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- Creators: Arizona State University
- Creators: Shiota, Michelle
- Resource Type: Text
- Status: Published
Description
The purpose of the current study was to use structural equation modeling-based quantitative genetic models to characterize latent genetic and environmental influences on proneness to three discrete negative emotions in middle childhood, according to mother-report, father-report and in-home observation. One primary aim was to test the extent to which covariance among the three emotions could be accounted for by a single, common genetically- and environmentally-influenced negative emotionality factor. A second aim was to examine the extent to which different reporters appeared to be tapping into the same genetically- and environmentally-influenced aspects of each emotion. According to mother- and father-report, moderate to high genetic influences were evident for all emotions, with mother- and father-report of fear and father-report of anger showing the highest heritability. Significant common environmental influences were also found for mother-report of anger and sadness in both univariate and multivariate models. For observed emotion, anger was moderately heritable with no evidence for common environmental variance, but sadness, object fear and social fear all showed modest to moderate common environmental influences and no significant genetic variance. In addition, cholesky decompositions examining genetic and environmental influences across reporter suggested that despite considerable overlap between mother-report and father-report, there was also reporter-specific variance on anger, sadness, and fear. Specifically, there were significant common environmental influences on mother-report of anger- and sadness that were not shared with father-report, and genetic influences on father-report of sadness and fear that were not shared with mother-report. In-home observations were not highly correlated enough with parent-report to support multivariate analysis for any emotion. Finally, according to both mother- and father-report, a single set of genetic and environmental influences was sufficient to account for covariance among all three negative emotions. However, fear was primarily explained by genetic influences not shared with other emotions, and anger also showed considerable emotion-specific genetic variance. In both cases, findings support the value of a more emotion-specific approach to temperament, and highlight the need to consider distinctions as well as commonalities across emotions, reporters and situations.
ContributorsClifford, Sierra (Author) / Lemery, Kathryn (Thesis advisor) / Shiota, Michelle (Committee member) / Eisenberg, Nancy (Committee member) / Arizona State University (Publisher)
Created2013
Description
A variety of studies have shown that the tendency toward nicotine dependence has a genetic component. The work described in this thesis addresses three separate questions: i) are there unidentified SNPs in the nicotinic receptors or other genes that contribute to the risk for nicotine dependence; ii) is there evidence of ongoing selection at nicotinic receptor loci; and, iii) since nicotine dependence is unlikely to be the phenotype undergoing selection, is a positive effect on memory or cognition the selected phenotype. I first undertook a genome –wide association scan of imputed data using samples from the Collaborative Study of the Genetics of Nicotine Dependence (COGEND). A novel association was found between nicotine dependence and SNPs at 13q31. The genes at this newly associated locus on chromosome 13 encode a group of micro-RNAs and a member of the glypican gene family. These are among the first findings to implicate a non-candidate gene in risk for nicotine dependence. I applied several complimentary methods to sequence data from the 1000 Genomes Project to test for evidence of selection at the nicotinic receptor loci. I found strong evidence for selection for alleles in the nicotinic receptor cluster on chromosome 8 that confer risk of nicotine dependence. I then used the dataset from the Collaborative Studies on the Genetics of Alcoholism (COGA) and looked for an association between neuropsychological phenotypes and SNPs conferring risk of nicotine dependence. One SNP passed multiple test correction for association with WAIS digit symbol score. This SNP is not itself associated with nicotine dependence but is in reasonable (r 2 = 0.75) LD with SNPs that are associated with nicotine dependence. These data suggest at best, a weak correlation between nicotine dependence and any of the tested cognitive phenotypes. Given the reproducible finding of an inverse relationship between SNPs associated with risk for nicotine dependence and cocaine dependence, I hypothesize that the apparently detrimental phenotype of nicotine dependence may confer decreased risk for cocaine dependence. As cocaine use impairs the positive rewards associated with social interactions, reducing the risk of cocaine addiction may be beneficial to both the individual and the group.
ContributorsSadler, Brooke (Author) / Hurtado, Ana Magdalena (Thesis advisor) / Goate, Alison (Thesis advisor) / Hill, Kim (Committee member) / Nagoshi, Craig (Committee member) / Arizona State University (Publisher)
Created2014
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
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
Sport is a widespread phenomenon across human cultures and history. Unfortunately, positive emotions in sport have been long vaguely characterized as happy or pleasant, or ignored altogether. Recent emotion research has taken a differentiated approach, however, suggesting there are distinct positive emotions with diverse implications for behavior. The present study applied this evolutionarily informed approach in the context of sport to examine which positive emotions are associated with play. It was hypothesized that pride, amusement, and enthusiasm, but not contentment or awe, would increase in Ultimate Frisbee players during a practice scrimmage. Further, it was hypothesized that increases in pride and amusement during practice would be differentially associated with sport outcomes, including performance (scores, assists, and defenses), subjective social connectedness, attributions of success, and attitudes toward the importance of practice. It was found that all positive emotions decreased during practice. It was also found that increases in pride were associated with more scores and greater social connectedness, whereas increases in amusement were associated with more assists. The present study was one of the first to examine change in positive emotions during play and to relate them to specific performance outcomes. Future studies should expand to determine which came first: emotion or performance.
ContributorsKuna, Jacob Anthony (Author) / Shiota, Michelle (Thesis director) / Glenberg, Arthur (Committee member) / Danvers, Alexander (Committee member) / Barrett, The Honors College (Contributor) / Department of Psychology (Contributor)
Created2014-05
Description
The purpose of this study was to examine the effects of two positive discrete emotions, awe and nurturant love, on implicit prejudices. After completing an emotion induction task, participants completed Implicit Association Test blocks where they paired photos of Arab and White individuals with "good" and "bad" evaluations. We hypothesized that nurturant love would increase the strength of negative evaluations of Arab individuals and positive evaluations of White individuals, whereas awe would decrease the strength of these negative evaluations when compared to a neutral condition. However, we found that both awe and nurturant love increased negative implicit prejudices toward Arab individuals when compared to the neutral condition.
ContributorsCarrasco, Mia Annette (Author) / Shiota, Michelle (Thesis director) / O'Neil, Makenzie (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
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
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
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