Our analysis of three annual assessments in a community sample of early adolescents supports the striatal imbalance model for the relation between two forms of impulsivity (sensation seeking and acting without thinking) and their relations to risk behavior and working memory performance. We found that although risk behavior and impulsivity increased across assessments, working memory performance also increased. This pattern suggests that not all risk taking need be accompanied by deficits in executive function. Indeed, we expected that the two forms of impulsivity would be positively related to each other at each assessment and positively related to risk behavior. However, we expected them to be differentially related to working memory performance with sensation seeking related positively and acting without thinking negatively related. In addition, because acting without thinking is linked to a deficit in executive function relative to subcortical impulse motivation, we expected it to be more strongly related to risk behavior than sensation seeking. Confirmation of all these predictions supported the proposed role of relative deficits in executive function as a precursor to risk behavior and associated externalizing problems.
Our findings supported a unique prediction of the striatal imbalance model, namely that adolescent risk taking is a product of both a dysfunctional form of impulsivity, associated with deficits in executive function and the tendency to act without thinking, and of a more controlled form of impulsivity associated with sensation seeking and relatively greater executive function. Indeed, at the same time that sensation seeking predicted increases in risk behavior (from time 1 to 2), it was accompanied by stronger working memory performance, as indicated by the prospective relation between working memory at time 1 and sensation seeking at time 2.
We also found that working memory performance was inversely related to subsequent risk behavior. Although this relation was not predicted by the striatal imbalance model, it is consistent with models that posit early weakness in executive cognitive function as increasing susceptibility to later problem behavior (Nigg, et al., 2006
; Tarter et al., 2003
). Furthermore, we could not rule out the effects of other forms of impulsivity that may mediate effects of working memory deficits on subsequent emergence of risk behavior. For example, a third form of impulsivity, temporal discounting, has also been found to be independent of sensation seeking (Wilson & Daly, 2006
) and acting without thinking (Reynolds, Penfold, & Patak, 2008
) and to predict drug use and other risky behavior (Reynolds, 2006
). Although we did not measure this form of impulsivity, it has also been found to be inversely related to working memory performance (Shamosh et al., 2008
). It is possible therefore that after controlling for prior influence of sensation seeking and acting without thinking, this or other forms of impulsivity could also influence risk taking in mid-adolescence.
Although acting without thinking was not associated with later emergence of risk behavior, this form of impulsivity was highly related to risk behavior at each assessment, suggesting that its effects were already evident at the first assessment in the study. This pattern is consistent with Tarter and colleagues (2003
model of neurobehavioral disinhibition, which predicts that early forms of externalizing problems and executive function deficits are associated with a pattern of increased risk for later problem behaviors. We suspect that this tendency is well under way prior to adolescence given evidence from studies that observe children as young as age 3 who exhibit impulsive traits that predict later problems in behavior (Caspi, Henry, McGee, Moffitt, & Silva, 1995
; Caspi, Moffitt, Newman, & Silva, 1996
; White, Moffitt, Caspi, Bartusch, Needles, & Stouthamer-Loeber 1994
Despite the strong relation between risk taking and acting without thinking that was evident at all three assessments, the direct path from sensation seeking at time 1 to risk behavior at time 2 indicates that atleast some of the risk taking that occurs during adolescence is the unique result of sensation seeking. While the size of this relation was not large after controlling for acting without thinking, it is likely to continue to grow as adolescents age. Indeed, many studies find a robust relation between sensation seeking and risk taking during later adolescence (e.g., Crawford, Pentz, Chou, Li, & Dwyer, 2003
; Romer & Hennessy, 2007
). The finding that working memory was positively related to sensation seeking is also consistent with research that finds a positive relation between sensation seeking and IQ. Indeed, IQ tends to have a small but persistent negative relation with maladaptive forms of risk taking (Henry & Moffitt, 1997
), Although the size of the relation between working memory and sensation seeking was not large, it is also likely to grow as adolescents age. As seen in the correlations in , the relation between working memory at time 1 and sensation seeking increased from .05 to .23 over the course of three years.
The separate effect of sensation seeking on risk taking suggests that later emergence of risk behavior associated with sensation seeking is actually marked by greater executive function. In this form of risk taking, attraction to risky activities is promoted by a combination of executive function and interest in novel and exciting stimuli of all kinds. Such a tendency would have clear adaptive benefits to adolescents who are expected to leave home, find mates, and start on a path toward self-sufficiency (Spear, 2007
). It would also encourage engaging in new experiences that could permit the adolescent to identify unique strengths and abilities as an independent actor (Jessor, 1992
). Unfortunately in a modern society with many hazards associated with risk taking during adolescence, such behavior is not without its perils, including risk for substance abuse and injury. However, it appears to be of a different sort from the risk taking that is implicated in the early emergence of weak executive function that may lead to more serious forms of disorder. Strategies designed to prevent those outcomes will need to distinguish between the two forms of impulsivity.
An alternative explanation for early weakness in executive function among high risk takers concerns the possibility that engagement in problem behavior disrupts the normal development of executive cognitive function. For example, heavy alcohol use during adolescence might affect the development of the hippocampus and thereby disrupt executive functioning (Medina, Schweinburg, Cohen-Zion, Nagel, & Tapert, 2007
). This explanation seems unlikely given that our early risk takers were not engaging in high levels of alcohol use. In addition, we found no effect of early risk taking on working memory. Furthermore, the finding that early weakness in working memory predicted later increases in risk behavior suggests that this deficit predates the heavier uptake of drug use that occurs later in the adolescence. Hence, the data are more consistent with the hypothesis that early deficits in working memory relative to motivational circuits is partly responsible for high levels of early risk taking.
Our results are also interesting in the context of theories that attribute increased risk and externalizing behavior during adolescence to a structural imbalance between dorsolateral PFC and mesolimbic control over behavior. These theories tend to focus on increasing dopamine transmission in the ventral mesolimbic system and to overlook the other major (dorsal striatal) dopamine pathway that subserves more controlled cognitive processes related to working memory ability. Our results suggest that this pathway also exhibits increasing activation during adolescence. As a result, rather than reflecting universally slower adolescent maturation of dorsal versus ventral control systems, such differences may primarily affect a subset of adolescents who tend to exhibit greater ventral than dorsal striatal maturation early in development. This imbalance appears to continue into mid-adolescence placing youth with these characteristics at increased risk for drug dependence and other externalizing problems. At the same time, youth who also experience increasing ventral striatal activation but who do not suffer from relative weakness in executive function appear to be less susceptible to impulsive outcomes. Indeed, the striatal imbalance model predicts that some risk taking is accompanied by stronger executive function, a prediction that is clearly at odds with models that attribute all adolescent risk taking to weak executive function. Nevertheless, it will be important to continue to follow these youth as they enter later adolescence to determine whether the two types of impulsivity lead to different risks to healthy development. It would be expected that youth who are high in acting without thinking would experience more serious risks to healthy development than those who are high in sensation seeking.
Limitations in this study should also be noted. We did not have direct measures of dopamine or striatal function in either of the pathways that were proposed to be critical to risk taking in our model. We assumed that variation in dopamine synthesis in the ventral striatum played a role in both forms of impulsivity we measured. However, the precise role of dopamine function in the dorsal pathway is less clear. In particular, the effects of drugs that increase dopamine function in this system appear to depend on the resting levels of dopamine activity, in keeping with the Yerkes-Dodson principle (Cools & Robbins, 2004
). Hence, it could be that dopamine function in this pathway is weak leading to poor executive function, or it could be that it is overly active, also leading to the same result. Future research should be directed to observing such activation more directly in youth who exhibit high versus low levels of the two forms of impulsivity.
We primarily base our conclusions regarding risk behavior on the self-report of our participants. However, in regard to many forms of risk behavior in adolescents, youth reports are more sensitive than those of parents (or teachers), who often do not know what drugs their children use, or what they do with their peers (Crouter, Bumpus, Davis, & McHale, 2005
; Herjanic & Reich, 1997
). Finally, an analysis that identifies unique trajectories over time and tests relations between them should also be conducted as this cohort ages to determine whether an early risk-taking trajectory has different relations with trajectories in impulsivity and executive function. It would be expected that such an analysis would show that an early risk-taking trajectory is more highly related to an early trajectory in acting without thinking and weak executive function than to later emerging trajectories in risk behavior.
Implications for Intervention
Our results suggest that interventions to prevent adverse consequences for either of the pathways we have identified will need to consider the differences between the two types of impulsivity. Interventions to prevent adverse effects of acting without thinking will need to focus on weaknesses in executive function that appear to emerge early in development. Our results indicate that if untreated such deficits will lead to increasing levels of risk and externalizing behavior as youth age. Interventions to reduce weaknesses in executive function include training in working memory (Klingberg, et al., 2005
) as well as in cognitive strategies of self-control and problem solving (Botvin & Schinke, 1997
). Interventions for those high in sensation seeking might more fruitfully focus on diverting sensation seeking drives to less harmful activities, such as sports that can also satisfy needs for novelty and excitement. However, cognitive control strategies may also be appropriate for such youth as these abilities can help to channel impulsive drives into more constructive activity.