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Description
The present study tested the factor structure of the externalizing disorders (e.g. attention-deficit hyperactivity disorder (ADHD), conduct disorder (SE), and substance experimentation (SE) ) in adolescence. In addition, this study tested the influence of the GABRA2 gene on the factors of the externalizing spectrum. Confirmatory factor analyses were used to

The present study tested the factor structure of the externalizing disorders (e.g. attention-deficit hyperactivity disorder (ADHD), conduct disorder (SE), and substance experimentation (SE) ) in adolescence. In addition, this study tested the influence of the GABRA2 gene on the factors of the externalizing spectrum. Confirmatory factor analyses were used to test the factor structure of the externalizing spectrum. Specifically, three competing alternate confirmatory factor analytic models were tested: a one-factor model where all disorders loaded onto a single externalizing factor, a two-factor model where CD and SE loaded onto one factor and ADHD loaded onto another, and a three-factor model, where all three disorders loaded onto separate factors. Structural equation modeling was used to test the effect of a GABRA2 SNP, rs279858, on the factors of the externalizing spectrum. Analyses revealed that a three-factor model of externalizing disorders with correlated factors fit the data best. Additionally, GABRA2 had a significant effect on the SE factor in adolescence, but not on the CD or ADHD factors. These findings demonstrate that the externalizing disorders in adolescence share commonalities but also have separate sources of systematic variance. Furthermore, biological mechanisms may act as a unique etiological factor in the development of adolescent substance experimentation.
ContributorsWang, Frances L (Author) / Chassin, Laurie (Thesis advisor) / Lemery-Chalfant, Kathryn (Committee member) / Geiser, Christian (Committee member) / Arizona State University (Publisher)
Created2012
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Description
Research has consistently shown that gay/lesbian/bisexual (GLB) or sexual minority youth are at an increased risk for adverse outcomes resulting from the stress caused by continual exposure to negative events (e.g., victimization, discrimination). The present study used a nationally representative sample of adolescents to test mechanisms that may be responsible

Research has consistently shown that gay/lesbian/bisexual (GLB) or sexual minority youth are at an increased risk for adverse outcomes resulting from the stress caused by continual exposure to negative events (e.g., victimization, discrimination). The present study used a nationally representative sample of adolescents to test mechanisms that may be responsible for the differences in offending behaviors among sexual minority and heterosexual adolescents. Specifically, this study tested whether bisexual adolescents received less maternal support than did heterosexual adolescents because of their sexual orientation, thus increasing the likelihood that they run away from home. This study then examined whether the greater likelihood that bisexual adolescents running away would lead to them committing a significantly higher variety of income-based offenses, but not a significantly higher variety of aggression-based offenses. This study tested the hypothesized mediation model using two separate indicators of sexual orientation measured at two different time points, modeled outcomes in two ways, as well as estimated the models separately for boys and girls. Structural equation modeling was used to test the hypothesized direct and indirect relations. Results showed support for maternal support and running away mediating the relations between sexual orientation and offending behaviors for the model predicting the likelihood of committing either an aggressive or an income offense, but only for girls who identified as bisexual in early adulthood. Results did not support these relations for the other models, suggesting that bisexual females have unique needs when it comes to prevention and intervention. Results also highlight the need for a greater understanding of sexual orientation measurement methodology.
ContributorsMansion, Andre (Author) / Chassin, Laurie (Thesis advisor) / Barrera, Manuel (Committee member) / Grimm, Kevin J. (Committee member) / Toomey, Russell B (Committee member) / Arizona State University (Publisher)
Created2018
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Description
The current study utilized data from two longitudinal samples to test mechanisms in the relation between a polygenic risk score indexing serotonin functioning and alcohol use in adolescence. Specifically, this study tested whether individuals with lower levels of serotonin functioning as indexed by a polygenic risk score were vulnerable to

The current study utilized data from two longitudinal samples to test mechanisms in the relation between a polygenic risk score indexing serotonin functioning and alcohol use in adolescence. Specifically, this study tested whether individuals with lower levels of serotonin functioning as indexed by a polygenic risk score were vulnerable to poorer self-regulation, and whether poorer self-regulation subsequently predicted the divergent outcomes of depressive symptoms and aggressive/antisocial behaviors. This study then examined whether depressive symptoms and aggressive/antisocial behaviors conferred risk for later alcohol use in adolescence, and whether polygenic risk and effortful control had direct effects on alcohol use that were not mediated through problem behaviors. Finally, the study examined the potential moderating role of gender in these pathways to alcohol use.

Structural equation modeling was used to test hypotheses. Results from an independent genome-wide association study of 5-hydroxyindoleacetic acid in the cerebrospinal fluid were used to create serotonin (5-HT) polygenic risk scores, wherein higher scores reflected lower levels of 5-HT functioning. Data from three time points were drawn from each sample, and all paths were prospective. Findings suggested that 5-HT polygenic risk did not predict self-regulatory constructs. However, 5-HT polygenic risk did predict the divergent outcomes of depression and aggression/antisociality, such that higher levels of 5-HT polygenic risk predicted greater levels of depression and aggression/antisociality. Results most clearly supported adolescents’ aggression/antisociality as a mechanism in the relation between 5-HT polygenic risk and later alcohol use. Deficits in self-regulation also predicted depression and aggression/antisociality, and indirectly predicted alcohol use through aggression/antisociality. These pathways to alcohol use might be the most salient for boys with low levels of socioeconomic status.

Results are novel contributions to the literature. The previously observed association between serotonin functioning and alcohol use might be due, in part, to the fact that individuals with lower levels of serotonin functioning are predisposed towards developing earlier aggression/antisociality. Results did not support the hypothesis that serotonin functioning predisposes individuals to deficits in self-regulatory abilities. Findings extend previous research by suggesting that serotonin functioning and self-regulation might be transdiagnostic risk factors for many types of psychopathology.
ContributorsWang, Frances Lynn (Author) / Chassin, Laurie (Thesis advisor) / Eisenberg, Nancy (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / MacKinnon, David (Committee member) / Arizona State University (Publisher)
Created2017
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Description

The purpose of this study is to examine the social and communicative barriers LGBTQIA+ students face when seeking healthcare at campus health and counseling services at Arizona State University. Social barriers relate to experiences and internalizations of societal stigma experienced by sexual and gender minority individuals as well as the

The purpose of this study is to examine the social and communicative barriers LGBTQIA+ students face when seeking healthcare at campus health and counseling services at Arizona State University. Social barriers relate to experiences and internalizations of societal stigma experienced by sexual and gender minority individuals as well as the anticipation of such events. Communication between patient and provider was assessed as a potential barrier with respect to perceived provider LGBTQIA+ competency. This study applies the minority stress model, considering experiences of everyday stigma and minority stress as a predictor of healthcare utilization among sexual and gender minority students. The findings suggest a small but substantial correlation between minority stress and healthcare use with 23.7% of respondents delaying or not receiving one or more types of care due to fear of stigma or discrimination. Additionally, communication findings indicate a lack of standardization of LGBTQIA+ competent care with experiences varying greatly between respondents.

ContributorsZahn, Jennica (Author) / Davis, Olga (Thesis director) / LeMaster, Benny (Committee member) / Watts College of Public Service & Community Solut (Contributor) / School of Art (Contributor) / Barrett, The Honors College (Contributor)
Created2021-05
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Description
Pediatric chronic pain is pervasive and associated with myriad adverse consequences, yet due consideration has not been given to the mental health disturbances that often present alongside chronic pain and the etiological mechanisms that potentially underlie both. The current study examined the etiology underlying chronic pain and internalizing symptomology in

Pediatric chronic pain is pervasive and associated with myriad adverse consequences, yet due consideration has not been given to the mental health disturbances that often present alongside chronic pain and the etiological mechanisms that potentially underlie both. The current study examined the etiology underlying chronic pain and internalizing symptomology in middle childhood, considering both independent and co-occurring symptom presentations. Phenotypic parent-offspring associations across chronic pain and internalizing symptomology were also examined. Lastly, nuclear twin family models were tested to determine the extent to which genetic and environmental factors underlie parent-offspring transmission. The sample comprised 795 children (399 families; Mage= 9.7 years; SD = 0.92) and their parents drawn from the Arizona Twin Project. Results indicated that chronic pain was highly heritable (78%), whereas internalizing symptomology was modestly heritable (32%) and further subject to moderate shared environmental influence (50%). Moreover, 9% of the variance in chronic pain was explained by additive genetic factors shared with internalizing symptomology. Maternal chronic pain and internalizing symptomology were positively associated with both child chronic pain and internalizing symptomology. The association between maternal chronic pain and child chronic pain was more pronounced for girls than boys, whereas the association between maternal internalizing symptomology and child internalizing symptomology was more pronounced for boys than girls. Paternal chronic pain was not significantly associated with child chronic pain but was unexpectedly associated with lower child internalizing symptomology. The negative association between paternal chronic pain and child internalizing symptomology was more pronounced for boys than girls. Paternal internalizing symptomology was not significantly associated with child chronic pain but was positively associated with child internalizing symptomology. Lastly, the best fitting reduced nuclear twin family models for both chronic pain and internalizing symptomology retained additive genetic, sibling-specific shared environmental, and nonshared environmental parameters, where parent-offspring transmission was solely explained by shared genetics and sibling-specific shared environmental factors further accounted for co-twin resemblance. Results provide novel insight into common liabilities underlying chronic pain and internalizing symptomology in middle childhood, parent-offspring associations across chronic pain and internalizing symptomology, and the etiological mechanisms that explain symptom aggregation across generations.
ContributorsOro, Veronica (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Chassin, Laurie (Committee member) / Davis, Mary (Committee member) / Su, Jinni (Committee member) / Arizona State University (Publisher)
Created2021