In this study, we set out to investigate whether introducing molecular genetic measures into an analysis of sexual partner variety will yield novel sociological insights. The data source is the white male DNA sample in the National Longitudinal Study of Adolescent Health. Our empirical analysis has produced a robust protective effect of the 9R/9R genotype relative to the Any10R genotype in the dopamine transporter gene (DAT1). The gene-environment interaction analysis demonstrates that the protective effect of 9R/9R tends to be lost in schools in which higher proportions of students start having sex early or among those with relatively low levels of cognitive ability. Our genetics-informed sociological analysis suggests that the "one size" of a single social theory may not fit all. Explaining a human trait or behavior may require a theory that accommodates the complex interplay between social contextual and individual influences and genetic predispositions.Risky sexual behavior often plays a critical role in the spread of sexually transmitted diseases (STD), including HIV among adolescents and young adults (IOM 1997). Sociological work on risky sexual behavior has demonstrated the importance of social contexts at the levels of individual, family, neighborhood, and school (Brewster 1994;Browning et al 2005;Furstenberg et al 1987). In this study, we set out to investigate whether introducing molecular genetic measures into analysis of sexual partner variety will lead to novel sociological insights.The notion that individuals may differ with respect to genetic predispositions is not new. Twins and siblings have long been used to estimate the proportion of variance in an outcome due to innate influences, but the findings have frequently been questioned because the two fundamental assumptions of equal environment and assortative mating remain controversial.Earlier efforts linking genetic variants and human outcomes often suffer from small sample sizes, population admixture, multiple testing, inappropriate controls, and non-replication (Cardon and Palmer 2003;Ioannidis et al 2001;Ioannidis et al 2003). Convincing evidence arrived recently. The year 2007 saw an unprecedented succession of discoveries in the genomics of complex traits (e.g., Frayling et al 2007;Pennisi 2007;Scott et al 2007;Sladek et al 2007;Steinthorsdottir et al 2007;Zeggini et al 2007). These discoveries identified genetic variants associated with acute lymphoblastic leukemia, obesity, type 2 diabetes mellitus, prostate cancer, breast cancer, and coronary heart disease. All of the evidence has been replicated multiple times in large independent samples. These discoveries in human genetic NIH Public Access
Author ManuscriptAJS. Author manuscript; available in PMC 2010 June 3. If individuals do differ in genetic susceptibilities for diseases, it will be a small stretch to suggest that individuals may also differ in genetic propensities for other traits and behaviors that are of interest to sociologists. The important question, however, is wheth...