To save this undefined to your undefined account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you used this feature, you will be asked to authorise Cambridge Core to connect with your undefined account.
Find out more about saving content to .
To save this article to your Kindle, first ensure firstname.lastname@example.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
The field of psychopathology is in a transformative phase, and is witnessing a renewed surge of interest in theoretical models of mental disorders. While many interesting proposals are competing for attention in the literature, they tend to focus narrowly on the proximate level of analysis and lack a broader understanding of biological function. In this paper, we present an integrative framework for mental disorders built on concepts from life history theory, and describe a taxonomy of mental disorders based on its principles, the fast–slow–defense model (FSD). The FSD integrates psychopathology with normative individual differences in personality and behavior, and allows researchers to draw principled distinctions between broad clusters of disorders, as well as identify functional subtypes within current diagnostic categories. Simulation work demonstrates that the model can explain the large-scale structure of comorbidity, including the apparent emergence of a general “p factor” of psychopathology. A life history approach also provides novel integrative insights into the role of environmental risk/protective factors and the developmental trajectories of various disorders.
In this article, we consider an often overlooked model that combines mediation and moderation to explain how a third variable can relate to a risk factor–psychopathology relationship. We refer to it as moderation and mediation in a three-variable system. We describe how this model is relevant to studying vulnerability factors and how it may advance developmental psychopathology research. To illustrate the value of this approach, we provide several examples where this model may be applicable, such as the relationships among parental externalizing pathology, harsh parenting, and offspring psychopathology as well as between neuroticism, stressful life events, and depression. We discuss possible reasons why this model has not gained traction and attempt to clarify and dispel those concerns. We provide guidance and recommendations for when to consider this model for a given data set and point toward existing resources for testing this model that have been developed by statisticians and other methodologists. Lastly, we describe important caveats, limitations, and considerations for making this approach most useful for developmental research. Overall, our goal in presenting this information to developmental psychopathology researchers is to encourage testing moderation and mediation in a three-variable system with the aim of advancing analytic strategies for studying vulnerability factors.
This study examined the intergenerational transmission of parental invalidation and whether parental difficulties in emotion regulation mediated the association between past experiences of invalidation and current invalidating parenting practices. We also aimed to investigate whether gender might influence the transmission of parental invalidation. We recruited a community sample of 293 dual-parent families (adolescent and their parents) based in Singapore. Parents and adolescents each completed measures of childhood invalidation, whereas parents additionally reported on their difficulties in emotion regulation. Results based on path analyses demonstrated that past parental invalidation experienced by fathers positively predicted current perceived invalidation by their children. The association between mothers’ childhood invalidation and current invalidating practices was fully mediated by mothers’ difficulties with emotion regulation. Further analyses revealed that parents’ current invalidating behaviors were not predicted by their past experiences of paternal or maternal invalidation. These findings point to the importance of considering the family invalidating environment as a whole when examining the influence of past experienced parental invalidation on emotion regulation and invalidating behaviors of second-generation parents. Our study provides empirical support for the intergenerational transmission of parental invalidation and highlights the need to address childhood experiences of parental invalidation in parenting programs.
The COVID-19 pandemic is a global traumatic experience for citizens, especially during sensitive time windows of heightened plasticity such as pregnancy and neonatal life. Pandemic-related stress experienced by mothers during pregnancy may act as an early risk factor for infants’ regulatory capacity development by altering maternal psychosocial well-being (e.g., increased anxiety, reduced social support) and caregiving environment (e.g., greater parenting stress, impaired mother–infant bonding). The aim of the present longitudinal study was to assess the consequences of pandemic-related prenatal stress on infants’ regulatory capacity. A sample of 163 mother–infant dyads was enrolled at eight maternity units in northern Italy. They provided complete data about prenatal stress, perceived social support, postnatal anxiety symptoms, parenting stress, mother–infant bonding, and infants’ regulatory capacity at 3 months of age. Women who experienced emotional stress and received partial social support during pregnancy reported higher anxious symptoms. Moreover, maternal postnatal anxiety was indirectly linked to the infants’ regulatory capacity at 3 months, mediated by parenting stress and mother–infant bonding. Dedicated preventive interventions should be delivered to mothers and should be focused on protecting the mother–infant dyad from the detrimental effects of pandemic-related stress during the COVID-19 healthcare emergency.
To date, a deficit-oriented approach dominates autism spectrum disorder (ASD) research, including studies of infant siblings of children with ASD at high risk (HR) for the disabilities associated with this disorder. Despite scientific advances regarding early ASD-related risk, there remains little systematic investigation of positive development, limiting the scope of research and quite possibly a deeper understanding of pathways toward and away from ASD-related impairments. In this paper, we argue that integrating a resilience framework into early ASD research has the potential to enhance knowledge on prodromal course, phenotypic heterogeneity, and developmental processes of risk and adaptation. We delineate a developmental systems resilience framework with particular reference to HR infants. To illustrate the utility of a resilience perspective, we consider the “female protective effect” and other evidence of adaptation in the face of ASD-related risk. We suggest that a resilience framework invites focal questions about the nature, timing, levels, interactions, and mechanisms by which positive adaptation occurs in relation to risk and developmental pathways toward and away from ASD-related difficulties. We conclude with recommendations for future research, including more focus on adaptive development and multisystem processes, pathways away from disorder, and reconsideration of extant evidence within an integrated risk-and-resilience framework.
Families of youth with autism spectrum disorder (ASD) are vulnerable to maladaptive psychosocial experiences, including elevated youth emotional and behavioral problems (EBPs) and poor parent couple relationship outcomes. Yet, the extent to which these family psychosocial experiences are intertwined has been given little research attention. The present study longitudinally investigated the bidirectional associations between parent couple conflict (PCC) and youth EBPs in 188 families of children and adolescents with ASD (initially aged 5 to 12 years) across four time points (T1, T2, T3, T4), each spaced 12 months apart. Mother- and father-report of youth EBPs and PCC were entered into a cross-lagged panel model. After adjusting for youth age and intellectual disability status and parent education and couple relationship length, the results indicated that father-report of PCC predicted increased youth EBPs 12 months later (T1→T2 and T2→T3). In addition, father-report of youth EBPs predicted increased PCC 12 months later (T3→T4). Mother-report did not demonstrate cross-lagged effects. The findings suggest that fathers’ perceptions of PCC and youth emotional and behavioral functioning are transactionally related, highlighting the need for family-wide interventions.
A variety of childhood experiences can lead to anxious/depressed (A/D) symptoms. The aim of the present study was to explore the brain morphological (cortical thickness and surface area) correlates of A/D symptoms and the extent to which these phenotypes vary depending on the quality of the parenting context in which children develop. Structural magnetic resonance imaging (MRI) scans were acquired on 45 children with Child Protective Services (CPS) involvement due to risk of not receiving adequate care (high-risk group) and 25 children without CPS involvement (low-risk group) (rangeage = 8.08–12.14; Mage = 10.05) to assess cortical thickness (CT) and cortical surface area (SA). A/D symptoms were measured using the Child Behavioral Checklist. The association between A/D symptoms and CT, but not SA, differed by risk status such that high-risk children showed decreasing CT as A/D scores increased, whereas low-risk children showed increasing CT as A/D scores increased. This interaction was specific to CT in prefrontal, frontal, temporal, and parietal cortical regions. The groups had marginally different A/D scores, in the direction of higher risk being associated with lower A/D scores. Results suggest that CT correlates of A/D symptoms are differentially shaped by the quality of early caregiving experiences and should be distinguished between high- and low-risk children.
Behavioral regulation problems have been associated with daily-life and mental health challenges in children with neurodevelopmental conditions such as attention-deficit/hyperactivity disorder (ADHD) and developmental coordination disorder (DCD). Here, we investigated transdiagnostic brain signatures associated with behavioral regulation. Resting-state fMRI data were collected from 115 children (31 typically developing (TD), 35 ADHD, 21 DCD, 28 ADHD-DCD) aged 7–17 years. Behavioral regulation was measured using the Behavior Rating Inventory of Executive Function and was found to differ between children with ADHD (i.e., children with ADHD and ADHD-DCD) and without ADHD (i.e., TD children and children with DCD). Functional connectivity (FC) maps were computed for 10 regions of interest and FC maps were tested for correlations with behavioral regulation scores. Across the entire sample, greater behavioral regulation problems were associated with stronger negative FC within prefrontal pathways and visual reward pathways, as well as with weaker positive FC in frontostriatal reward pathways. These findings significantly increase our knowledge on FC in children with and without ADHD and highlight the potential of FC as brain-based signatures of behavioral regulation across children with differing neurodevelopmental conditions.
Parenting behaviors are significantly linked to youths’ behavioral adjustment, an association that is moderated by youths’ and parents’ self-regulation. The biological sensitivity to context theory suggests that respiratory sinus arrhythmia (RSA) indexes youths’ varying susceptibility to rearing contexts. However, self-regulation in the family context is increasingly viewed as a process of “coregulation” that is biologically embedded and involves dynamic Parent×Child interactions. No research thus far has examined physiological synchrony as a dyadic biological context that may moderate associations between parenting behaviors and preadolescent adjustment. Using a two-wave sample of 101 low-socioeconomic status (SES) families (children and caretakers; mean age 10.28 years), we employed multilevel modeling to examine dyadic coregulation during a conflict task, indicated by RSA synchrony, as a moderator of the linkages between observed parenting behaviors and preadolescents’ internalizing and externalizing problems. Results showed that high dyadic RSA synchrony resulted in a multiplicative association between parenting and youth adjustment. High dyadic synchrony intensified the relations between parenting behaviors and youth behavior problems, such that in the context of high dyadic synchrony, positive and negative parenting behaviors were associated with decreased and increased behavioral problems, respectively. Parent–child dyadic RSA synchrony is discussed as a potential biomarker of biological sensitivity in youth.
In an effort to elucidate new factors that may contribute to developmental psychopathology, the current study examined whether accelerated epigenetic aging at birth related to children's differential susceptibility to the effects of aversive parenting on early emerging mental health risk. Using data from a multiethnic birth cohort, the interaction between Horvath's methylation age in umbilical cord blood and hostile parenting behaviors was examined in relation to perceptions of infant's temperament at 6 months and to children's psychological symptoms at 3 years in 154 families. Results broadly revealed that children with higher levels of accelerated methylation aging evinced more unpredictable temperaments and more psychological symptoms if their mothers reported more hostile parenting, but showed fewer difficulties if mothers engaged in less hostile parenting; children with lower levels of accelerated methylation age did not show associations between hostility and temperament or psychological symptoms. Effects were not accounted for by gestational age at birth, demographic factors, or the distribution of cell subtypes. These findings suggest that accelerated epigenetic age may function as a form of differential susceptibility, signaling increased risk for psychopathology in more aversive contexts but decreased risk in less aversive early environments. Taken together, they point to a novel biological process to consider within risk for psychopathology.
This study examines the link between behavior in kindergarten and adult-life welfare receipt. Teacher-rated behavioral assessments were obtained for inattention, hyperactivity, aggression–opposition, anxiety, and prosociality when children (n=2960) were aged 5–6 years and linked to their tax return records from age 18–35 years. We used group-based based trajectory modeling to identify distinct trajectories of welfare receipt and multinomial logistic regression models to examine the association between behaviors and trajectory group membership. The child's sex, IQ, and family background were adjusted for. Four trajectories of welfare receipt were identified: low (n = 2,390, 80.7%), declining (n = 260, 8.8%), rising (n = 150, 5.2%), and chronic (n = 160, 5.4%). Relative to the low trajectory, inattention and aggression–opposition at age 6 years were associated with increased risk of following a declining, rising, and chronic trajectory of welfare receipt, independent of hyperactivity and anxiety. Prosocial behaviors were independently associated with a lower risk of following a chronic trajectory. This study shows that kindergarten children exhibiting high inattention and aggression–opposition and low prosocial behaviors may be at increased risk of long-term welfare receipt in adulthood. The implications for early screening, monitoring, and prevention are discussed.
The functioning of the hypothalamic–pituitary–adrenal (HPA) axis is implicated in the etiology and maintenance of depressive and posttraumatic stress disorder (PTSD) symptoms. However, different maltreatment experiences as well as the increased sensitivity of the HPA axis during puberty may alter associations between the HPA axis and mental health. To address these gaps, the current study examined the potential bidirectional associations between cortisol reactivity to a stressor, PTSD symptoms, and depressive symptoms among early adolescents across two time points, 1 year apart (n = 454; Mage = 10.98 at Time 1 and Mage = 12.11 at Time 2). Multiple-group path models tested the pathways between cortiol reactivity and mental health prior to and during puberty, for different types of maltreatment . Overall, the results showed that associations between cortisol output and symptoms of PTSD and depression were driven by those in the midst of puberty. Specifically, higher cortisol output at Time 1 was linked with higher levels of subsequent PTSD and depressive symptoms for neglected youth who had reached puberty. However, depressive symptoms predicted subsequent lower cortisol output for the physical abuse and emotional abuse groups. These findings demonstrate longitudinal links between cortisol, depressive symptoms, and PTSD symptoms among youth with different types of maltreatment histories and highlight the need to consider the reorganization of the stress system during puberty in order to advance our understanding of the HPA axis and mental health.
Adolescent pregnancy (AP) is a significant public health issue. Child maltreatment (CM) represents an established risk factor, yet little is known about the explanatory mechanisms linking the phenomena. Informed by developmental theory, this study prospectively tested seven multi-level, indirect pathways that could plausibly explain the relationship between CM and AP: (1) substance use (polysubstance use and frequency); (2) sexual risk behavior; (3) depressive symptoms; (4) posttraumatic stress disorder symptoms; (5) cognitive dysregulation; (6) pregnancy desire and difficulty expectancies; and (7) age at menarche. Data came from a prospective, longitudinal cohort study of 469 ethnically diverse, nulliparous adolescent females, designed to examine the impact of substantiated CM on reproductive outcomes such as pregnancy and childbirth (265 maltreated and 204 demographically matched comparison adolescents). A multiple-mediator structural equation model was conducted to simultaneously test multiple indirect effects while accounting for confounding variables. Maltreatment had an indirect effect on pregnancy via substance use and higher pregnancy desire/lower perceived difficulty. Findings represent a step towards elucidating pathways linking CM with AP. Recommendations are offered to prevent pregnancy by addressing the pregnancy-specific mechanisms that are part of the maltreatment sequelae.
Child abuse is associated with elevated risk for psychopathology. The current study examined the role of automatic emotion regulation as a potential mechanism linking child abuse with internalizing psychopathology. A sample of 237 youth aged 8–16 years and their caregivers participated. Child abuse severity was assessed by self-report questionnaires, and automatic emotion regulation was assessed using an emotional Stroop task designed to measure adaptation to emotional conflict. A similar task without emotional stimuli was also administered to evaluate whether abuse was uniquely associated with emotion regulation, but not cognitive control applied in a nonemotional context. Internalizing psychopathology was assessed concurrently and at a 2-year longitudinal follow-up. Child abuse severity was associated with lower emotional conflict adaptation but was unrelated to cognitive control. Specifically, the severity of emotional and physical abuse, but not sexual abuse, were associated with lower emotional conflict adaptation. Emotional conflict adaptation was not associated with internalizing psychopathology prospectively. These findings suggest that childhood emotional and physical abuse, in particular, may influence automatic forms of emotion regulation. Future work exploring the socioemotional consequences of altered automatic emotion regulation among youth exposed to child abuse is clearly needed.
Guided by developmental psychopathology and dual-risk frameworks, the present study examined the interplay between childhood maltreatment and maternal major depression history in relation to neural reward responsiveness in youth. The sample consisted of 96 youth (ages 9–16; M = 12.29 years, SD = 2.20; 68.8% female) drawn from a large metropolitan city. Youth were recruited based on whether their mothers had a history of major depressive disorder (MDD) and were categorized into two groups: youth with mothers with a history of MDD (high risk; HR; n = 56) and youth with mothers with no history of psychiatric disorders (low risk; LR; n = 40). The reward positivity (RewP), an event-related potential component, was utilized to measure reward responsiveness and the Childhood Trauma Questionnaire measured childhood maltreatment. We found a significant two-way interaction between childhood maltreatment and risk group in relation to RewP. Simple slope analysis revealed that in the HR group, greater childhood maltreatment was significantly associated with reduced RewP. The relationship between childhood maltreatment and RewP was not significant among the LR youth. The present findings demonstrate that the association between childhood maltreatment and blunted reward responsiveness is dependent on whether offspring have mothers with histories of MDD.
Most research has studied self-regulation by presenting experimenter-controlled test stimuli and measuring change between baseline and stimulus. In the real world, however, stressors do not flash on and off in a predetermined sequence, and there is no experimenter controlling things. Rather, the real world is continuous and stressful events can occur through self-sustaining interactive chain reactions. Self-regulation is an active process through which we adaptively select which aspects of the social environment we attend to from one moment to the next. Here, we describe this dynamic interactive process by contrasting two mechanisms that underpin it: the “yin” and “yang” of self-regulation. The first mechanism is allostasis, the dynamical principle underlying self-regulation, through which we compensate for change to maintain homeostasis. This involves upregulating in some situations and downregulating in others. The second mechanism is metastasis, the dynamical principle underling dysregulation. Through metastasis, small initial perturbations can become progressively amplified over time. We contrast these processes at the individual level (i.e., examining moment-to-moment change in one child, considered independently) and also at the inter-personal level (i.e., examining change across a dyad, such as a parent–child dyad). Finally, we discuss practical implications of this approach in improving the self-regulation of emotion and cognition, in typical development and psychopathology.
This study focused on generality versus specificity of susceptibility of effects of eight family and child-care exposures measured between 3 and 54 months of age (e.g., sensitive parenting, child-care quality) on five child development outcomes assessed at age 4.5 years (e.g. behavior problems, preacademic skill), using data from The National Institute of Child Health and Human Development (NICHD) Study of Early Child Care and Youth Development (n = 1,364, boys = 705; White = 1,097, Black = 176, other = 91), while applying a novel influence-statistics method. Results indicated that susceptibility across the environment-predictor:child-outcome associations is normally rather than bimodally (i.e., orchid–dandelion) distributed. Analysis of susceptibility documents both domain generality and specificity of developmental plasticity, with effect sizes proving small in the former case. As predicted, children who as infants had difficult temperaments or who scored higher on a polygenic-plasticity score (serotonin-transporter-linked promoter region [5-HTTLPR], dopamine receptor D4 [DRD4], brain-derived neurotrophic factor [BDNF]) proved somewhat more susceptible to some of the environmental effects investigated. Results lead to the recommendation that two-types-of-individuals vis-a-vis susceptibility to environmental influences be questioned and general-trait conceptions of susceptibility be further investigated.
Previous studies have established that individual characteristics such as violent behavior, substance use, and high-risk sexual behavior, as well as negative relationships with parents and friends, are all risk factors for intimate partner violence (IPV). In this longitudinal prospective study, we investigated whether violent behavior, substance use, and high-risk sexual behavior in early adulthood (ages 22–23 years) mediated the link between family conflict and coercive relationship talk with friends in adolescence (ages 16–17 years) and dyadic IPV in adulthood (ages 28–30 years). A total of 998 individuals participated in multimethod assessments, including observations of interactions with parents and friends. Data from multiple reporters were used for variables of interest including court records, parental and self-reports of violence, self-reports of high-sexual-risk behaviors and substance use, and self- and romantic partner-reports of IPV. Longitudinal mediation analyses showed that violent behavior during early adulthood mediated the link between coercive relationship talk with friends in adolescence and dyadic IPV in adulthood. No other mediation paths were found and there was no evidence of gender differences. Results are discussed with attention to the interpersonal socialization processes by which IPV emerges relative to individual risk factors.
Cross-species evidence suggests that the ability to exert control over a stressor is a key dimension of stress exposure that may sensitize frontostriatal-amygdala circuitry to promote more adaptive responses to subsequent stressors. The present study examined neural correlates of stressor controllability in young adults. Participants (N = 56; Mage = 23.74, range = 18–30 years) completed either the controllable or uncontrollable stress condition of the first of two novel stressor controllability tasks during functional magnetic resonance imaging (fMRI) acquisition. Participants in the uncontrollable stress condition were yoked to age- and sex-matched participants in the controllable stress condition. All participants were subsequently exposed to uncontrollable stress in the second task, which is the focus of fMRI analyses reported here. A whole-brain searchlight classification analysis revealed that patterns of activity in the right dorsal anterior insula (dAI) during subsequent exposure to uncontrollable stress could be used to classify participants' initial exposure to either controllable or uncontrollable stress with a peak of 73% accuracy. Previous experience of exerting control over a stressor may change the computations performed within the right dAI during subsequent stress exposure, shedding further light on the neural underpinnings of stressor controllability.
Although indirectly aggressive behavior and anxiety symptoms can co-occur, it is unclear whether anxiety is an antecedent or outcome of indirect aggression at the individual level and whether other personality traits can contribute to these longitudinal associations. Therefore, the between- and within-person associations among indirect aggression, anxiety symptoms, and empathic concern were examined across adolescence from ages 11 to 16 in a cohort of individuals followed annually (N = 700; 52.9% girls; 76.0% White) controlling for direct aggression and demographic variables. Results of autoregressive latent trajectory models with structured residuals supported an acting out model at the within-person level. Specifically, anxiety symptoms positively predicted indirect aggression and indirect aggression negatively predicted empathic concern at each adjacent time point. These findings suggest that methods of reducing worries about the self and increasing healthy self-confidence could prevent indirect aggression and help build concern and compassion toward others.