ASU Electronic Theses and Dissertations
This collection includes most of the ASU Theses and Dissertations from 2011 to present. ASU Theses and Dissertations are available in downloadable PDF format; however, a small percentage of items are under embargo. Information about the dissertations/theses includes degree information, committee members, an abstract, supporting data or media.
In addition to the electronic theses found in the ASU Digital Repository, ASU Theses and Dissertations can be found in the ASU Library Catalog.
Dissertations and Theses granted by Arizona State University are archived and made available through a joint effort of the ASU Graduate College and the ASU Libraries. For more information or questions about this collection contact or visit the Digital Repository ETD Library Guide or contact the ASU Graduate College at gradformat@asu.edu.
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- All Subjects: Parental influences
- Creators: Chassin, Laurie
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
Description
Family disruption, or the separation of children from caregivers, has been well-established in prior literature as a risk factor for child maladjustment; however, little is known about how family disruption impacts youth into adulthood, particularly how it influences children’s later parenting of their own offspring. The present study examined whether cumulative family disruption (i.e., parental hospitalization, death, incarceration, divorce) in childhood exerts effects on children’s parenting of their own offspring in adulthood, beyond other demographic characteristics and risk factors. Further, several potential mechanisms were hypothesized to underlie the association between family disruption in the first and second generation (G1-G2) family and later parenting provided from second-generation (G2) adults to third-generation (G3) children. Mediators included conflict and disorganization in the G1-G2 family and dysregulation in the G2 child.
Participants (N = 236 in models that included multiple G2 siblings; N = 110 in models without siblings) were drawn from a larger sample of at-risk (i.e., alcoholic) and comparison families followed longitudinally for over 30 years and across three generations. Four mediation models were estimated to examine effects of two separate G1-G2 family disruption components (deviance-related and health-related disruption) on parenting of G3, mediated by family conflict, family disorganization, and G2 dysregulation. Results indicated that health-related disruption impairs consistency of parenting provided to G3 offspring through conflict in the G1-G2 family. A direct effect of health-related disruption was also seen on parental monitoring. There were no direct or mediated effects of deviance-related disruption on parenting. Implications and future directions will be discussed.
Participants (N = 236 in models that included multiple G2 siblings; N = 110 in models without siblings) were drawn from a larger sample of at-risk (i.e., alcoholic) and comparison families followed longitudinally for over 30 years and across three generations. Four mediation models were estimated to examine effects of two separate G1-G2 family disruption components (deviance-related and health-related disruption) on parenting of G3, mediated by family conflict, family disorganization, and G2 dysregulation. Results indicated that health-related disruption impairs consistency of parenting provided to G3 offspring through conflict in the G1-G2 family. A direct effect of health-related disruption was also seen on parental monitoring. There were no direct or mediated effects of deviance-related disruption on parenting. Implications and future directions will be discussed.
ContributorsBlake, Austin Joy (Author) / Chassin, Laurie (Thesis advisor) / Meier, Madeline (Committee member) / Wolchik, Sharlene (Committee member) / McNeish, Daniel (Committee member) / Arizona State University (Publisher)
Created2019