Theses and Dissertations

Prior research has established a relation between parenting behaviors and symptoms of child psychopathology, and this association may be influenced by both genetic and environmental factors. Gene-environment correlation, or the influence of a child’s genes on the environment they receive, represents one possible mechanism through which genes and environment combine to influence child outcomes. This study examined evocative gene-environment correlation in the relation between parenting and symptoms of child psychopathology in a sample of 676 twins (51.5% female, 58.5% Caucasian, 23.7% Hispanic/Latinx, primarily middle class, MAge=8.43, SD=.62) recruited from Arizona birth records. Using univariate ACE twin biometric models, genetic influences were found to moderately contribute to internalizing symptoms (A=.47, C=.25, E=.28), while externalizing (A=.86, E=.14) and ADHD (A=.84, E=.16) symptoms were found to be highly heritable. The genetic influences for positive (C=.54, E=.46) and negative (C=.44, E=.56) parenting were smaller and found to be nonsignificant. The correlations between parenting and types of psychopathology were examined and bivariate Cholesky decompositions were conducted for statistically significant correlations. Negative parenting was moderately positively correlated with externalizing and ADHD symptoms; the relation between externalizing symptoms and negative parenting was found to be due to shared genetics, whereas the relation between negative parenting and ADHD symptoms was due to the shared environment. The mixed results regarding the role of gene environment correlation in relations between parenting and child psychopathology indicate that further research on the mechanisms of this relation is needed.

This thesis proposes an extension of David Lewis's causal influence account of causation, providing a method to calculate the `degrees of causal influence.' By providing a quantitative approach to causal influence, I find that that the influence approach can assess statements that involve causal redundancies, allowing the assessor to attribute primary causal responsibility to the contending cause with a higher net influence value. The causal influence calculation also addresses criticisms towards Lewis's influence account, namely those involving `inert zones' of influence, the use of the term `might,' trumping versus symmetric overdetermination, and Lewis's clause requiring stepwise influence. This thesis also compares the results of causal influence in multiple toy cases including Two Rocks, both the asymmetric and symmetric variants, demonstrating that causal influence overcomes many of the core issues in Lewis's initial counterfactual account of causation. Using the asymmetric Two Rocks variant, this thesis also provides a detailed example of how to use the calculation and a discussion of the calculation's limitations. The main drawbacks of the quantitative method for causal influence seems to be the effort that it requires and issues in finding measurable qualities to compare the similarity/difference between possible worlds. Using the Two Rocks case, however, the causal influence calculation reaches the same conclusions as what Lewis suggests. A primary remaining issue is applying the calculation to instances of causation by omission, however this seems to only be a problem in using the equations rather than a problem within the idea of causal influence itself. Also, there may still be issues in justifying comparative overall similarity. However, this is an issue that both the counterfactual and influence accounts face.