Prenatal maternal anxiety is considered a risk factor for the development of child internalizing problems. However, little is known about potential mechanisms that account for these associations. The current study examined whether prenatal maternal anxiety was indirectly associated with toddler internalizing problems via prenatal maternal physiology and infant negative affectivity. We examined these associations in a longitudinal study of 162 expectant mothers from their third trimester until 18 months postpartum. Path analyses showed that higher prenatal anxiety was associated with higher infant negative affectivity at 7 months, which in turn was associated with higher toddler internalizing problems at 18 months. Prenatal anxiety was not indirectly associated with child outcomes via baseline or task-evoked respiratory sinus arrhythmia (RSA) in response to an infant cry while pregnant. However, pregnant women with greater decreases in task-evoked RSA had toddlers with greater internalizing problems, which was mediated by infant negative affectivity at 7 months. Findings suggest that prenatal anxiety and RSA reactivity to an infant cry may be independent risk factors for the development of infant negative affectivity, which in turn increases risk for toddler internalizing problems. These findings contribute to a growing literature on mechanisms that underlie intergenerational transmission of internalizing problems.

Challenges with childhood emotion regulation may have origins in infancy and forecast later social and cognitive developmental delays, academic difficulties, and psychopathology. This study tested whether markers of emotion dysregulation in infancy predict emotion dysregulation in toddlerhood, and whether those associations depended on maternal sensitivity. When children (N = 111) were 7 months, baseline respiratory sinus arrhythmia (RSA), RSA withdrawal, and distress were collected during the Still Face Paradigm (SFP). Mothers’ reports of infant regulation and orientation and maternal sensitivity were also collected at that time. Mothers’ reports of toddlers’ dysregulation were collected at 18 months. A set of hierarchical regressions indicated that low baseline RSA and less change in RSA from baseline to stressor predicted greater dysregulation at 18 months, but only for infants who experienced low maternal sensitivity. Baseline RSA and RSA withdrawal were not significantly associated with later dysregulation for infants with highly sensitive mothers. Infants who exhibited low distress during the SFP and who had lower regulatory and orienting abilities at 7 months had higher dysregulation at 18 months regardless of maternal sensitivity. Altogether, these results suggest that risk for dysregulation in toddlerhood has biobehavioral origins in infancy but may be buffered by sensitive caregiving.

From its inception, development and psychopathology theorists have sought to uncover the earliest forms of risk for mental health challenges in children, to prevent the development of more severe, intractable manifestations of psychopathology. Large familial risk registries have advanced our understanding of early, potentially modifiable factors that could prevent or mitigate the expression of challenging symptoms of neurodevelopmental conditions, and similar registries have been proposed to advance understanding of ADHD and related phenotypes. Data from single-site studies, largely focused on perinatal exposure to maternal mood disorders, reveal that a robust predictor of child psychopathology is parental psychopathology. However, early developmental trajectories of psychopathology risk may be better captured using transdiagnostic approaches in pregnancy, capturing the full range of mental health symptoms. We describe here the need for a parental mental health registry that begins prenatally that includes deep behavioral phenotyping across a range of transdiagnostic indicators of mental health risk to prevent psychopathology in children. This registry has the potential to uncover pathways to psychopathology risk in childhood and support the discovery of novel mechanisms to be targeted for prevention and intervention.

Despite recent applications of a developmental psychopathology perspective to the perinatal period, these conceptualizations have largely ignored the role that childbirth plays in the perinatal transition. Thus, we present a conceptual model of childbirth as a bridge between prenatal and postnatal health. We argue that biopsychosocial factors during pregnancy influence postnatal health trajectories both directly and indirectly through childbirth experiences, and we focus our review on those indirect effects. In order to frame our model within a developmental psychopathology lens, we first describe “typical” biopsychosocial aspects of pregnancy and childbirth. Then, we explore ways in which these processes may deviate from the norm to result in adverse or traumatic childbirth experiences. We briefly describe early postnatal health trajectories that may follow from these birth experiences, including those which are adaptive despite traumatic childbirth, and we conclude with implications for research and clinical practice. We intend for our model to illuminate the importance of including childbirth in multilevel perinatal research. This advancement is critical for reducing perinatal health disparities and promoting health and well-being among birthing parents and their children.

In 2010, the Research Domain Criteria (RDoC) were developed to advance our understanding of the pathophysiology of mental illness across multiple levels of analysis, ranging from cells to circuits to self-report instruments. Several conceptual RDoC-informed manuscripts have highlighted the importance of studying how developmental processes give rise to psychopathology. However, there are few empirical studies that integrate the RDoC framework with development and psychopathology principles. This special issue was developed to fill this empirical gap. In this introduction to the special issue, we describe how the developmental psychopathology field predates and informs the RDoC framework. We highlight three important ways in which developmental psychopathology and the RDoC framework can mutually inform one another, leading to novel discoveries to identify, prevent, and treat mental health problems across the life span.

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.

The World Health Organization recently reported that maternal mental health is a major public health concern. As many as one in four women suffer from psychiatric disorders at some point during pregnancy or the first postpartum year. Furthermore, self-injurious thoughts and behaviors (SITBs) represent one of the leading causes of death among women during this time. Thus, efforts to identify women at risk for serious forms of psychopathology and especially for SITBs are of utmost importance. Despite this urgency, current single-diagnostic approaches fail to recognize a significant subset of women who are vulnerable to perinatal stress and distress. The current study was among the first to investigate emotion dysregulation—a multilevel, transdiagnostic risk factor for psychopathology—and its associations with stress, distress, and SITBs in a sample of pregnant women (26–40 weeks gestation) recruited to reflect a range of emotion dysregulation. Both self-reported emotion dysregulation and respiratory sinus arrhythmia, a biomarker of emotion dysregulation, demonstrated expected associations with measures of mental health, including depression, anxiety, borderline personality pathology, and SITBs. In addition, self-reported emotion dysregulation was associated with blunted respiratory sinus arrhythmia responsivity to an ecologically valid infant cry task. Findings add to the literature considering transdiagnostic risk during pregnancy using a multiple-levels-of-analysis approach.

We investigated whether neurobehavioral markers of risk for emotion dysregulation were evident among newborns, as well as whether the identified markers were associated with prenatal exposure to maternal emotion dysregulation. Pregnant women (N = 162) reported on their emotion dysregulation prior to a laboratory assessment. The women were then invited to the laboratory to assess baseline respiratory sinus arrhythmia (RSA) and RSA in response to an infant cry. Newborns were assessed after birth via the NICU Network Neurobehavioral Scale. We identified two newborn neurobehavioral factors—arousal and attention—via exploratory factor analysis. Low arousal was characterized by less irritability, excitability, and motor agitation, while low attention was related to a lower threshold for auditory and visual stimulation, less sustained attention, and poorer visual tracking abilities. Pregnant women who reported higher levels of emotion dysregulation had newborns with low arousal levels and less attention. Larger decreases in maternal RSA in response to cry were also related to lower newborn arousal. We provide the first evidence that a woman's emotion dysregulation while pregnant is associated with risks for dysregulation in her newborn. Implications for intergenerational transmission of emotion dysregulation are discussed.

Decades of fetal programming research indicates that we may be able to map the origins of many physical, psychological, and medical variations and morbidities before the birth of the child. While great strides have been made in identifying associations between prenatal insults, such as undernutrition or psychosocial stress, and negative developmental outcomes, far less is known about how adaptive responses to adversity regulate the developing phenotype to match stressful conditions. As the application of epigenetic methods to human behavior has exploded in the last decade, research has begun to shed light on the role of epigenetic mechanisms in explaining how prenatal conditions shape later susceptibilities to mental and physical health problems. In this review, we describe and attempt to integrate two dominant fetal programming models: the cumulative stress model (a disease-focused approach) and the match–mismatch model (an evolutionary–developmental approach). In conjunction with biological sensitivity to context theory, we employ these two models to generate new hypotheses regarding epigenetic mechanisms through which prenatal and postnatal experiences program child stress reactivity and, in turn, promote development of adaptive versus maladaptive phenotypic outcomes. We conclude by outlining priority questions and future directions for the fetal programming field.

Following recent advances in behavioral and psychiatric epigenetics, researchers are increasingly using epigenetic methods to study prenatal exposure to maternal mood disorder and its effects on fetal and newborn neurobehavior. Despite notable progress, various methodological limitations continue to obscure our understanding of the epigenetic mechanisms underpinning prenatal exposure to maternal mood disorder on newborn neurobehavioral development. Here we detail this problem, discussing limitations of the currently dominant analytical approaches (i.e., candidate epigenetic and epigenome-wide association studies), then present a solution that retains many benefits of existing methods while minimizing their shortcomings: epigenetic pathway analysis. We argue that the application of pathway-based epigenetic approaches that target DNA methylation at transcription factor binding sites could substantially deepen our mechanistic understanding of how prenatal exposures influence newborn neurobehavior.

Low resting respiratory sinus arrhythmia (RSA), and to a lesser extent excessive RSA reactivity to emotion evocation, are observed in many psychiatric disorders characterized by emotion dysregulation, including syndromes spanning the internalizing and externalizing spectra, and other conditions such as nonsuicidal self-injury. Nevertheless, some inconsistencies exist. For example, null outcomes in studies of RSA–emotion dysregulation relations are sometimes observed among younger participants. Such findings may derive from use of age inappropriate frequency bands in calculating RSA. We combine data from five published samples (N = 559) spanning ages 4 to 17 years, and reanalyze RSA data using age-appropriate respiratory frequencies. Misspecifying respiratory frequencies results in overestimates of resting RSA and underestimates of RSA reactivity, particularly among young children. Underestimates of developmental shifts in RSA and RSA reactivity from preschool to adolescence were also observed. Although correlational analyses revealed weak negative associations between resting RSA and aggression, those with clinical levels of externalizing exhibited lower resting RSA than their peers. No associations between RSA reactivity and externalizing were observed. Results confirm that age-corrected frequency bands should be used when estimating RSA, and that literature-wide overestimates of resting RSA, underestimates of RSA reactivity, and underestimates of developmental shifts in RSA and RSA reactivity may exist.

Self-inflicted injury (SII) is a continuum of intentionally self-destructive behaviors, including nonsuicidal self-injuries, suicide attempts, and death by suicide. These behaviors are among the most pressing yet perplexing clinical problems, affecting males and females of every race, ethnicity, culture, socioeconomic status, and nearly every age. The complexity of these behaviors has spurred an immense literature documenting risk and vulnerability factors ranging from individual to societal levels of analysis. However, there have been relatively few attempts to articulate a life span developmental model that integrates ontogenenic processes across these diverse systems. The objective of this review is to outline such a model with a focus on how observed patterns of comorbidity and continuity can inform developmental theories, early prevention efforts, and intervention across traditional diagnostic boundaries. Specifically, when SII is viewed through the developmental psychopathology lens, it becomes apparent that early temperamental risk factors are associated with risk for SII and a range of highly comorbid conditions, such as borderline and antisocial personality disorders. Prevention efforts focused on early-emerging biological and temperamental contributors to psychopathology have great potential to reduce risk for many presumably distinct clinical problems. Such work requires identification of early biological vulnerabilities, behaviorally conditioned social mechanisms, as well as societal inequities that contribute to self-injury and underlie intergenerational transmission of risk.

The term allostasis, which is defined as stability through change, has been invoked repeatedly by developmental psychopathologists to describe long-lasting and in some cases permanent functional alterations in limbic–hypothalamic–pituitary–adrenal axis responding following recurrent and/or prolonged exposure to stress. Increasingly, allostatic load models have also been invoked to describe psychological sequelae of abuse, neglect, and other forms of maltreatment. In contrast, neural adaptations to stress, including those incurred by monoamine systems implicated in (a) mood and emotion regulation, (b) behavioral approach, and (c) social affiliation and attachment, are usually not included in models of allostasis. Rather, structural and functional alterations in these systems, which are exquisitely sensitive to prolonged stress exposure, are usually explained as stress mediators, neural plasticity, and/or programming effects. Considering these mechanisms as distinct from allostasis is somewhat artificial given overlapping functions and intricate coregulation of monoamines and the limbic–hypothalamic–pituitary–adrenal axis. It also fractionates literatures that should be mutually informative. In this article, we describe structural and functional alterations in serotonergic, dopaminergic, and noradrenergic neural systems following both acute and prolonged exposure to stress. Through increases in behavioral impulsivity, trait anxiety, mood and emotion dysregulation, and asociality, alterations in monoamine functioning have profound effects on personality, attachment relationships, and the emergence of psychopathology.

Although antisocial personality disorder (ASPD) is more common among males and borderline PD (BPD) is more common among females, some authors have suggested that the two disorders reflect multifinal outcomes of a single etiology. This assertion is based on several overlapping symptoms and features, including trait impulsivity, emotional lability, high rates of depression and suicide, and a high likelihood of childhood abuse and/or neglect. Furthermore, rates of ASPD are elevated in the first degree relatives of those with BPD, and concurrent comorbidity rates for the two disorders are high. In this article, we present a common model of antisocial and borderline personality development. We begin by reviewing issues and problems with diagnosing and studying PDs in children and adolescents. Next, we discuss dopaminergic and serotonergic mechanisms of trait impulsivity as predisposing vulnerabilities to ASPD and BPD. Finally, we extend shared risk models for ASPD and BPD by specifying genetic loci that may confer differential vulnerability to impulsive aggression and mood dysregulation among males and impulsive self-injury and mood dysregulation among females. Although the precise mechanisms of these sex-moderated genetic vulnerabilities remain poorly understood, they appear to interact with environmental risk factors including adverse rearing environments to potentiate the development of ASPD and BPD.

Although parasuicidal behavior in adolescence is poorly understood, evidence suggests that it may be a developmental precursor of borderline personality disorder (BPD). Current theories of both parasuicide and BPD suggest that emotion dysregulation is the primary precipitant of self-injury, which serves to dampen overwhelmingly negative affect. To date, however, no studies have assessed endophenotypic markers of emotional responding among parasuicidal adolescents. In the present study, we compare parasuicidal adolescent girls (n = 23) with age-matched controls (n = 23) on both psychological and physiological measures of emotion regulation and psychopathology. Adolescents, parents, and teachers completed questionnaires assessing internalizing and externalizing psychopathology, substance use, trait affectivity, and histories of parasuicide. Psychophysiological measures including electrodermal responding (EDR), respiratory sinus arrhythmia, and cardiac pre-ejection period (PEP) were collected at baseline, during negative mood induction, and during recovery. Compared with controls, parasuicidal adolescents exhibited reduced respiratory sinus arrhythmia (RSA) at baseline, greater RSA reactivity during negative mood induction, and attenuated peripheral serotonin levels. No between-group differences on measures of PEP or EDR were found. These results lend further support to theories of emotion dysregulation and impulsivity in parasuicidal teenage girls.This work was supported by grants from the Seattle Children's Hospital and Regional Medical Center, the Pediatric Clinical Research Center at Seattle Children's Hospital (M01-RR 00037), and the National Foundation for Suicide Prevention to Cindy J. Smith, and by a grant from the National Institute of Mental Health to Theodore P. Beauchaine (R01 MH63699). We express thanks to Trevor Aerts, Anna Amen, Tyson Bailey, Jordan Campbell, Breyen Engelhardt, Ashleigh Freize, Jennifer Gross, Barbara Kleine, Dana Kovalchick, Jenna Lee, Eileen Magill, Elise Mallman, Emily Miller, Andrea Moore, Seamus Morrone, Shelby Soike, and Aubriana Teeley.