Bullying Involvement and Adolescent Substance Use: A Study of Multilevel Risk and Protective Factors

Bullying, frequent drunkenness, and frequent cannabis use are significant health-risk behaviours among youth. While many studies have demonstrated that bullying involvement may initiate a developmental pathway to both types of frequent substance use, there is a limited understanding of the connection between these behaviours. The presence of risk and protective factors within youths’ relationships and within their neighbourhoods may alter the associations between bullying involvement and both types of frequent substance use. A systemic approach is needed to assess the complex, social environments in which youth are embedded. The current thesis consists of two studies that examined the associations between bullying and both types of frequent substance use within the context of youths’ social environments. In Study 1, multilevel modeling was used to examine the associations between bullying and frequent substance use within the context of individual and neighbourhood risk factors. Our results indicated that the risk factors associated with both frequent drunkenness and frequent cannabis use exist at both levels, with neighbourhoods altering the association of individual risk factors. Moreover, bullying was a unique risk factor associated with both types of frequent substance use, whereas indirect associations were observed for victimization. Study 2 used a similar methodology to examine the association between bullying and both types of frequent substance use within the context of individual and neighbourhood protective factors. Once again, our results indicated that the protective factors associated with both types of frequent substance use exist at multiple levels, and that neighbourhoods altered the association of individual protective factors. Additionally, positive relationship characteristics interacted with the link between bullying and both types of frequent substance use. Together, these findings clarify the nature of the bullying-substance use link and emphasize the need to study adolescent development in context.

ENVIRONMENTAL INFLUENCES AND EPIGENETIC MECHANISMS IN RISK FOR DEPRESSION

Genetic and environmental factors interact to influence vulnerability for internalizing psychopathology, including Major Depressive Disorder (MDD). The mechanisms that account for how environmental stress can alter biological systems are not yet well understood yet are critical to develop more accurate models of vulnerability and targeted interventions. Epigenetic influences, and more specifically, DNA methylation, may provide a mechanism by which stress could program gene expression, thereby altering key systems implicated in depression, such as frontal-limbic circuitry and its critical role in emotion regulation. This thesis investigated the role of environmental factors from infancy and throughout the lifespan affecting the serotonergic (5-HT) system in the vulnerability to and treatment of depression and anxiety and potential underlying DNA methylation processes. First, we investigated the contributions of additive genetic vs. environmental factors on an early trait phenotype for depression (negative emotionality) in infants and their stability over time in the first 2 years of life. We provided evidence of the substantial contributions of both genetic and shared environmental factors to this trait, as well as genetically- and environmentally- mediated stability and innovation. Second, we studied how childhood environmental stress is associated with peripheral DNA methylation of the serotonin transporter gene, SLC6A4, as well as long-term trajectories of internalizing behaviours. There was a relationship between childhood psychosocial adversity and SLC6A4 methylation in males, as well as between SLC6A4 methylation and internalizing trajectory in both sexes. Third, we investigated changes in emotion processing and epigenetic modification of the SLC6A4 gene in depressed adolescents before and after Mindfulness-Based Cognitive Therapy (MBCT). The alterations from pre- to post-treatment in connectivity between the ACC and other network regions and SLC6A4 methylation suggested that MBCT may work to optimize the connectivity of brain networks involved in cognitive control of emotion as well as also normalize the relationship between SLC6A4 methylation and activation patterns in frontal-limbic circuitry. Our results from these three studies strengthen the theory that environmental influences are critical in establishing early vulnerability factors for MDD, driving epigenetic processes, and altering brain processes as an individual undergoes treatment, or experiences relapse.