Continuity of psychopathology v. resilience across the transition to adolescence: role of hair cortisol and sensitive caregiving.

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, Mage = 9.3 years ± 1.41), early adolescence (N = 111, Mage = 11 0.66 years ± 1.23), and late adolescence (N = 138, Mage = 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.

Chronic early trauma impairs emotion recognition and executive functions in youth; specifying biobehavioral precursors of risk and resilience.

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.

From mothers to children and back: Bidirectional processes in the cross-generational transmission of anxiety from early childhood to early adolescence.

BACKGROUND: Maternal psychopathology and caregiving behavior are linked with child anxiety and these associations may be particularly salient when families face mass trauma together and members influence each other's symptomatology and resilience. Despite the well-known mother-to-child effects, less research addressed the longitudinal bidirectional effects of maternal and child's anxiety symptoms on each other. METHODS: Mothers and children exposed to chronic war-related trauma from Sderot, Israel, and comparison group were followed at three time-points; Early childhood (T1:N = 232, MAge = 2.76 years), late childhood (T3:N = 176, MAge = 9.3 years), and early adolescence (T4:N = 110, MAge = 11.66 years). At each time-point maternal and child's anxiety symptoms were evaluated via questionnaires and maternal sensitivity was coded from videotaped observations of parent-child interactions. Bidirectional associations were examined using traditional cross-lagged panel model (CLPM) and CLPM with random intercepts (RI-CLPM). RESULTS: Trauma-exposed mothers and children exhibited more anxiety symptoms and lower maternal sensitivity. Cross-lagged panel models revealed cross-time bidirectional associations between maternal anxiety and child anxiety from early to late childhood. Child anxiety at each time-point predicted maternal anxiety and maternal sensitivity at the next stage; however, maternal sensitivity did not show longitudinal associations with child anxiety, highlighting children's role in shaping caregiving. CONCLUSIONS: Findings demonstrate bidirectional cross-generational influences of mother and child on each other's anxiety in contexts of trauma and pinpoint early childhood as a sensitive period for such mutual influences. Children's increased anxiety following trauma appears to be further exacerbated via its impact on increasing maternal anxiety and compromising sensitive caregiving, underscoring the potential benefits of parental and mother-child interventions for trauma-exposed populations.

Physiological and social synchrony as markers of PTSD and resilience following chronic early trauma.

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.

Human attachment triggers different social buffering mechanisms under high and low early life stress rearing.

Social buffering - the attenuation of stress by maternal safety signals - is a core mammalian-general stress management mechanism implicating two ancient systems: the oxytocinergic and HPA systems. Yet, because human attachments are representation-based, understanding social buffering mechanisms in humans requires the assessment of relationship history and consideration of early life stress (ELS), which alters stress responsivity. We followed a unique trauma-exposed cohort across childhood, versus a low-stress control group, and repeatedly observed maternal sensitive, safety-promoting style. In adolescence, we used an attachment induction paradigm that exposed children to both live and reminders of attachment safety signals and measured oxytocin and cortisol baseline and response, to test how maternal safety signals impact hormonal reactivity in children reared under high- versus low-stress conditions. Only safety-promoting mothers exhibited a stress-buffering function, but their effect was system-specific and depended on the rearing context. For oxytocin, safety-promoting mothers normalized the deficient baseline oxytocin levels observed in ELS youth by implicating a plasticity-by-affiliation mechanism. For cortisol, safety-promoting mothering reduced the initial stress response only among youth reared in low-stress contexts via the typical buffering-by-safety mechanism. Results suggest that human attachments require internalized security evolving over time to trigger a stress buffering function. Under conditions of chronic early stress, the stressful rearing context overrides the maternal safety signals, normative stress buffering mechanisms fail, and safety-promoting mothers switch to an immature, affiliation-based mechanism that relies on maternal presence.

Stress and immune biomarkers interact with parenting behavior to shape anxiety symptoms in trauma-exposed youth.

The relations between stress, HPA-axis, and the immune system have been extensively studied; however, no study to date addressed the joint contribution of immune and HPA biomarkers to the development of anxiety in youth exposed to chronic trauma as mediated by mother-child interaction patterns. A unique cohort of war-exposed children and their mothers, compared to matched controls, were followed from infancy and the current study reports findings from early adolescence (mean age = 11.66, SD = 1.23; N = 111; exposed = 58 control = 53). Youth and mothers' salivary cortisol (CT) and secretory immunoglobulin (s-IgA) levels were measured three times during a 4-hour lab visit, mother-child interaction patterns were quantified from a joint task, and children's anxiety symptoms diagnosed. Trauma-exposed children had higher levels of CT and s-IgA, exhibited more anxiety symptoms, and showed lower social collaboration with mother during the joint task. Trauma-exposed mothers had higher CT and s-IgA levels and showed less supportive parenting during mother-child interaction. Structural equation modeling defined three bio-behavioral paths by which trauma increases anxiety in youth. While the first path charted a behavioral link from exposure to child anxiety via diminished maternal support, the other two paths described mediated biological paths, one through HPA-axis functioning, the other via the immune system. Paths via the child's HPA and immune system were mediated by the parallel maternal variable. Findings are the first to describe the complex bio-behavioral interplay of stress and immune biomarkers and parenting behavior in shaping to the development of risk and resilience trajectories in youth growing up amidst chronic trauma.

Escitalopram and NHT normalized stress-induced anhedonia and molecular neuroadaptations in a mouse model of depression.

Anhedonia is defined as a diminished ability to obtain pleasure from otherwise positive stimuli. Anxiety and mood disorders have been previously associated with dysregulation of the reward system, with anhedonia as a core element of major depressive disorder (MDD). The aim of the present study was to investigate whether stress-induced anhedonia could be prevented by treatments with escitalopram or novel herbal treatment (NHT) in an animal model of depression. Unpredictable chronic mild stress (UCMS) was administered for 4 weeks on ICR outbred mice. Following stress exposure, animals were randomly assigned to pharmacological treatment groups (i.e., saline, escitalopram or NHT). Treatments were delivered for 3 weeks. Hedonic tone was examined via ethanol and sucrose preferences. Biological indices pertinent to MDD and anhedonia were assessed: namely, hippocampal brain-derived neurotrophic factor (BDNF) and striatal dopamine receptor D2 (Drd2) mRNA expression levels. The results indicate that the UCMS-induced reductions in ethanol or sucrose preferences were normalized by escitalopram or NHT. This implies a resemblance between sucrose and ethanol in their hedonic-eliciting property. On a neurobiological aspect, UCMS-induced reduction in hippocampal BDNF levels was normalized by escitalopram or NHT, while UCMS-induced reduction in striatal Drd2 mRNA levels was normalized solely by NHT. The results accentuate the association of stress and anhedonia, and pinpoint a distinct effect for NHT on striatal Drd2 expression.