Intimate partner violence (IPV), defined as psychological, physical, or sexual abuse within a current or former romantic relationship, has significant consequences for the health and well-being of men and women. Although there has been substantial research on IPV, much of the research has focused on risk and protective factors, and intervention activities for victims. A small body of research on perpetrators suggests the etiology of IPV perpetration is complex and multifactorial, but the dearth of research on perpetrators has resulted in a limited number of effective interventions for perpetrators of IPV. This dissertation contributes to the limited understanding of factors, especially modifiable risk and protective factors, associated with IPV perpetration, as informed by the Catalyst Model of Aggression and the IPV Contextual Framework. Improved understanding of modifiable risk and protective factors for IPV perpetration may inform the development of more effective intervention and prevention efforts. Using the nationally-representative sample collected in The National Longitudinal Study of Adolescent Health, the dissertation examined factors associated with IPV perpetration, including static antecedents (factors that remain stable over time), distal antecedents (factors that occur prior to the time of perpetration) and proximal antecedents (factors that occur near the time of perpetration), and the interaction of static antecedents with distal and proximal antecedents. For this dissertation, static antecedents were operationalized as personality traits and three dopamine genes. Distal antecedents were operationalized as adolescent exposure to violence and school social environment. Proximal antecedents were defined as financial stressors and job satisfaction. Logistic regression and multinomial logistic regression were used to examine these relationships. All analyses were weighted and clustered to allow for population-level estimates and were stratified by gender and race. My results suggest that personality, but not the three dopamine genes, was associated with IPV perpetration. There was some indication the genetic factors interact with environmental characteristics during adolescence and adulthood to increase the odds of perpetrating IPV during adulthood, in at least some circumstances and among some subpopulations. For example, there was a significant interaction between school social environment and genes among white men, white women, and non-white women. However, these relationships were not constant across strata and type of antecedent. Overall, the practical implications of this dissertation are unclear. As the field of violence prevention continues to develop, additional research on the genetic contribution to IPV perpetration will contribute to our understanding of these findings and provide additional context on the biological mechanisms underlying these relationships. Additional context may also contribute to the understanding of how to best develop intervention and prevention activities for individuals with the highest level of risk for IPV perpetration. Ultimately, it may be possible to tailor pharmacological or behavioral interventions based on the individual static, distal, and proximal antecedents associated with perpetration.