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- All Subjects: Genetics
- All Subjects: Temperament in children
- Genre: Academic theses
- Creators: Lemery-Chalfant, Kathryn
- Member of: ASU Electronic Theses and Dissertations
- Resource Type: Text
Description
Using data from an eight-year longitudinal study of 214 children's social and emotional development, I conducted three studies to (1) examine patterns of agreement for internalizing (INT) and externalizing (EXT) symptomatology among different informants (mothers, fathers, teachers, and adolescents) using a recently developed structural equation modeling approach for multi-trait, multi-method data; (2) examine the developmental trajectories for INT and EXT and predict individual differences in symptom development using temperament and parenting variables; and (3) describe patterns of INT and EXT co-occurrence and predict these patterns from temperament and parenting. In Study 1, longitudinal invariance was established for mothers', fathers' and teachers' reports over a six-year period. Sex, age, and SES did not substantially moderate agreement among informants, although both sex and age were differentially related to symptomatology depending on the informant. Agreement among teachers and mothers, but not among mothers and fathers, differed by domain of symptomatology, and was greater for EXT than for INT. In Study 2, latent profile analysis, a person-centered analytic approach, did not provide easily interpretable patterns of symptom development, a failure that is likely the result of the relatively modest sample size. Latent growth curve models, an alternative analytic approach, did provide good fit to the data. Temperament and parenting variables were examined as predictors of the latent growth parameters in these models. Although there was little prediction of the slope, effortful control was negatively related to overall levels of EXT, whereas impulsivity and anger were positively related. Mutually responsive orientation, a measure of the parent-child relationship, was a more consistent predictor of EXT than was parental warmth. Furthermore, the relation between mutually responsive orientation and EXT was partially mediated by inhibitory control. Across informants, there were few consistent predictors of INT. In Study 3, latent profile analysis was used to classify individuals into different patterns of INT and EXT co-occurrence. In these models, a similar class structure was identified for mothers and for teachers. When temperament and parenting were examined as predictors of co-occurring symptomatology, few significant interactions were found and results largely replicated prior findings from this data set using arbitrary symptom groups.
ContributorsSulik, Michael John (Author) / Eisenberg, Nancy (Thesis advisor) / Spinrad, Tracy L (Thesis advisor) / Lemery-Chalfant, Kathryn (Committee member) / Wolchik, Sharlene A (Committee member) / Arizona State University (Publisher)
Created2013
Description
Fibromyalgia (FM) is a chronic musculoskeletal disorder characterized by widespread pain, fatigue, and a variety of other comorbid physiological and psychological characteristics, including a deficit of positive affect. Recently, the focus of research on the pathophysiology of FM has considered the role of a number of genomic variants. In the current manuscript, case-control analyses did not support the hypothesis that FM patients would differ from other chronic pain groups in catechol-O-methyltransferase (COMT) and mu-opioid receptor (OPRM1) genotype. However, evidence is provided in support of the hypothesis that functional single nucleotide polymorphisms on the COMT and OPRM1 genes would be associated with risk and resilience, respectively, in a dual processing model of pain-related positive affective regulation in FM. Forty-six female patients with a physician-confirmed diagnosis of FM completed an electronic diary that included once-daily assessments of positive affect and soft tissue pain. Multilevel modeling yielded a significant gene X environment interaction, such that individuals with met/met genotype on COMT experienced a greater decline in positive affect as daily pain increased than did either val/met or val/val individuals. A gene X environment interaction for OPRM1 also emerged, indicating that individuals with at least one asp allele were more resilient to elevations in daily pain than those homozygous for the asn allele. In sum, the findings offer researchers ample reason to further investigate the contribution of the catecholamine and opioid systems, and their associated genomic variants, to the still poorly understood experience of FM.
ContributorsFinan, Patrick Hamilton (Author) / Zautra, Alex (Thesis advisor) / Davis, Mary (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / Presson, Clark (Committee member) / Arizona State University (Publisher)
Created2011
Description
Externalizing behaviors are pervasive, widespread, and disruptive across a multitude of settings and developmental contexts. While the conventional diathesis-stress model typically measures the disordered end of the spectrum, studies that span the range of behavior, from externalizing to competence behaviors, are necessary to see the full picture. To that end, this study examined the additive and nonadditive relations of a dimension of parenting (ranging from warm to rejecting), and variants in dopamine, vasopressin, and neuropeptide-y receptor genes on externalizing/competence in a large sample of predominantly Caucasian twin children in toddlerhood, middle childhood, and early adolescence. Variants within each gene were hypothesized to increase biological susceptibility to both negative and positive environments. Consistent with prediction, warmth related to lower externalizing/higher competence at all ages. Earlier levels of externalizing/competence washed out the effect of parental warmth on future externalizing/competence with the exception of father warmth in toddlerhood marginally predicting change in externalizing/competence from toddlerhood to middle childhood. Warmth was a significant moderator of the heritability of behavior in middle childhood and early adolescence such that behavior was less heritable (mother report) and more heritable (father report) in low warmth environments. Interactions with warmth and the dopamine and vasopressin genes in middle childhood and early adolescence emphasize the moderational role gene variants play in relations between the rearing environment and child behavior. For dopamine, the long variant related to increased sensitivity to parent warmth such that the children displayed more externalizing behaviors when exposed to rejection but they also displayed more competence behaviors when exposed to high warmth. Vasopressin moderation was only present under conditions of parental warmth, not rejection. Interactions with neuropeptide-y and warmth were not significant. The picture that emerges is one of gene-environment interplay, wherein the influence of both parenting and child genotype each depend on the level of the other. As genetic research moves forward, gene variants previously implicated as conferring risk for disorder should be reexamined in conjunction with salient aspects of the environment on the full range of the behavioral outcome of interest.
ContributorsO'Brien, T. Caitlin (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Eisenberg, Nancy (Committee member) / Enders, Craig (Committee member) / Nagoshi, Craig (Committee member) / Arizona State University (Publisher)
Created2011
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 examines the relations among three aspects of temperament (shyness, impulsivity, and effortful control), resting respiratory sinus arrhythmia (RSA) recorded during a calming film and RSA suppression during three behavioral measures of effortful control, and adjustment (anxiety and externalizing behavior) in a sample of 101 preschool-age children. Principal components analysis was used to create composites for effortful control, shyness, impulsivity, anxiety, and externalizing behavior, and hierarchical regression analysis was used to test the study hypotheses. As expected, baseline RSA was negatively related to effortful control in shy children, but was unrelated to effortful control in children who were not shy. It was hypothesized that high baseline RSA would reduce the relation between shyness and anxiety, and between impulsivity and externalizing behavior; this hypothesis was supported for externalizing behavior, but not for anxiety. The interaction between impulsivity and RSA as a predictor of externalizing was statistically independent of effortful control, indicating that these are unique effects. Finally, it was hypothesized that RSA suppression would be positively related to effortful control for children low, but not high, in shyness. There was a marginal interaction between shyness and RSA suppression, with RSA suppression marginally negatively related to EC for children low in shyness, but unrelated to effortful control for children high in shyness; the direction of this association was opposite predictions. These findings indicate that RSA is more strongly related to effortful control for children high in shyness, and that it consequently may not be appropriate to use RSA as an index of EC for all children. This study also draws attention to the need to consider the context in which baseline RSA is measured because a true baseline may not be obtained for shy children if RSA is measured in an unfamiliar laboratory context. The finding that high RSA moderated (but did not eliminate) the relation between impulsivity and externalizing behavior is consistent with the conceptualization of RSA as a measure of self-regulation, but further research is needed to clarify the mechanism underlying this effect.
ContributorsSulik, Michael John (Author) / Eisenberg, Nancy (Thesis advisor) / Spinrad, Tracy L. (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / Arizona State University (Publisher)
Created2012
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
Prior research has established associations between sleep duration and body mass index (BMI) scores and risk for obesity in middle childhood, but it is less clear whether other objectively- and subjectively-measured sleep indicators may be associated with BMI scores, weight status (e.g., obesity), and other estimates of weight and body fat such as waist circumference (WC) and percent body fat. Empirical studies have also demonstrated independent associations between broad self-regulation and sleep indicators and BMI scores, but no study to date has tested these factors in a model together and the extent to which associations between normative sleep problems, weight indicators, and effortful control (EC) may be explained by shared genetic or environmental influences. Data from a large longitudinal study of twins was used to test phenotypic associations between sleep problems at eight years and weight indicators at nine years, including whether EC at eight years moderates these associations. Additionally, multiple quantitative behavior genetic models were used to estimate unique and shared genetic and environmental covariances among normative sleep problems, weight indicators, and EC at eight years of age and whether additive genetic influence on weight in middle childhood differs by child weight status group. Phenotypic findings showed that greater sleep duration at eight years predicted greater decreases BMI at nine years of age for children with low levels of EC at eight years. Greater sleep midpoint variability at eight years predicted greater increases in percent body fat from eight to nine years of age for children with low EC at eight years. Behavior genetic findings showed greater environmental influences on parent-reported sleep duration and quality, as well as objective sleep midpoint variability. Similarly, associations between parent-reported sleep duration and sleep midpoint variability and other sleep indicators and EC were primarily accounted for by shared environmental factors. In contrast, there was high additive genetic influence on objective sleep quantity and quality, all weight indicators, and EC. Many of the associations between sleep indicators, sleep and weight indicators, and among weight indicators were entirely accounted for by shared additive genetic factors, suggesting that common, underlying sets of genes explain these relations.
ContributorsBreitenstein, Reagan Styles (Author) / Doane, Leah D. (Thesis advisor) / Lemery-Chalfant, Kathryn (Committee member) / Perez La Mar, Marisol (Committee member) / Grimm, Kevin (Committee member) / Arizona State University (Publisher)
Created2019
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