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- All Subjects: Genetics
- Creators: Lemery-Chalfant, Kathryn
- Creators: Chassin, Laurie
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 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
It has been theorized that cultural variation within the family shapes children’s self-regulatory competence, yet there is a dearth of research examining the relation between culture and self-regulation. Family orientation refers to the emphasis on providing support, respect, and obligation to the family system, and is important for children’s functioning, yet existing literature on related constructs relies on parent-reported measures. Additionally, quantitative genetic research has neglected the role of culture in the genetic and environmental contributions on children’s self-regulation. There were three main aims of this study: 1) to propose novel coding schemes and factor analytic approaches to capture family orientation, 2) to examine the relation between family orientation and self-regulation in middle childhood, and 3) to examine whether family orientation moderates the genetic and environmental influences on self-regulation in middle childhood. The sample was drawn from the Arizona Twin Project (N=710) where children (49.1% female, 55.6% White, 28.3% Hispanic/Latino) were assessed at approximately eight years of age (Mage = 8.38 years, SD = 0.66). Family orientation values were indexed by parent-reported familism, whereas family orientation behaviors comprised coded measures of children’s family orientation and experimenter ratings of caregiver and child behavior. Outcome measures of self-regulation included the Continuous Performance Task, Flanker Task, Digit Span Backward, and parent- and teacher-reported effortful control (Temperament in Middle Childhood Questionnaire). Higher family orientation behaviors predicted positively predicted children’s self-regulation, with the exception of Digit Span Backward performance, and associations were not moderated by child sex, family SES, or race/ethnicity. Twin models revealed that differences in family orientation behaviors could be attributed to genetic, shared, and nonshared environmental influences, and additive genetic and nonshared environmental influences explained the variation across measures of self-regulation. Finally, there was no evidence that family orientation values nor behaviors moderated the genetic or environmental influences on children’s self-regulation. This study highlights the complex nature of cultural variation within the family and its importance for children’s self-regulatory abilities.
ContributorsRea-Sandin, Gianna (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Doane, Leah D (Committee member) / Causadias, Jose (Committee member) / Grimm, Kevin J (Committee member) / Arizona State University (Publisher)
Created2022
Description
Pediatric chronic pain is pervasive and associated with myriad adverse consequences, yet due consideration has not been given to the mental health disturbances that often present alongside chronic pain and the etiological mechanisms that potentially underlie both. The current study examined the etiology underlying chronic pain and internalizing symptomology in middle childhood, considering both independent and co-occurring symptom presentations. Phenotypic parent-offspring associations across chronic pain and internalizing symptomology were also examined. Lastly, nuclear twin family models were tested to determine the extent to which genetic and environmental factors underlie parent-offspring transmission. The sample comprised 795 children (399 families; Mage= 9.7 years; SD = 0.92) and their parents drawn from the Arizona Twin Project. Results indicated that chronic pain was highly heritable (78%), whereas internalizing symptomology was modestly heritable (32%) and further subject to moderate shared environmental influence (50%). Moreover, 9% of the variance in chronic pain was explained by additive genetic factors shared with internalizing symptomology. Maternal chronic pain and internalizing symptomology were positively associated with both child chronic pain and internalizing symptomology. The association between maternal chronic pain and child chronic pain was more pronounced for girls than boys, whereas the association between maternal internalizing symptomology and child internalizing symptomology was more pronounced for boys than girls. Paternal chronic pain was not significantly associated with child chronic pain but was unexpectedly associated with lower child internalizing symptomology. The negative association between paternal chronic pain and child internalizing symptomology was more pronounced for boys than girls. Paternal internalizing symptomology was not significantly associated with child chronic pain but was positively associated with child internalizing symptomology. Lastly, the best fitting reduced nuclear twin family models for both chronic pain and internalizing symptomology retained additive genetic, sibling-specific shared environmental, and nonshared environmental parameters, where parent-offspring transmission was solely explained by shared genetics and sibling-specific shared environmental factors further accounted for co-twin resemblance. Results provide novel insight into common liabilities underlying chronic pain and internalizing symptomology in middle childhood, parent-offspring associations across chronic pain and internalizing symptomology, and the etiological mechanisms that explain symptom aggregation across generations.
ContributorsOro, Veronica (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Chassin, Laurie (Committee member) / Davis, Mary (Committee member) / Su, Jinni (Committee member) / Arizona State University (Publisher)
Created2021
Description
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
Although substantial research has examined individual, family, and peer factors that contribute to predicting adolescent alcohol use, limited attention has been devoted to the unique role of romantic partners and little consideration has been given to the potential importance of romantic relationship seriousness. Data from Waves I and II of the National Longitudinal Study of Adolescent Health (Add Health) were used to assess the relation between romantic relationship seriousness and binge drinking and drinking consequences one year later among 14-18 year-olds (n= 928 adolescents; 54.1% female). Main effects of relationship seriousness and moderating effects of adolescent age, partner age, adolescent age by partner age, parental alcoholism, and gender were examined separately for each drinking outcome using zero-inflated Poisson regression (ZIP) models. Relationship seriousness and study covariate interactions were also examined. ZIP models estimate (a) a logistic regression that distinguishes between individuals whose values can only be zero on the outcome (i.e., a structural zero class) and individuals with count values ranging from zero to any other positive integer (i.e., a non-structural zero class), and (b) a Poisson regression predicting count values among the non-structural zero class. Results showed trends towards significance for relations between relationship seriousness and binge drinking and drinking consequences among non-structural zero classes. As hypothesized, increased relationship seriousness predicted less frequent binge drinking and fewer drinking consequences. The relation between relationship seriousness and binge drinking was moderated by peer alcohol use; the negative relation between relationship seriousness and binge drinking frequency was significant among adolescents who reported 0-2, but not 3, close friends who drink. The relation between relationship seriousness and number of drinking consequences was moderated by gender, adolescent delinquency (covariate), peer alcohol use (covariate), and Wave I drinking consequences (control variable). Specifically, a significant relation between relationship seriousness and number of drinking consequences was revealed only for females and only for adolescents who reported high consequences at Wave I, and was significant among adolescents who reported 0-2 close friends who drink and low delinquency. Results indicate that relationship seriousness can protect adolescents in terms of drinking outcomes, which could have implications for prevention efforts.
ContributorsCarr, Colleen (Author) / Wolchik, Sharlene (Thesis advisor) / Chassin, Laurie (Thesis advisor) / Dishion, Thomas (Committee member) / Tein, Jenn-Yun (Committee member) / Arizona State University (Publisher)
Created2016
Description
The present study tested the respective mediating effects of sensation seeking and initial level of response (LR) to negative, sedative alcohol effects on the relation between the density of familial history of alcoholism and adolescent alcohol use. Additionally, the present study tested the direct effect of LR to negative, sedative alcohol effects on adolescent drinking over and above the effects of sensation seeking; and also tested the moderating effect of sensation seeking on the relation between level of response negative, sedative alcohol effects and adolescent drinking. Specifically, OLS regression models first estimated the effects of sensation seeking, LR to negative, sedative alcohol effects, and their interaction on alcohol outcomes, over and above the influence of covariates. Indirect effects were then tested using the PRODCLIN method through RMediation. Analyses failed to support sensation seeking as a mediator in the relation between familial history of alcoholism and adolescent drinking, and as a moderator of the relation between LR and adolescent drinking. However, analyses did support a robust direct effect of LR to negative, sedative alcohol effects on adolescent alcohol involvement. A significant mediating effect of initial LR to negative, sedative alcohol effects on the relation between familial alcoholism and adolescent drinking was found, however failed to maintain significance in post-hoc analyses attenuating the downward bias of the measure of initial LR. Initial LR to negative, sedative alcohol effects continued to predict adolescent drinking after attenuating measure bias. These findings strengthen research on initial LR to negative, sedative alcohol effects as a risk for greater alcohol involvement in adolescence, and underscore the complexity of studying the familial transmission of alcoholism in adolescent populations
ContributorsPandika, Danielle (Author) / Chassin, Laurie (Thesis advisor) / Corbin, William (Committee member) / Aiken, Leona (Committee member) / Arizona State University (Publisher)
Created2015
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