Although there is increasing attention for the interrelationship between obsessive–compulsive personality disorder (OCPD) and obsessive–compulsive disorder (OCD), their shared characteristics in terms of childhood trait antecedents remain understudied. Perfectionism may be a viable candidate trait antecedent, given its role in the clinical manifestation of both OCPD and OCD in adulthood, and the evidence that perfectionism reflects a dispositional tendency observable from childhood onwards. However, little is known about childhood trajectories of perfectionism with prospective links to later OCPD versus OCD. Using latent growth curve modeling, this study explored the baseline and growth of childhood perfectionism in 485 community and referred children (55.5% girls, 7.17–14.78 years old, Mage = 10.74, SD = 1.50) across three waves. Adolescent OCPD traits and OCD symptoms were measured in Wave 4. An overall decreasing trend of perfectionism from childhood through adolescence appeared, without inter-individual differences in growth. Individual differences in baseline levels of childhood perfectionism were significant, and equally predicting adolescent OCPD and OCD outcomes. At a more specific level, childhood perfectionism predicted most strongly the rigid perfectionism component of OCPD, and the orderliness/cleanliness/perfectionism and obsession domain of OCD. This demonstrates the value of childhood perfectionism for understanding differential outcomes of adolescent OCPD traits and OCD symptoms.

We examined whether Research Domain Criteria (RDoC)-informed measures of prenatal stress predicted newborn neurobehavior and whether these effects differed by newborn sex. Multilevel, prenatal markers of prenatal stress were obtained from 162 pregnant women. Markers of the Negative Valence System included physiological functioning (respiratory sinus arrhythmia [RSA] and electrodermal [EDA] reactivity to a speech task, hair cortisol), self-reported stress (state anxiety, pregnancy-specific anxiety, daily stress, childhood trauma, economic hardship, and family resources), and interviewer-rated stress (episodic stress, chronic stress). Markers of the Arousal/Regulatory System included physiological functioning (baseline RSA, RSA, and EDA responses to infant cries) and self-reported affect intensity, urgency, emotion regulation strategies, and dispositional mindfulness. Newborns’ arousal and attention were assessed via the Neonatal Intensive Care Unit (NICU) Network Neurobehavioral Scale. Path analyses showed that high maternal episodic and daily stress, low economic hardship, few emotion regulation strategies, and high baseline RSA predicted female newborns’ low attention; maternal mindfulness predicted female newborns’ high arousal. As for male newborns, high episodic stress predicted low arousal, and high pregnancy-specific anxiety predicted high attention. Findings suggest that RDoC-informed markers of prenatal stress could aid detection of variance in newborn neurobehavioral outcomes within hours after birth. Implications for intergenerational transmission of risk for psychopathology are discussed.

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.

Adolescents who hold an entity theory of personality – the belief that people cannot change – are more likely to report internalizing symptoms during the socially stressful transition to high school. It has been puzzling, however, why a cognitive belief about the potential for change predicts symptoms of an affective disorder. The present research integrated three models – implicit theories, hopelessness theories of depression, and the biopsychosocial model of challenge and threat – to shed light on this issue. Study 1 replicated the link between an entity theory and internalizing symptoms by synthesizing multiple datasets (N = 6,910). Study 2 examined potential mechanisms underlying this link using 8-month longitudinal data and 10-day diary reports during the stressful first year of high school (N = 533, 3,199 daily reports). The results showed that an entity theory of personality predicted increases in internalizing symptoms through tendencies to make fixed trait causal attributions about the self and maladaptive (i.e., “threat”) stress appraisals. The findings support an integrative model whereby situation-general beliefs accumulate negative consequences for psychopathology via situation-specific attributions and appraisals.

Incremental prediction of aggression from callous–unemotional (CU) traits is well established, but cross-cultural replication and studies of young children are needed. Little is understood about the contribution of CU traits in children who are already aggressive. We addressed these issues in prospective studies in the United Kingdom and Colombia. In a UK epidemiological cohort, CU traits and aggression were assessed at age 3.5 years, and aggression at 5.0 years by mothers (N = 687) and partners (N = 397). In a Colombian general population sample, CU traits were assessed at age 3.5 years and aggression at 3.5 and 5.0 years by mother report (N = 220). Analyses consistently showed prediction of age-5.0 aggression by age-3.5 CU traits controlling for age-3.5 aggression. Associations between age-3.5 CU traits and age-5.0 aggression were moderated by aggression at 3.5 years, with UK interaction terms, same informant, β = .07 p = .014 cross-informant, β = .14 p = .002, and in Colombia, β = .09 p = .128. The interactions arose from stronger associations between CU traits and later aggression in those already aggressive. Our findings with preschoolers replicated across culturally diverse settings imply a major role for CU traits in the maintenance and amplification of already established aggression, and cast doubt on their contribution to its origins.

In a career spanning six decades, Edward Zigler redefined developmental psychology as the equal integration of scientific inquiry and evidence with social policy formulation and analysis to improve child well-being. The theme of his accumulated work was advancing child development as social action for children and families. Besides early childhood intervention and policy, for which he devoted most of his time, Dr. Zigler did pioneering work in education and school reform, social policy, prevention, child maltreatment, family support, developmental disabilities, and in service to government. In this article, I reflect on four of Dr. Zigler's major contributions to science and society that are underrated and, in many respects, under-appreciated in the larger context of the field. These are (a) historical analysis of Head Start, (b) conceptualization and analysis of motivation as a key component of early childhood program impacts, (c) development of preschool-to-third-grade programs and school reforms, and (d) critical analysis of theory, research, policy, and practice. Together, these and other contributions by Dr. Zigler provide a strong foundation to build a better society for all.

Differential susceptibility theory stipulates that some children are more susceptible than others to both supportive and adverse developmental experiences/exposures. What remains unclear is whether the same individuals are most affected by different exposures (i.e., domain general vs. specific). We address this issue empirically for the first time using, for illustrative and proof-of-principle purposes, a novel influence-statistics’ method with data from the National Institute of Child Health and Human Development (NICHD) Study of Early Child Care. Results indicated that previously documented effects of greater quality of care on enhanced pre-academic skills and greater quantity of care on more behavior problems apply mostly to different children. Analyses validating the new method indicated, as predicted, that (a) the quantity-of-care effect applied principally to children from more socioeconomically advantaged families and that (b) being highly susceptible to both, one or neither childcare effect varied as a function of a three-gene, polygenic-plasticity score (serotonin transporter linked polymorphic region [5-HTTLPR], dopamine receptor D4 [DRD4], brain-derived neurotrophic factor [BDNF]) in a dose–response manner (i.e., 2>1>0). While domain-specific findings involving child-care effects cannot be generalized to other environmental influences, the influence-statistics’ approach appears well suited for investigating the generality–specificity of environment effects, that is, of “differential, differential susceptibility.”

Family Minds is a brief group psychoeducational parenting intervention designed to increase the reflective functioning (RF) and mentalization skills of foster parents. RF is important for foster parents who have to build relationships with children whose adverse experiences increase their risk for psychosocial challenges. A randomized controlled trial (RCT) for Family Minds was conducted in Texas with 89 foster parents. The main aims of this study were to examine whether the intervention could significantly increase the RF/mentalization skills of the foster parents and decrease their parenting stress. After 6 weeks, compared with the control group, intervention foster parents improved their RF via a lowering of pre-mentalizing and also significantly decreased parenting stress related to parent–child dysfunctional interactions. Other measures of RF and parenting stress showed no significant differences between groups. Foster child behavior was not significantly different between groups, although data at 6 months showed a possible lowering of internalizing symptoms for children of intervention parents. This RCT provides some encouraging evidence that Family Minds may increase RF in foster parents, improve parental sensitivity and their ability to emotionally regulate, decrease parenting stress related to challenging interactions with their foster children, and possibly decrease children's internalizing behavior.

Adverse childhood experiences are significant risk factors in the development of adolescent borderline personality disorder symptoms (BPDs). Theorists have posited that two personality vulnerabilities factors, self-criticism and dependency, may inform our understanding of this relationship. However, no research has examined the associations between early negative experiences, personality vulnerabilities, and adolescent BPDs. The current study aimed to identify profiles of dependency and self-criticism to examine the associations of these profiles with cumulative forms of childhood maltreatment (CM) and BPDs as well as to explore the mediating and moderating role of vulnerable personality profiles in the relationship between cumulative CM and BPDs. Two hundred and forty-one nonclinical and clinical adolescents participated in the study (Mage = 16.37, SD = 1.84). The findings indicated three different profiles: average dependent profile, dependent and self-critical profile, and self-critical profile. Individuals in the average dependent profile presented lower levels of CM and BPDs. Mediation analyses showed that relative to the average dependent profile, a higher cumulative CM history predicted a higher probability of belonging in the dependent and self-critical profile or the self-critical profile and, in turn, this was associated with higher levels of BPDs. No moderating effects of profiles of dependency and self-criticism were found.

While previous studies suggest that both genetic and environmental factors play an important role in the development of autism-related traits, little is known about potential biological mechanisms underlying these associations. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we examined prospective associations between DNA methylation (DNAm: nbirth = 804, nage 7 = 877) and trajectories of social communication deficits at age 8–17 years. Methylomic variation at three loci across the genome (false discovery rate = 0.048) differentiated children following high (n = 80) versus low (n = 724) trajectories of social communication deficits. This differential DNAm was specific to the neonatal period and not observed at 7 years of age. Associations between DNAm and trajectory membership remained robust after controlling for co-occurring mental health problems (i.e., hyperactivity/inattention, conduct problems). The three loci identified at birth were not replicated in the Generation R Study. However, to the best of our knowledge, ALSPAC is the only study to date that is prospective enough to examine DNAm in relation to longitudinal trajectories of social communication deficits from childhood to adolescence. Although the present findings might point to potentially novel sites that differentiate between a high versus low trajectory of social communication deficits, the results should be considered tentative until further replicated.

We examined whether adolescents’ loneliness and social withdrawal mediated the association between maternal depressive symptoms and adolescent suicidality. Secondary analyses on the Québec Longitudinal Study of Child Development data were conducted (n = 1,623). Each mother completed the Centre for Epidemiologic Studies Depression Scale (at child ages 5 months, 1.5, 3.5, 5, and 7 years). Adolescent's social withdrawal (adolescent, father, and teacher reported at 10, 12, and 13 years) and loneliness (adolescent reported at 10, 12, and 13 years), were assessed using items from the Social Behavior Questionnaire and the Loneliness and Social Satisfaction Questionnaire, respectively. Adolescents completed self-reports to assess suicidal thoughts and attempts at 13, 15, 17, and 20 years. Children of mothers with higher levels of maternal depressive symptoms had an increased risk for suicidality (OR = 1.15, 95% CI: 1.03–1.28). Loneliness explained 16% of the total effect of maternal depressive symptoms on adolescent suicidality (indirect effect OR = 1.02, 95% CI: 1.00–1.04). There was no indirect effect of maternal depressive symptoms on adolescent suicidal outcomes via social withdrawal (indirect effect OR = 1.00, 95% CI: 0.99–1.02). Interventions that target loneliness may be beneficial for decreasing the risk for suicidality among adolescents of mothers with depressive symptoms.

Childhood adversity is thought to undermine youth socioemotional development via altered neural function within regions that support emotion processing. These effects are hypothesized to be developmentally specific, with adversity in early childhood sculpting subcortical structures (e.g., amygdala) and adversity during adolescence impacting later-developing structures (e.g., prefrontal cortex; PFC). However, little work has tested these theories directly in humans. Using prospectively collected longitudinal data from the Fragile Families and Child Wellbeing Study (FFCWS) (N = 4,144) and neuroimaging data from a subsample of families recruited in adolescence (N = 162), the current study investigated the trajectory of harsh parenting across childhood (i.e., ages 3 to 9) and how initial levels versus changes in harsh parenting across childhood were associated with corticolimbic activation and connectivity during socioemotional processing. Harsh parenting in early childhood (indexed by the intercept term from a linear growth curve model) was associated with less amygdala, but not PFC, reactivity to angry facial expressions. In contrast, change in harsh parenting across childhood (indexed by the slope term) was associated with less PFC, but not amygdala, activation to angry faces. Increases in, but not initial levels of, harsh parenting were also associated with stronger positive amygdala–PFC connectivity during angry face processing.

This study evaluated whether Attachment and Biobehavioral Catch-up (ABC), a parenting intervention, altered the attachment representations of parents (average age of 34.2 years) who had been referred to Child Protective Services (CPS) due to risk for child maltreatment when their children were infants. Approximately 7 years after completing the intervention, parents who had been randomized to receive ABC (n = 43) exhibited greater secure base script knowledge than parents who had been randomized to receive a control intervention (n = 51). Low-risk parents (n = 79) exhibited greater secure base script knowledge than CPS-referred parents who had received a control intervention. However, levels of secure base script knowledge did not differ between low-risk parents and CPS-referred parents who had received the ABC intervention. In addition, secure base script knowledge was positively associated with parental sensitivity during interactions with their 8-year-old children among low-risk and CPS-referred parents. Mediational analyses supported the idea that the ABC intervention enhanced parents’ sensitivity 7 years later indirectly via increases in parents’ secure base script knowledge.

DNA methylation of the elongation of very long chain fatty acids protein 2 (ELOVL2) was suggested as a biomarker of biological aging, while childhood maltreatment (CM) has been associated with accelerated biological aging. We investigated the association of age and CM experiences with ELOVL2 methylation in peripheral blood mononuclear cells (PBMC). Furthermore, we investigated ELOVL2 methylation in the umbilical cord blood mononuclear cells (UBMC) of newborns of mothers with and without CM. PBMC and UBMC were isolated from 113 mother–newborn dyads and genomic DNA was extracted. Mothers with and without CM experiences were recruited directly postpartum. Mass array spectrometry and pyrosequencing were used for methylation analyses of ELOVL2 intron 1, and exon 1 and 5′ end, respectively. ELOVL2 5′ end and intron 1 methylation increased with higher age but were not associated with CM experiences. On the contrary, overall ELOVL2 exon 1 methylation increased with higher CM, but these changes were minimal and did not increase with age. Maternal CM experiences and neonatal methylation of ELOVL2 intron 1 or exon 1 were not significantly correlated. Our study suggests region-specific effects of chronological age and experienced CM on ELOVL2 methylation and shows that the epigenetic biomarker for age within the ELOVL2 gene does not show accelerated biological aging years after CM exposure.

Here we evaluate whether infant difficult temperament (6 months) functions as a vulnerability or more general plasticity factor when investigating effects of early-childhood parenting (8–42 months) on both positive and negative early-adolescent socioemotional development (age 8–11 years). Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC, N = 14,541) and a re-parameterized model-testing approach to distinguish alternative person × environment conceptual models, results indicated that temperament × parenting interacted in predicting externalizing (i.e., hyperactivity, conduct problems), but not other behavior (i.e., emotional symptoms, peer problems), in a (weak) differential susceptibility manner. While more and less supportive parenting predicted, respectively, fewer and more behavior problems, it did so more strongly for children who were more difficult as infants.

Although there has been significant work on the association between posttraumatic stress disorder (PTSD) and attachment orientation, this is less the case for complex PTSD (CPTSD). The primary aim of this paper was to assess the strength of the association between the four adult attachment styles (i.e., secure, dismissing, preoccupied, and fearful) and severity of CPTSD symptoms (i.e., symptoms of PTSD and disturbances in self-organization [DSO]). We hypothesized that attachment orientation would be more strongly associated with DSO symptoms compared to PTSD symptoms. A trauma exposed clinical sample (N = 331) completed self-report measures of traumatic life events, CPTSD symptoms, and attachment orientation. It was found that secure attachment and fearful attachment were significantly associated with DSO symptoms but not with PTSD symptoms. Dismissing attachment style was significantly associated with PTSD and DSO symptoms. Preoccupied attachment was not significantly associated with CPTSD symptoms. Treatment implications for CPTSD using an attachment framework are discussed.

Acute stress affects interoception, but it remains unclear if this is due to activation of the sympatho-adreno-medullary (SAM) or hypothalamic–pituitary–adrenocortical axis. This study aimed to investigate the effect of SAM axis activation on interoceptive accuracy (IAcc). Central alpha2-adrenergic receptors represent a negative feedback mechanism of the SAM axis. Major depressive disorder and adverse childhood experiences (ACE) are associated with alterations in the biological stress systems, including central alpha2-adrenergic receptors. Here, healthy individuals with and without ACE as well as depressive patients with and without ACE (n = 114; all without antidepressant medication) were tested after yohimbine (alpha2-adrenergic antagonist) and placebo. We assessed IAcc and sensibility in a heartbeat counting task. Increases in systolic and diastolic blood pressure after yohimbine confirmed successful SAM axis activation. IAcc decreased after yohimbine only in the healthy group with ACE, but remained unchanged in all other groups (Group × Drug interaction). This effect may be due to selective upregulation of alpha2-adrenergic receptors after childhood trauma, which reduces capacity for attention focus on heartbeats. The sympathetic neural pathway including alpha2-adrenergic circuitries may be essential for mediating interoceptive signal transmission. Suppressed processing of physical sensations in stressful situations may represent an adaptive response in healthy individuals who experienced ACE.

Supportive forensic interviews conducted in accordance with the National Institute of Child Health and Human Development Revised Protocol (RP) help many alleged victims describe abusive experiences. When children remain reluctant to make allegations, the RP guides interviewers to (a) focus on rapport building and nonsuggestive support in a first interview, and (b) plan a second interview to allow continued rapport building before exploring for possible abuse. We explored the dynamics of such two-session RP interviews. Of 204 children who remained reluctant in an initial interview, we focused on 104 who made allegations when re-interviewed a few days later. A structural equation model revealed that interviewer support during the first session predicted children's cooperation during the rapport-building phase of the second session, which, in turn, predicted more spontaneous allegations, which were associated with the interviewers’ enhanced use of open-ended questions. Together, these factors mediated the effects of support on children's free recall of forensically important information. This highlighted the importance of emphasizing rapport with reluctant children, confirming that some children may need more time to build rapport even with supportive interviewers.

An impairment in recognizing distress is implicated in the development and severity of antisocial behavior. It has been hypothesized that a lack of attention to the eyes plays a role, but supporting evidence is limited. We developed a computerized training to improve emotion recognition in children and examined the role of eye gaze before and after training. Children referred into an intervention program to prevent antisocial outcomes completed an emotion recognition task with concurrent eye tracking. Those with emotion recognition impairments (n = 54, mean age: 8.72 years, 78% male) completed the training, while others (n = 38, mean age: 8.95 years, 84% male) continued with their usual interventions. Emotion recognition and eye gaze were reassessed in all children 8 weeks later. Impaired negative emotion recognition was significantly related to severity of behavioral problems at pretest. Children who completed the training significantly improved in emotion recognition; eye gaze did not contribute to impairment or improvement in emotion recognition. This study confirms the role of emotion recognition in severity of disruptive behavior and shows that a targeted intervention can quickly improve emotion impairments. The training works by improving children's ability to appraise emotional stimuli rather than by influencing their visual attention.