Testing the role of adolescent sexual initiation in later-life sexual risk behavior: a longitudinal twin design

The consistent association between adolescent sexual initiation (ASI) and risky adult sexual behavior (RASB) has generally been assumed to indicate that ASI has a causal effect on RASB; consequently, it is assumed that delaying ASI will reduce RASB. Yet the ASI-RASB association might be better accounted for by some third variable. We evaluated the causal role of ASI (initiation of oral, anal, or vaginal sex at or before age 16) in influencing RASB in a longitudinal sample of 2,173 twins (followed from ages 11 to 24 or from ages 17 to 29) using two methods: the discordant-twin design and the propensity-score design. The former controlled for unmeasured genetic and shared environmental factors, and the latter controlled for measured nonshared environmental factors. We replicated the link between ASI and RASB reported in previous research, but results from the discordant-twin and propensity-score analyses suggested that this association is better explained by common genetic or environmental risk factors than as a causal effect. These findings suggest that preventing ASI is unlikely to reduce RASB.     

The Relationship between Parent-Child Conflict and Adolescent Antisocial Behavior: Confirming Shared Environmental Mediation

Prior studies have indicated that the relationship between parent-child conflict and adolescent antisocial behavior is at least partially shared environmental in origin. However, all available research on this topic (to our knowledge) relies exclusively on parent and/or adolescent informant-reports, both of which are subject to various forms of rater bias. As the presence of significant shared environmental effects has often been attributed to rater bias in the past (Baker et al. Journal of Abnormal Psychology 16:219–235, 2007; Bartels et al. Journal of the American Academy of Child and Adolescent Psychiatry 42:1351–1359, 2003, Twin Research 7:162–175, 2004; Hewitt et al. Behavior Genetics 22:293–317, 1992), it would be important to confirm that findings of shared environmental mediation persist when even examining (presumably more objective) observer-ratings of these constructs. The current study thus examined the origins of the relationship between parent-child conflict and adolescent acting-out behavior, as measured using both observer-ratings and various informant-reports. Participants included 1,199 adopted and non-adopted adolescents in 610 families from the Sibling Interaction and Behavior Study (SIBS). Results indicated that parent-child conflict consistently predicts acting-out behavior in adopted adolescents, and moreover, that this association is equivalent to that in biologically-related adolescents. Most importantly, these findings did not vary across parent- and adolescent-reported or observer-ratings of parent-child conflict and acting-out behavior. Such findings argue strongly against rater bias as a primary explanation of shared environmental mediation of the association between parent-child conflict and adolescent antisocial behavior.     

Schizophrenia: A Neurodevelopmental Perspective

Diverse lines of research suggest that schizophrenia is a genetically influenced neurodevelopmental disorder. Family, twin, and adoption studies suggest that most cases of schizophrenia involve a genetic diathesis that is necessary but not sufficient for development of the disorder. Histological, neuroimaging, and neuropsychological findings converge in providing evidence for medial-temporal and frontal lobe dysfunction that likely predates the onset of psychosis. Behavioral phenomenology and neurobiology suggest that dopamine plays a crucial moderating role between these structural abnormalities and functional impairment. Recently, investigators have used animal models and clinical syndromes to integrate these findings into neurodevelopmental models of schizophrenia that hold great potential for yielding etiological insight.     

Genetic relationships between personality and eating attitudes and behaviors

Genetic and environmental factors underlying relationships between personality traits and disordered eating were examined in 256 female adolescent twin pairs (166 monozygotic, 90 dizygotic). Eating behaviors were assessed with the Total Score, Body Dissatisfaction, Weight Preoccupation, Binge Eating, and Compensatory Behavior subscales from the Minnesota Eating Disorders Inventory (M-EDI; K. L. Klump, M. McGue, & W. G. Iacono, 2000). Personality characteristics were assessed with the Negative Emotionality, Positive Emotionality, and Constraint scales from the Multidimensional Personality Questionnaire (MPQ; A. Tellegen, 1982). Model-fitting analyses indicated that although genetic factors were more likely to contribute to MPQ and M-EDI phenotypic associations than environmental factors, shared genetic variance between the 2 phenotypes was limited. MPQ personality characteristics may represent only some of several genetic risk factors for eating pathology.     

How intelligence and education contribute to substance use: Hints from the Minnesota Twin family study

In old and even middle age, there are associations between physical health and both intelligence and education. This may occur because intelligence and/or education exert effects on lifestyle choices that, in turn, affect later health. Substance use is one aspect of lifestyle choice in young adulthood that could play such a role. The effects of intelligence and/or education on substance use could be direct and environmental, or indirect due to the presence of confounding genetic and shared family influences. We used the Minnesota Twin Family Study to distinguish these effects in males and females at age 24. In contrast to prevailing expectations, there were moderately negative direct nonshared environmental effects of both IQ and education on both smoking and drinking in both males and females. That is, controlling for family background effects in the form of both genetic and shared environmental influences, both higher IQ and greater education were associated with greater alcohol and nicotine use. These effects were accounted for by alcohol and nicotine use at age 17. Our results suggest that genetic and family-culture variables confound the associations between intelligence and education and substance use in young adults, rendering them indirect. Further research is needed to understand the roles of IQ and education in alcohol and nicotine use and their relative impacts on physical health throughout the lifespan.     

Genetic and environmental transactions underlying educational attainment

This report used a population-representative longitudinal twin study with two birth cohorts to explore the association between intelligence and education by understanding how genetic and environmental influences on intelligence moderate genetic and environmental influences on school grades and educational attainment. Nonshared environmental influences on grades were strong when IQ was low, but decreased across the range of IQ. Shared environmental influences common to age 24 educational attainment and age 17 IQ were strong when IQ was low, but genetic influences common to IQ and education were strong when IQ was high. These results suggest that the causal mechanisms linking educational variables with intelligence differ for people with different levels of intelligence.     

Age-of-Onset or Behavioral Sub-Types? A Prospective Comparison of Two Approaches to Characterizing the Heterogeneity within Antisocial Behavior

There are two common approaches to sub-typing the well-documented heterogeneity within antisocial behavior: age-of-onset (i.e., childhood-onset versus adolescence-onset; see Moffitt 1993) and behavioral (i.e., physical aggression versus non-aggressive rule-breaking). These approaches appear to be associated, such that aggression is more characteristic of childhood-onset antisocial behavior whereas rule-breaking is linked to both child- and adolescence-onset antisocial behavior. However, it remains unclear which approach, if either, better explains the heterogeneity within antisocial behavior. We examined this question in a prospective sample of male twins, assessed at the ages of 11, 14, 17, and 24 years. Although the age-of-onset subtypes predicted adult antisocial behavior in the expected direction when analyzed alone, this association dissipated once we controlled for aggression and rule-breaking. Such findings suggest that the behavioral sub-types of antisocial behavior may be a stronger predictor of later antisocial outcomes than is its age-of-onset.     

Environmental Contributions to the Stability of Antisocial Behavior over Time: Are They Shared or Non-shared?

It has recently been argued that shared environmental influences are moderate, identifiable, and persistent sources of individual differences in most forms of child and adolescent psychopathology, including antisocial behavior. Unfortunately, prior studies examining the stability of shared environmental influences over time were limited by possible passive gene-environment correlations, shared informants effects, and/or common experiences of trauma. The current study sought to address each of these limitations. We examined adolescent self-reported antisocial behavior in a 3.5 year longitudinal sample of 610 biological and adoptive sibling pairs from the Sibling Interaction and Behavior Study (SIBS). Results revealed that 74–81% of shared environmental influences present at time 1 were also present at time 2, whereas most non-shared environmental influences (88–89%) were specific to a particular assessment period. Such results provide an important constructive replication of prior research, strongly suggesting that shared environmental contributions to antisocial behavior are systematic in nature.