A dual taxonomy is presented to reconcile 2 incongruous facts about antisocial behavior: (a) It shows impressive continuity over age, but (b) its prevalence changes dramatically over age, increasing almost 10-fold temporarily during adolescence. This article suggests that delinquency conceals 2 distinct categories of individuals, each with a unique natural history and etiology: A small group engages in antisocial behavior of 1 sort or another at every life stage, whereas a larger group is antisocial only during adolescence. According to the theory of life-course-persistent antisocial behavior, children's neuropsychological problems interact cumulatively with their criminogenic environments across development, culminating in a pathological personality. According to the theory of adolescence-limited antisocial behavior, a contemporary maturity gap encourages teens to mimic antisocial behavior in ways that are normative and adjustive.

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We report data that support the distinction between childhood-onset and adolescent-onset type conduct problems. Natural histories are described from a representative birth cohort of 457 males studied longitudinally from age 3 to 18 years. Childhood-and adolescent-onset cases differed on temperament as early as age 3 years, but almost half of childhood-onset cases did not become seriously delinquent. Type comparisons were consistent with our contention that males whose antisocial behavior follows a life-course-pcrsistent path differ from males who follow an adolescence-limited path. As adolescents, the two types differed on convictions for violent crime, personality profiles, school leaving, and bonds to family. These differences can be attributed to developmental history because the two groups were well matched on measures of antisocial conduct at age 18 years: parent-reports, self-reports, and adjudication records. By age 18 years, many conduct-problem boys had encountered factors that could ensnare them in an antisocial future: substance dependence, unsafe sex, dangerous driving habits, delinquent friends, delinquent perceptions, and unemployment. Implications for theory, research design, prevention, and therapeutic treatment of conduct problems are highlighted.Theantisocial behavior of adolescents bears in the face of evidence that most serious serious consequences for individuals, fami-property and violent crimes are now cornlies, communities, and society. The general mitted by teenaged offenders and evidence public has forsaken its credulous notions that almost all violent and predatory adult of "teenaged hijinks" and "boyish pranks" antisocial careers originate in juvenile conduct problems. Despite a sense of urgency -.about reducing adolescent antisocial behavThis research was supported by USPHS Grant MH-j o r > scientific progress toward that goal has to T. Moffitt from the Violence and Traumatic h a m p e r e d by great diversity inherent stress Branch of the National Institute of Mentalr j i , Health and by the William Freeman Vilas Trust at the within the broad class of adolescents who University of Wisconsin. The Dunedin Multidiscipli-engage in antisocial behaviors. Apportionnary Health and Development Research Unit is sup-j n g this heterogeneity into meaningful subported by the New Zealand Health Research Council. t y p e s n a s ^e n the focus of much taxonomic Gee, and Charlotte Paul, and the New Zealand Police Motfitt, 1993a; Quay, 1987). generously shared data with us. We arc grateful to our " Developmentalists are now reaching a staff, and to the study members and their parents and consensus that antisocial behavior follows tcac l 1 " sat least two primary developmental courses, Address correspondence and reprint requests to: ... , . , , , , "_ "_,. t u~. ~tu*.m,uu Terrie E. Moffitt, University of Wisconsin-Madison, o n e W l t h childhood-onset and the other with Dpt. of Psychology, 1202 W.Johnson St.. Madison, later, generally postpubertal onset (e.g., 53706. Farrington et al., 1990; Loeber &...

Over the past half century two competing hypotheses in sociological inquiry have provided interpretations of the well-documented association between low socioeconomic status and mental disorders. The selection hypothesis asserts that mental disorders impair status attainment, whereas the causation hypothesis states that conditions of life associated with low socioeconomic status markedly increase the risk of mental disorders. Using data from the longitudinal Dunedin Multidisciplinary Health and Development Study (n=1037), we examine selection and causation processes during the transition to young adulthood by investigating the mutual influence of mental disorders and educational attainment, a core element of socioeconomic status. The Dunedin Study follows a cohort from birth to age 21, and includes psychiatric diagnoses for study members at ages 15 and 21 using DSM criteria. We focus on the four disorders of anxiety, depression, anti-social disorder, and attention deficit disorder and find a unique relationship with socioeconomic status for each one. These findings highlight the need for (a) greater consideration of antisocial disorders in the status attainment process and (b) more theoretical development in the sociology of mental disorders to account for disorder-specific relations with socioeconomic status.

Evidence of marked variability in response among people exposed to the same environmental risk implies that individual differences in genetic susceptibility might be at work. The study of such Gene-by-Environment (GxE) interactions has gained momentum. In this article, the authors review research about one of the most extensive areas of inquiry: variation in the promoter region of the serotonin transporter gene (SLC6A4; also known as 5-HTT) and its contribution to stress sensitivity. Research in this area has both advanced basic science and generated broader lessons for studying complex diseases and traits. The authors evaluate four lines of evidence about the 5-HTT stress-sensitivity hypothesis: 1) observational studies about the serotonin transporter linked polymorphic region (5-HTTLPR), stress sensitivity, and depression in humans; 2) experimental neuroscience studies about the 5-HTTLPR and biological phenotypes relevant to the human stress response; 3) studies of 5-HTT variation and stress sensitivity in nonhuman primates; and 4) studies of stress sensitivity and genetically engineered 5-HTT mutations in rodents. The authors then dispel some misconceptions and offer recommendations for GxE research. The authors discuss how GxE interaction hypotheses can be tested with large and small samples, how GxE research can be carried out before as well as after replicated gene discovery, the uses of GxE research as a tool for gene discovery, the importance of construct validation in evaluating GxE research, and the contribution of GxE research to the public understanding of genetic science.