Extant literature has demonstrated that self-control is critical for health and adjustment in adolescence. Questions remain regarding whether there are individuals that may be most vulnerable to impaired self-control development and whether aspects of the structural home environment may predict membership in these subgroups, as well as the behavioral consequences of impaired self-control trajectories. The present study utilized growth mixture modeling and data from 1083 individuals (50% female, 82% White) from age 8.5 to 15 years to identify four latent classes of self-control development. Additionally, higher household chaos and lower socioeconomic status at age 8.5 were associated with maladaptive trajectories of self-control at ages 8.5-11.5. In turn, maladaptive self-control trajectories at ages 8.5-11.5 were associated with higher risk taking at age 15. The results highlight the importance of increased structure and support for at-risk youth.

Background: Current theories in neuroscience emphasize the crucial role of individual differences in the brain contributing to the development of risk taking during adolescence. Yet, little is known about developmental pathways through which family risk factors are related to the neural processing of risk during decision making, ultimately contributing to health risk behaviors. Using a longitudinal design, we tested whether neural risk processing, as affected by family multi-risk index, predicted delay discounting and substance use. Method: One hundred and fiftyseven adolescents (aged 13-14 years at Time 1, 52% male) were assessed annually three times. Family multi-risk index was measured by socioeconomic adversity, household chaos, and family risk-taking behaviors. Delay discounting was assessed by a computerized task, substance use by questionnaire data, and risk-related neural processing by blood-oxygen-level-dependent (BOLD) responses in the amygdala during a lottery choice task. Results: Family multi-risk index at Time 1 was related to adolescent substance use at Time 3 (after controlling for baseline substance use) indirectly through heightened amygdala sensitivity to risks and greater delay discounting. Conclusions: Our results elucidate the crucial role of neural risk processing in the processes linking family multirisk index and the development of substance use. Furthermore, risk-related amygdala activation and delay discounting are important targets in the prevention and treatment of substance use among adolescents growing up in high-risk family environments.

Executive functioning (EF) may be transmitted across generations such that strengths or deficiencies in parent EF are similarly manifested in the child. The present study examined the contributions of parent EF and impulsivity on adolescent EF, and investigated whether household chaos is an environmental moderator that alters these transmission processes. American adolescents (N = 167, 47% female, 13–14 years old at Time 1) completed behavioral measures of EF and reported household chaos at Time 1 and one year later at Time 2. Parents completed behavioral measures of EF and self-reported impulsivity at Time 1. Results indicated that lower parent EF at Time 1 predicted lower adolescent EF at Time 2 (controlling for adolescent EF and IQ at Time 1), but only in the context of high household chaos. Findings suggest that household chaos may be a risk factor that compounds influences of poor parent EF and compromises adolescent EF development.

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.

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.