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dc.contributor.authorMazurka, Raegan
dc.contributor.otherQueen's University (Kingston, Ont.). Theses (Queen's University (Kingston, Ont.))en
dc.date2013-09-05 08:50:17.51en
dc.date2013-09-05 11:24:45.764en
dc.date.accessioned2013-09-05T15:34:12Z
dc.date.available2013-09-05T15:34:12Z
dc.date.issued2013-09-05
dc.identifier.urihttp://hdl.handle.net/1974/8250
dc.descriptionThesis (Master, Psychology) -- Queen's University, 2013-09-05 11:24:45.764en
dc.description.abstractChildhood adversity is often associated with devastating physical, cognitive, and psychosocial outcomes, and is a major public health problem in terms of its prevalence and economic cost. Childhood adversity is associated with increased risk for psychopathology, as well as with dysregulation of the neurobiological stress response. An additional factor known to alter neuroendocrine functioning and increase psychopathology risk is polymorphisms within the FKBP5 gene. The goal of the current study was to examine the gene-environment interaction of childhood adversity and variation in the FKBP5 gene on the cortisol response to a psychosocial stress task (i.e., the Trier Social Stress Test). The final sample consisted of 90 depressed and non-depressed adolescents and young adults (11 - 21 years). Childhood adversity was assessed using the Childhood Experience and Abuse Scale (CECA; Bifulco et al., 1994), and was defined as the presence versus absence prior to 18 years of age of severe physical, sexual, or emotional abuse or neglect, witness to domestic discord/violence, or peer-perpetrated bullying. Participants were genotyped at the rs1360780 site of the FKBP5 gene and grouped according to whether they had at least one risk T allele (i.e., TT or TC genotype versus the CC genotype). Controlling for depression and anxiety psychopathology, I found a significant interaction of FKBP5 and childhood adversity status such that individuals with the FKBP5 risk allele (i.e., TT or TC genotype) and a history of childhood adversity showed a distinct cortisol response pattern characterized by decreasing cortisol from baseline and less cortisol output compared to individuals without childhood adversity. This relationship was specific to the experience of severe adversity and appeared to be strongest when adversity was defined as witnessing domestic discord/violence. These results are consistent with a diathesis-stress model in which the FKBP5 risk allele leaves individuals vulnerable to neurobiological dysregulation in the face of severe adverse experience in childhood. The implications of this research for understanding stress-related psychopathology and the limitations of this gene-environment interaction design are discussed.en_US
dc.languageenen
dc.language.isoenen_US
dc.relation.ispartofseriesCanadian thesesen
dc.rightsThis publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner.en
dc.subjectFKBP5en_US
dc.subjectChildhood Adversityen_US
dc.subjectCortisolen_US
dc.subjectTrier Social Stress Testen_US
dc.titleInteraction of Polymorphisms in the FKBP5 Gene & Childhood Adversity on the Cortisol Response to a Psychosocial Stress Task in Adolescents and Young Adultsen_US
dc.typethesisen_US
dc.description.degreeMasteren
dc.contributor.supervisorHarkness, Kateen
dc.contributor.departmentPsychologyen


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