Matching Items (9)
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- All Subjects: Genetics
- All Subjects: Individual & Family Studies
- Genre: Academic theses
- Creators: Bradley, Robert
- Creators: Chassin, Laurie
- Member of: ASU Electronic Theses and Dissertations
- Resource Type: Text
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 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
Description
This study drew upon a bioecological framework to empirically investigate the relations between environmental chaos and preschoolers' language across time, including the potentially mediating roles of children's effortful control and parenting. Child sex also was examined as a moderator of these relations. For this study, the following data were collected at 30, 42, and 54 months of age. Household chaos and (at 30 months) socioeconomic status (SES) were reported by mothers. Children's effortful control (EC) was rated by mothers and nonparental caregivers, and was observed during a number of laboratory tasks. Maternal vocalizations were assessed during free play sessions with their children (at 30 and 42 months), and supportive and unsupportive parenting behaviors and affect were observed during free play and teaching tasks at each age. Mothers also reported on their own reactions to children's negative emotions. Finally, (at 54 months) children's expressive and receptive language was measured with a standard assessment. Structural equation modeling and path analyses indicated that SES at 30 months and greater levels of household chaos at 42 months predicted not only poorer language skills, but also deficits in children's EC and less supportive parenting in low-income mothers at 54 months, even when controlling for stability in these constructs. Children's effortful control at 42 months, but not parenting, positively predicted later language, suggesting that EC may play a mediating role in the relations between household chaos, as well as SES, and preschoolers' language abilities. Child sex did not moderate the pattern of relations. Post-hoc analyses also indicated that the negative relation between chaos and language was significant only for children who had low EC at 42 months. This study represents a much-needed addition to the currently limited longitudinal research examining environmental chaos and children's developmental outcomes. Importantly, findings from this study elucidate an important process underlying the links between chaos and children's language development, which can inform interventions and policies designed to support families and children living in chaotic home environments.
ContributorsGaertner, Bridget Maria (Author) / Spinrad, Tracy L. (Thesis advisor) / Eisenberg, Nancy (Committee member) / Hanish, Laura (Committee member) / Bradley, Robert (Committee member) / Arizona State University (Publisher)
Created2012
Description
Understanding how interpersonal relationships, such as parenting and sibling relationships, may contribute to early sleep development is important, as early sleep dysregulation has been shown to impact later sleep behavior (Sadeh & Anders, 1993), as well as cognitive and behavioral functioning (Gregory et al., 2006; Soffer-Dudek et al., 2011). In addition, twin studies provide an optimal opportunity to estimate genetic and environmental contributions to parenting, sibling relationships and child sleep, as they are influenced by both genetic and contextual factors. As such, the current thesis examined whether parental punitive discipline and sibling conflict were associated with child sleep duration, dysregulation and daytime sleepiness at 12 months, 30 months, and five years in a longitudinal sample of young twins recruited through birth records (Lemery-Chalfant et al., 2013). Mixed model regression analyses and quantitative behavioral genetic models (univariate and bivariate) were conducted to explore bidirectional relations and estimate genetic and environmental contributions to parental punitive punishment, sibling conflict and child sleep parameters. Sleep duration and dysregulation showed stability over time. Parental punitive discipline did not predict concurrent or future sleep parameters, nor were there bidirectional relations between punitive discipline and child sleep behaviors. Greater sibling conflict at five years was associated with shorter concurrent child sleep duration and greater daytime sleepiness, suggesting that sibling conflict may be a critical interpersonal stressor that negatively impacts child sleep. Shared environmental factors also accounted for the greatest proportion of the covariance between sibling conflict and sleep duration and daytime sleepiness at five years. These findings hold promise for sleep and sibling interaction interventions, including educating parents about fostering positive sibling relations and teaching caregivers to utilize specific parenting behaviors that may encourage better child sleep behaviors (e.g., establishing bedtime routines). Future studies should aim to understand the nuances of associations between family relationships (like punitive discipline and sibling conflict) and child sleep, as well as other explore person- and family-level factors, such as child negative emotions and parenting, that may influence associations between family relationships and child sleep.
ContributorsBreitenstein, Reagan Styles (Author) / Doane, Leah D (Thesis advisor) / Lemery, Kathryn (Committee member) / Bradley, Robert (Committee member) / Arizona State University (Publisher)
Created2015
Description
This study examined whether early adversity at 30-months moderated the heritability of common and individual components of EF at 8 years. It was hypothesized that early adversity would not moderate the common EF factor, but instead moderate individual EF components. The sample included 208 twin pairs from the Arizona Twin Project. Early Adversity, assessed at 30 months of age, included Parenting Daily Hassles, low perceived MOS social support, punitive punishment (Parental Responses to Child Misbehavior), home chaos (Confusion, Hubbub, and Order Scale), CES-D maternal depression, and low maternal emotional availability. EF at 8 years included the Eriksen Flanker Task, Continuous Performance Task, Digit Span Forward and Backward, and parent-reported Attentional Focusing and Inhibitory Control (Temperament in Middle Childhood Questionnaire). For both early adversity and EF, the first principal components were extracted as composites. A confirmatory factor analysis was also conducted to index common EF. Genetic analyses were tested on the common EF composites as well as each individual task using umx. Univariate models revealed genetic influences on all individual measures and common EF, with broad sense heritability from .22 (Digit Span Backwards) to .61 (parent-reported inhibitory control). Shared environmental influences were found for the Flanker Task (.13) and parent-reported inhibitory control (.24), and E was moderate to high (.40-.73) for all measures except parent-report inhibitory control (.15) and attentional focusing (.31). Moderation of heritability was not observed in for Digit Span Forward, Digit Span Backward, and Attentional Focusing. However, the nonshared environment was moderated for Common EF, and the Flanker Task, and additive genes and the nonshared environment were moderated for the Continuous Performance Task and Inhibitory Control. Generally, total variance decreased as early adversity increased, suggesting that homes with low levels of adversity may allow children to interact with more proximal processes that can promote EF development.
ContributorsRea-Sandin, Gianna (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Elam, Kit (Committee member) / Bradley, Robert (Committee member) / Arizona State University (Publisher)
Created2018
Description
Adolescent substance use carries a considerable public health burden, and early initiation into use is especially problematic. Research has shown that sensation seeking traits increase risk for substance use experimentation, but less is known about individual and contextual factors that can potentially protect against this risk. This study utilized a longitudinal sub sample of youth (N=567) from a larger study of familial alcoholism to examine sensation seeking in early adolescence (ages 10-15) and its relations to later substance use experimentation. Hypotheses tested whether individual executive control, parenting consistency, neighborhood disadvantage, and neighborhood ethnic concentration moderated sensation seeking’s effects on substance use experimentation using multilevel zero-inflated Poisson modeling. Across models, higher levels of sensation seeking were predictive of a higher likelihood of having initiated substance use, but sensation seeking was not significantly related to the number of different substance use classes tried. Only neighborhood disadvantage emerged as a significant moderator of the path from sensation seeking to substance use initiation. The strength of sensation seeking effects on substance use initiation increased as neighborhood disadvantage decreased below average levels, with the most advantaged neighborhoods exhibiting the strongest link between sensation seeking and substance use. There was also a trend towards the most disadvantaged neighborhoods exhibiting increased sensation seeking effects on substance use initiation. These results highlight the importance of focusing on relatively more advantaged areas as potentially risky environments for the externalizing pathway to substance use.
ContributorsJensen, Michaeline R (Author) / Gonzales, Nancy A. (Thesis advisor) / Chassin, Laurie (Thesis advisor) / Enders, Craig (Committee member) / White, Rebecca (Committee member) / Arizona State University (Publisher)
Created2016
Description
In species with highly heteromorphic sex chromosomes, the degradation of one of the sex chromosomes can result in unequal gene expression between the sexes (e.g., between XX females and XY males) and between the sex chromosomes and the autosomes. Dosage compensation is a process whereby genes on the sex chromosomes achieve equal gene expression which prevents deleterious side effects from having too much or too little expression of genes on sex chromsomes. The green anole is part of a group of species that recently underwent an adaptive radiation. The green anole has XX/XY sex determination, but the content of the X chromosome and its evolution have not been described. Given its status as a model species, better understanding the green anole genome could reveal insights into other species. Genomic analyses are crucial for a comprehensive picture of sex chromosome differentiation and dosage compensation, in addition to understanding speciation.
In order to address this, multiple comparative genomics and bioinformatics analyses were conducted to elucidate patterns of evolution in the green anole and across multiple anole species. Comparative genomics analyses were used to infer additional X-linked loci in the green anole, RNAseq data from male and female samples were anayzed to quantify patterns of sex-biased gene expression across the genome, and the extent of dosage compensation on the anole X chromosome was characterized, providing evidence that the sex chromosomes in the green anole are dosage compensated.
In addition, X-linked genes have a lower ratio of nonsynonymous to synonymous substitution rates than the autosomes when compared to other Anolis species, and pairwise rates of evolution in genes across the anole genome were analyzed. To conduct this analysis a new pipeline was created for filtering alignments and performing batch calculations for whole genome coding sequences. This pipeline has been made publicly available.
In order to address this, multiple comparative genomics and bioinformatics analyses were conducted to elucidate patterns of evolution in the green anole and across multiple anole species. Comparative genomics analyses were used to infer additional X-linked loci in the green anole, RNAseq data from male and female samples were anayzed to quantify patterns of sex-biased gene expression across the genome, and the extent of dosage compensation on the anole X chromosome was characterized, providing evidence that the sex chromosomes in the green anole are dosage compensated.
In addition, X-linked genes have a lower ratio of nonsynonymous to synonymous substitution rates than the autosomes when compared to other Anolis species, and pairwise rates of evolution in genes across the anole genome were analyzed. To conduct this analysis a new pipeline was created for filtering alignments and performing batch calculations for whole genome coding sequences. This pipeline has been made publicly available.
ContributorsRupp, Shawn Michael (Author) / Wilson Sayres, Melissa A (Thesis advisor) / Kusumi, Kenro (Committee member) / DeNardo, Dale (Committee member) / Arizona State University (Publisher)
Created2016
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 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.
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
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 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
Description
Sibling relationships are important units of socialization during adolescence. These involuntary relationships consist of positive and negative relationship qualities (Buist & Vermande, 2014; Deater-Deckard et al., 2002; Updegraff et al., 2005a), and some dimensions of these relationships are less understood than other dimensions. One dimension in need of attention is that of sibling relational victimization, which includes behaviors aimed at harming one’s sibling relationship during a period in which interpersonal relationships are developmentally salient (Collins & Steinberg, 2006; Crick, 1995; Crick & Grotpeter, 1995). In my dissertation, I examine the associations between family and friendship dynamics and sibling relational victimization longitudinally during adolescence. In study 1, I examined the developmental change in sibling relational victimization experiences during adolescence, and tested the associations between parent-youth and sibling conflict and intimacy and sibling relational victimization longitudinally. Sibling structural characteristics were explored as moderators. Using longitudinal growth and multi-level modeling, I found that sibling relational victimization decreased across adolescence for both siblings, with younger siblings reporting higher frequency of sibling relational victimization relative to older siblings. On a general level, parent-adolescent and sibling intimacy and conflict were associated with sibling relational victimization, albeit in different ways for mixed- and same-gender dyads and older and younger siblings. Overall, findings from study 1 highlight the importance of examining parent-youth and sibling relationship dynamics, the vulnerability of younger siblings as victims of sibling relational victimization, and the interplay of sibling gender dynamics and father-youth relationships on sibling relational victimization experiences in adolescence.
In study 2, I examined whether sibling relational victimization and negativity moderate the associations between parent-adolescent conflict and friendship control, conflict, and perspective taking in adolescence. Variation by sibling birth order and gender also was explored. Using path analytic models, I found that mother-adolescent, sibling, and friendship dynamics were interlinked, such that mother-adolescent conflict in combination with sibling negativity and sibling relational aggression were associated with friendship outcomes, albeit differently by sibling gender and friendship outcome. Findings from study 2 suggest the importance of addressing negative mother-adolescent and sibling relationship dynamics in prevention and intervention curricula aimed at promoting positive friendship dynamics during adolescence.
ContributorsSarama, Annabella Gallagher (Author) / Updegraff, Kimberly (Thesis advisor) / Kochenderfer-Ladd, Becky (Committee member) / Thompson, Marilyn (Committee member) / Bradley, Robert (Committee member) / Arizona State University (Publisher)
Created2021