Family socioeconomic status and adolescent substance use: The role of parent-adolescent brain similarity and parental monitoring.

Greater neural similarity between parents and adolescents may reduce adolescent substance use. Among 70 parent-adolescent dyads, we tested a longitudinal path model in which family economic environment is related to adolescent substance use, directly and indirectly through parent-adolescent neural similarity and parental monitoring. Neural similarity was measured as parent-adolescent pattern similarity in functional brain connectivity at Time 1. Parents reported socioeconomic status and parental monitoring at Time 1. Adolescents reported parental monitoring at Time 1 and substance use at Time 2. Higher family socioeconomic status was associated with greater neural similarity. Greater neural similarity was associated with lower adolescent substance use, mediated through greater adolescent-perceived parental monitoring. Parent-adolescent neural similarity may attenuate adolescent substance use by bolstering parental monitoring. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Leveraging multivariate approaches to advance the science of early-life adversity.

Since the landmark Adverse Childhood Experiences (ACEs) study, adversity research has expanded to more precisely account for the multifaceted nature of adverse experiences. The complex data structures and interrelated nature of adversity data require robust multivariate statistical methods, and recent methodological and statistical innovations have facilitated advancements in research on childhood adversity. Here, we provide an overview of a subset of multivariate methods that we believe hold particular promise for advancing the field's understanding of early-life adversity, and discuss how these approaches can be practically applied to explore different research questions. This review covers data-driven or unsupervised approaches (including dimensionality reduction and person-centered clustering/subtype identification) as well as supervised/prediction-based approaches (including linear and tree-based models and neural networks). For each, we highlight studies that have effectively applied the method to provide novel insight into early-life adversity. Taken together, we hope this review serves as a resource to adversity researchers looking to expand upon the cumulative approach described in the original ACEs study, thereby advancing the field's understanding of the complexity of adversity and related developmental consequences.

Psychopathology as long-term sequelae of maltreatment and socioeconomic disadvantage: Neurocognitive development perspectives.

Neuroscience research underscores the critical impact of adverse experiences on brain development. Yet, there is limited understanding of the specific pathways linking adverse experiences to accelerated or delayed brain development and their ultimate contributions to psychopathology. Here, we present new longitudinal data demonstrating that neurocognitive functioning during adolescence, as affected by adverse experiences, predicts psychopathology during young adulthood. The sample included 167 participants (52% male) assessed in adolescence and young adulthood. Adverse experiences were measured by early maltreatment experiences and low family socioeconomic status. Cognitive control was assessed by neural activation and behavioral performance during the Multi-Source Interference Task. Psychopathology was measured by self-reported internalizing and externalizing symptomatology. Results indicated that higher maltreatment predicted heightened frontoparietal activation during cognitive control, indicating delayed neurodevelopment, which, in turn predicted higher internalizing and externalizing symptomatology. Furthermore, higher maltreatment predicted a steeper decline in frontoparietal activation across adolescence, indicating neural plasticity in cognitive control-related brain development, which was associated with lower internalizing symptomatology. Our results elucidate the crucial role of neurocognitive development in the processes linking adverse experiences and psychopathology. Implications of the findings and directions for future research on the effects of adverse experiences on brain development are discussed.

Neural Circuit Markers of Familial Risk for Depression Among Healthy Youths in the Adolescent Brain Cognitive Development Study.

BACKGROUND: Family history of depression is a robust predictor of early-onset depression, which may confer risk through alterations in neural circuits that have been implicated in reward and emotional processing. These alterations may be evident in youths who are at familial risk for depression but who do not currently have depression. However, the identification of robust and replicable findings has been hindered by few studies and small sample sizes. In the current study, we sought to identify functional connectivity (FC) patterns associated with familial risk for depression. METHODS: Participants included healthy (i.e., no lifetime psychiatric diagnoses) youths at high familial risk for depression (HR) (n = 754; at least one parent with a history of depression) and healthy youths at low familial risk for psychiatric problems (LR) (n = 1745; no parental history of psychopathology) who were 9 to 10 years of age and from the Adolescent Brain Cognitive Development (ABCD) Study sample. We conducted whole-brain seed-to-voxel analyses to examine group differences in resting-state FC with the amygdala, caudate, nucleus accumbens, and putamen. We hypothesized that HR youths would exhibit global amygdala hyperconnectivity and striatal hypoconnectivity patterns primarily driven by maternal risk. RESULTS: HR youths exhibited weaker caudate-angular gyrus FC than LR youths (α = 0.04, Cohen's d = 0.17). HR youths with a history of maternal depression specifically exhibited weaker caudate-angular gyrus FC (α = 0.03, Cohen's d = 0.19) as well as weaker caudate-dorsolateral prefrontal cortex FC (α = 0.04, Cohen's d = 0.21) than LR youths. CONCLUSIONS: Weaker striatal connectivity may be related to heightened familial risk for depression, primarily driven by maternal history. Identifying brain-based markers of depression risk in youths can inform approaches to improving early detection, diagnosis, and treatment.

Brain Similarity as a Protective Factor in the Longitudinal Pathway Linking Household Chaos, Parenting, and Substance Use.

BACKGROUND: Socioecological factors such as family environment and parenting behaviors contribute to the development of substance use. While biobehavioral synchrony has been suggested as the foundation for resilience that can modulate environmental effects on development, the role of brain similarity that attenuates deleterious effects of environmental contexts has not been clearly understood. We tested whether parent-adolescent neural similarity-the level of pattern similarity between parent-adolescent functional brain connectivity representing the level of attunement within each dyad-moderates the longitudinal pathways in which household chaos (a stressor) predicts adolescent substance use directly and indirectly via parental monitoring. METHODS: In a sample of 70 parent-adolescent dyads, similarity in resting-state brain activity was identified using multipattern connectivity similarity estimation. Adolescents and parents reported on household chaos and parental monitoring, and adolescent substance use was assessed at a 1-year follow-up. RESULTS: The moderated mediation model indicated that for adolescents with low neural similarity, but not high neural similarity, greater household chaos predicted higher substance use over time directly and indirectly via lower parental monitoring. Our data also indicated differential susceptibility in the overall association between household chaos and substance use: Adolescents with low neural similarity exhibited high substance use under high household chaos but low substance use under low household chaos. CONCLUSIONS: Neural similarity acts as a protective factor such that the detrimental effects of suboptimal family environment and parenting behaviors on the development of adolescent health risk behaviors may be attenuated by neural similarity within parent-adolescent bonds.

Characterizing the dimensional structure of early-life adversity in the Adolescent Brain Cognitive Development (ABCD) Study.

Early-life adversity has profound consequences for youth neurodevelopment and adjustment; however, experiences of adversity are heterogeneous and interrelated in complex ways that can be difficult to operationalize and organize in developmental research. We sought to characterize the underlying dimensional structure of co-occurring adverse experiences among a subset of youth (ages 9-10) from the Adolescent Brain Cognitive Development (ABCD) Study (N = 7115), a community sample of youth in the United States. We identified 60 environmental and experiential variables that reflect adverse experiences. Exploratory factor analysis identified 10 robust dimensions of early-life adversity co-occurrence, corresponding to conceptual domains such as caregiver substance use and biological caregiver separation, caregiver psychopathology, caregiver lack of support, and socioeconomic disadvantage / neighborhood lack of safety. These dimensions demonstrated distinct associations with internalizing problems, externalizing problems, cognitive flexibility, and inhibitory control. Non-metric multidimensional scaling characterized qualitative similarity among the 10 identified dimensions. Results supported a nonlinear three-dimensional structure representing early-life adversity, including continuous gradients of "perspective", "environmental uncertainty", and "acts of omission/commission". Our findings suggest that there are distinct dimensions of early-life adversity co-occurrence in the ABCD sample at baseline, and the resulting dimensions may have unique implications for neurodevelopment and youth behavior.

Parenting, emotion regulation, and externalizing symptomatology as adolescent antecedents to young adult health risk behaviors.

This study used longitudinal data to elucidate how trajectories of negative parenting across adolescence are associated with young adult health risk behaviors (HRBs) by testing difficulties with emotion regulation and externalizing symptomatology as sequential underlying mediators. The sample included 167 adolescents (53% males, Mage  = 14 at Time 1 and Mage  = 18 at Time 5) who were assessed five times. Adolescents self-reported on negative parenting, emotion regulation, externalizing symptomatology, and engagement in HRBs. Results suggest that increasingly negative parenting across adolescence has adverse consequences for emotion regulation development and in turn, externalizing symptomatology, which confers risk for young adult HRBs. Results offer insights towards mechanisms for prevention and intervention and public health policy aimed at reducing the prevalence and consequences of engagement in HRBs.

Differential Associations of Adversity Profiles with Adolescent Cognitive Control and Psychopathology.

Adverse childhood experiences are common and have long-term consequences for biological and psychosocial adjustment. We used a person-centered approach to characterize distinct profiles of adversity in early adolescence and examined associations with later cognitive control and psychopathology. The sample included 167 adolescents (47% female) and their primary caregivers who participated in a longitudinal study across four time points (approximately one year between assessments). At Time 1 (Mage = 14 years), we measured seven indicators of adversity: socioeconomic disadvantage, abuse, neglect, household chaos, parent substance use, parent depression, and negative life events. At Times 2-4, adolescents' behavioral performance and functional activation during a cognitive control task were measured. At Time 5, adolescents and their caregiver reported on adolescent internalizing and externalizing symptomatology. Using latent profile analysis, we identified four distinct adversity subgroups: a low exposure group, a neglect group, a household instability group, and a poly-adversity group. These groups significantly differed on subsequent levels of psychopathology, but not cognitive control. Specifically, the poly-adversity group reported significantly higher levels of both internalizing and externalizing symptomatology relative to the low exposure group, and the household instability group demonstrated elevated risk for externalizing symptomatology. When using a cumulative risk approach, higher levels of adversity exposure were associated with significantly worse cognitive control performance (but not neural activation). These results suggest that psychopathology outcomes may be differentially predicted by distinct patterns of risk, and that cognitive control impairment may be more strongly predicted by cumulative risk.

Associations between early-life stress exposure and internalizing symptomatology during the COVID-19 pandemic: Assessing the role of neurobehavioral mediators.

Background: The ongoing COVID-19 pandemic is a major stressor that has been associated with increased risk for psychiatric illness in the general population. Recent work has highlighted that experiences of early-life stress (ELS) may impact individuals' psychological functioning and vulnerability for developing internalizing psychopathology in response to pandemic-related stress. However, little is known about the neurobehavioral factors that may mediate the association between ELS exposure and COVID-related internalizing symptomatology. The current study sought to examine the mediating roles of pre-pandemic resting-state frontoamygdala connectivity and concurrent emotion regulation (ER) in the association between ELS and pandemic-related internalizing symptomatology. Methods: Retrospective life-stress histories, concurrent self-reported ER strategies (i.e., reappraisal and suppression), concurrent self-reported internalizing symptomatology (i.e., depression- and anxiety-related symptomatology), and resting-state functional connectivity data from a sample of adults (N = 64, M age = 22.12, female = 68.75%) were utilized. Results: There were no significant direct associations between ELS and COVID-related internalizing symptomatology. Neither frontoamygdala functional connectivity nor ER strategy use mediated an association between ELS and COVID-related internalizing symptomatology (ps > 0.05). Exploratory analyses identified a significant moderating effect of reappraisal use on the association between ELS and internalizing symptomatology (ß = -0.818, p = 0.047), such that increased reappraisal use buffered the impact of ELS on psychopathology. Conclusions: While frontoamygdala connectivity and ER do not appear to mediate the association between ELS and COVID-related internalizing symptomatology, our findings suggest that the use of reappraisal may buffer against the effect of ELS on mental health during the pandemic.

Neural cognitive control moderates the longitudinal link between hedonia and substance use across adolescence.

Hedonic dysregulation is evident in addiction and substance use disorders, but it is not clearly understood how hedonic processes may interact with brain development related to cognitive control to influence risky decision making and substance use during adolescence. The present study used prospective longitudinal data to clarify the role of cognitive control in the link between hedonic experiences and the development of substance use during adolescence. Participants included 167 adolescents (53% male) assessed at four time points, annually. Adolescents participated in a functional magnetic resonance imaging (fMRI) session where blood-oxygen level dependent (BOLD) response was monitored during the Multi-Source- Interference Task to assess cognitive control. Substance use and hedonia were assessed using self-report. A two-group growth curve model of substance use with hedonia as a time-varying covariate indicated that higher levels of hedonia predicted higher substance use, but only in adolescents with higher activation in the frontoparietal regions and in the rostral anterior cingulate cortex during cognitive control. Results elucidate the moderating effects of neural cognitive control on associations between hedonia and adolescent substance use, suggesting that lower cognitive control functioning in the brain may exacerbate risk for substance use promoted by hedonia.

Transactional relations between developmental trajectories of executive functioning and internalizing and externalizing symptomatology in adolescence.

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.

Associations between developmental patterns of negative parenting and emotion regulation development across adolescence.

Research has documented changes in parenting practices and in emotion regulation (ER) during adolescence. However, developmental trajectories of these constructs and how they may be linked are not clearly known. The present study examined longitudinal associations between developmental trajectories of negative parenting and developmental trajectories of ER (e.g., abilities and strategy use, including cognitive reappraisal and suppression). The sample included 167 adolescents (53% males) who were first recruited at age 13 or 14 years and assessed annually four times. Adolescents self-reported on the perceived degree of their parent's negative parenting and ER. Growth mixture modeling revealed two distinct trajectories of negative parenting across adolescence: Class 1 contained the majority of adolescents (84%), with moderate initial levels of negative parenting that decreased across adolescence; Class 2 contained a smaller group of adolescents (16%), reporting moderate initial levels of negative parenting that increased across adolescence. Though growth curve modeling did not reveal significant growth in ER across time in the sample as a whole, results from a two-group model demonstrated that ER development significantly differs depending on adolescents' experiences of negative parenting trajectories. Adolescents experiencing decreases in negative parenting showed significant increases in ER abilities and no significant changes in suppression. Adolescents experiencing increases in negative parenting exhibited significant decreases in ER abilities. Adolescent's cognitive reappraisal was unaffected by negative parenting. The findings underscore the significant role of differential parenting environments in the development of ER abilities during adolescence. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Associations among negative life events, changes in cortico-limbic connectivity, and psychopathology in the ABCD Study.

Adversity exposure is a risk factor for psychopathology, which most frequently onsets during adolescence, and prior research has demonstrated that alterations in cortico-limbic connectivity may account in part for this association. In a sample of youth from the Adolescent Brain Cognitive Development (ABCD) Study (N = 4006), we tested a longitudinal structural equation model to examine the indirect effect of adversity exposure (negative life events) on later psychopathology via changes in cortico-limbic resting-state functional connectivity (rsFC). We also examined the potential protective effects of parental acceptance. Generally, cortico-limbic connectivity became more strongly negative between baseline and year 2 follow-up, suggesting that stronger negative correlations within these cortico-limbic networks may reflect a more mature phenotype. Exposure to a greater number of negative life events was associated with stronger negative cortico-limbic rsFC which, in turn, was associated with lower internalizing (but not externalizing) symptoms. The indirect effect of negative life events on internalizing symptoms via cortico-limbic rsFC was significant. Parental acceptance did not moderate the association between negative life events and rsFC. Our findings highlight how stressful childhood experiences may accelerate neurobiological maturation in specific cortico-limbic connections, potentially reflecting an adaptive process that protects against internalizing problems in the context of adversity.

A 4-year longitudinal neuroimaging study of cognitive control using latent growth modeling: developmental changes and brain-behavior associations.

Despite theoretical models suggesting developmental changes in neural substrates of cognitive control in adolescence, empirical research has rarely examined intraindividual changes in cognitive control-related brain activation using multi-wave multivariate longitudinal data. We used longitudinal repeated measures of brain activation and behavioral performance during the multi-source interference task (MSIT) from 167 adolescents (53% male) who were assessed annually over four years from ages 13 to 17 years. We applied latent growth modeling to delineate the pattern of brain activation changes over time and to examine longitudinal associations between brain activation and behavioral performance. We identified brain regions that showed differential change patterns: (1) the fronto-parietal regions that involved bilateral insula, bilateral middle frontal gyrus, left pre-supplementary motor area, left inferior parietal lobule, and right precuneus; and (2) the rostral anterior cingulate cortex (rACC) region. Longitudinal confirmatory factor analyses of the fronto-parietal regions revealed strong measurement invariance across time implying that multivariate functional magnetic resonance imaging data during cognitive control can be measured reliably over time. Latent basis growth models indicated that fronto-parietal activation decreased over time, whereas rACC activation increased over time. In addition, behavioral performance data, age-related improvement was indicated by a decreasing trajectory of intraindividual variability in response time across four years. Testing longitudinal brain-behavior associations using multivariate growth models revealed that better behavioral cognitive control was associated with lower fronto-parietal activation, but the change in behavioral performance was not related to the change in brain activation. The current findings suggest that reduced effects of cognitive interference indicated by fronto-parietal recruitment may be a marker of a maturing brain that underlies better cognitive control performance during adolescence.

Maltreatment and brain development: The effects of abuse and neglect on longitudinal trajectories of neural activation during risk processing and cognitive control.

The profound effects of child maltreatment on brain functioning have been documented. Yet, little is known about whether distinct maltreatment experiences are differentially related to underlying neural processes of risky decision making: valuation and control. Using conditional growth curve modeling, we compared a cumulative approach versus a dimensional approach (relative effects of abuse and neglect) to examine the link between child maltreatment and brain development. The sample included 167 adolescents (13-14 years at Time 1, 53 % male), assessed annually four times. Risk processing was assessed by blood-oxygen-level-dependent responses (BOLD) during a lottery choice task, and cognitive control by BOLD responses during the Multi-Source Interference Task. Cumulative maltreatment effects on insula and dorsolateral anterior cingulate cortex (dACC) activation during risk processing were not significant. However, neglect (but not abuse) was associated with slower developmental increases in insula and dACC activation. In contrast, cumulative maltreatment effects on fronto-parietal activation during cognitive control were significant, and abuse (but not neglect) was associated with steeper developmental decreases in fronto-parietal activation. The results suggest neglect effects on detrimental neurodevelopment of the valuation system and abuse effects on accelerated neurodevelopment of the control system, highlighting differential effects of distinct neglect versus abuse adverse experiences on neurodevelopment.

Processes linking socioeconomic disadvantage and neural correlates of cognitive control in adolescence.

Socioeconomic status (SES) is broadly associated with self-regulatory abilities across childhood and adolescence. However, there is limited understanding of the mechanisms underlying this association, especially during adolescence when individuals are particularly sensitive to environmental influences. The current study tested perceived stress, household chaos, parent cognitive control, and parent-adolescent relationship quality as potential proximal mediators of the association between family SES and neural correlates of cognitive control. A sample of 167 adolescents and their primary caregivers participated in a longitudinal study across four years. SES was indexed by caregivers' education and income-to-needs ratio at Time 1. At Time 2, adolescents reported on their perceived stress, household chaos, and relationship with parents, and parents completed a cognitive control task. Two years later, adolescents completed the same cognitive control task while blood-oxygenation-level-dependent (BOLD) response was monitored with functional magnetic resonance imaging (fMRI). A parallel mediation model indicated that parent cognitive control, but not other proximal factors, explained the relation between SES and adolescents' activation in the middle frontal gyrus during a cognitive control task. The results suggest potential targets for intervention and prevention efforts that may positively alter neurocognitive outcomes related to socioeconomic disadvantage.

Socioeconomic Risk for Adolescent Cognitive Control and Emerging Risk-Taking Behaviors.

This study examined whether cognitive control mediated the association between socioeconomic status (SES; composite of income-to-needs ratio and parent education) and changes in risk-taking behaviors. The sample included 167 dyads of adolescents (53% male; Mage  = 14.07 years at Time 1) and their parents, assessed annually across 4 years. Parents reported socioeconomic variables at Time 1. Adolescents reported risk-taking behaviors at Times 1 and 4, and completed a functional magnetic resonance imaging cognitive control task at Times 2 and 3. Lower SES was associated with lower behavioral (but not neural) cognitive control, which was associated with increases in risk-taking behaviors. The findings suggest that elevated socioeconomic risk may compromise cognitive control which can cascade into maladaptive behaviors in adolescence.

Bidirectional links between adolescent brain function and substance use moderated by cognitive control.

BACKGROUND: No clear consensus exists as to whether neurodevelopmental abnormalities among substance users reflect predisposing neural risk factors, neurotoxic effects of substances, or both. Using a longitudinal design, we examined developmental patterns of the bidirectional links between neural mechanisms and substance use throughout adolescence. METHOD: 167 adolescents (aged 13-14 years at Time 1, 53% male) were assessed annually four times. Risk-related neural processing was assessed by blood-oxygen-level-dependent responses in the insula during a lottery choice task, cognitive control by behavioral performance during the Multi-Source Interference Task, and substance use by adolescents' self-reported cigarette, alcohol, and marijuana use. RESULTS: Latent change score modeling indicated that greater substance use predicted increased insula activation during risk processing, but the effects of insula activation on changes in substance use were not significant. The coupling effect from substance use to insula activation was particularly strong for adolescents with low cognitive control, which supports the theorized moderating role of cognitive control. CONCLUSIONS: Our results elucidate how substance use may alter brain development to be biased toward maladaptive decision-making, particularly among adolescents with poor cognitive control. Furthermore, the current findings underscore that cognitive control may be an important target in the prevention and treatment of adolescent substance use given its moderating role in the neuroadaptive effects of substance use on brain development.

Religious Social Support Protects against Social Risks for Adolescent Substance Use.

We used a social developmental perspective to identify how prominent social contexts influence substance use during adolescence. Longitudinal data were collected annually from 167 parent-adolescent dyads over four years. We investigated whether parent substance use was related to adolescent substance use directly and indirectly via peer substance use and whether these associations were moderated by religious social support. Structural equation modeling (SEM) analysis indicated significant moderated mediation: Greater parent substance use predicted increases in adolescent substance use indirectly via increased peer substance use when adolescent religious social support was low or average, but not high. These results suggest religious social support may protect adolescents against prominent social risks for intergenerational substance use.