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- All Subjects: Genetics
- All Subjects: Parent and child
- 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
The current study delineated the developmental trajectories of early childhood externalizing and internalizing symptoms reported by mothers and fathers, and examined the role of the 18-month observed parenting quality × Respiratory Sinus Arrhythmia
(RSA) interaction in predicting these trajectories. Child sex was tested as a covariate and moderator. It was found that children's low baseline RSA or high RSA reactivity , in comparison to high baseline RSA or low RSA reactivity , was more reactive as a function
of early parenting quality when predicting the development of early childhood problem symptoms. Differential patterns of the interaction between parenting quality and RSA were detected for mothers' and fathers' reports. Mother-reported models showed a diathesis-stress pattern, whereas the father-reported model showed a vantage-sensitivity pattern, especially for internalizing symptoms. This may imply the potential benefit of fathers' active engagement in children's early development. In addition, the effect of the parenting quality × RSA interaction in predicting the mother-reported models was found
to be further moderated by child sex. Specifically, the parenting quality × baseline RSA interaction was significantly predictive of girls' 54-month internalizing, and the parenting quality × RSA reactivity interaction significantly predicted boys' internalizing slope. Girls with low baseline RSA or boys with high RSA reactivity were vulnerable to the less positive parenting, exhibiting high levels of 54-month internalizing symptoms or slow decline in internalizing over time, respectively. Future research directions were discussed in terms of integrating the measures of SNS and PNS in psychopathology study,
exploring the mechanisms underlying the sex difference in parenting quality × RSA interaction, and comparing the findings of children's typical and atypical development.
(RSA) interaction in predicting these trajectories. Child sex was tested as a covariate and moderator. It was found that children's low baseline RSA or high RSA reactivity , in comparison to high baseline RSA or low RSA reactivity , was more reactive as a function
of early parenting quality when predicting the development of early childhood problem symptoms. Differential patterns of the interaction between parenting quality and RSA were detected for mothers' and fathers' reports. Mother-reported models showed a diathesis-stress pattern, whereas the father-reported model showed a vantage-sensitivity pattern, especially for internalizing symptoms. This may imply the potential benefit of fathers' active engagement in children's early development. In addition, the effect of the parenting quality × RSA interaction in predicting the mother-reported models was found
to be further moderated by child sex. Specifically, the parenting quality × baseline RSA interaction was significantly predictive of girls' 54-month internalizing, and the parenting quality × RSA reactivity interaction significantly predicted boys' internalizing slope. Girls with low baseline RSA or boys with high RSA reactivity were vulnerable to the less positive parenting, exhibiting high levels of 54-month internalizing symptoms or slow decline in internalizing over time, respectively. Future research directions were discussed in terms of integrating the measures of SNS and PNS in psychopathology study,
exploring the mechanisms underlying the sex difference in parenting quality × RSA interaction, and comparing the findings of children's typical and atypical development.
ContributorsLi, Yi (Author) / Eisenberg, Nancy (Thesis advisor) / Spinrad, Tracy (Thesis advisor) / Lemery-Chalfant, Kathryn (Committee member) / Wilkens, Natalie (Committee member) / Arizona State University (Publisher)
Created2014
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 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
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
This study examined whether social support available to parents moderated the heritability of parent-reported social approach at 12 months (N = 286 twin pairs, 52.00% female) and social competence at 30 months (N = 259 twin pairs, 53.30% female). Genetic and environmental covariance across age is also reported. Social support consistently moderated genetic influences on children’s social approach and competence, such that heritability was highest when parents reported low social support. Shared environment was not moderated by social support and explained continuity across age. Findings provide further evidence that genetic and environmental influences on development vary across context. When parents are supported, environmental influences on children’s social competence are larger, perhaps because support helps parents provide a broadly promotive environment.
ContributorsClifford, Sierra (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Doane, Leah (Committee member) / Shiota, Michelle (Committee member) / Grimm, Kevin (Committee member) / Arizona State University (Publisher)
Created2017
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
Several decades of research have concluded that child social functioning is a critical predictor of wellbeing across various developmental domains. Most scientists agree that both genetic and environmental influences play defining roles in social behavior; the processes by which they concurrently affect child development, however, has been the subject of less research. This work examines distinct mechanisms that shape child prosociality by examining genetic and environmental influences on development, via two empirical studies. The first study analyzed the evocative-reactive and the evocative-socially-mediated hypotheses as gene-environment correlation (rGE) mechanisms connecting the arginine vasopressin receptor 1a (AVPR1a) and dopamine receptor D2 (DRD2) genes, child prosocial behavior, and parent differential treatment (PDT). Findings present modest evidence for the evocative-reactive rGE hypothesis; specifically, AVPR1a marginally influenced child prosociality, which subsequently predicted mother preference in adolescence. The second study examined several gene-environment interactions (GxEs) in exploring how social environmental variables- positive and negative parenting- predicted child prosociality, as moderated by socially-implicated child genes, DRD2 and dopamine receptor D4 (DRD4). Findings indicated that while positive parenting was predictive of child prosociality regardless of genetic variants, the effects of negative parenting on child prosociality were dependent on child genetic variants. Together, findings from these studies suggest modest genetic and environmental influences on child behavior in middle childhood and adolescence, consistent with previous research and theory. Directions for future research are offered, and intervention and policy implications are discussed.
ContributorsMeek, Shantel E (Author) / Jahromi, Laudan B (Thesis advisor) / Lemery-Chalfant, Kathryn (Thesis advisor) / Valiente, Carlos (Committee member) / Iida, Masumi (Committee member) / Arizona State University (Publisher)
Created2013