Matching Items (3)
Filtering by

Clear all filters

157208-Thumbnail Image.png
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

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
168281-Thumbnail Image.png
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

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
161993-Thumbnail Image.png
Description
Negative Urgency and Positive Urgency are important subfacets of a propensity to rash action. There is currently limited research on parental antecedents of Negative Urgency and Positive Urgency. The current study investigated whether parent personality and parenting behaviors predict adolescent Negative Urgency and Positive Urgency. Data were taken from a

Negative Urgency and Positive Urgency are important subfacets of a propensity to rash action. There is currently limited research on parental antecedents of Negative Urgency and Positive Urgency. The current study investigated whether parent personality and parenting behaviors predict adolescent Negative Urgency and Positive Urgency. Data were taken from a community sample with parent personality, positive parenting behaviors, and child Negative Urgency and Positive Urgency measured at separate timepoints. Structural equation models were used to examine whether parent personality predicted adolescent Negative Urgency and Positive Urgency and whether positive parenting mediated this relationship. There was no evidence for a relationship between parent personality and children’s Negative Urgency and Positive Urgency. In addition, there was no relationship between parenting behaviors and child Negative and Positive Urgency in cross-reporter models, but child-reported parenting predicted later adolescent-reported Negative and Positive Urgency. Greater positive parenting, as perceived by children, was related to less Negative and Positive Urgency when they were adolescents. More research is needed to understand whether the current results are due to reporter bias or whether child-perceived parenting behaviors influence the development of adolescent Negative and Positive Urgency.
ContributorsBui, Leena (Author) / Chassin, Laurie (Thesis advisor) / Corbin, William (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / McNeish, Daniel (Committee member) / Arizona State University (Publisher)
Created2022