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Description
Methods to test hypotheses of mediated effects in the pretest-posttest control group design are understudied in the behavioral sciences (MacKinnon, 2008). Because many studies aim to answer questions about mediating processes in the pretest-posttest control group design, there is a need to determine which model is most appropriate to

Methods to test hypotheses of mediated effects in the pretest-posttest control group design are understudied in the behavioral sciences (MacKinnon, 2008). Because many studies aim to answer questions about mediating processes in the pretest-posttest control group design, there is a need to determine which model is most appropriate to test hypotheses about mediating processes and what happens to estimates of the mediated effect when model assumptions are violated in this design. The goal of this project was to outline estimator characteristics of four longitudinal mediation models and the cross-sectional mediation model. Models were compared on type 1 error rates, statistical power, accuracy of confidence interval coverage, and bias of parameter estimates. Four traditional longitudinal models and the cross-sectional model were assessed. The four longitudinal models were analysis of covariance (ANCOVA) using pretest scores as a covariate, path analysis, difference scores, and residualized change scores. A Monte Carlo simulation study was conducted to evaluate the different models across a wide range of sample sizes and effect sizes. All models performed well in terms of type 1 error rates and the ANCOVA and path analysis models performed best in terms of bias and empirical power. The difference score, residualized change score, and cross-sectional models all performed well given certain conditions held about the pretest measures. These conditions and future directions are discussed.
ContributorsValente, Matthew John (Author) / MacKinnon, David (Thesis advisor) / West, Stephen (Committee member) / Aiken, Leona (Committee member) / Enders, Craig (Committee member) / Arizona State University (Publisher)
Created2015
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Description
Anxiety and depression are among the most prevalent disorders in youth, with prevalence rates ranging from 15% to 25% for anxiety and 5% to 14% for depression. Anxiety and depressive disorders cause significant impairment, fail to spontaneously remit, and have been prospectively linked to problematic substance use and legal problems

Anxiety and depression are among the most prevalent disorders in youth, with prevalence rates ranging from 15% to 25% for anxiety and 5% to 14% for depression. Anxiety and depressive disorders cause significant impairment, fail to spontaneously remit, and have been prospectively linked to problematic substance use and legal problems in adulthood. These disorders often share a high-degree of comorbidity in both clinical and community samples, with anxiety disorders typically preceding the onset of depression. Given the nature and consequences of anxiety and depressive disorders, a plethora of treatment and preventative interventions have been developed and tested with data showing significant pre to post to follow-up reductions in anxiety and depressive symptoms. However, little is known about the mediators by which these interventions achieve their effects. To address this gap in the literature, the present thesis study combined meta-analytic methods and path analysis to evaluate the effects of youth anxiety and depression interventions on outcomes and four theory-driven mediators using data from 55 randomized controlled trials (N = 11,413). The mediators included: (1) information-processing biases, (2) coping strategies, (3) social competence, and (4) physiological hyperarousal. Meta-analytic results showed that treatment and preventative interventions reliably produced moderate effect sizes on outcomes and three of the four mediators (information-processing biases, coping strategies, social competence). Most importantly, findings from the path analysis showed that changes in information-processing biases and coping strategies consistently mediated changes in outcomes for anxiety and depression at both levels of intervention, whereas gains in social competence and reductions in physiological hyperarousal did not emerge as significant mediators. Knowledge of the mediators underlying intervention effects is important because they can refine testable models of treatment and prevention efforts and identify which anxiety and depression components need to be packaged or strengthened to maximize intervention effects. Allocating additional resources to significant mediators has the potential to reduce costs associated with adopting and implementing evidence-based interventions and improve dissemination and sustainability in real-world settings, thus setting the stage to be more readily integrated into clinical and non-clinical settings on a large scale.
ContributorsStoll, Ryan (Author) / Pina, Armando A (Thesis advisor) / MacKinnon, David (Committee member) / Knight, George (Committee member) / Arizona State University (Publisher)
Created2015
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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

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.
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
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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

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.
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
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Description
Mediation analysis is integral to psychology, investigating human behavior’s causal mechanisms. The diversity of explanations for human behavior has implications for the estimation and interpretation of statistical mediation models. Individuals can have similar observed outcomes while undergoing different causal processes or different observed outcomes while receiving the same treatment. Researchers

Mediation analysis is integral to psychology, investigating human behavior’s causal mechanisms. The diversity of explanations for human behavior has implications for the estimation and interpretation of statistical mediation models. Individuals can have similar observed outcomes while undergoing different causal processes or different observed outcomes while receiving the same treatment. Researchers can employ diverse strategies when studying individual differences in multiple mediation pathways, including individual fit measures and analysis of residuals. This dissertation investigates the use of individual residuals and fit measures to identify individual differences in multiple mediation pathways. More specifically, this study focuses on mediation model residuals in a heterogeneous population in which some people experience indirect effects through one mediator and others experience indirect effects through a different mediator. A simulation study investigates 162 conditions defined by effect size and sample size for three proposed methods: residual differences, delta z, and generalized Cook’s distance. Results indicate that analogs of Type 1 error rates are generally acceptable for the method of residual differences, but statistical power is limited. Likewise, neither delta z nor gCd could reliably distinguish between contrasts that had true effects and those that did not. The outcomes of this study reveal the potential for statistical measures of individual mediation. However, limitations related to unequal subpopulation variances, multiple dependent variables, the inherent relationship between direct effects and unestimated indirect effects, and minimal contrast effects require more research to develop a simple method that researchers can use on single data sets.
ContributorsSmyth, Heather Lynn (Author) / MacKinnon, David (Thesis advisor) / Tein, Jenn-Yun (Committee member) / McNeish, Daniel (Committee member) / Grimm, Kevin (Committee member) / Arizona State University (Publisher)
Created2022