Longitudinal Associations Among Socioeconomic Status, Delay Discounting, and Substance Use in Adolescence.

It is unclear how delay discounting and substance use develop across adolescence and whether contextual factors alter their trajectories. The present study used a longitudinal design to examine whether socioeconomic status is related to developmental trajectories of delay discounting and substance use across adolescence. The sample included 167 adolescents (Mage = 14 at Time 1; 53% male) and their parents who participated annually across four years. Parents reported SES at Time 1 and adolescents completed delay discounting behavioral assessments and substance use questionnaires at Times 1 to 4. Bivariate latent growth curve modeling revealed that low SES was related to steeper increases in substance use from age 14 through 17, mediated through elevated delay discounting at age 14. The findings clarify the mediating role of delay discounting in linking family economic environment to the progression of substance use.

Negative Affect, Sensation Seeking, and Adolescent Substance Use Development: The Moderating Role of Executive Function.

It is unknown how the Addictions Neuroclinical Assessment markers-negative affect, sensation seeking, and executive function-contribute to substance use development. This study examined whether associations of negative affect and sensation seeking with substance use vary by executive function. Participants were 167 adolescents (47% female) who participated annually for four years (Mage = 14.07, SDage = 0.54 at Time 1). There were within-person bidirectional associations between higher negative affect and higher substance use for adolescents with lower executive function. Adolescents with higher sensation seeking at age 14 exhibited increasing substance use trajectories from age 14 to 17, regardless of executive function level. Negative affect and substance use influence each other within individuals, whereas sensation seeking predicts substance use between individuals.

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.

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.

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.

Longitudinal pathways linking family risk, neural risk processing, delay discounting, and adolescent substance use.

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 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 fifty-seven 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 multi-risk 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.

Intergenerational transmission of delay discounting: The mediating role of household chaos.

INTRODUCTION: Adolescence is a period when impulsive decision making may be especially vulnerable to environmental influences. Impulsive decision making is often assessed using a delay discounting paradigm, which measures the preference for smaller rewards sooner over larger rewards with a delay. Research is needed to clarify the relationship between parents' and adolescents' delay discounting and to identify related environmental processes that might facilitate the intergenerational transmission of delay discounting. The current prospective longitudinal study examined the competing mediating processes of household chaos and harsh parenting in the intergenerational transmission of delay discounting between parents and adolescents. METHODS: Participants included 167 adolescents (mean age = 14.07 years at Time 1; 53% male) and their parents (mean age = 41.98 years at Time 1; 87% female) recruited from the southeast United States. Parents' delay discounting was collected at Time 1, and adolescents' delay discounting was collected both at Time 1 and at Time 3 via a computerized delay discounting task. Parents and adolescents reported household chaos and harsh parenting at Time 2. RESULTS: A parallel mediation model indicated that parents' delay discounting at Time 1 indirectly predicted adolescents' delay discounting Time 3 residualized change scores (regressing Time 3 delay discounting onto baseline delay discounting) through household chaos but not through harsh parenting at Time 2. CONCLUSIONS: These results underline the importance of household chaos in facilitating the intergenerational transmission of delay discounting between parents and adolescents. Furthermore, our findings point to household chaos as a potential environmental target for interrupting intergenerational impulsivity.

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.