Date of Award

12-31-2018

Document Type

Campus Access Thesis

Degree Name

Master of Arts (MA)

Department

Clinical Psychology

First Advisor

Paul G. Nestor

Second Advisor

Alice Carter

Third Advisor

Richard Hunter

Abstract

Experiences of childhood adversity have long been associated with poor mental health functioning (Anda et al., 2006) and with impairments in learning and memory (Homberg, Molteni, Calabrese, & Riva, 2014). How these experiences increase risk of mental illness and cognitive dysfunction remains an active area of research; much less is known about how protective factors alter trajectories and contribute to wellbeing. Participants (N=100) completed self-report measures of adverse childhood events, current wellbeing, emotional functioning, and neuropsychological tests of executive functioning. DNA samples were collected and analyzed for functional polymorphisms of the Serotonin Transporter Receptor (5-HTTLPR) and Brain-Derived Neurotrophic Factor (BDNF) genes. This study examined the moderating effect of candidate gene polymorphic variation in the associations between childhood adversity, mental health, and cognitive functioning. We hypothesized that greater exposure to adverse childhood events would be associated with increased psychiatric symptomatology and lower levels of wellbeing. Significant associations were observed between experiences of childhood adversity and psychiatric symptomatology, such that endorsements of greater childhood adversity were correlated with lower levels of wellbeing, higher ratings of global psychiatric symptom severity and distress, as well as higher ratings of psychotic-like experiences. Additionally, adverse childhood events were negatively correlated with scores on measures of attention and working memory. Each genetic polymorphism was examined as a predictor and moderator of psychiatric symptomatology and wellbeing through Gene x Environment (G x E) interactions. Counter to our expectations, polymorphism group did not predict mental health functioning. Last, G x G x E interactions were tested to examine whether childhood adversity and polygenic susceptibility predicted symptoms and wellbeing. Three-way interaction of selected polymorphisms and adversity were not predictive of outcomes. However, endorsement of childhood adversity and being a carrier of the Short 5-HTTLPR alleles and Val/Met or Met/Met BDNF alleles each independently predicted both higher ratings on psychiatric symptoms and lower wellbeing. Taken together, these findings indicate strong evidence to support the influence of individual genetic variation in G x G models predicting psychiatric symptoms and wellbeing, although do not confirm the hypothesized G x E interactions with childhood adversity, despite strong evidence of adversity as predictor of outcomes.

Comments

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