Previous research has shown that personality characteristics, such as sensation seeking (SS), are strong predictors of risk-taking behavior during adolescence. However, the relationship between levels of SS and brain response has not been studied during this time period. Given the prevalence of risky behavior during adolescence, it is important to understand neurobiological differences in reward sensitivity between youth with high and low SS personalities. To this end, we used functional magnetic resonance imaging (fMRI) to examine differences in brain activity in an adolescent sample that included 27 high (HSS) and 27 low sensation seekers (LSS), defined by the Impulsive Sensation Seeking scale of the Zuckerman-Kuhlman Personality Questionnaire (Zuckerman et al., 1993). In the scanner, participants played a modified Wheel of Fortune decision-making task (Cservenka and Nagel, 2012) that resulted in trials with monetary Wins or No Wins. We compared age- and sex-matched adolescent HSS and LSS (mean age = 13.94 ± 1.05) on brain activity by contrasting Win versus No Win trials. Our findings indicate that HSS show greater bilateral insular and prefrontal cortex (PFC) brain response on Win vs. No Win compared to LSS. Analysis of simple effects showed that while LSS showed comparable brain activity in these areas during Wins and No Wins, HSS showed significant differences in brain response to winning (activation) versus not winning (deactivation), with between-group comparison suggesting significant differences in brain response, largely to reward absence. Group differences in insular activation between reward receipt and absence may suggest weak autonomic arousal to negative outcomes in HSS compared with LSS. Additionally, since the PFC is important for goal-directed behavior and attention, the current results may reflect that HSS allocate fewer attentional resources to negative outcomes than LSS. This insensitivity to reward absence in HSS may lead to a greater likelihood of maladaptive choices when negative consequences are not considered, and may be an early neural marker of decreased loss sensitivity that has been seen in addiction. This neurobiological information may ultimately be helpful in establishing prevention strategies aimed at reducing youth risk-taking and suggests value in further examination of neural associations with personality characteristics during adolescence.
Although adolescents are developmentally distinct from adults, they often receive addiction treatment based on adult models. This is problematic because adolescents face significantly different conditions in addiction treatment, including distinct basic biological and neurodevelopmental stages, unique sociodevelopmental concerns, distinctive addiction trajectories, and, in turn, disparate treatment goals and outcomes. In sum, it can be difficult for even savvy clinicians to know how to approach addiction treatment with this important age group. In an effort to help clinicians and researchers consider substance use via a neurodevelopmental lens, we approached this review with 4 goals: (i) characterize the prevalence, and related health and safety implications of substance use within this age group; (ii) identify the nature of the adolescent brain, including characteristic features of this phase of neurodevelopment relevant to adolescent substance use treatment; (iii) provide an overview of current adolescent addiction interventions and avenues to improve clinical treatment and clinical research efforts for adolescents; and (iv) examine the intersection between the nature of the developing brain and adolescent substance use, and utilize that information to inform alternative routes and directions for substance use treatment in this critical age group. This review concludes by offering a novel neurodevelopmental model and framework to examine substance use interventions, along with a series of recommendations to optimize adolescent substance use treatment and clinical research.
An increasing number of studies have implicated network functional connectivity with addiction. Yet, none have examined functional connectivity as a potential mechanism of adolescent behavior change. We examined the underlying neural mechanisms of a promising treatment for adolescents, motivational interviewing (MI). We began by employing psychophysiological interaction (PPI) to evaluate network response in a sample of adolescent cannabis users (N = 30). Next, we examined correlations between network connectivity and clinical metrics of treatment outcome. PPI analyses seeded on the orbitofrontal cortex (OFC) showed significant increases in functional connectivity across the inferior frontal gyrus (IFG), precentral gyrus, anterior and posterior cingulate gyrus, supplementary motor area (SMA), superior frontal gyrus, pallidus, caudate, and parahippocampal gyrus. Further, greater functional connectivity between the OFC and anterior cingulate/medial frontal gyrus was associated with less behavior change (e.g., greater post-treatment cannabis problems). These data support the role of the OFC network as a mechanism of adolescent addiction treatment response.
Many adolescents struggle with overweight/obesity, which exponentially increases in the transition to adulthood. Overweight/obesity places youth at risk for serious health conditions, including type 2 diabetes. In adults, neural substrates implicated in addiction (e.g., orbitofrontal cortex (OFC), striatum, amygdala, and ventral tegmental area) have been found to be relevant to risk for overweight/obesity. In this study, we examined three hypotheses to disentangle the potential overlap between addiction and overweight/obesity processing by examining (1) brain response to high vs. low calorie beverages, (2) the strength of correspondence between biometrics, including body mass index (BMI) and insulin resistance, and brain response and (3) the relationship between a measure of food addiction and brain response using an established fMRI gustatory cue exposure task with a sample of overweight/obese youth (M age = 16.46; M BMI = 33.1). Greater BOLD response was observed across the OFC, inferior frontal gyrus (IFG), nucleus accumbens, right amygdala, and additional frontoparietal and temporal regions in neural processing of high vs. low calorie beverages. Further, BMI scores positively correlated with BOLD activation in the high calorie > low calorie contrast in the right postcentral gyrus and central operculum. Insulin resistance positively correlated with BOLD activation across the bilateral middle/superior temporal gyrus, left OFC, and superior parietal lobe. No relationships were observed between measures of food addiction and brain response. These findings support the activation of parallel addiction-related neural pathways in adolescents’ high calorie processing, while also suggesting the importance of refining conceptual and neurocognitive models to fit this developmental period.
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