Several researchers have suggested that the nature of the covariation between internalizing and externalizing disorders may be understood better by examining the associations between temperament or personality and these disorders. The present study examined neuroticism as a potential common feature underlying both internalizing and externalizing disorders and novelty seeking as a potential broad-band specific feature influencing externalizing disorders alone. Participants were 12- to 18-year-old twin pairs (635 monozygotic twin pairs and 691 dizygotic twin pairs; 48% male and 52% female) recruited from the Colorado Center for Antisocial Drug Dependence. Genetic and nonshared environmental influences shared in common with neuroticism influenced the covariation among distinct internalizing disorders, the covariation among distinct externalizing disorders, and the covariation between internalizing and externalizing disorders. Genetic influences shared in common with novelty seeking influenced the covariation among externalizing disorders and the covariation between major depressive disorder and externalizing disorders, but not the covariation among internalizing disorders or between anxiety disorders and externalizing disorders. Also, after accounting for genetic and environmental influences shared in common with neuroticism and novelty seeking, there were no significant common genetic or environmental influences among the disorders examined, suggesting that the covariance among the disorders is sufficiently explained by neuroticism and novelty seeking. We conclude that neuroticism is a heritable common feature of both internalizing disorders and externalizing disorders, and that novelty seeking is a heritable broadband specific factor that distinguishes anxiety disorders from externalizing disorders. Keywords: internalizing, externalizing, neuroticism, novelty-seeking, genetics, environment

The present study examined empathy deficits in toddlerhood (age 14 to 36 months) as predictors of antisocial personality disorder (ASPD) symptoms and psychopathy measured by the Levenson Self-Report Psychopathy scale (Levenson, Kiehl, & Fitzpatrick, 1995) in adulthood (age 23 years) in 956 individuals from the Colorado Longitudinal Twin Study. Consistent with the hypothesis that antisocial behavior is associated with “active” rather than “passive” empathy deficits, early disregard for others, not lack of concern for others, predicted later ASPD symptoms. Early disregard for others was also significantly associated with factor 1 of the Levenson Self-Report Psychopathy Scale, which includes items assessing interpersonal and affective deficits, but not with factor 2, which includes items assessing impulsivity and poor behavioral control. The association between early disregard for others and psychopathy factor 2 was near zero after controlling for the shared variance between psychopathy factors 1 and 2. These results suggest that there is a propensity toward adulthood ASPD symptoms and psychopathy factor 1 that can be assessed early in development, which may help identify individuals most at risk for stable antisocial outcomes.

The present study tested specific hypotheses advanced by the developmental propensity model of the etiology of conduct problems in the Colorado Longitudinal Twin Study, a prospective, longitudinal, genetically informative sample. High negative emotionality, low behavioral inhibition, low concern and high disregard for others, and low cognitive ability assessed during toddlerhood (age 14 to 36 months) were examined as predictors of conduct problems in later childhood and adolescence (age 4 to 17 years). Each hypothesized antisocial propensity dimension predicted conduct problems, but some predictions may be context specific or due to method covariance. The most robust predictors were observed disregard for others (i.e., responding to others’ distress with active, negative responses such as anger and hostility), general cognitive ability, and language ability, which were associated with conduct problems reported by parents, teachers, and adolescents, and change in observed negative emotionality (i.e., frustration tolerance), which was associated with conduct problems reported by teachers and adolescents. Furthermore, associations between the most robust early predictors and later conduct problems were influenced by the shared environment rather than genes. We conclude that shared environmental influences that promote disregard for others and detract from cognitive and language development during toddlerhood also predispose individuals to conduct problems in later childhood and adolescence. The identification of those shared environmental influences common to early antisocial propensity and later conduct problems is an important future direction, and additional developmental behavior genetic studies examining the interaction between children’s characteristics and socializing influences on conduct problems are needed.

We examined the magnitude of genetic and environmental influences on observed negative emotionality at age 14, 20, and 24 months. Participants were 403 same-sex twin pairs recruited from the Longitudinal Twin Study whose emotional responses to four different situations were coded by independent raters. Negative emotionality showed significant consistency across settings, and there was evidence of a latent underlying negative emotionality construct. Heritability decreased, and the magnitude of shared environmental influences increased, for the latent negative emotionality construct from age 14 to 24 months. There were significant correlations between negative emotionality assessed at age 14, 20, and 24 months, and results suggested common genetic and shared environmental influences affecting negative emotionality across age, and that age-specific influences are limited to non-shared environmental influences, which include measurement error.