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The generalist genes specialist environment model, when applied to developmental psychopathology, predicts that genetic influences should explain variance that is shared across internalizing and externalizing problems, whereas environmental influences should explain variance that distinguishes the two overarching problem types. The present study is a direct test of this hypothesis, leveraging a sample of 708 twins and siblings (aged 10–18 years, 93% White) from the United States. Measures of severity of symptoms, regardless of type, and of directionality of symptoms – whether the adolescent tended to exhibit more externalizing or internalizing problems – were subjected to genetic (A), shared environmental (C), and nonshared environmental (E) (ACE) variance decompositions. As expected, severity of problems was under substantial genetic influence, but there were also significant shared and nonshared environmental influences. Contrary to the generalist genes specialist environment model, directionality of problem type was also under considerable genetic influence, with modest nonshared environmental influence. Findings corroborate existing evidence from other designs highlighting the role of familial influences (including generalist genes) in comorbidity of adolescent internalizing and externalizing problems, but suggest that the specialist environments hypothesis may not be the key factor in distinguishing problem type.
Adolescence is a period of social, physical, and neurobiological transitions that may leave individuals more vulnerable to the development of internalizing and externalizing symptomatology. Extant research demonstrates that executive functioning (EF) is associated with psychopathology outcomes in adolescence; however, it has yet to be examined how EF and psychopathology develop transactionally over time. Data were collected from 167 adolescents (47% female, 13–14 years old at Time 1) and their primary caregiver over 4 years. At each time point, adolescents completed three behavioral tasks that capture the underlying dimensions of EF, and both adolescents and their primary caregiver completed measures of adolescent psychopathology. Latent growth curve modeling was used to test the associations between initial levels and trajectories of EF and psychopathology. Results indicated that higher initial levels of internalizing and externalizing symptomatology were associated with lower EF at Time 4 (controlling for Time 1 EF). Initial levels of EF did not predict changes in internalizing and externalizing symptomatology. These findings suggest that early psychopathology may be a risk factor for maladaptive EF development in adolescence.
The constructs now subsumed under the label “internalizing disorders” had garnered the attention of researchers and practitioners long before the recent terminology was coined in the 1980s. Spanning decades of research, intervention, and practice, this chapter describes childhood internalizing disorders by their traits and prevalence, and then highlights the important contribution of factor analysis in marking their scientific evolution. We learn how exposure of the underlying dimensionality of internalizing disorders, along with critical refinements to terminology, precipitated the identification of early (subsyndromal) symptoms of depression and anxiety, and paved the way for the development of assessment scales that would ultimately expand our ability to intervene with precision, refine research, develop methods for prevention, identify moderator variables, and discover the potential of universal screening. The chapter concludes by providing a brief sampler of tools currently in use by practitioners and schools for the treatment, reduction of symptoms, and prevention of internalizing disorders.
Individual differences in temperament have been well-described, but individual differences in temperament trajectories require elaboration. Specifically, it is unknown if subgroups of infants display different developmental patterns and if these patterns relate to later behavioral problems. The aims were to identify distinct developmental patterns in broad dimensions of temperament among typically developing infants, to determine whether these developmental patterns differ by sex, to evaluate how developmental patterns within each dimension of temperament relate to developmental patterns within other dimensions of temperament, and to determine whether developmental patterns of infant temperament are associated with internalizing and externalizing behavior at 2 years of age. Data from the longitudinal Alberta Pregnancy Outcomes and Nutrition study (n = 1,819) were used to model latent class trajectories of parent-reported infant temperament at 3, 6, and 12 months. Four to five unique latent trajectories were identified within each temperament dimension. Sex was not associated with trajectory groups. Developmental coordination was observed between trajectories of negative emotionality and regulatory capacity, and between regulatory capacity and positive affect, but not between positive affect and negative emotionality. Negative emotionality and regulatory capacity predicted internalizing and externalizing behavior. Patterns of development in infant temperament, and not just intensity of temperament, contribute toward later problem behavior.
Several aspects of mother–child relationships are associated with children's internalizing problems. We examined longitudinal associations between mother–child conflict and children's internalizing problems in middle childhood. Specifically, we examined whether conflict and children's internalizing problems predict each other longitudinally in a sample of children from 3rd through 6th grade (N = 1,364) and their mothers using a cross-lagged panel model with random intercepts. In line with expectations, we found stable between-family differences in both mother–child conflict and children's internalizing problems. Contrary to expectations, we did not find that mother–child conflict and children's internalizing problems showed significant cross-lagged associations. However, mother–child conflict and children's internalizing problems had correlated errors at each wave, indicating that these two constructs covary with each other concurrently at multiple times across development, independent of stable between-family associations (i.e., as one increases, so does the other, and vice versa). The results of this study point to the importance of using statistical approaches that can disentangle between-family differences from within-family processes. In future studies, shorter time scales (e.g., weeks or months) may better capture dynamic associations between parent–child conflict and internalizing problems.
This paper reviews and synthesizes key areas of research related to the etiology, development, and maintenance of internalizing symptoms in children, adolescents, and adults with autism spectrum disorder (ASD). In developing an integrated conceptual model, we draw from current conceptual models of internalizing symptoms in ASD and extend the model to include factors related to internalizing within other populations (e.g., children that have experienced early life stress, children with other neurodevelopmental conditions, typically developing children) that have not been systematically examined in ASD. Our review highlights the need for more research to understand the developmental course of internalizing symptoms, potential moderators, and the interplay between early risk and protective factors. Longitudinal studies incorporating multiple methods and both environmental and biological factors will be important in order to elucidate these mechanisms.
Inhibitory control (IC) deficits have been associated with psychiatric symptoms in all ages. However, longitudinal studies testing the direction of the associations in childhood are scarce. We used a sample of 2,874 children (7 to 9 years old) to test the following three hypotheses: (a) IC deficits are an underlying risk factor with a potentially causal role for psychopathology, (b) IC deficits are a complication of psychopathology, and (c) IC deficits and psychopathology are associated at the trait level but not necessarily causally related. We used the go/no-go task to assess IC, the parent-rated Strengths and Difficulties Questionnaire to evaluate externalizing/internalizing symptoms, and the random intercepts cross-lagged panel model to test the hypotheses. The results showed no support for the underlying risk factor hypothesis, suggesting that IC unlikely has a causal role in this age group's psychopathology. The complication hypothesis received support for externalizing symptoms, suggesting that externalizing symptoms may hamper the normal development of IC. IC deficits and both externalizing and internalizing symptoms were correlated at the trait level, indicating a possible common origin. We suggest that it may be useful to support children with externalizing symptoms to promote and protect their IC development.
The current study examined a bifactor model of affective dimensions of withdrawal. Specifically, a model which specified a general factor of anxious-avoidant withdrawal (i.e., withdrawal with negative affect), a specific factor of unsociability (i.e., withdrawal without negative affect), and a specific factor of negative affect without withdrawal was specified in the primary sample (n = 238, 56.3% boys, M age = 44.92 months, SD = 5.32 months) and a validation sample (n = 332, 52.6% boys, M age = 47.11 months, SD = 7.32 months). The model provided a good fit to the data in both samples. In the primary sample, longitudinal relations between the bifactor model and peer victimization were examined across three time points (Time 1 in the spring, Time 2 in the fall, and Time 3 in the spring). Results showed that negative affect without withdrawal was concurrently associated with higher levels of relational and physical victimization at T1, unsociability predicted reductions in relational victimization from T1 to T2 as children entered a new classroom, and anxious-avoidant withdrawal predicted reductions in relational and physical victimization from T2 to T3 as children acclimated to the new classroom. Developmental considerations and clinical implications are discussed.
Affect reactivity to stress may play a role in the development of internalizing symptoms during the college transition, a critical developmental juncture for Latinx adolescents, the largest ethnic minority group on college campuses. This study examined whether affect reactivity during high school is associated with internalizing symptoms in college and explored two potential protective factors, perceived family and peer support. Participants were 209 Latinx adolescents (Mage = 18.10; 64.4% female) who completed standard surveys and four diary assessments per day over 7 days (N > 4,500 momentary observations). First, to measure affect reactivity, we assessed whether perceived stress was associated with negative affect at the momentary level during high school (senior year). Second, we tested whether affect reactivity predicted internalizing symptoms during the first year of college. Third, we tested whether perceived family or peer support buffered the negative consequences of affect reactivity. Results indicated statistically significant within- and between-person associations between stress and negative affect. Moreover, affect reactivity significantly predicted depressive, but not anxiety, symptoms. Buffering was found for family, but not peer, support. Findings extend previous research by detecting associations between momentary affect reactivity and internalizing symptoms during a sociocultural shift in Latinx adolescents’ lives and have implications for culturally appropriate programs to prevent depressive symptoms.
Fearful inhibition and impulsivity-anger significantly predict internalizing and externalizing problems, respectively. An important moderator that may affect these associations is frontal EEG asymmetry (FA). We examined how temperament and FA at 6 years interactively predicted behavioral problems at 9 years. A community sample of 186 children (93 boys, 93 girls) participated in the study. Results indicated that the effect of fearful inhibition on parent-reported internalizing problems increased as children exhibited greater right FA. The effect of impulsivity-anger on parent-reported externalizing problems increased as children showed greater left FA. Because FA was allowed to vary rather than children being dichotomized into membership in left FA and right FA groups, we observed that children’s FA contributed to the resilience process only when FA reached specific asymmetry levels. These findings highlight the importance of considering the different functions of FA in combination with specific dimensions of temperament in predicting children’s socioemotional outcomes. Clinical implications include providing suggestions for intervention services by demonstrating the role of FA in developing behavioral problems and inspiring research on whether it is possible to alter EEG activation and thus potentially improve developmental outcomes.
Neurophysiological patterns may distinguish which youth are at risk for the well-documented increase in internalizing symptoms during adolescence. Adolescents with internalizing problems exhibit altered resting-state functional connectivity (RSFC) of brain regions involved in socio-affective processing. Whether connectivity-based biotypes differentiate adolescents’ levels of internalizing problems remains unknown.
Sixty-eight adolescents (37 females) reported on their internalizing problems at ages 14, 16, and 18 years. A resting-state functional neuroimaging scan was collected at age 16. Time-series data of 15 internalizing-relevant brain regions were entered into the Subgroup-Group Iterative Multi-Model Estimation program to identify subgroups based on RSFC maps. Associations between internalizing problems and connectivity-based biotypes were tested with regression analyses.
Two connectivity-based biotypes were found: a Diffusely-connected biotype (N = 46), with long-range fronto-parietal paths, and a Hyper-connected biotype (N = 22), with paths between subcortical and medial frontal areas (e.g. affective and default-mode network regions). Higher levels of past (age 14) internalizing problems predicted a greater likelihood of belonging to the Hyper-connected biotype at age 16. The Hyper-connected biotype showed higher levels of concurrent problems (age 16) and future (age 18) internalizing problems.
Differential patterns of RSFC among socio-affective brain regions were predicted by earlier internalizing problems and predicted future internalizing problems in adolescence. Measuring connectivity-based biotypes in adolescence may offer insight into which youth face an elevated risk for internalizing disorders during this critical developmental period.
Teenage childbearing (age 15–19 years) represents a significant public health issue that can generate considerable deleterious, multigenerational consequences for teen-childbearing mothers and their offspring. However, few studies have examined the potential mediating mechanisms that may explain if and how teen childbearing is associated with the development of offspring psychopathology. The current study used a developmental model to test the mediating role of chronic child maltreatment in the relationship between teen childbearing and offspring internalizing symptoms in childhood and emerging adulthood. The study participants were 384 individuals from socioeconomically disadvantaged, ethnically diverse backgrounds, assessed across two longitudinal waves of data (i.e., ages 10–12 and 18–20). The sample included maltreated and nonmaltreated children, all of whom were comparable in terms of family income. Structural equation modeling was conducted to test direct and indirect pathways from teen childbearing to offspring psychopathology. A multigenerational developmental cascade was found such that individuals born to mothers who began their childbearing in adolescence were more likely to experience chronic maltreatment during childhood, which in turn predicted greater internalizing symptoms throughout childhood and emerging adulthood. Using a developmental psychopathology framework, the results are discussed with regard to implications for prevention and early intervention.
This rejoinder is aimed at responding to the respective commentaries by Vernberg and Abel and Beauchaine; however, most of the rejoinder focuses on the commentary by Vernberg and Abel given the fact that Vernberg and Abel appear to challenge the basic premise that maladaptive traits denote personality disturbance beyond that of externalizing and internalizing disorder, which according to them, renders the concept of youth BPD obsolete. The authors of this rejoinder provide two points of rebuttal in this regard. First, while it is true that Axis I and II show a very similar empirical structure and can thus be represented from a unified perspective, the construct of youth BPD lies in the co-occurrence and interplay of specific symptoms. BPD is therefore more than a sum of its symptoms, and assessing these symptoms individually from established internalizing-externalizing measures (as Vernberg and Abel suggest) would not adequately capture the dynamics between symptoms that largely account for the downward spiral of BPD functioning. Second, they view the DSM-5 Criterion A function as the feature of personality pathology that distinguishes it from trait function; in particular the self-concept manifestations of Criterion A that are not readily captured by trait (Criterion B) personality function.
Children who are adopted from care are more likely to experience enduring emotional and behavioral problems across development; however, adoptees’ trajectories of mental health problems and factors that impact their trajectories are poorly understood. Therefore, we used multilevel growth analyses to chart adoptees’ internalizing and externalizing problems across childhood, and examined the associations between preadoptive risk and postadoptive protective factors on their trajectories. This was investigated in a prospective longitudinal study of case file records (N = 374) and questionnaire-based follow-ups (N = 96) at approximately 5, 21, and 36 months postadoptive placement. Preadoptive adversity (indexed by age at placement, days in care, and number of adverse childhood experiences) was associated with higher internalizing and externalizing scores; the decrease in internalizing scores over childhood was accelerated for those exposed to lower levels of preadoptive risk. Warm adoptive parenting was associated with a marked reduction in children's internalizing and externalizing problems over time. Although potentially limited by shared methods variance and lack of variability in parental warmth scores, these findings demonstrate the deleterious impact of preadoptive risk and the positive role of exceptionally warm adoptive parenting on children's trajectories of mental health problems and have relevance for prevention and intervention strategies.
Given the equivocal literature on the relationship between internalizing symptoms and early adolescent alcohol use (AU) and AU disorder (AUD), the present study took a developmental perspective to understand how internalizing and externalizing symptoms may operate together in the etiology of AU and AUD. We pit the delayed onset and rapid escalation hypothesis (Hussong et al., 2011) against a synthesis of the dual failure model and the stable co-occurring hypothesis (Capaldi, 1992; Colder et al., 2013, 2018) to test competing developmental pathways to adolescent AU and AUD involving problem behavior, peer delinquency, and early initiation of AU. A latent transactional and mediational framework was used to test pathways to AUD spanning developmental periods before AU initiation (Mage = 11) to early and high risk for AUD (Mage = 14–15 and Mage = 17–18). The results supported three pathways to AUD. The first started with “pure” externalizing symptoms in early childhood and involved multiple mediators, including the subsequent development of co-occurring symptoms and peer delinquency. The second pathway involved stable co-occurring symptoms. Interestingly, chronically elevated pure internalizing symptoms did not figure prominently in pathways to AUD. Selection and socialization effects between early AU and peer delinquency constituted a third pathway.
Resting pulse is robustly and inversely associated with the risk for externalizing disorders and may be positively associated with internalizing disorders. We know little about the causal nature of these associations.
We examined resting pulse at conscription examination in 369 301 males born 1960–80 with a mean (s.d.) follow-up of 29.1 (7.7) years. From pulse rates, we predicted, using Cox models, the risk for criminal behavior (CB), drug abuse (DA), alcohol use disorder (AUD), major depression (MD), and anxiety disorders (AD), assessed from medical, criminal, and pharmacy registries. Co-relative analyses were conducted on the general population, cousin, half-sibling, full-sibling, and monozygotic pairs discordant for the outcome. Twin/sibling modeling for pulse was performed using OpenMX.
Familial resemblance for pulse resulted entirely from genetic factors. In the general population, the risk for externalizing disorders (CB, DA, and AUD) and internalizing disorders (MD and AD) were, respectively, significantly associated with low and high resting pulse rate. For CB, DA, and AUD, co-relative analyses showed that the inverse association with pulse resulted entirely from familial common causes (aka ‘confounders’). By contrast, co-relative analyses found that the association between higher pulse and MD and AD resulted from direct causal effects.
Resting pulse has a negative and positive association with, respectively, the risk for externalizing and for internalizing disorders. Co-relative analyses indicate that the nature of these associations differ, suggesting that elevated pulse appears to directly increase the risk for internalizing disorders while the reduced pulse is a risk index for underlying traits that predispose to externalizing disorders.
Hierarchical structural models of psychopathology rarely extend to obsessive-compulsive spectrum disorders. The current study sought to examine the higher-order structure of the obsessive-compulsive and related disorders (OCRDs) in DSM-5: obsessive-compulsive disorder (OCD), hoarding disorder (HD), body dysmorphic disorder (BDD), trichotillomania (hair-pulling disorder; HPD) and excoriation (skin-picking) disorder (SPD).
Adult patients in a partial hospital program (N = 532) completed a dimensional measure of the five OCRDs. We used confirmatory factor analysis to identify the optimal model of the comorbidity structure. We then examined the associations between the transdiagnostic factors and internalizing and externalizing symptoms (i.e. depression, generalized anxiety, neuroticism, and drug/alcohol cravings).
The best fitting model included two correlated higher-order factors: an obsessions-compulsions (OC) factor (OCD, BDD, and HD), and a body-focused repetitive behavior (BFRB) factor (HPD and SPD). The OC factor, not the BFRB factor, had unique associations with internalizing symptoms (standardized effects = 0.42–0.66) and the BFRB factor, not the OC factor, had small marginally significant unique association with drug/alcohol cravings (standardized effect = 0.22, p = 0.088).
The results mirror findings from twin research and indicate that OCD, BDD, and HD share liability that is significantly associated with internalizing symptoms, but this liability may be relatively less important for BFRBs. Further research is needed to better examine the associations between BFRBs and addictive disorders.
Prior research has documented elevations in levels of internalizing and externalizing behaviors among children in lower income families in comparison to more advantaged peers. However, most studies focus on behavior problems at a single point in time or within a short developmental period. Associations between income dynamics and developmental trajectories of behavior problems over time are less understood. To address this, the current study uses data from the National Longitudinal Study of Youth (N = 7,476; 50.8% male) to examine how income dynamics (annual income and income volatility) across three distinct developmental periods from early childhood to early adolescence relate to trajectories of externalizing and internalizing problems. Group-based mixture modeling revealed a five-group trajectory model for externalizing behavior and a four-group trajectory model for internalizing behavior. Higher cumulative annual income predicted greater likelihood of belonging to the low-stable group compared to the other, more problematic groups for both externalizing and internalizing trajectories. In addition, income losses predicted higher risk of membership in any group other than the low-stable group for internalizing and externalizing behavior. Developmental period-specific income dynamics, though not as consistent as cumulative dynamics, also predicted trajectory group membership.
This study examined the long-term effects of a randomized controlled trial of the Family Check-Up (FCU) intervention initiated at age 2 on inhibitory control in middle childhood and adolescent internalizing and externalizing problems. We hypothesized that the FCU would promote higher inhibitory control in middle childhood relative to the control group, which in turn would be associated with lower internalizing and externalizing symptomology at age 14. Participants were 731 families, with half (n = 367) of the families assigned to the FCU intervention. Using an intent-to-treat design, results indicate that the FCU intervention was indirectly associated with both lower internalizing and externalizing symptoms at age 14 via its effect on increased inhibitory control in middle childhood (i.e., ages 8.5–10.5). Findings highlight the potential for interventions initiated in toddlerhood to have long-term impacts on self-regulation processes, which can further reduce the risk for behavioral and emotional difficulties in adolescence.
There is an expanding literature on the theoretical and empirical connections between personality and psychopathology, and their shared neurobiological correlates. Recent cybernetic theories of personality and psychopathology, as well as affective neuroscience theory, provide grounding for understanding neurobiological–personality–psychopathology (NPP) associations. With the emergence of large sample datasets (e.g., Human Connectome Project) advanced quantitative modeling can be used to rigorously test dynamic statistical representations of NPP connections. Also, research suggests that these connections are influenced by sex, and large samples provide the opportunity to examine how NPP associations might be moderated by sex. The current study used a large sample from the Duke Neurogenetics Study (DNS) to examine how amygdala activation to facial expressions was linked with self-report of personality traits and clinical interviews of internalizing and externalizing symptoms of psychopathology. Structural equation modeling results revealed direct associations of amygdala activation with personality trait expression, as well as indirect associations (though personality) with symptoms of psychopathology. Moreover, the NPP links were moderated by sex. The current results are in line with research that identifies a broader role played by the amygdala in personality and provide potential insights for continued research in personality neuroscience and recent theories on the neurobiology of personality.