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

ABSTRACT: 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.

SUBMITTER: Kim-Spoon J

PROVIDER: S-EPMC6791121 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature

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Project description:BackgroundDelay discounting is a potential etiological factor in adolescents' alcohol use, making it important to understand its antecedents. Family disorganization might contribute to delay discounting, but few studies have tested this relation. Moreover, because delay discounting is heritable, the effects of family disorganization on delay discounting might be moderated by adolescents' genetic risk for delay discounting. Thus, the current study examined the role of family disorganization, in interaction with genetic risk, in predicting adolescents' delay discounting and subsequent alcohol use.MethodsAdolescents participated in 4 waves of data collection. Adolescents self-reported their family disorganization at T1, completed a delay discounting questionnaire at T3, and self-reported their alcohol use both at T2 (covariate) and T4 (outcome). Using results from an independent sample, we created a polygenic risk score consisting of dopaminergic genes to index genetic risk for delay discounting.ResultsGreater family disorganization predicted adolescents' greater delay discounting, but only for adolescents with low levels of genetic risk for delay discounting. Adolescents with high and mean levels of genetic risk for delay discounting showed elevated delay discounting regardless of their family's disorganization. Greater delay discounting prospectively predicted adolescents' greater alcohol use. Finally, the effects of family disorganization on adolescents' alcohol use were mediated through delay discounting, but only for adolescents with low levels of genetic risk.ConclusionsResults suggest multiple pathways to delay discounting. Although there are genetically influenced pathways to delay discounting, family disorganization might represent an environmental pathway to delay discounting (and subsequent alcohol use) for a subset of adolescents at low genetic risk. These findings reinforce the utility of family interventions for reducing adolescents' delay discounting and alcohol use, at least for a subgroup of adolescents. Because higher family organization did not buffer against delay discounting among adolescents with high genetic risk, future research should explore other early environmental influences that could protect these high-risk adolescents from developing these risky behaviors.

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

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