Given clear connections between mental and physical health, the impact of dysfunctional brain-body communication on emotional behavior and psychopathology is garnering increased attention. Vagal circuits comprise a major neural substrate for communication between the brain and peripheral organs, and evidence suggests that these circuits are developmentally plastic and sensitive to stress and other environmental challenges. Here, we review historic and current literature regarding how early life experience shapes the development of vagal circuitry in rodents and in humans. We discuss the anatomical intricacies of the sensory and motor vagal systems in rodents and outline their pre- and postnatal windows of developmental plasticity. We then focus on how two core features of early life experience, i.e., nutrition and maternal care, alter vagal circuit development in rodents. We discuss human studies that use differing psychological frameworks for measuring, interpreting, and contextualizing vagal contributions to the development of emotional control and stress response systems. We focus on infant, child, and adolescent research that test relations between parental care and/or early life adversity and vagal function, and how these factors impact emotional regulation and development of psychopathology. By synthesizing literature across species, we draw attention to novel insights and testable hypotheses that can be explored using different model systems. We emphasize the importance of considering environmental context and developmental timing for study design and interpretation of results. We conclude that vagal circuitry is an environmentally sensitive system for encoding stressful experiences during early life in rodents and in humans, with lifespan health consequences.
Tuberous sclerosis complex (TSC) is a rare genetic disorder caused by pathogenic variants in the TSC1 or TSC2 genes. Apart from multisystem physical manifestations, most individuals with TSC experience TSC-associated neuropsychiatric disorders (TAND). Little is known about how TAND severity changes over time and what factors may predict these changes. Preliminary data suggest the presence of differential TAND severity trajectories. Caregiver well-being may act as a mediator of TAND severity, and a well-being intervention designed for caregivers of children with developmental disabilities may improve caregiver well-being. The study aims are to (1) examine longitudinal trajectories of TAND severity in a large sample of individuals with TSC and to examine potential predictors of differential trajectories, (2) evaluate the association between caregiver well-being characteristics, TAND severity, and severity trajectories, and (3) adapt and evaluate the feasibility, acceptability, and potential efficacy of a brief, online group-based well-being intervention for family caregivers. For the first 2 aims, 500 individuals with TSC or their caregivers will be recruited in an accelerated longitudinal design to document TAND severity at 5 time points over 12 months via a web-based app. At each time point, participants will complete demographic, TSC characteristics, intervention, and well-being questionnaires. Data will be analyzed using latent class mixed and multinomial regression modeling (aim 1) and structural equation and mediation modeling (aim 2). Participatory methods will be used to adapt an existing caregiver well-being intervention for the TSC community (aim 3). Thirty caregivers will be invited to participate in the adapted group-based online well-being intervention. This study was funded from July 2024 (HT94252410790 and HT94252410791), and ethics approvals were obtained from the University of Cape Town (July 2024), Vrije Universiteit Brussel (November 2024), and the Department of Defense Office of Human Research Oversight (December 2024). The TAND Toolkit app was adapted for longitudinal data collection (aims 1 and 2). Recruitment started in December 2025 and will continue until 500 participants are enrolled (anticipated December 2026). Primary outputs are expected by July 2028. For aim 3, experiential and adaptation workshops were completed in June 2025, the pilot intervention was delivered in November 2025, and data collection will continue till May 2026. Outputs are expected by December 2026. Identification of differential longitudinal TAND trajectories and their correlates will stimulate research in TSC and generate evidence for the self-report quantified TAND checklist as a clinical outcome measure. Understanding the association between caregiver well-being and TAND severity will provide support for targeted well-being interventions. A successful pilot trial will provide preliminary data for larger-scale clinical trials, with the potential to support caregivers and improve TAND outcomes. Together, the findings from the study will help close the gap in interventions for TAND. ClinicalTrials.gov NCT06879665; https://clinicaltrials.gov/study/NCT06879665. DERR1-10.2196/91726.
Organisational gradients refer to a continuous low-dimensional embedding of brain regions and can quantify core organisational principles of complex systems like the human brain. Mapping how these organisational principles are altered or refined across development and phenotypes is essential to understanding the relationship between brain and behaviour. Taking a developmental approach and leveraging longitudinal and cross-sectional data from two multi-modal neuroimaging datasets, spanning the full neurotypical-neurodivergent continuum, we charted the organisational variability of structural (610 participants, N=390 with one observation, N=163 with two observations and N=57 with three) and functional (512 participants, N=340 with one observation, N=128 with two observations and N=44 with three). Across datasets, despite differing phenotypes, we observe highly similar structural and functional gradients. These gradients, or organisational principles, are highly stable across development, with the exact same ordering across early childhood into mid-adolescence. However, there is substantial developmental change in the strength of embedding within those gradients: by modelling developmental trajectories as non-linear splines, we show that structural and functional gradients are refined across development. Specifically, structural gradients gradually contract in low-dimensional space as networks become more integrated, whilst the functional manifold expands, indexing functional specialisation. The coupling of these structural and functional gradients follows a unimodal-association axis and varies across individuals, with developmental effects concentrated in the more plastic higher-order networks. Importantly, these developmental effects on coupling, in these higher-order networks, are attenuated in the neurodivergent sample. Finally, we mapped structure-function coupling onto dimensions of psychopathology and cognition and demonstrate that dimensions of cognition, such as working memory, are robust predictors of coupling. In summary, across clinical and community samples, we demonstrate consistent principles of structural and functional brain organisation, with progressive structural integration and functional segregation. These gradients are established early in life, refined through development, and their coupling is predicted by working memory.
The development of psychopathology during childhood and adolescence is complex and likely to follow diverse patterns. Mapping trajectories of psychopathological difficulties may improve our understanding of the nature of emerging, resolving and persistent psychopathology. The purpose of this study is to examine trajectories of psychopathology throughout childhood and adolescence by examining multiple data sources, including questionnaire-based reports of emotional and behavioural difficulties, psychiatric diagnoses and prescribed psychotropic medications. Group-based multi-trajectory modelling was used to identify the psychopathological trajectories. This study included 49,361 full-term live-born singleton children born between 1996 and 2003, recruited into the Danish National Birth Cohort. Strengths and Difficulties Questionnaire data were collected when the children/adolescents were 7, 11 and 18 years old. Annual information about psychiatric diagnoses and redeemed prescriptions for psychotropic medication was retrieved from nationwide registries between the ages of 1 and 18. We included six predefined dimensions to identify the trajectories: internalizing behavioural problems, externalizing behavioural problems, neurodevelopmental diagnoses, affective diagnoses, mixed psychiatric diagnoses and psychotropic medications. Six distinct trajectory groups were identified for both boys and girls. Approximately 6% of the boys and 8% of the girls receive the bulk of the psychiatric diagnoses and psychotropic medications. We found no support for 'pure' internalizing or externalizing patterns in any identified trajectory, as problems in one dimension often indicated the presence of problems in another dimension. Our results demonstrate substantial psychiatric comorbidity and add new insights to the understanding of child and adolescent well-being and the complex patterns of developmental psychopathology.
Eating disorders (ED) are dangerous psychiatric conditions that can emerge in youth. In previous work, child psychopathology increased risk for elevated body dissatisfaction and ED. Although parent psychopathology contributes to a range of psychological disorders, it has not yet been tested as a risk factor for youth body dissatisfaction and ED symptoms. The current prospective study tested whether lifetime parent anxiety and depression (measured when the child was ages 3 and 9) predicted adolescent body dissatisfaction at age 12 and 15 and symptoms of anorexia nervosa (AN) or bulimia nervosa (BN) at age 15 in a community sample of youth. We also examined whether child psychopathology at age 3 or 6 (anxiety, depression, and oppositional defiant disorder [ODD]) moderated, and body dissatisfaction mediated, these relationships. Maternal anxiety and depression predicted youth body dissatisfaction at age 12, and maternal and paternal depression predicted youth body dissatisfaction at age 15. Preregistered moderation and mediation analyses (https://osf.io/s8a6y) identified that child ODD moderated relationships between maternal anxiety and youth AN symptoms at age 15 and between paternal anxiety and youth body dissatisfaction at age 12. In addition, youth body dissatisfaction at age 12 mediated relationships between both maternal anxiety and depression and youth AN symptoms at age 15. The present study demonstrates additional vulnerability factors in early childhood that may increase risk for the development of body dissatisfaction and ED symptoms in early and middle adolescence. These data suggest that parent psychopathology should be an area of focus when evaluating early childhood risk factors for EDs.
Childhood is a period of peak developmental plasticity, involving drastic changes in the maturation of the neural circuitry underlying fear learning. Disruption and atypical development of fear learning are candidate mechanisms underlying child psychopathology. While there is a lack of understanding behind the maturation of fear learning systems in humans, rodent studies in this area delineate the normative development of fear learning systems early in life, and the effects of early threatening and fearful experiences on this developmental trajectory. Here, we review the rodent literature on developmental fear learning, as well as human studies that show translational convergence in typical development and children exposed to early life threat. We identify several gaps in research, including the role that caregivers play in regulating fear learning at different developmental stages and the intergenerational transmission of learned fear. Finally, we provide recommendations on how to address these gaps in a way that would improve our developmental frameworks of fear learning.
Studies persuasively show that parental power assertion contributes to children's hostile (defensive) mindsets, but most examined severe forms of control (abuse, harsh punishment) and aggressive children. Less is known about processes linking power assertion with children's hostile mindsets in typical, low-risk families. Further, specific mechanisms accounting for associations between parenting and hostile mindsets are unclear; children's theory of mind (ToM) and regulation have been suggested, implying equifinality in developmental cascades. Finally, factors that moderate impact of parenting on children's hostile mindsets, implying multifinality, are unclear. In a study of 200 mothers, fathers, and children, we proposed that links between parental power assertion and children's hostile mindsets are (a) accounted for by two parallel mediators - children's poor ToM and poor regulation, and (b) moderated by their representations of parents. We expected links between power assertion and hostile mindset to be significant for children with negative representations, but defused, or absent, for children with positive representations. Parental power assertion was assessed at toddler and preschool age, ToM and regulation at preschool age, and hostile mindsets and representations of parents at early school age. We supported both mediated paths for mother-child dyads, mediation via child regulation for father-child dyads, and moderation for both.
Parental differential treatment is associated with higher levels of psychopathology symptoms in children. Both higher overall levels of differential treatment (absolute/magnitude of differential treatment) and consistently favoring one child over another (relative differential treatment) are associated with risk in children. This study enhances understanding of parental differential treatment using a genetically informed twin design that clarifies child- and parent-driven effects. Participants included 632 twin pairs (Mage = 7.6 years, SD = 0.94; 96% White, 44% Rural) and parents. Parental differential treatment was assessed using an observed card game interaction and reports from mothers, fathers, and children. Twin modeling indicated heritable influences on parental hostility (h2 = .34 for females, .06 for males) and intrusiveness (h2 = .51 across the sample), suggesting that children's heritable traits elicit parenting. Observed intrusiveness differences predicted ADHD. Absolute and relative differences in maternal discipline predicted externalizing, internalizing, and ADHD symptoms, with a similar but less strong pattern for paternal discipline. However, absolute differences in paternal affection and paternal partiality proved especially important for children's psychopathology. Findings show children's behavior can elicit maladaptive differences in parenting, informing interventions.
Negative urgency is a transdiagnostic risk factor for a plethora of mental disorders. Internalizing symptoms are embedded in theories of negative urgency, yet we know little regarding how developmental changes in each coincide, and if changes in one predict changes in the other across middle adolescence. This study filled these voids in the literature, with N = 754 (52% female) community-recruited youth from the National Consortium on Alcohol NeuroDevelopment in Adolescence (NCANDA) study reporting internalizing symptoms and negative urgency annually. Negative urgency and internalizing symptoms were highly correlated at the between-person level, and between-person correlations were nearly double in size within male versus female adolescents. At the within-person level, changes in negative urgency and internalizing symptoms co-occurred across ages 14-18 but not age 13. Age 14 within-person changes in negative urgency prospectively predicted age 15 within-person changes in internalizing symptoms, and this effect was nearly double in size within female versus male adolescents. Findings held when accounting for externalizing symptoms, other impulsive personality traits, parenting, and school transitions. Results indicate that relations between negative urgency and internalizing symptoms were demonstrated across and within adolescents, with time-varying changes in negative urgency at age 14 being particularly impactful in terms of future internalizing symptoms.
Effectiveness of prevention programmes to reduce suicidal-related behaviours among adolescents could improve when systematically involve interventions for parents/caregivers to enhance family functioning and parental skills. We aim to systematically review parental or family-based family prevention interventions and meta-analyse its effectiveness, as evidence on this topic has not been recently and systematically synthesised. We will conduct a systematic review and meta-analysis of randomised controlled trials of parent-based prevention interventions to reduce suicidal-related behaviours in adolescents aged 10-19 years. Studies involving a comparison group, postintervention and/or follow-up assessments of suicidal ideation, self-harm, suicidal attempts, psychopathology, emotional regulation and behavioural and functional outcomes will be reviewed. The CINAHL, CENTRAL, PubMed, Scopus and Web of Science (WOS) databases were searched, without time limits, for eligible studies in English or Spanish, and with results available. Databases were searched from November 2025 to March 2026. The study selection process, the data extraction and the critical evaluation-with the Cochrane risk-of-bias tool-of included studies will be conducted independently and in duplicate by teams of reviewers, with the assistance of a third party, until reaching a high degree of agreement. If substantial heterogeneity is observed (I2>75%), we will use a narrative synthesis of the study results. If feasible, we will conduct a quality effects model for the statistical synthesis of results. If sufficient data are available, we will assess potential sources of heterogeneity. Doi plots, the Rosenthal's N test and Egger's Z test will be used to assess publication bias. The Grades of Recommendation, Assessment, Development and Evaluation approach will be used to assess the confidence in the evidence reviewed. Results are expected to be published in a peer-reviewed journal in the field of adolescent and/or youth mental health. This study will be conducted using published data and does not involve human participants directly. Therefore, it is exempt from ethical review. Therefore, it is exempt from ethical review. CRD420251183954.
This study investigates the dynamic, time-varying associations between multiple socio-ecological stressors and internalizing symptoms among Mexican-origin youth from low-income immigrant families. Grounded in a socioecological framework and employing time-varying effect modeling (TVEM), we examine how stressors at the interpersonal, family, and neighborhood levels differentially influence anxiety and depressive symptoms across early adolescence (ages 11-13), middle adolescence (ages 14-17), and late adolescence/emerging adulthood (ages 18-20). Participants included 604 Mexican-origin adolescents (54% female) from low-income immigrant families, assessed across three waves spanning nine years. Five distinct stressors were identified: discrimination, foreigner stress, economic stress, language brokering stress, and neighborhood violence/non-safety. Results from TVEM analyses revealed that the impact of discrimination on internalizing symptoms was more pronounced during early and middle adolescence, while foreigner stress became increasingly more pronounced in late adolescence/emerging adulthood. Economic hardship and language brokering stress consistently predicted internalizing symptoms across all developmental periods, whereas neighborhood violence/non-safety exerted the greatest influence during early adolescence. These findings underscore the importance of considering how stressor type and developmental timing intersect to shape mental health outcomes. Moreover, the results suggest that identifying sensitive windows for specific socio-ecological stressors can inform the optimal timing of tailored, developmentally sensitive interventions to mitigate their adverse effects.
Background: Bullying victimization is associated with serious short- and long-term consequences, including mental health problems. The close link between victimization and psychopathology underscores the necessity of examining potential risk factors that may increase vulnerability to victimization. The present study sought to enhance understanding of the mechanisms underlying a transgenerational transmission of the risk for victimization by examining the interplay between genes and environment.Methods: This study extended previous research by employing a nuclear twin family design comprising monozygotic and dizygotic twins, their parents, and siblings. Using data from 1,915 German population-based twin families, structural equation modelling was applied to estimate genetic and environmental components of vulnerability to bullying victimization. Longitudinal path analyses were further conducted to examine how parenting style and children's problem behaviour interact as risk factors contributing to the likelihood of being bullied.Results: Results indicated that genetic factors accounted for approximately one-third of the variance, which is most likely attributable to genetically predisposed characteristics that augment an individual's risk of being bullied by peers. Environmental influences not shared by family members accounted for the remaining variance, emphasizing the significance of environmental factors that are unique to each sibling. Furthermore, longitudinal path analyses revealed that the relationship between a positive parenting style and children's bullying victimization was mediated by children's externalizing and internalizing problem behaviour.Conclusions: The findings emphasize a complex interplay between genetically influenced risk factors and environmental conditions in explaining the development of bullying victimization. Knowledge on risk factors is crucial for effective preventions and interventions. Evidence of the negative and temporally persistent consequences of bullying victimization underscores the importance of a thoroughful examination of the etiology of bullying victimization.The genetic risk for bullying victimization is about 30% (and 50% after correction for attenuation due to error of measurement) highlighting the significance of genetically predisposed characteristics that augment an individual’s risk of being bullied by peersThe primary proportion of the variance is attributable to environmental factors that are effectively not shared by members of a family, suggesting that they are unique to each sibling.Interventions targeting children’s problematic characteristics might not only prevent children from being bullied but also mitigate the risk of long-term negative consequences. Antecedentes: La victimización por bullying se asocia a consecuencias serias a corto y largo plazo, incluyendo problemas de salud mental. La estrecha relación entre la victimización y la psicopatología resalta la necesidad de examinar los posibles factores de riesgo que pueden aumentar la vulnerabilidad a la victimización. El presente estudio buscó profundizar en la comprensión de los mecanismos subyacentes a la transmisión transgeneracional del riesgo de victimización mediante el examen de la interacción entre los genes y el ambiente. Métodos: Este estudio amplió investigaciones previas empleando un diseño de familia nuclear de gemelos, comprendiendo gemelos monocigóticos y dicigóticos (mellizos), sus padres y hermanos. Utilizando datos de 1.915 familias gemelares de la población alemana, se aplicó un modelo de ecuaciones estructurales para estimar los componentes genéticos y ambientales de la vulnerabilidad a la victimización por bullying. Se realizaron análisis de trayectoria longitudinal para examinar cómo el estilo parental y la conducta problemática de los niños interactúan como factores de riesgo que contribuyen a la probabilidad de sufrir bullying. Resultados: Los resultados indicaron que los factores genéticos explicaron aproximadamente un tercio de la varianza, probablemente atribuible a características genéticamente predispuestas que aumentan el riesgo de un individuo de ser víctima de bullying por parte de sus compañeros. Las influencias ambientales no compartidas por los miembros de la familia explicaron la varianza restante, lo que resalta la importancia de los factores ambientales únicos para cada hermano. Además, los análisis de trayectoria longitudinal revelaron que la relación entre un estilo parental positivo y la victimización por acoso escolar estaba mediada por la externalización e internalización de la conducta problemática de los niños. Conclusiones: Los hallazgos enfatizan una compleja interacción entre los factores de riesgo genéticamente influenciados y las condiciones ambientales para explicar el desarrollo de la victimización por bullying. El conocimiento de los factores de riesgo es crucial para una prevención e intervención eficaces.
Studies indicate that alterations in gut microbiota composition (GMC) during the first 1,000 days of life are associated with neurodevelopment and further behavioral development. However, research on the associations between GMC and executive functions (EFs) in childhood is scarce. This study aims to improve the understanding of the biological processes underlying behavioral development by exploring the associations between GMC and EFs early in life. Study population (n = 373) is part of the longitudinal FinnBrain Birth Cohort Study. GMC was analyzed using infant and toddler stool sample 16S rRNA sequencing and targeted and untargeted metabolomic assays. EF was assessed using the Spin the Pots and Snack Delay tasks at 2.5 years and the Spin the Pots task, Delay of Gratification task, EF Touch battery and BRIEF-2 questionnaire at 5 years. Alpha diversity in infancy was negatively associated with preschool EF. Additionally, EFs differed between microbial groups based on dominant genera. Bacterial genera abundances were related to some EFs, but no associations were found between microbial metabolites and EF. This study is among the first to investigate associations between GMC and EF in childhood, a crucial developmental stage characterized by significant changes in both the brain and microbiota.
Recent research suggests that maternal mood entropy, a novel measure of mood dysfunction, is associated with child outcomes. However, the link between maternal mood entropy and children's structural brain development, and how this association may change across childhood, remains unclear. In a longitudinal study with neuroimaging data collected at ages 4.5, 6, 7.5, and 10.5 years (n = 1,498; n = 674 with neuroimaging), we examined whether maternal mood entropy is associated with children's hippocampal and amygdala volumes over time. Mothers reported on negative mood symptoms at several assessments between ages 3 months and 4.5 years. We calculated maternal mood levels as the sum of mood symptoms and computed maternal mood entropy by applying Shannon's entropy to the distributions of mood questionnaire responses. Maternal mood measures were not associated with amygdala volumes; however, mood entropy was directly associated with smaller hippocampal volumes at age 4.5 years and indirectly associated with smaller hippocampal volumes at 10.5 years through rank-order stability over time. These effects were present beyond the effects of socioeconomic status and intracranial volume and were specific to mood entropy, not mood levels. Our findings indicate that patterns of maternal mood are embedded in early childhood brain structure, setting the stage for subsequent neurodevelopment.
This study evaluated whether young adult romantic relationship quality is an intergenerational mechanism linking Generation 1-2 (G1-G2) family climate and G2 social problem-solving skills during adolescence to G2-G3 parenting and family level-functioning and ultimately G3 child maladjustment and social-emotional competence. Our sample included 396 families with a parent (Mage = 28.29; 94% White) from a longitudinal study starting when they were in 6th grade. Participants completed annual assessments through high school, three assessments in young adulthood, and surveys after becoming parents. Two intergenerational pathways emerged: Positive G1-G2 family climates in adolescence predicted less young adult relationship violence; in turn, violence was associated with lower G2-G3 harsh discipline, abusive parenting, and family conflict. Of these, harsh discipline and abusive parenting were associated with G3 children's adjustment. In addition, G2 social problem-solving skills in adolescence were associated with stronger couple problem-solving skills in young adulthood and with better G2-G3 family routines; in turn, G2-G3 family routines were associated with G3 child social-emotional competence. Finally, moderation effects were observed in which youth who received the PROSPER interventions exhibited associations between adolescent social problem-solving skills and young adult couple problem-solving and G2-G3 parental warmth and (lower) lax discipline.
Background: The ICD-11 introduced distinct criteria for Posttraumatic Stress Disorder (PTSD) and Complex PTSD (CPTSD), necessitating validated assessment tools. While the International Trauma Questionnaire (ITQ) is a widely used self-report measure, the International Trauma Interview (ITI) is a structured clinician-administered interview considered a gold standard. This study investigated the correspondence between ITQ and ITI symptom and diagnostic classifications in a treatment-seeking veteran population.Methods: A sample of 108 Danish veterans completed both the ITQ and ITI. We calculated descriptive statistics, bivariate correlations, and Cohen's κ values to assess agreement for individual symptom items and diagnostic categories (ICD-11 PTSD, CPTSD, and PTSD or CPTSD combined), using the ITI as the reference standard. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were also determined.Results: ITQ scores were consistently higher than ITI scores across all symptom domains. Total symptom scores for PTSD, DSO, and CPTSD showed strong associations between instruments (r = .74 to .82, all p < .001). Agreement for individual symptom items varied from fair to substantial (κ = .33 to .70). The combined diagnosis of PTSD or CPTSD showed moderate agreement (κ = .60) with high sensitivity (0.94) and PPV (0.90). However, agreement for ICD-11 PTSD alone was fair (κ = .38), with low PPV (0.39) despite good sensitivity (0.65).Conclusion: The ITQ consistently reported higher symptom endorsement than the ITI. While the ITQ shows strong convergent validity for overall symptom burden and high sensitivity for screening trauma-related psychopathology (PTSD or CPTSD combined), its limited agreement for standalone ICD-11 PTSD diagnosis suggests it should not be used as a sole diagnostic tool. Comprehensive clinical interviews remain crucial for definitive diagnosis, while the ITQ can serve as an effective screening instrument. The ITQ consistently indicated higher symptom level endorsement than the ITI.On an item level, agreement between the ITQ and ITI items varied from fair to substantial.The ITQ provides good sensitivity in identifying cases with PTSD or CPTSD, but have limited specificity as it will capture a substantial number of false positive cases. Antecedentes: La CIE-11 introdujo criterios distintos para el Trastorno de Estrés Postraumático (TEPT) y el TEPT Complejo (TEPT-C), lo que hace necesarios instrumentos de evaluación validados. Mientras que el Cuestionario Internacional de Trauma (ITQ por sus siglas en inglés) es una medida de autoinforme ampliamente utilizada, la Entrevista Internacional de Trauma (ITI por sus siglas en inglés) es una entrevista estructurada administrada por un clínico, considerada un estándar de referencia. Este estudio investigó la correspondencia entre las clasificaciones sintomáticas y diagnósticas del ITQ y del ITI en una población de veteranos que buscaban tratamiento. Métodos: Una muestra de 108 veteranos daneses completó tanto el ITQ como la ITI. Se calcularon estadísticas descriptivas, correlaciones bivariadas y valores κ de Cohen para evaluar el acuerdo en los ítems sintomáticos individuales y en las categorías diagnósticas (TEPT según la CIE-11, TEPT-C, y TEPT o TEPT-C combinados), utilizando la ITI como estándar de referencia. También se determinaron la sensibilidad, la especificidad, el valor predictivo positivo (VPP) y el valor predictivo negativo (VPN). Resultados: Las puntuaciones del ITQ fueron sistemáticamente más altas que las de la ITI en todos los dominios sintomáticos. Las puntuaciones totales de síntomas para TEPT, DSO y TEPT-C mostraron asociaciones fuertes entre los instrumentos (r = .74 a .82, todos p < .001). La concordancia para los ítems de síntomas individuales varió de moderado a sustancial (κ = .33 a .70). El diagnóstico combinado de TEPT o TEPT-C mostró un acuerdo moderado (κ = .60), con alta sensibilidad (0.94) y VPP (0.90). Sin embargo, el acuerdo para el TEPT según la CIE-11 por sí solo fue regular (κ = .38), con un VPP bajo (0.39) a pesar de una buena sensibilidad (0.65). Conclusión: El ITQ reportó sistemáticamente una mayor presencia de síntomas que la ITI. Si bien el ITQ muestra una fuerte validez convergente para la carga global de síntomas y una alta sensibilidad para el tamizaje de psicopatología relacionada con el trauma (TEPT o TEPT-C combinados), su escasa concordancia para el diagnóstico independiente de TEPT según la CIE-11 sugiere que no debería utilizarse como única herramienta diagnóstica. Las entrevistas clínicas integrales siguen siendo fundamentales para un diagnóstico definitivo, mientras que el ITQ puede servir como un instrumento de tamizaje eficaz.
In youth remitted from anxiety and depressive disorders, lower daytime positive (PA) or higher negative affect (NA) and suboptimal sleep could reinforce one another in bidirectional vicious feedback loops. The strength of these loops may contribute to increase of anxiety or depressive symptoms four months later. Remitted 13-to-21-year-olds engaged in a two-week app-based daily diary with affect items, wearing a wrist-worn accelerometer assessing sleep, and completed anxiety (RCADS), depression (BDI) and sleep (SRSQ) questionnaires at baseline and four-month follow-up. Autoregressive models using lagged correlation estimated PA and NA from daily means and fluctuations, sleep from total sleep time and sleep efficiency, and assessed overall and individual bidirectional associations. Regression analyses examined bidirectional and exploratively unidirectional associations as predictors of the four-month anxiety and depression symptom course. Subgroups with and without clinically relevant sleep problems were exploratively compared. In 118 youth (89.8% female; Mage = 19.37; SDage = 1.70), daytime PA was negatively associated to subsequent nighttime sleep (β = -0.07, p = .03), especially in the no self-reported clinical sleep problems group (β = -0.14, p < .01). No other associations were significant, and no associations were robust significant symptom course predictors. Instead of a feedback loop, found patterns only suggest that youth who feel higher daytime PA subsequently sleep shorter and less efficiently. The interplay of objective sleep and affect may not be caught in a day-to-day pattern in youth, and may require studying longer cumulative or delayed effects of low sleep quality.
Personality disorders are highly prevalent worldwide imposing substantial personal and social challenges. Schema Therapy is an effective psychotherapeutic approach for personality pathology and other complex characterological problems. New scientific insights prompted a re-evaluation of its theoretical underpinnings leading to a reformulated Schema Therapy theory. Furthermore, the assumed cross-cultural universality of the Schema Therapy model has not been tested. This project has two primary aims: (1) To develop revised instruments based on the reformulated theory that are psychometrically sound and valid across diverse cultures and languages. (2) To validate the Schema Therapy-related constructs and their inter-relationships across cultures. New draft versions of the Young Schema Questionnaire, Schema Coping Inventory, and Schema Mode Inventory were developed. Before dissemination, these instruments will undergo rigorous psychometric evaluation to refine item sets and ensure linguistic and conceptual consistency. A minimum of 100 adult mental health patients and 100 non-patients from each participating country will complete the revised instruments. Sociodemographic and mental health-related variables will also be assessed. Statistical analyses will evaluate (a) internal consistency, (b) unidimensionality, (c) cross-cultural invariance, (d) factorial validity (if possible), and (e) known-group validity. Malfunctioning items will be deleted, and subscales will be shortened, if possible, targeting internal consistency of ≥.80. This study is expected to yield optimized versions of the three instruments aligned with the reformulated theory. These findings will inform subsequent international studies to further assess the structural and cross-cultural validity of the revised scales. The resulting empirically validated scales will be openly accessible, facilitating worldwide utilization. This protocol outlines the first international study based on the reformulated theory, aiming to extend the psychopathological coverage and enhance the cross-cultural application of evidence-based treatments for personality pathology. Results will be disseminated through peer-reviewed publications and conference presentations. Potential limitations are discussed.
Theorists conceptualize reactive aggression as emotional (especially angry) and proactive aggression as unemotional (although it is unclear whether relations between proactive aggression and emotion are null or negative). Goals of the current study were to: (a) examine links between reactive aggression and a range of emotions (happiness, sadness, anger, and anxiety), and (b) include neutral emotion to address whether proactive aggression is unrelated or negatively related to emotion. To assess emotion, playgroups of four same-sex, unfamiliar, nine-year-old children (N = 158; 52.5% males; racially/ethnically diverse) interacted as round-robin dyads while completing challenging and cooperative tasks; observers coded emotions second-by-second. To assess both behavioral and observational reactive-versus-proactive aggression, children completed video games with virtual peers. Reactive aggression was positively related to happiness, anger, and anxiety and negatively related to neutral emotion, for at least one task and one aggression measure. Proactive aggression was positively related to neutral emotion but negatively related to happiness, for both tasks and aggression measures. Findings enhance theoretical understanding of: (a) reactive aggression as broadly emotional by relating it to happiness and anxiety as well as anger, and (b) proactive aggression as unemotional by linking it to the display of neutral emotion and the lack of display of happiness.
Methylenedioxymethamphetamine (MDMA)-assisted psychotherapy (MDMA-AP) is a potentially transformative intervention for post-traumatic stress disorder (PTSD). Despite encouraging Phase III trial results, the psychological mechanisms underpinning MDMA's therapeutic effects remain insufficiently understood. Existing research on MDMA has emphasised neurobiological processes but has not adequately incorporated subjective, relational, and experiential processes that are likely to be central to optimising psychedelic-assisted treatments. In the absence of an established clinical psychological theory of MDMA-AP, qualitative approaches can support theory development to refine and optimise MDMA-AP, and identify cross-diagnostic change processes that may broaden its therapeutic scope. Approximately 25 experienced psychodynamically trained psychotherapists will receive two doses of MDMA (80-120 mg, oral), separated by ≥1 week, under controlled research conditions in an open-label, qualitative mechanistic study. Clinician-participants will complete baseline interviews examining beliefs and attitudes toward MDMA-AP, brief phenomenological interviews during MDMA sessions, in-depth phenomenological and theory-oriented follow-up interviews examining experience and understandings of MDMA-associated change processes, and daily reflective journals between dosing sessions. Additional standardised measures will assess reflective functioning and related constructs. Qualitative data will be analysed using phenomenological and thematic approaches, and grounded theory-inspired techniques will be used to develop a theoretically coherent model of MDMA's psychological mechanisms of action grounded in the full dataset. In this study of MDMA's potential mechanisms-of-action, we treat psychotherapists as expert observers of their own psychological processes. By examining first-hand experience in participants selected for their well-developed capacity for self-reflection, meta-awareness, and advanced theoretical and clinical frameworks for understanding mental phenomena, psychopathology, and psychological treatment, we anticipate generating novel insights into MDMA's therapeutic mechanisms-of-action. The primary study output will be a theoretically grounded model of MDMA's psychological mechanisms of action, intended to inform novel treatment models amenable to future experimental evaluation. The study also offers a transferable framework for qualitative mechanistic investigations of psychedelic compounds, supporting the development of integrative and evidence-based models of psychedelic therapy.