Emotion dysregulation is defined as patterns of emotional experience or expression that interfere with goal-directed activity. This paper considers this functionalist definition from a developmental perspective with the goal of elaborating this approach with respect to its central questions. What are the goals that are impeded by emotionally dysregulated responding, and what alternative goals might motivate emotion dysregulation? What are the developmental processes by which these goals take shape, and what are the influences of the family context, and especially of central relationships in the family, in their emergence? How does this functionalist account address the complex interaction of experience and developing biological processes that also influence emotion regulation and dysregulation? Drawing on research literature concerning children at risk for affective psychopathology and considering relevant examples of the interaction of biology and context, this discussion offers a portrayal of emotion dysregulation as a biologically dynamic, experience-based aspect of adaptation to environments and relationships that, in conditions of risk for the emergence of developmental psychopathology, motivates patterns of emotional responding that serve immediate coping often at the cost of long-term maladaptation. Implications for emotions theory and the study of developmental psychopathology are also considered.

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.

Maltreatment increases risk for psychopathology in childhood and adulthood, thus identifying mechanisms that influence these associations is necessary for future prevention and intervention. Emotion dysregulation resulting from maltreatment is one potentially powerful mechanism explaining risk for psychopathology. This study tests a conceptual model that distinguishes deprivation and threat as distinct forms of exposure with different pathways to psychopathology. Here we operationalize threat as exposure to physical and/or sexual abuse and deprivation as exposure to neglect. We test the hypothesis that threat and deprivation differentially predict use of avoidant strategies and total regulation. Data were drawn from the Longitudinal Studies on Child Abuse and Neglect (LONGSCAN study; N = 866), which followed high-risk children from age 4 to 18. At age 6, children and their parents reported on adversity exposure. Case records documented exposure to abuse and neglect. At 18, adolescents reported on regulation strategies and psychopathology. Regression analyses indicated that greater exposure to threat, but not deprivation, predicted greater use of avoidant strategies in adolescence. Moreover, avoidance partially mediated the longitudinal association between exposure to threat in early childhood and symptoms of internalizing psychopathology in adolescence. Results suggest that abuse and neglect differentially predict regulation strategy use and that regulation strategy use predicts psychopathology.

While emotional dysregulation is a broad construct, the current paper adopts a narrow approach to facilitate translational neuroscience research on pediatric anxiety. The paper first presents data on an adapted version of the antisaccade task and then integrates these data into a research framework. Data on an adapted version of the antisaccade task were collected in 57 youth, including 35 seeking treatment for an anxiety disorder. Associations were examined between performance on the antisaccade task and (a) age, (b) performance on other cognitive-control tasks (i.e., the stop-signal delay and flanker tasks), and (c) level of anxiety symptoms. Better performance on the antisaccade task occurred in older relative to younger subjects and correlated with better performance on the flanker task. Across the 57 youth, higher levels of anxiety correlated with shorter latency for correct antisaccades. These data can be placed within a three-step framework for translational neuroscience research. In the first step, a narrow index of emotion dysregulation is targeted. In the second step, this narrow index is linked to other correlated indicators of the same underlying narrow latent construct. In the third and final step, associations are examined with clinical outcomes and response to treatment.

As early as infancy, caregivers’ facial expressions shape children's behaviors, help them regulate their emotions, and encourage or dissuade their interpersonal agency. In childhood and adolescence, proficiencies in producing and decoding facial expressions promote social competence, whereas deficiencies characterize several forms of psychopathology. To date, however, studying facial expressions has been hampered by the labor-intensive, time-consuming nature of human coding. We describe a partial solution: automated facial expression coding (AFEC), which combines computer vision and machine learning to code facial expressions in real time. Although AFEC cannot capture the full complexity of human emotion, it codes positive affect, negative affect, and arousal—core Research Domain Criteria constructs—as accurately as humans, and it characterizes emotion dysregulation with greater specificity than other objective measures such as autonomic responding. We provide an example in which we use AFEC to evaluate emotion dynamics in mother–daughter dyads engaged in conflict. Among other findings, AFEC (a) shows convergent validity with a validated human coding scheme, (b) distinguishes among risk groups, and (c) detects developmental increases in positive dyadic affect correspondence as teen daughters age. Although more research is needed to realize the full potential of AFEC, findings demonstrate its current utility in research on emotion dysregulation.

Childhood exposure to stress can induce prolonged negative effects on health, which in turn confer risks for the next generation, but greater specificity is needed to inform intervention. A first step is to measure individual differences in emotional reactivity to stress early in life in ways that can account for heterogeneity in child exposure. The present study tested the hypothesis that mothers’ childhood exposure to stress would be differentially associated with patterns of positive and negative emotional reactivity in their offspring, suggesting transmission of stress response across generations. Participants were 268 young mothers (age 14–23 years) followed longitudinally since childhood, and their infants aged 3–9 months. Latent class analysis of infant emotions expressed before and during the still-face paradigm yielded five subgroups that varied in valence, intensity, and reactivity. After accounting for sociodemographic factors, infant temperament, and postpartum depression, multinomial regression models showed that, relative to an emotionally regulated still-face response, infants showing low negative reactivity were more likely to have mothers exposed to childhood emotional abuse, and infants showing high and increasing negative reactivity were more likely to have mothers exposed to childhood emotional neglect. Mechanisms by which early maternal stress exposure influences emotional reactivity in offspring are discussed.

Childhood maltreatment is associated with increased risk for most forms of psychopathology. We examine emotion dysregulation as a transdiagnostic mechanism linking maltreatment with general psychopathology. A sample of 262 children and adolescents participated; 162 (61.8%) experienced abuse or exposure to domestic violence. We assessed four emotion regulation processes (cognitive reappraisal, attention bias to threat, expressive suppression, and rumination) and emotional reactivity. Psychopathology symptoms were assessed concurrently and at a 2-year longitudinal follow-up. A general psychopathology factor (p factor), representing co-occurrence of psychopathology symptoms across multiple internalizing and externalizing domains, was estimated using confirmatory factor analysis. Maltreatment was associated with heightened emotional reactivity and greater use of expressive suppression and rumination. The association of maltreatment with attention bias varied across development, with maltreated children exhibiting a bias toward threat and adolescents a bias away from threat. Greater emotional reactivity and engagement in rumination mediated the longitudinal association between maltreatment and increased general psychopathology over time. Emotion dysregulation following childhood maltreatment occurs at multiple stages of the emotion generation process, in some cases varies across development, and serves as a transdiagnostic mechanism linking child maltreatment with general psychopathology.

Irritability and anxiety are two common clinical phenotypes that involve high-arousal negative affect states (anger and fear), and that frequently co-occur. Elucidating how these two forms of emotion dysregulation relate to perturbed neurodevelopment may benefit from alternate phenotyping strategies. One such strategy applies a bifactor latent variable approach that can parse shared versus unique mechanisms of these two phenotypes. Here, we aim to replicate and extend this approach and examine associations with neural structure in a large transdiagnostic sample of youth (N = 331; M = 13.57, SD = 2.69 years old; 45.92% male). FreeSurfer was used to extract cortical thickness, cortical surface area, and subcortical volume. The current findings replicated the bifactor model and demonstrate measurement invariance as a function of youth age and sex. There were no associations of youth's factor scores with cortical thickness, surface area, or subcortical volume. However, we found strong convergent and divergent validity between parent-reported irritability and anxiety factors with clinician-rated symptoms and impairment. A general negative affectivity factor was robustly associated with overall functional impairment across symptom domains. Together, these results support the utility of the bifactor model as an alternative phenotyping strategy for irritability and anxiety, which may aid in the development of targeted treatments.

Autism spectrum disorder (ASD) is associated with pervasive social deficits as well as marked emotion dysregulation across the life span. Decreased social motivation accounts in part for social difficulties, but factors moderating its influence are not fully understood. In this paper, we (a) characterize social and emotional functioning among children and adolescents with ASD, (b) explore contributions of social motivation and emotion dysregulation to social skill, and (c) consider biological sex and intellectual functioning as moderators of these associations. In a sample of 2,079 children and adolescents with ASD from the Simons Simplex Collection, we document direct effects of social motivation, internalizing symptoms, aggression, attention problems, irritability, and self-injurious behavior on children's social skills. Furthermore, dysregulation in several domains moderated the association between social motivation and social skill, suggesting a blunting effect on social motivation in the context of emotional difficulties. Moreover, when considering only individuals with intellectual skills in the average range or higher, biological sex further moderated these associations. Findings add to our understanding of social–emotional processes in ASD, suggest emotion dysregulation as a target of intervention in the service of social skill improvements, and build on efforts to understand sources of individual difference that contribute to heterogeneity among individuals with ASD.

Grounded in self-determination theory's (SDT; Ryan & Deci, 2017) organismic perspective, we present a process view of integrative emotion regulation. SDT describes three general types of emotion regulation: integrative emotion regulation, which focuses on emotions as carrying information that is brought to awareness; controlled emotion regulation, which is focused on diminishing emotions through avoidance, suppression, or enforced expression or reappraisal; and amotivated emotion regulation, in which emotions are uncontrolled or dysregulated. We review survey and experimental research contrasting these emotion regulation styles, providing evidence for the benefits of integrative emotion regulation for volitional functioning, personal well-being, and high-quality relationships, and for the costs of controlled emotion regulation and dysregulation. The development of emotion regulation styles is discussed, especially the role of autonomy-supportive parenting in fostering more integrative emotion regulation, and the role of controlling parenting in contributing to controlled or dysregulated emotion processing. Overall, integrative emotion regulation represents a beneficial style of processing emotions, which develops most effectively in a nonjudgmental and autonomy-supportive environment, an issue relevant to both development and psychotherapy.

Emotion dysregulation characterizes many forms of psychopathology. Patterns of dysregulation occur as a function of a developmental process in which normative and adaptive emotion regulation skills fail to become part of the child's behavioral repertoire due to biological, psychological, and contextual processes and experiences. Here we highlight the processes involved in the dysregulation of temperamental anger and frustration that become core features of externalizing problems and place children at risk for more serious forms of psychopathology. We imbed these processes in a larger self-regulatory framework, and we discuss how they influence mental as well as physical health, using data from our 20-year longitudinal study following a large cohort of children into young adulthood. Recommendations are made for future research involving the integration of biological systems with mental and physical health outcomes.

Behavioral Inhibition (BI) is a temperament type that predicts social withdrawal in childhood and anxiety disorders later in life. However, not all BI children develop anxiety. Attention bias (AB) may enhance the vulnerability for anxiety in BI children, and interfere with their development of effective emotion regulation. In order to fully probe attention patterns, we used traditional measures of reaction time (RT), stationary eye-tracking, and recently emerging mobile eye-tracking measures of attention in a sample of 5- to 7-year-olds characterized as BI (N = 23) or non-BI (N = 58) using parent reports. There were no BI-related differences in RT or stationary eye-tracking indices of AB in a dot-probe task. However, findings in a subsample from whom eye-tracking data were collected during a live social interaction indicated that BI children (N = 12) directed fewer gaze shifts to the stranger than non-BI children (N = 25). Moreover, the frequency of gazes toward the stranger was positively associated with stationary AB only in BI, but not in non-BI, children. Hence, BI was characterized by a consistent pattern of attention across stationary and ambulatory measures. We demonstrate the utility of mobile eye-tracking as an effective tool to extend the assessment of attention and regulation to social interactive contexts.

Adverse caregiving, for example, previous institutionalization (PI), is often associated with emotion dysregulation that increases anxiety risk. However, the concept of developmental multifinality predicts heterogeneity in anxiety outcomes. Despite this well-known heterogeneity, more work is needed to identify sources of this heterogeneity and how these sources interact with environmental risk to influence mental health. Here, working memory (WM) was examined during late childhood/adolescence as an intra-individual factor to mitigate the risk for separation anxiety, which is particularly susceptible to caregiving adversities. A modified “object-in-place” task was administered to 110 youths (10–17 years old), with or without a history of PI. The PI youths had elevated separation anxiety scores, which were anticorrelated with morning cortisol levels, yet there were no group differences in WM. PI youths showed significant heterogeneity in separation anxiety symptoms and morning cortisol levels, and WM moderated the link between caregiving and separation anxiety and mediated the association between separation anxiety and morning cortisol in PI youth. Findings suggest that (a) institutional care exerts divergent developmental consequences on separation anxiety versus WM, (b) WM interacts with adversity-related emotion dysregulation, and (c) WM may be a therapeutic target for separation anxiety following early caregiving adversity.

Difficulties with emotion regulation can take many forms, including increased sensitivity to emotional cues and habitual use of maladaptive cognitive or behavioral regulation strategies. Despite extensive research on emotion regulation and youth adjustment, few studies integrate multiple measures of emotion regulation. The present study evaluated the underlying structure of emotion regulation processes in adolescence using both task- and survey-based measures and determined whether differences in these emotion regulation latent factors mediated the association between peer victimization and internalizing psychopathology. Adolescents aged 16–17 years (n = 287; 55% female; 42% White) recruited in three urban centers in the United States completed baseline and follow-up assessments 4 months apart. Three models of emotion regulation were evaluated with confirmatory factor analysis. A three-factor model fit the data best, including cognitive regulation, behavioral regulation, and emotional reactivity latent factors. Task-based measures did not load onto these latent factors. Difficulties with behavioral regulation mediated the association between peer victimization and depression symptoms, whereas cognitive regulation difficulties mediated the association with anxiety symptoms. Findings point to potential targets for intervention efforts to reduce risk for internalizing problems in adolescents following experiences of peer victimization.

Early life stress (ELS) is a risk factor for the development of depression in adolescence; the mediating neurobiological mechanisms, however, are unknown. In this study, we examined in early pubertal youth the associations among ELS, cortisol stress responsivity, and white matter microstructure of the uncinate fasciculus and the fornix, two key frontolimbic tracts; we also tested whether and how these variables predicted depressive symptoms in later puberty. A total of 208 participants (117 females; M age = 11.37 years; M Tanner stage = 2.03) provided data across two or more assessment modalities: ELS; salivary cortisol levels during a psychosocial stress task; diffusion magnetic resonance imaging; and depressive symptoms. In early puberty there were significant associations between higher ELS and decreased cortisol production, and between decreased cortisol production and increased fractional anisotropy in the uncinate fasciculus. Further, increased fractional anisotropy in the uncinate fasciculus predicted higher depressive symptoms in later puberty, above and beyond earlier symptoms. In post hoc analyses, we found that sex moderated several additional associations. We discuss these findings within a broader conceptual model linking ELS, emotion dysregulation, and depression across the transition through puberty, and contend that brain circuits implicated in the control of hypothalamic–pituitary–adrenal axis function should be a focus of continued research.

Although numerous studies reveal altered respiratory sinus arrhythmia (RSA) among children, adolescents, and adults who exhibit emotion dysregulation, effects of temperamental vulnerability and parental mental health on RSA remain unclear. We evaluated the relationship among emotion regulation, RSA, and RSA reactivity in a pooled sample of 24 vulnerable and 31 resilient adolescents (mean age = 13.69 years; 60% girls), including associations with temperamental vulnerability and parental depressive symptoms. Participants watched a neutral film clip while their resting RSA was recorded, and then completed a reward and frustration task, using an affective Posner paradigm. Temperament and emotion regulation were assessed via self-report and parent report, and parents reported on their own depressive symptoms. Low resting RSA was associated with temperamental negative emotionality, whereas greater RSA reactivity to frustration was associated with maladaptive emotion regulation strategies. No significant relations were found between RSA and parental depressive symptoms. This study elucidates the role of RSA as a biomarker of individual differences in emotion dysregulation and temperamental vulnerability and stresses the importance of considering multiple units of analyses, as well as functional domains, when studying emotional responding and regulation in adolescents.

Aberrant face emotion processing has been demonstrated in youth with and at a familial risk for bipolar and major depressive disorders. However, the neurobiological factors related to emotion processing that underlie resilience from youth-onset mood disorders are not well understood. Functional magnetic resonance imaging data during an implicit emotion processing task were collected at baseline from a sample of 50 youth, ages 8–17, who were healthy but also familially at high risk for either bipolar disorder or major depressive disorder, and 24 healthy controls with no family history of psychopathology (HCL). Participants were reevaluated 3 years later and classified into three groups for analysis: high-risk youth who converted to a psychiatric diagnosis (CVT; N = 23), high-risk youth who were resilient from developing any psychopathology (RES; N = 27), and HCL youth (N = 24) who remained healthy at follow-up. For happy > calm faces, the CVT and RES groups had significantly lower activation in the left inferior parietal lobe (IPL), while the RES group had lower activation in the right supramarginal gyrus. For fear > calm faces, the RES group had lower activation in the right precuneus and inferior frontal gyrus (IFG) compared to the CVT group. Connectivity analyses revealed the RES group exhibited higher left IPL connectivity with visual cortical regions for happy > calm faces, and higher IFG connectivity with frontal, temporal, and limbic regions for fear > calm faces. These connectivities were correlated with improvements in prosocial behaviors and global functioning. Our findings suggest that differential activation and connectivity in the IPL, IFG, and precuneus in response to emotional stimuli may represent distinct resilience and risk markers for youth-onset mood disorders.

While child poverty is a significant risk factor for poor mental health, the developmental pathways involved with these associations are poorly understood. To advance knowledge about these important linkages, the present study examined the developmental sequelae of childhood exposure to poverty in a multiyear longitudinal study. Here, we focused on exposure to poverty, neurobiological circuitry connected to emotion dysregulation, later exposure to stressful life events, and symptoms of psychopathology. We grounded our work in a biopsychosocial perspective, with a specific interest in “stress sensitization” and emotion dysregulation. Motivated by past work, we first tested whether exposure to poverty was related to changes in the resting-state coupling between two brain structures centrally involved with emotion processing and regulation (the amygdala and the ventromedial prefrontal cortex; vmPFC). As predicted, we found lower household income at age 10 was related to lower resting-state coupling between these areas at age 15. We then tested if variations in amygdala–vmPFC connectivity interacted with more contemporaneous stressors to predict challenges with mental health at age 16. In line with past reports showing risk for poor mental health is greatest in those exposed to early and then later, more contemporaneous stress, we predicted and found that lower vmPFC–amygdala coupling in the context of greater contemporaneous stress was related to higher levels of internalizing and externalizing symptoms. We believe these important interactions between neurobiology and life history are an additional vantage point for understanding risk and resiliency, and suggest avenues for prediction of psychopathology related to early life challenge.