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- All Subjects: psychology
- Genre: Academic theses
- Creators: Lemery-Chalfant, Kathryn
- Member of: ASU Electronic Theses and Dissertations
Description
The interplay of genes and environment on children's development is a complex dynamic process. As behavior geneticists begin to model protective as well as risk factors, and interactive as well as main effect influences, development is elucidated. It was hypothesized that positive parenting, a quality home environment, and high family cohesion would moderate the heritability of three components of temperament: Effortful Control, Negative Affectivity, and Extraversion/Surgency. Participants were drawn from the Wisconsin Twin Project and consisted of 1573 twins (51% boys), 88.5% Caucasian, M=7.93 years (SD=0.87). Higher order composites for the parenting and family environment moderators were formed from mother and father reports of Behavior Management Self-Assessment, Child Rearing Practices Report, Family Assessment Device, and Family Conflict Scale. Measures of the home environment (LEOS Living Environment Observation Scale and CHAOS Confusion, Hubbub, and Order Scale) were not composited due to the nature of the variables. Correlational analyses showed a majority of the temperament and environmental measures to be correlated (rs = -.49-.57). For Effortful Control, Negative Affectivity, and Extraversion/Surgency, estimates for the heritability and nonshared environment were 0.60 and 0.40, 0.80 and 0.20, and 0.59 and 0.41, respectively, with no significant main effects of the shared environment. Models incorporating environmental moderation of these estimates yielded parenting as a significant moderator for Negative Affectivity, LEOS for Effortful Control and Extraversion/Surgency, and CHAOS for Effortful Control and Extraversion/Surgency. Results suggest that the quality of the family environment may act as a permissive or determinative influence on the heritability and expression of temperament. Future analyses include the examination of interactive genetic influences. These findings underscore the importance of shared environment, and support the recent literature on the benefits of positive influences on children's development.
ContributorsKao, Karen (Author) / Bradley, Robert H. (Thesis advisor) / Lemery-Chalfant, Kathryn (Thesis advisor) / Nagoshi, Craig (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
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
The hypothalamus pituitary adrenal (HPA) axis and the human genome are important components of the biological etiology of externalizing disorders. By studying the associations between specific genetic variants, diurnal cortisol, and externalizing symptoms we can begin to unpack this complex etiology. It was hypothesized that genetic variants from the corticotropine releasing hormone receptor 1 (CRHR1), FK506 binding protein 51 (FKBP5), catechol-O-methyl transferase (COMT), and dopamine transporter (DAT1) genes and diurnal cortisol intercepts and slopes would separately predict externalizing symptoms. It was also hypothesized that genetic variants would moderate the association between cortisol and externalizing. Participants were 800 twins (51% boys), 88.5% Caucasian, M=7.93 years (SD=0.87) participating in the Wisconsin Twin Project. Hierarchical Linear Modeling (HLM) was used to separate the variance associated with state and trait cortisol measured across three consecutive days and trait cortisol measures were used. There were no main effects of genes on externalizing symptoms. The evening cortisol intercept, the morning cortisol slope and the evening cortisol slope predicted externalizing, but only in boys, such that boys with higher cortisol and flatter slopes across the day also had more externalizing symptoms. The morning cortisol intercept and CRHR1 rs242924 interacted to predict externalizing in both boys and girls, with GG carriers significantly higher compared to TT carriers at one standard deviation below the mean of morning cortisol. For boys only there was a significant interaction between the DAT1 variable number tandem repeat (VNTR) and the afternoon slope and a significant slope for 9/9 carriers and 9/10 carriers such that when the slope was more steep, boys carrying a nine had fewer externalizing symptoms but when the slope was less steep, they had more. Results confirm a link between diurnal trait cortisol and externalizing in boys, as well as moderation of that association by genetic polymorphisms. This is the first study to empirically examine this association and should encourage further research on the biological etiology of externalizing disorder symptoms.
ContributorsSwann, Gregory (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Chassin, Laurie (Committee member) / Doane-Sampey, Leah (Committee member) / Arizona State University (Publisher)
Created2012
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
Background: Premature infants may be at risk for lower effortful control, and subsequent lower academic achievement, peer competence, and emotional and physical wellness throughout the lifespan. However, because prematurity is related to obstetrical and neonatal complications, it is unclear what may drive the effect. Effortful control also has a strong heritable component; therefore, environmental factors during pregnancy and the neonatal period may interact with genetic factors to predict effortful control development. In this study, I aimed to dissect the influences of genetics, prematurity, and neonatal and obstetrical complications on the development of effortful control from 12 months to 10 years using a twin cohort. Methods: This study used data from the Arizona Twin Project, an ongoing longitudinal study of approximately 350 pairs of twins. Twins were primarily Hispanic/Latinx (23.8%-27.1%) and non-Hispanic/Latinx White (53.2%-57.8%), and families ranged in socioeconomic status with around one-third falling below or near the poverty line. Of the twins, 62.6% were born prematurely. Effortful control was assessed via parent report at six waves. Results: There was not a significant relationship between gestational age and effortful control regardless of whether obstetrical and neonatal complications were controlled for. Biometric twin modeling revealed that the attentional focusing subdomain of effortful control was highly heritable. Gestational age did not moderate genetic and environmental estimates. Conclusions: The findings help inform the risk assessment of prematurity and provide evidence for differing etiology of each subdomain of effortful control and the strong role of genetics in effortful control development.
ContributorsPickett, Janna (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Su, Jinni (Committee member) / Eggum, Natalie D (Committee member) / Arizona State University (Publisher)
Created2023
Description
Aggressive and violent behavior is expressed differently across development, but for some adolescents, this behavior leads to criminal justice involvement through arrests and incarceration. Further, according to the biopsychosocial model, aggressive behavior is influenced by both genetics and the environment. This study sought to examine the differential impacts of early childhood environmental cumulative risk and genetic risk on the developmental cascade from middle childhood behavioral aggression and lack of control to adolescent antisocial behavior or callous-unemotional traits, to emerging adult involvement with the criminal justice system, and whether the effects of risk were mitigated by receiving the Family Check-Up (FCU) prevention program in childhood. The sample included high-risk youth (N = 731; 50% female, 50% White, 28% Black, 13% Hispanic, 9% Indigenous, Native Hawaiian, or Asian; of these 13% were multiracial; Mincome = $28,993; representative 515 genotyped) involved in a randomized-controlled trial of the Family Check-Up and followed longitudinally across 11 waves from ages 2 through 19 years. Behavioral measures included parent-report of behavioral aggression and observational lack of control in middle childhood, self-report of antisocial behavior and callous-unemotional (CU) traits in adolescence, and self-report of involvement with the legal system at age 19. Results of longitudinal structural equation modeling (SEM) supported a developmental cascade from middle childhood behavioral aggression to antisocial behavior in adolescence to legal system involvement. Early cumulative environmental risk and polygenic risk tolerance (RT PGS) significantly predicted involvement with the legal system at age 19, while RT PGS also predicted antisocial behavior in adolescence. Further, intervention effects were found for the FCU, such that the FCU disrupted the effects of RT PGS and middle childhood aggression on antisocial behavior and CU traits in adolescence. This study showed that the FCU can mitigate polygenic risk, supporting the benefit of early psychosocial prevention programs. Importantly, this study showed initial evidence that prevention programs targeting early childhood conduct problems could potentially reduce rates of justice system involvement, including arrests and incarceration, by the age of 19.
ContributorsOstner, Savannah Grace (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Tein, Jenn-Yun (Committee member) / Davis, Mary C (Committee member) / Arizona State University (Publisher)
Created2024
Description
This study investigated whether the patterns of direct association, and of gene-environment interaction (GxE), between family variables (i.e., parenting, family conflict, and attitudinal familism) and youth externalizing behaviors differed across racial/ethnic groups. The sample was composed of 772 twin pairs from the Adolescent Brain Development Study (ABCD) and analyses were run on three racial/ethnic groups (White [n=1023], Black/African American [n=220], Hispanic [n=152]; Mage=10.14 years). Youth reports of parental warmth, parental monitoring, family conflict, parent-reported attitudinal familism, and parent reports of youth externalizing behaviors were collected at baseline when children were 10 years old. Regression analyses tested the direct association between the family variables and youth externalizing behaviors, and moderated heritability models tested for GxE. Family conflict was associated with more externalizing behaviors for White youth, and parental warmth was associated with fewer externalizing behaviors for Hispanic youth. Parental attitudinal familism composite and familism support were associated with fewer externalizing behaviors for Black youth but more externalizing behaviors for Hispanic youth. We found no effects for parental monitoring, familism obligations, and familism referent on youth externalizing behaviors. Additive genetic and non-shared environmental influences explained the variance in youth externalizing behaviors across all groups. For White youth, parental warmth, parental monitoring, and familism support moderated additive genetic (A), shared-environmental (C), and non-shared environmental (E) influences on externalizing behaviors, and familism obligations moderated C and E influences. Results from exploratory moderated heritability analyses conducted for the Black/African American and Hispanic samples are discussed. Altogether, these findings highlight the multiple avenues through which the family context can impact the development of youth externalizing behaviors, and reinforce the need to examine how these relations differ across racial/ethnic groups.
ContributorsTrevino, Angel Daniel (Author) / Su, Jinni (Thesis advisor) / Lemery-Chalfant, Kathryn (Committee member) / Causadias, Jose (Committee member) / Arizona State University (Publisher)
Created2023
Description
The tendency for psychopathology to aggregate within families is well-documented, though little is known regarding the level of specificity at which familial transmission of symptomology occurs. The current study first tested competing higher-order structures of psychopathology in adolescence, indexing general and more specific latent factors. Second, parent-offspring transmission was tested for broadband domain specificity versus transmission of a general liability for psychopathology. Lastly, genetic and environmental mechanisms underlying the familial aggregation of psychopathology were examined using nuclear twin-family models. The sample was comprised of five hundred adolescent twin pairs (mean age 13.24 years) and their parents drawn from the Wisconsin Twin Project. Twins and parents completed independent diagnostic interviews. For aim 1, correlated factors, bifactor, and general-factor models were tested using adolescent symptom count data. For aim 2, structural equation modeling was used to determine whether broadband domain-specific transmission effects were necessary to capture parent-offspring resemblance in psychopathology above and beyond a general transmission effect indexed by the latent correlation between a parental internalizing factor and offspring P-factor. For aim 3, general factor models were fitted in both generations, and factor scores were subsequently extracted and used in nuclear twin-family model testing. Results indicated that the bifactor model exhibited the best fit to the adolescent data. Familial aggregation of psychopathology was sufficiently accounted for by the transmission of a general liability. Lastly, the best fitting reduced nuclear twin-family model indicated that additive genetic, sibling-specific shared environmental, and nonshared environmental influences contributed to general psychopathology. Parent-offspring transmission was accounted for by shared genetics only, whereas co-twin aggregation was additionally explained by sibling-specific shared environmental factors. Results provide novel insight into the specificity and etiology of the familial aggregation of psychopathology.
ContributorsOro, Veronica (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Chassin, Laurie (Committee member) / Doane, Leah D (Committee member) / Arizona State University (Publisher)
Created2019
Description
The present study utilized longitudinal data from a high-risk community sample (n=254, 52.8% female, 47.2% children of alcoholics, 74% non-Hispanic Caucasian) to test questions concerning the effects of genetic risk, parental knowledge, and peer substance use on emerging adult substance use disorders (SUDs). Specifically, this study examined whether parental knowledge and peer substance use mediated the effects of parent alcohol use disorder (AUD) and genetic risk for behavioral undercontrol on SUD. The current study also examined whether genetic risk moderated effects of parental knowledge and peer substance use on risk for SUD. Finally, this study examined these questions over and above a genetic "control" which explained a large proportion of variance in the outcome, thereby providing a stricter test of environmental influences.
Analyses were performed in a path analysis framework. To test these research questions, the current study employed two polygenic risk scores. The first, a theory-based score, was formed using single-nucleotide polymorphisms (SNPs) from receptor systems implicated in the amplification of positive effects in the presence of new/exciting stimuli and/or pleasure derived from using substances. The second, an empirically-based score, was formed using a data-driven approach that explained a large amount of variance in SUDs. Together, these scores allowed the present study to test explanations for the relations among parent AUD, parental knowledge, peer substance use, and SUDs.
Results of the current study found that having parents with less knowledge or an AUD conferred greater risk for SUDs, but only for those at higher genetic risk for behavioral undercontrol. The current study replicated research findings suggesting that peer substance use mediated the effect of parental AUD on SUD. However, it adds to this literature by suggesting that some mechanism other than increased behavioral undercontrol explains relations among parental AUD, peer substance use, and emerging adult SUD. Taken together, these findings indicate that children of parents with AUDs comprise a particularly risky group, although likelihood of SUD within this group is not uniform. These findings also suggest that some of the most important environmental risk factors for SUDs exert effects that vary across level of genetic propensity.
Analyses were performed in a path analysis framework. To test these research questions, the current study employed two polygenic risk scores. The first, a theory-based score, was formed using single-nucleotide polymorphisms (SNPs) from receptor systems implicated in the amplification of positive effects in the presence of new/exciting stimuli and/or pleasure derived from using substances. The second, an empirically-based score, was formed using a data-driven approach that explained a large amount of variance in SUDs. Together, these scores allowed the present study to test explanations for the relations among parent AUD, parental knowledge, peer substance use, and SUDs.
Results of the current study found that having parents with less knowledge or an AUD conferred greater risk for SUDs, but only for those at higher genetic risk for behavioral undercontrol. The current study replicated research findings suggesting that peer substance use mediated the effect of parental AUD on SUD. However, it adds to this literature by suggesting that some mechanism other than increased behavioral undercontrol explains relations among parental AUD, peer substance use, and emerging adult SUD. Taken together, these findings indicate that children of parents with AUDs comprise a particularly risky group, although likelihood of SUD within this group is not uniform. These findings also suggest that some of the most important environmental risk factors for SUDs exert effects that vary across level of genetic propensity.
ContributorsBountress, Kaitlin (Author) / Chassin, Laurie (Thesis advisor) / Crnic, Keith (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / MacKinnon, David (Committee member) / Arizona State University (Publisher)
Created2015