INTRODUCTION

Genes and experience jointly contribute to individual differences in social behavior, lifestyle, and disease risk. Once controversial, that statement is now accepted throughout the behavioral sciences. Evidence from decades of research in behavioral and psychiatric genetics (McGue & Bouchard, 1998; Martin, Boomsma, & Machin, 1997; Plomin, DeFries, Craig, & McGuffin, 2003; Rose, 1995; Rutter & Silberg, 2002) has fostered an integrated perspective in developmental science, a perspective that acknowledges the interplay of nature and nurture from prenatal life, through the acquisition and development of behaviors in infancy, to individual differences in cognitive decline and well-being in senescence.

Few if any dimensions of social behavior and health are insulated from some genetic influence, however indirect, but the timing, magnitude, and nature of genetic influences differ across health and social behaviors, and genetic effects are modulated by complex interactions of age, gender, environmental exposure, family circumstance, and family history of disease. It is equally true that no dimension of health and social behavior is independent of variation in one's cumulative experience, but identifying environmental effects, assessing their magnitude, and articulating their pathways of causal influence are invariably confounded with correlated genetic differences between families and individuals. For that reason, incisive appraisal of environmental factors and disease risk require research designs that control, to the degree possible, between-family genetic confounds.

Contemporary analyses of the differences within and between human twins, analyses first suggested by Sir Francis Galton 125 years ago, offer fundamental data with which to address the causes of familial and individual variation in behavioral development and behavioral disorder.