Terrie E. Moffitt

Adolescence-limited and life-course-persistent antisocial behavior: a developmental taxonomy.

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, childrens 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.

A gradient of childhood self-control predicts health, wealth, and public safety

Policy-makers are considering large-scale programs aimed at self-control to improve citizens’ health and wealth and reduce crime. Experimental and economic studies suggest such programs could reap benefits. Yet, is self-control important for the health, wealth, and public safety of the population? Following a cohort of 1,000 children from birth to the age of 32 y, we show that childhood self-control predicts physical health, substance dependence, personal finances, and criminal offending outcomes, following a gradient of self-control. Effects of childrens self-control could be disentangled from their intelligence and social class as well as from mistakes they made as adolescents. In another cohort of 500 sibling-pairs, the sibling with lower self-control had poorer outcomes, despite shared family background. Interventions addressing self-control might reduce a panoply of societal costs, save taxpayers money, and promote prosperity.

Development of Depression From Preadolescence to Young Adulthood: Emerging Gender Differences in a 10-Year Longitudinal Study

The authors investigated the emergence of gender differences in clinical depression and the overall development of depression from preadolescence to young adulthood among members of a complete birth cohort using a prospective longitudinal approach with structured diagnostic interviews administered 5 times over the course of 10 years. Small gender differences in depression (females greater than males) first began to emerge between the ages of 13 and 15. However, the greatest increase in this gender difference occurred between ages 15 and 18. Depression rates and accompanying gender differences for a university student subsample were no different than for a nonuniversity subsample. There was no gender difference for depression recurrence or for depression symptom severity. The peak increase in both overall rates of depression and new cases of depression occurred between the ages of 15 and 18. Results suggest that middle-to-late adolescence (ages 15-18) may be a critical time for studying vulnerability to depression because of the higher depression rates and the greater risk for depression onset and dramatic increase in gender differences in depression during this period.

Males on the life-course-persistent and adolescence-limited antisocial pathways: Follow-up at age 26 years

This article reports a comparison on outcomes of 26-year-old males who were defined several years ago in the Dunedin longitudinal study as exhibiting childhood-onset versus adolescent-onset antisocial behavior and who were indistinguishable on delinquent offending in adolescence. Previous studies of these groups in childhood and adolescence showed that childhood-onset delinquents had inadequate parenting, neurocognitive problems, undercontrolled temperament, severe hyperactivity, psychopathic personality traits, and violent behavior. Adolescent-onset delinquents were not distinguished by these features. Here followed to age 26 years, the childhood-onset delinquents were the most elevated on psychopathic personality traits, mental-health problems, substance dependence, numbers of children, financial problems, work problems, and drug-related and violent crime, including violence against women and children. The adolescent-onset delinquents at 26 years were less extreme but elevated on impulsive personality traits, mental-health problems, substance dependence, financial problems, and property offenses. A third group of men who had been aggressive as children but not very delinquent as adolescents emerged as low-level chronic offenders who were anxious, depressed, socially isolated, and had financial and work problems. These findings support the theory of life-course-persistent and adolescence-limited antisocial behavior but also extend it. Findings recommend intervention with all aggressive children and with all delinquent adolescents, to prevent a variety of maladjustments in adult life.

Childhood predictors differentiate life-course persistent and adolescence-limited antisocial pathways among males and females

This article reports a comparison on childhood risk factors of males and females exhibiting childhood-onset and adolescent-onset antisocial behavior, using data from the Dunedin longitudinal study. Childhood-onset delinquents had childhoods of inadequate parenting, neurocognitive problems, and temperament and behavior problems, whereas adolescent-onset delinquents did not have these pathological backgrounds. Sex comparisons showed a male-to-female ratio of 10:1 for childhood-onset delinquency but a sex ratio of only 1.5:1 for adolescence-onset delinquency. Showing the same pattern as males, childhood-onset females had high-risk backgrounds but adolescent-onset females did not. These findings are consistent with core predictions from the taxonomic theory of life-course persistent and adolescence-limited antisocial behavior.

Developmental Trajectories of Childhood Disruptive Behaviors and Adolescent Delinquency: A Six-Site, Cross-National Study

This study used data from 6 sites and 3 countries to examine the developmental course of physical aggression in childhood and to analyze its linkage to violent and nonviolent offending outcomes in adolescence. The results indicate that among boys there is continuity in problem behavior from childhood to adolescence and that such continuity is especially acute when early problem behavior takes the form of physical aggression. Chronic physical aggression during the elementary school years specifically increases the risk for continued physical violence as well as other nonviolent forms of delinquency during adolescence. However, this conclusion is reserved primarily for boys, because the results indicate no clear linkage between childhood physical aggression and adolescent offending among female samples despite notable similarities across male and female samples in the developmental course of physical aggression in childhood.

Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of a gene X environment interaction.

BACKGROUND Recent evidence documents that cannabis use by young people is a modest statistical risk factor for psychotic symptoms in adulthood, such as hallucinations and delusions, as well as clinically significant schizophrenia. The vast majority of cannabis users do not develop psychosis, however, prompting us to hypothesize that some people are genetically vulnerable to the deleterious effects of cannabis. METHODS In a longitudinal study of a representative birth cohort followed to adulthood, we tested why cannabis use is associated with the emergence of psychosis in a minority of users, but not in others. RESULTS A functional polymorphism in the catechol-O-methyltransferase (COMT) gene moderated the influence of adolescent cannabis use on developing adult psychosis. Carriers of the COMT valine158 allele were most likely to exhibit psychotic symptoms and to develop schizophreniform disorder if they used cannabis. Cannabis use had no such adverse influence on individuals with two copies of the methionine allele. CONCLUSIONS These findings provide evidence of a gene x environment interaction and suggest that a role of some susceptibility genes is to influence vulnerability to environmental pathogens.

Gene-environment interactions in psychiatry: joining forces with neuroscience.

Gene–environment interaction research in psychiatry is new, and is a natural ally of neuroscience. Mental disorders have known environmental causes, but there is heterogeneity in the response to each causal factor, which gene–environment findings attribute to genetic differences at the DNA sequence level. Such findings come from epidemiology, an ideal branch of science for showing that gene–environment interactions exist in nature and affect a significant fraction of disease cases. The complementary discipline of epidemiology, experimental neuroscience, fuels gene–environment hypotheses and investigates underlying neural mechanisms. This article discusses opportunities and challenges in the collaboration between psychiatry, epidemiology and neuroscience in studying gene–environment interactions.

Genetic Sensitivity to the Environment: The Case of the Serotonin Transporter Gene and Its Implications for Studying Complex Diseases and Traits

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.

Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study.

Papers pp 1195, 1199 The strongest evidence that cannabis use may be a risk factor for later psychosis comes from a Swedish cohort study which found that heavy cannabis use at age 18 increased the risk of later schizophrenia sixfold. 1 2 This study could not establish whether adolescent cannabis use was a consequence of pre-existing psychotic symptoms rather than a cause. We present the first prospective longitudinal study of adolescent cannabis use as a risk factor for adult schizophreniform disorder, taking into account childhood psychotic symptoms3 antedating cannabis use. View this table: Association between cannabis use in adolescence and schizophrenia and depressive symptoms and disorders at age 26 (n=759), controlling for childhood psychotic symptoms and use of other drugs in adolescence The Dunedin multidisciplinary health and development study (a study of a general population birth cohort of 1037 individuals born in Dunedin, New Zealand, in 1972-3)4 has a 96% follow up rate at age 26. It obtained information on psychotic symptoms at age 11 and drug use at ages 15 and 18 from self reports and assessed …