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Polygenic indices (PGI)—the new recommended label for polygenic scores in social science applications—are genetic summary scales often used to represent an individual's liability for a disease, trait, or behavior on the basis of the additive effects of measured genetic variants. Enthusiasm for linking genetic data with social outcomes and the inclusion of premade PGIs in social science data sets have facilitated increased uptake of PGIs in social science research, a trend that will likely continue. Yet most social scientists lack the expertise to interpret and evaluate PGIs in social science research. Here, I provide a primer on PGIs for social scientists focusing on key concepts, unique statistical genetic considerations, and best practices in calculation, estimation, reporting, and interpretation. I summarize recommended best practices as a checklist to aid social scientists in evaluating and interpreting studies with PGIs. I conclude by discussing the similarities between PGIs and standard social science scales and unique interpretative considerations.

Unfortunately, the nature‐versus‐nurture debate continues in criminology. Over the past 5 years, the number of heritability studies in criminology has surged. These studies invariably report sizeable heritability estimates (∼50 percent) and minimal effects of the so‐called shared environment for crime and related outcomes. Reports of such high heritabilities for such complex social behaviors are surprising, and findings indicating negligible shared environmental influences (usually interpreted to include parenting and community factors) seem implausible given extensive criminological research demonstrating their significance. Importantly, however, the models on which these estimates are based have fatal flaws for complex social behaviors such as crime. Moreover, the goal of heritability studies—partitioning the effects of nature and nurture—is misguided given the bidirectional, interactional relationship among genes, cells, organisms, and environments. This study provides a critique of heritability study methods and assumptions to illuminate the dubious foundations of heritability estimates and questions the rationale and utility of partitioning genetic and environmental effects. After critiquing the major models, we call for an end to heritability studies. We then present what we perceive to be a more useful biosocial research agenda that is consonant with and informed by recent advances in our understanding of gene function and developmental plasticity.

This study assesses self‐control theory's stability postulate. We advance research on self‐control stability in three ways. First, we extend the study of stability beyond high school, estimating GBTMs of self‐control from ages 10 to 25. Second, drawing on advances in developmental psychology and social neuroscience, especially the dual systems model of risk taking, we investigate whether two distinct personality traits—impulsivity and sensation seeking—often conflated in measures of self‐control, exhibit divergent developmental patterns. Finding that they do, we estimate multitrajectory models to identify latent classes of co‐occurring developmental patterns. We supplement GBTM stability analyses with hierarchical linear models and reliable variance estimates. Lastly, using fixed effects models, we explore whether the observed within‐individual changes are associated with changes in crime net of overall age trends. These ideas are tested using five waves of data from the Family and Community Health Study. Results suggest that self‐control is unstable, that distinct patterns of development exist for impulsivity and sensation seeking, and that these changes are uniquely consequential for crime. We conclude by comparing our findings with extant research and discussing the implications for self‐control theory.

AbstractRecent studies evince that interpersonal racial discrimination (IRD) increases the risk of crime among African Americans and familial racial socialization fosters resilience to discrimination's criminogenic effects. Yet, studies have focused on the short‐term effects of IRD and racial socialization largely among adolescents. In this study, we seek to advance knowledge by elucidating how racialized experiences—in interactions and socialization—influence crime for African Americans over time. Elaborating Simons and Burt's (2011) social schematic theory, we trace the effects of childhood IRD and familial racial socialization on adult offending through cognitive and social pathways and their interplay. We test this life‐course SST model using data from the FACHS, a multisite study of Black youth and their families from ages 10 to 25. Consistent with the model, analyses reveal that the criminogenic consequences of childhood IRD are mediated cognitively by a criminogenic knowledge structure and socially through the nature of social relationships in concert with ongoing offending and discrimination experiences. Specifically, by increasing criminogenic cognitive schemas, IRD decreases embeddedness in supportive romantic, educational, and employment relations, which influence social schemas and later crime. Consonant with expectations, the findings also indicate that racial socialization provides enduring resilience by both compensating for and buffering discrimination's criminogenic effects.

Simons and Burt's (2011) social schematic theory (SST) of crime posits that adverse social factors are associated with offending because they promote a set of social schemas (i.e., a criminogenic knowledge structure) that elevates the probability of situational definitions favorable to crime. This study extends the SST model by incorporating the role of contexts for action. Furthermore, the study advances tests of the SST by incorporating a measure of criminogenic situational definitions to assess whether such definitions mediate the effects of schemas and contexts on crime. Structural equation models using 10 years of panel data from 582 African American youth provided strong support for the expanded theory. The results suggest that childhood and adolescent social adversity fosters a criminogenic knowledge structure as well as selection into criminogenic activity spaces and risky activities, all of which increase the likelihood of offending largely through situational definitions. Additionally, evidence shows that the criminogenic knowledge structure interacts with settings to amplify the likelihood of situational definitions favorable to crime.