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This study investigates the common‐family environmental (CE), within‐family environmental (WE), and hereditary (H) components of antisocial behavior and its correlates using a twin study design. The subjects are 265 adolescent twin pairs who reported in a mail survey on their antisocial behavior, deceitfulness, parental rejection (as perceived), anger, impulsivity, and value placed on school achievement. These six variables are intercorrelated in two ways: between‐families (twin pairs' sums) and within‐families (twin pairs' differences). The former covariance structure captures the twins' resemblances: the latter, the twins' differences in behavior. LISREL is used to model the observed relationships using structural equations containing CE, WE, and H factors. The best‐fitting model requires only H and WE factors to explain the variables' relationships. Within this population, delinquent behavior is unaffected by CE influences such as social class, child rearing styles, parental attitudes, parental religion, and other factors equally affecting the twins. The principal genetic correlates of delinquency appear to be deceitfullness and temperamental traits.

The relationship between the quality of twins'mutual attachment and delinquency is examined in a study of 265 twin pairs. It is predicted that twins with stronger mutual attachments will have lower rates of delinquent behavior. Contrary to this prediction, twins'mutual attachment (that is, the frequency with which the twins saw each other in teenage activities) is found to be unrelated to delinquent behavior. The twins often cooperated, however, in their delinquent acts: 61 % of the girls and 79% of the boys reported committing one or more delinquent acts with their twins. In accord with social control theory, social bonds (normlessness, perceived parental acceptance‐rejection, and value placed on academic achievement) are strongly associated with delinquent behavior. Except for male DZ twins, however, these same variables are only weakly associated with twins'mutual attachments. A behavioral genetic analysis of the social bonds indicate both genetic and specific environmental components to their variation but fail to show evidence of a shared environmental component. Implications of these findings are discussed.

This article examines the familial transmission of criminal convictions in families in the Cambridge Study in Delinquent Development. Our main analyses focus on the 344 families in the Cambridge Study with two or more children. Criminal convictions were highly familial because convictions in a parent increased the risk of convictions in a child. Correlations between siblings were stronger in same‐sex siblings (.45 to .50) than in opposite‐sex ones (.27). Sibling correlations did not vary by birth order. Convictions of mothers and father correlated .55. Parent‐child correlations were about the same as within‐generation correlations between siblings. LISREL models were used to assess whether the effect of parental convictions on child convictions was direct or mediated through the quality of the family environment (i.e., supervision. child rearing, and family size). The best fitting LISREL models suggested a direct effect of parental convictions on child convictions, without any mediation by family environment. These data on fill biological siblings, however, did not permit separate estimation of family environmental versus genetic effects. One environmental effect appeared, however—a socialization effect among siblings; in families with three sons, there appeared to be mutual influence of one sibling on another. Also, regression models based on the boys suggested that family environmental variables did add to parental criminality.

Our goal is to build bridges between theoretical criminology, the study of criminal careers, and policy‐relevant research. Insights from the criminal career and propensity positions lead us to seek (1) a comprehensive means of incorporating theoretical variables in research on criminal careers, (2) statistical models that yield meaningful projections relevant to public policy issues, and (3) methods for comparing findings for different measures of offending. We present a conceptual framework accomplishing this by applying the general linear model to the study of crime and criminal careers. This framework differentiates the elements of (1) a curvilinear function linking the scale of the linear model and the scale of the measure of offending, (2) a probabilistic relationship between a latent tendency to offend and the measure of offending, (3) a probability distribution of individual differences on the latent dimension, and (4) relationships among repeated observations for the same individual. We describe numerous versions of the general linear model that do not require special statistical expertise and are appropriate for the full range of measures of offending. We conclude by addressing strategies for comparing results across measures.

Sibling effects refer to the immediate influence one sibling may have on another or to indirect influences through their embeddedness in a common friendship network We used three aspects of sibling mutual interaction—warmth, conflict, and frequency of contact with mutual friends—to evaluate sibling effects on delinquency and substance use in 135 brother pairs, 142 sister pairs, and 141 mixed‐sex pairs in the Arizona Sibling Study (primarily aged 10–16 years). We hypothesized that sibling relationship variables would condition the behavioral resemblance of the younger and older sibling. For both substance use and delinquency, this prediction was confirmed for warmth and mutual friends: Sibling pairs who reported warmer mutual relationships or greater contact with mutual friends were more alike behaviorally. The statistical sibling effects were not explained by social class, parental substance use, or rearing styles. We interpret them as the influence of one sibling on the other and as the influence arising from sharing common friends. Given the existence of sibling effects, the strength of shared familial influences of other origins must be revised downward.

SummaryThis paper applies models of the onset of adolescent sexual intercourse using national data from Denmark and the USA. The model gave excellent fits to data on Danish Whites and a good fit to American Whites, but the model-fits for American Blacks and Hispanics were not as good. The weakness of the latter model fits may reflect either real processes that the model does not capture or problems in the reliability of adolescent sexuality data.

This study presents a multivariate behavioural genetic analysis of the relationship between education, intelligence and age of first birth. Analyses investigated the mediational role of education in explaining the relationship between intelligence and age of first birth at both the phenotypic and behavioural genetic level. The data come from the National Longitudinal Survey of Youth (NLSY), a nationally representative survey that included genetically informative full- and half-sibling pairs (n=1423 pairs). Respondents were aged 14 to 22 when contacted in 1979. Heritability estimates were 0·32, 0·50 and 0·06 for IQ, education and age of first birth, respectively. Shared environment estimates were 0·35, 0·23 and 0·20 respectively. Common genetic and shared environmental factors were substantial in explaining the relationship between intelligence and education, and also education and age of first birth. Education partially mediated the relationship between intelligence and age of first birth only in the phenotypic analyses. After considering the genetic and shared environmental factors that influence all three variables, evidence for mediation was less convincing. This pattern of results suggests that the apparent mediational role of education at the phenotypic level is in fact the result of underlying genetic and shared environmental influences that affect education, IQ and age of first birth in common.

Fisher (1930) presented both theoretical and empirical results concerning genetic influences on fertility. Since then, only sparse research has been done on the genetics of fertility, although more sophisticated methodogy and data now exist than were available to Fisher. This paper presents a behavioural genetic analysis of age at first intercourse, accounting for genetic, shared environmental, and selected non-shared environmental influences. The data came from the nationally representative National Longitudinal Survey of Youth (NLSY). A newly developed kinship linking procedure was used that identifies links for cousins, half-siblings, full-siblings and twins in the NLSY. The results suggest a genetic influence in the overall dataset, and also among whites and in male–male and opposite-sex pairs. Genetic influences were extremely small or non-existent for blacks and for female–female pairs. Shared environmental influences were small for most subsets of the data, but moderate for female–female pairs. Two specific non-shared environmental influences – self-esteem and locus of control – were ruled out as accounting for any meaningful variance, although other general sources of non-shared environmental influence appear potentially important. Analysis of selected samples from upper and lower tails suggested that genetic influences are important in accounting for both early and late non-virginity. These findings are consistent with work reported by Miller et al. (1999), who used molecular genetic methods. Generally, these findings support the existence of genetic influences and implicate non-shared environmental influences as being important determinants of the timing of loss of virginity among US adolescents and young adults.