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

Abstract

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.

A developmental perspective on personality and psychopathology across the life span

“…However, adolescents with higher levels of disinhibition are more likely than their peers to escalate use, use problematically, and eventually develop a substance use disorder (Iacono et al., 2008; Young et al., 2009). Continued exposure to environmental risk, including impaired parenting, suboptimal schooling, peer rejection, or an antisocial peer group, some of which elicited or selected by children themselves, as well as substance use itself, will exacerbate both disinhibition and externalizing psychopathology, and may have direct effects on the developing adolescent brain, leading to further deviations in control, reward, and emotionality processes (e.g., Kim‐Spoon et al, in press; Malone et al., 2014; Wilson et al, in press). And these processes will continue to play out into adulthood, with persistently high levels of disinhibition, increased likelihood of antisocial behavior and ongoing substance use, and associated psychosocial impairment.…”

Understanding patterns of heterogeneity in executive functioning during adolescence: Evidence from population‐level data

“…For example, EF predicts a host of behavioral and clinical outcomes including academic achievement (Miller et al, 2012), social skills (Miller & Hinshaw, 2010), and wellbeing (Cotrena et al, 2016. Deficits in adolescent EF have also been linked to substance use (Kim-Spoon et al, 2020), depression…”

“…For example, EF predicts a host of behavioral and clinical outcomes including academic achievement (Miller et al., 2012), social skills (Miller & Hinshaw, 2010), and wellbeing (Cotrena et al., 2016). Deficits in adolescent EF have also been linked to substance use (Kim‐Spoon et al., 2020), depression (Melendez‐Torres et al., 2016), as well as conduct disorders (Nigg & Huang‐Pollock, 2003), and are considered a key transdiagnostic risk factor for the development of psychopathology (Nolen‐Hoeksema & Watkins, 2011; Snyder et al., 2015).…”

“…For example, EF predicts a host of behavioral and clinical outcomes including academic achievement (Miller et al, 2012), social skills (Miller & Hinshaw, 2010), and wellbeing (Cotrena et al, 2016. Deficits in adolescent EF have also been linked to substance use (Kim-Spoon et al, 2020), depressionThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.…”

Neural substrates of substance use disorders

“…There is some evidence that frontostriatal, frontolimbic and frontocerebellar systems are altered as a consequence of use [27]. Others have reported increasing risk-related insular cortex activation with prolonged substance use [28 ▪▪ ]. Using longitudinal cohorts to predict the emergence of substance use, investigators reported that both decreased anterior cingulate cortex volume [29] and blunted orbitofrontal cortex activation during reward outcome [30 ▪▪ ] predicted greater risk for substance and alcohol use initiation.…”