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Background: The transition to adolescence implicates heightened vulnerability alongside increased opportunities for resilience. Contexts of early life stress (ELS) exacerbate risk; still, little research addressed biobehavioral mediators of risk and resilience across the adolescent transition following ELS. Utilizing a unique cohort, we tested biosocial moderators of chronicity in adolescents' internalizing disorders v. resilience. Method: Families exposed to chronic war-related trauma, v. controls, were followed. We utilized data from three time-points framing the adolescent transition: late childhood (N = 177, M age = 9.3 years ± 1.41), early adolescence (N = 111, M age = 11 0.66 years ± 1.23), and late adolescence (N = 138, M age = 15.65 years ± 1.31). In late childhood and late adolescence children's internalizing disorders were diagnosed. At early adolescence maternal and child's hair cortisol concentrations (HCC), maternal sensitivity, and mothers' post-traumatic symptoms evaluated. Results: War-exposed children exhibited more internalizing disorders of chronic trajectory and mothers were less sensitive and more symptomatic. Three pathways elucidated the continuity of psychopathology: (a) maternal sensitivity moderated the risk of chronic psychopathology, (b) maternal post-traumatic symptoms mediated continuity of risk, (c) trauma exposure moderated the association between child internalizing disorders at late childhood and maternal HCC, which linked with child HCC. Child HCC linked with maternal post-traumatic symptoms, which were associated with child disorders in late adolescence. Conclusion: Results demonstrate the complex interplay of maternal and child's biosocial factors as mediators and moderators of risk chronicity across the adolescent transition following trauma. Findings are first to utilize maternal and child's HCC as biomarkers of chronic stress v. resilience during adolescence, a period of neural reorganization and personal growth that shapes the individual's lifetime adaptation. [ABSTRACT FROM AUTHOR]

Simple Summary: Premature birth disrupts the continuity of bodily contact between mother and newborn, leading to greater prevalence of physiological, cognitive, and behavioral difficulties among prematurely born children. We followed a group of mothers and preterm infants who received skin-to-skin contact (Kangaroo Care, KC) in the neonatal period, as compared to a matched group who received standard incubator care, from birth to adulthood. Our aim was to investigate how a touch-based neonatal intervention shaped three outcomes in young adulthood: anxiety and depressive symptoms, levels of oxytocin, and markers of the immune system. Findings indicated that the effects of KC on adult outcomes were indirect and stemmed from its impact on mother, child, and the dyad across infancy, childhood, and adolescence. KC reduced maternal anxiety and depression in infancy, improved infant attention and child executive functions, and increased mother–child synchrony across development. These effects were interconnected and led to improved outcomes in adulthood. Our study uniquely describes mechanisms by which a birth intervention can influence adult outcomes through step-by-step enhancement and provides valuable insights into the topic of "developmental continuity", a key controversy in developmental research. Premature birth disrupts the continuity of maternal–newborn bodily contact, which underpins the development of physiological and behavioral support systems. Utilizing a unique cohort of mother–preterm dyads who received skin-to-skin contact (Kangaroo Care, KC) versus controls, and following them to adulthood, we examined how a touch-based neonatal intervention impacts three adult outcomes; anxiety/depressive symptoms, oxytocin, and secretory immunoglobulin A (s-IgA), a biomarker of the immune system. Consistent with dynamic systems' theory, we found that links from KC to adult outcomes were indirect, mediated by its effects on maternal mood, child attention and executive functions, and mother–child synchrony across development. These improvements shaped adult outcomes via three mechanisms; (a) "sensitive periods", where the infancy improvement directly links with an outcome, for instance, infant attention linked with higher oxytocin and lower s-IgA; (b) "step-by-step continuity", where the infancy improvement triggers iterative changes across development, gradually shaping an outcome; for instance, mother–infant synchrony was stable across development and predicted lower anxiety/depressive symptoms; and (c) "inclusive mutual-influences", describing cross-time associations between maternal, child, and dyadic factors; for instance, from maternal mood to child executive functions and back. Findings highlight the long-term impact of a birth intervention across development and provide valuable insights on the mechanisms of "developmental continuity", among the key topics in developmental research. [ABSTRACT FROM AUTHOR]

Exposure to chronic early trauma carries lasting effects on children's well-being and adaptation. Guided by models on resilience, we assessed the interplay of biological, emotional, cognitive, and relational factors in shaping two regulatory outcomes in trauma-exposed youth: emotion recognition (ER) and executive functions (EF). A unique war-exposed cohort was followed from early childhood to early adolescence. At preadolescence (11–13 years), ER and EF were assessed and respiratory sinus arrhythmia (RSA), biomarker of parasympathetic regulation, was quantified. Mother–child dyadic reciprocity, child's avoidance symptoms, and cortisol (CT) were measured in early childhood. Trauma-exposed youth displayed impaired ER and EF abilities. Conditional process analysis described two differential indirect paths leading from early trauma to regulatory outcomes. ER was mediated by avoidance symptoms in early childhood and modulated by cortisol, such that this path was evident only for preadolescents with high, but not low, CT. In comparison, EF was mediated by the degree of dyadic reciprocity experienced in early childhood and modulated by RSA, observed only among youth with lower RSA. Findings pinpoint trauma-related disruptions to key regulatory support systems in preadolescence as mediated by early-childhood relational, clinical, and physiological factors and highlight the need to specify biobehavioral precursors of resilience toward targeted early interventions. [ABSTRACT FROM AUTHOR]

Objective: Although resilience is a key topic in clinical theory and research, few studies focused on biobehavioral mechanisms that underpin resilience. Guided by the biobehavioral synchrony frame, we examined the dynamic interplay of physiological and behavioral synchrony as marker of risk and resilience in trauma‐exposed youth. Methods: A unique cohort of war‐exposed versus control children was followed at four time‐points from early childhood to preadolescence and child posttraumatic stress disorder (PTSD) repeatedly assessed. At preadolescence (11–13 years), mother and child were observed in several social and nonsocial tasks while cardiac data collected and measures of respiratory sinus arrhythmia (RSA) and RSA synchrony computed. The social interactive task was microcoded for behavioral synchrony and the second‐by‐second balance of behavioral and physiological synchrony was calculated. War‐exposed preadolescents were divided into those diagnosed with PTSD at any time‐point across childhood versus resilient children. Results: Group differences in behavioral synchrony, RSA synchrony, and their interplay emerged. PTSD dyads exhibited the tightest autonomic synchrony combined with the lowest behavioral synchrony, whereas resilient dyads displayed the highest behavioral and lowest autonomic synchrony. Hierarchical Linear Model analysis pinpointed two resilience‐promoting mechanisms. First, for resilient and control dyads, moments of behavioral synchrony were coupled with decreased RSA synchrony. Second, only among resilient dyads, moments of behavioral synchrony increased child RSA levels. Conclusion: Findings specify mechanisms by which biobehavioral synchrony promotes resilience. As children grow, the tightly coupled mother–child physiology must be replaced by loosely coordinated behavioral attunement that buttresses maturation of the child's allostatic self‐regulation. Our findings highlight the need for synchrony‐based interventions to trauma‐exposed mothers. [ABSTRACT FROM AUTHOR]

Objective: Identifying biomarkers that can distinguish trauma-exposed youth at risk for developing posttraumatic pathology from resilient individuals is essential for targeted interventions. As trauma can alter the microbiome with lasting effects on the host, our longitudinal, multimeasure, cross-species study aimed to identify the microbial signature of posttraumatic stress disorder (PTSD)., Method: We followed children exposed to war-related trauma and matched controls from early childhood ( M age = 2.76 years, N = 232) to adolescence ( M age = 16.13 years, N = 84), repeatedly assessing posttraumatic symptomatology and maternal caregiving. In late adolescence, we collected fecal samples from mothers and youth and assessed microbiome composition, diversity, and mother-child microbial synchrony. We then transplanted adolescents' fecal samples into germ-free mice to determine if behavioral changes are observed., Results: Youth with PTSD exhibited a distinct gut microbiome profile and lower diversity compared to resilient individuals, and microbiome diversity mediated the continuity of posttraumatic symptomatology throughout development. Low microbiome diversity correlated with more posttraumatic symptoms in early childhood, more emotional and behavioral problems in adolescence, and poor maternal caregiving. Youth with PTSD demonstrated less mother-child microbial synchrony, suggesting that low microbial concordance between mother and child may indicate susceptibility to posttraumatic illness. Germ-free mice transplanted with microbiomes from individuals with PTSD displayed increased anxious behavior., Conclusions: Our findings provide evidence that the trauma-associated microbiome profile is at least partially responsible for the anxiety component of the PTSD phenotype and highlight microbial underpinnings of resilience. Further, our results suggest that the microbiome may serve as additional biological memory of early life stress and underscore the potential for microbiome-related diagnosis and treatment following trauma. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Breastfeeding has long been known to improve infants' health and mental development and to enhance the mother-infant bond, but much less research focused on the biological composition of breast milk and its associations with the infant's biomarkers and social development. In this exploratory study, we measured oxytocin (OT) and secretory immunoglobulin-A (s-IgA), the most abundant antibody in breast milk, and evaluated their associations with the same biomarkers in infant saliva and, consequently, with infant social engagement behavior. Fifty-five mother-infant dyads were home-visit and OT and s-IgA were assessed from breast milk and from infant saliva before and after a free-play interaction. Infant social behavior was coded offline using the Coding Interactive Behavior (CIB) and maternal anxiety self-reported. A path model revealed that mother's breast milk s-IgA impacted child social engagement via its links with child OT. In parallel, maternal breast milk OT was linked with infant social behavior through its association with the infant's immunity. This path was moderated by maternal anxiety; only in cases of high anxiety breast milk OT was positively connected to infant s-IgA. Our study, the first to measure OT and s-IgA in both breast milk and infant saliva in relation to observed social behavior, underscores the need for much further research on the dynamic interplay between breast milk composition, infant biomarkers, maternal mental health, and infant social outcomes. Results may suggest that biological systems in breast milk integrate to prepare infants to function in their social ecology through bio-behavioral feedback loops that signal the degree of stress in the environment., Competing Interests: no conflict., (© 2023 The Authors.)