Adolescent resilience to addiction: a social plasticity hypothesis

Abstract

The prevalence of substance use disorders is highest during adolescence; however, many adolescents experience a natural resolution of their substance use by early adulthood, without any formal intervention. Something appears to be unique and adaptive about the adolescent brain. In this Review, we examine the roles of the social environment and neurocognitive development in adolescents' natural resilience to substance use disorders. At present, little is known about the neurocognitive mechanisms that underlie this adaptive phenomenon, since neurodevelopmental studies have mainly focused on the risk side of the substance use equation: escalation of substance use. To provide a framework for future studies, we put forth a social plasticity model that includes developmentally limited enhanced social attunement (ie, the need to harmonise with the social environment), affective processing, and brain plasticity, which underlie adolescents' capacity to learn from and adapt to their constantly evolving social environments.

Figure 1:. Substance use and dependence across adolescence and adulthood

Results from the latest available US household survey in 2001 on drug abuse show that the prevalence of substance use, abuse, and dependence peak during adolescence and early adulthood. Reproduced from Dennis and Scott.

Figure 2:. Brain networks involved in adolescent risk and resilience to substance use and substance use disorders

The executive control network includes the dorsolateral prefrontal cortex (dlPFC), dorsal anterior cingulate cortex (dACC), posterior parietal cortex (PPC), dorsal premotor cortex (dPMC), pre-supplementary motor area (preSMA), and inferior frontal gyrus (IFG). The salience network includes the amygdala (A), ventral striatum (VS), dorsal striatum (DS), orbitofrontal cortex (OFC), ventral ACC (vACC), and anterior insula (AI). The reinforcement learning network includes the VS, DS, A, and AI, as well as the medial prefrontal cortex (mPFC), and hippocampus and parahippocampal gyrus (H & PHG). The social cognition network includes the mPFC, posterior ACC (pACC), temporoparietal junction (TPJ), superior temporal sulcus (STS), and temporal pole (TP).

Figure 3:. Social plasticity model of adolescent resilience to substance use and substance use disorders

Age-limited increase and subsequent decrease in substance use and related problems are explained by the developmentally changing interactions between the social reinforcing value of substance use, social attunement (SA), learning and plasticity (L&P), and behavioural control (BC). Social attunement and experimentation: onset of puberty marks a shift in brain plasticity and surge in social attunement, and the need to belong and to attune to peer behaviours increases the social reinforcing value of substance use as adolescence progresses. Facilitated social learning and escalation: enhanced associative learning strengthens the association between substance use and the rewarding social outcomes, which can lead to escalation of substance use in social contexts. Social devaluation of substance use and proactive behavioural control: the transition to adulthood parallels social devaluation of substance use, increased importance of long-term goals, improved emotional control, and decreased impulsive decision making. De-escalation of substance use: high social attunement, brain plasticity, and behavioural control integratively allow youths to implicitly notice change in the social reinforcing value of substance use and successfully adapt their behaviour accordingly. The increasing thickness of the arrows refers to the hypothesised increasing strength of the interactions between social attunement, learning and plasticity, and behavioural control across development.