpreted cautiously and require confirmation in larger controlled studies. These findings contribute preliminary evidence to an underexplored area in the underrepresented female ADHD population and highlight the potential value of integrating narrative processes within group interventions to support both individual meaning-making and interpersonal validation. Full article

For many decades, the regulation of immune responses, namely, the maintenance of self-tolerance and the prevention of pro-inflammatory processes, was attributed to the suppressive function of T and/or B regulatory cells. However, the field of immune regulation was recently expanded to include not only many membrane-bound regulatory molecules on immune cells but also the release of many soluble molecules playing a role in the modulation of immune responses. Soluble checkpoint molecules are the subject of many recent studies, in which they were reported to function as both regulatory and stimulatory molecules. They are involved in the pathogenesis of immune-mediated disorders, infections, and cancer, and are involved in balancing immune effector responses with regulatory reactions. Many of them have become relevant targets in treating these diseases. In this review, we chose to focus on those soluble molecules whose role is attributed to immune-mediated diseases, namely in modulating autoimmunity by enhancing mechanisms of self-tolerance and immunosuppressive signals. The understanding of these mechanisms might facilitate the development of future therapeutic approaches. Full article

Background/Objectives: Disordered eating behaviours are increasingly common among young adults, yet nutrition-focused, region-specific data from Romania and Central and Eastern Europe (CEE) remain scarce. We characterised nutritional patterns, weight-control practices, disordered-eating indicators, body image, and psychosocial factors among Romanian young adults and tested how these differed across body mass index (BMI) categories. Methods: In a cross-sectional online survey (March–April 2026), 753 Romanian adults aged 18–30 years (93.5% female) completed a 30-item questionnaire. Self-reported anthropometric measurements were classified using WHO BMI cutoffs. Prevalences (with Wilson 95% confidence intervals [CIs]) were compared across BMI categories using the chi-square test, and multivariable logistic regression, adjusted for age and sex, estimated odds ratios (ORs). Results: Most participants were normal weight (59.1%); 11.6% were underweight, 29.3% were overweight or obese, and 86.3% were omnivorous. Dietary restriction (57.4%) and physical exercise (46.7%) were the leading weight-control methods; self-induced vomiting (6.4%) and medication (4.5%) were less frequent. Lifetime compulsive/emotional eating was reported by 50.1%, current stress-related eating by 49.1%, and guilt after eating by 66.1%. Lifetime night eating reached 31.9% (current, 12.9%). Body dissatisfaction (36.1% “not at all satisfied”), difficulty looking in the mirror (66.7%) and self-reported stress (82.2%) were widespread. In adjusted models, dietary restriction, emotional eating and guilt after eating rose steeply and monotonically with BMI (overweight/obesity vs. normal weight: aOR 2.34, 2.49 and 2.73, respectively; all p < 0.001), whereas current night eating and frequent self-weighing did not differ across BMI categories (p = 0.92 and p = 0.82). Dietary restriction increased from 24.1% in underweight to 55.5% in normal-weight and 74.2% in overweight/obesity participants; corresponding gradients were also observed for emotional eating and food-related guilt. Conclusions: In this predominantly female, largely urban online convenience sample of Romanian young adults, self-reported behavioural risk indicators related to disordered eating were common. Restriction, emotional eating and food-related guilt increased with BMI, whereas night eating and self-weighing showed no clear BMI gradient. These findings should be interpreted cautiously and should not be generalised to Romanian young men or rural populations without confirmation in more representative samples. Full article

Background/Objectives: Binge eating (BE)—eating an objectively large amount of food with a subjective loss of control—occurs broadly beyond formal eating disorder diagnoses. However, its real-time occurrence in the general population remains poorly understood due to reliance on retrospective, clinic-based self-reporting. Ecological momentary assessment (EMA) captures repeated, real-time reports of BE and may overcome these limitations. This scoping review mapped EMA studies of BE in non-clinical, general population samples, paying attention to population characteristics, methodological approaches, and key findings. Methods: This review followed PRISMA-ScR guidelines. PubMed and Scopus were searched for studies published between January 2016 and January 2026, with eligibility independently assessed by two reviewers. Results: Twenty-three studies met the inclusion criteria. Twenty studies (87%) comprised predominantly female samples, and most participants were in their twenties; men, middle-aged adults, and racially diverse populations were underrepresented. Regarding EMA methodology, BE was assessed either by measuring overeating and loss of control of eating separately (15 studies) or through direct, instructed self-report (8 studies); most studies used signal-contingent designs, with response rates generally being between 60% and 85%. Across studies, BE was most consistently linked to negative affect, weight stigma, and body dissatisfaction, while dietary restraint and food insecurity—a more recently emerging focus—were each examined in only one or two studies. Conclusions: This review maps the range of EMA methodologies used to assess BE, offering a methodological reference point for future studies. However, the existing evidence remains concentrated in young, female, and predominantly White samples, and further research in underrepresented populations is needed to clarify the broader determinants of BE in everyday life. Full article