ABSTRACT
The Southern California Twin Register at the University of Southern California (USC) was initiated in 1984 and continues to provide an important resource for studies investigating genetic and environmental influences on human behavior. This article provides an update on the current register and its potential for future twin studies using recruitment through school district databases and voter records. An overview is also provided for an ongoing longitudinal twin study investigating the development of externalizing psychopathology from childhood to young adulthood, the USC Study of Risk Factors for Antisocial Behavior. Characteristics of the twins and their families are presented, including recruitment and participation rates, as well as attrition analyses and a summary of key findings to date.
Subject(s)
Antisocial Personality Disorder/epidemiology , Diseases in Twins/epidemiology , Genetics, Behavioral , Mental Disorders/epidemiology , Registries , Twins, Dizygotic/genetics , Twins, Monozygotic/genetics , Adolescent , Adult , Aged , Antisocial Personality Disorder/genetics , Antisocial Personality Disorder/psychology , California/epidemiology , Child , Diseases in Twins/genetics , Diseases in Twins/psychology , Female , Gene-Environment Interaction , Humans , Longitudinal Studies , Male , Mental Disorders/genetics , Mental Disorders/psychology , Middle Aged , Patient Selection , Prospective Studies , Risk Factors , Twins, Dizygotic/statistics & numerical data , Twins, Monozygotic/statistics & numerical data , Young AdultABSTRACT
PURPOSE: This twin study examined the structure of genetic and environmental influences on aggression and rule-breaking in order to examine change and stability across the span of childhood to mid-adolescence. METHODS: Behavioral assessments were conducted at two time points: age 9-10 years and 14-15 years. Using behavioral genetics biometric modeling, the longitudinal structure of influences was investigated. RESULTS: Aggression and rule-breaking were found to be influenced by a latent common factor of antisocial behavior (ASB) within each wave of data collection. The childhood-age common factor of ASB was influenced by 41% genetics, 40% shared environment and 19% nonshared environment. In adolescence, 41% of influences on the common factor were novel and entirely genetic, while the remainder of influences were stable across time. Additionally, both aggression and rule-breaking within each wave were found to have unique influences not common across subscales or across waves, highlighting specificity of influences on different problem behaviors at both ages. CONCLUSIONS: This research sheds light on the commonality of influences on etiology of different forms of antisocial behavior, and suggests future directions for research into intervention for antisocial behavior problems in youth, such as investigation of adolescence-specific environmental influences on the development of antisocial behavior problems.
ABSTRACT
PURPOSE: This study investigated genetic and environmental commonalities and differences between aggressive and non-aggressive antisocial behavior (ASB) in male and female child and adolescent twins, based on a newly developed self-report questionnaire with good reliability and external validity - the Self-Report Delinquency Interview (SR-DI). METHODS: Subjects were 780 pairs of twins assessed through laboratory interviews at three time points in a longitudinal study, during which the twins were: (1) ages 9-10 years; (2) age 11-13 years, and (3) age 16-18 years. RESULTS: Sex differences were repeatedly observed for mean levels of ASB. In addition, diverse change patterns of genetic and environmental emerged, as a function of sex and form of ASB, during the development from childhood to adolescence. Although there was some overlap in etiologies of aggressive and non-aggressive ASB, predominantly in shared environmental factors, their genetic overlap was moderate and the non-shared environmental overlap was low. CONCLUSIONS: Taken together, these results reinforced the importance of differentiating forms of ASB and further investigating sex differences in future research. These results should be considered in future comparisons between youth self-report and parental or teacher report of child and adolescent behavior, and may help elucidate commonalities and differences among informants.
ABSTRACT
Impulsivity is a multifaceted personality construct that plays an important role throughout the lifespan in psychopathological disorders involving self-regulated behaviors. Its genetic and environmental etiology, however, is not clearly understood during the important developmental period of adolescence. This study investigated the relative influence of genes and environment on self-reported impulsive traits in adolescent twins measured on two separate occasions (waves) between the ages of 11 and 16. An adolescent version of the Barratt Impulsiveness Scale (BIS) developed for this study was factored into subscales reflecting inattention, motor impulsivity, and non-planning. Genetic analyses of these BIS subscales showed moderate heritability, ranging from 33-56% at the early wave (age 11-13 years) and 19-44% at the later wave (age 14-16 years). Moreover, genetic influences explained half or more of the variance of a single latent factor common to these subscales within each wave. Genetic effects specific to each subscale also emerged as significant, with the exception of motor impulsivity. Shared twin environment was not significant for either the latent or specific impulsivity factors at either wave. Phenotypic correlations between waves ranged from r = 0.25 to 0.42 for subscales. The stability correlation between the two latent impulsivity factors was r = 0.43, of which 76% was attributable to shared genetic effects, suggesting strong genetic continuity from mid to late adolescence. These results contribute to our understanding of the nature of impulsivity by demonstrating both multidimensionality and genetic specificity to different facets of this complex construct, as well as highlighting the importance of stable genetic influences across adolescence.
Subject(s)
Impulsive Behavior/genetics , Impulsive Behavior/psychology , Adolescent , Analysis of Variance , Child , Factor Analysis, Statistical , Female , Humans , Longitudinal Studies , Male , Models, Genetic , Neuropsychological Tests , Twins, Dizygotic , Twins, MonozygoticABSTRACT
High EEG frontal alpha power (FAP) is thought to represent a state of low arousal in the brain, which has been related in past research to antisocial behavior (ASB). We investigated a longitudinal sample of 900 twins in two assessments in late childhood and mid-adolescence to verify whether relationships exist between FAP and both aggressive and nonaggressive ASB. ASB was measured by the Child Behavioral Checklist, and FAP was calculated using connectivity analysis methods that used principal components analysis to derive power of the most dominant frontal activation. Significant positive predictive relationships emerged in males between childhood FAP and adolescent aggressive ASB using multilevel mixed modeling. No concurrent relationships were found. Using bivariate biometric twin modeling analysis, the relationship between childhood FAP and adolescent aggressive ASB in males was found to be entirely due to genetic factors, which were correlated r=0.22.
Subject(s)
Adolescent Behavior/physiology , Aggression/physiology , Antisocial Personality Disorder/diagnosis , Conduct Disorder/diagnosis , Frontal Lobe/physiopathology , Twins/genetics , Adolescent , Antisocial Personality Disorder/genetics , Antisocial Personality Disorder/physiopathology , Child , Conduct Disorder/genetics , Conduct Disorder/physiopathology , Diseases in Twins/diagnosis , Diseases in Twins/genetics , Diseases in Twins/physiopathology , Electroencephalography , Female , Humans , MaleABSTRACT
AIMS: Clinical studies demonstrate attenuation of trigeminal-related pain states such as migraine by intranasal CO(2) application. This study investigated the underlying mechanisms of this observation and its potential use to reverse trigeminal pain and hypersensitivity. MAIN METHODS: We used a behavioral rat model of capsaicin-induced trigeminal thermal hyperalgesia, intranasal CO2 application and several pharmacologic agents such as carbonic anhydrase, acid-sensing ion channels (ASICs), and TRPV1 blocker as well as acidic buffer solutions to investigate and mimic the underlying mechanism. KEY FINDINGS: Intranasal CO(2) application produced a robust dose-dependent antihyperalgesic effect in rats that lasted at least one hour. Blockade of nasal carbonic anhydrase with a dorzolamide solution (Trusopt ophthalmic solution) showed only a non-significant decrease of the antihyperalgesic effect of intranasal CO(2) application. Pharmacologic blockade of ASICs or TRPV(1) receptor significantly attenuated the antihyperalgesic effect of CO(2) application. The effect of intranasal CO(2) application could be mimicked by application of pH 4, but not pH 5, buffer solution to the nasal mucosa. As with CO(2) application, the antihyperalgesic effect of intranasal pH 4 buffer was blocked by nasal application of antagonists to ASICs and TRPV(1) receptors. SIGNIFICANCE: Our results indicate that intranasal CO(2) application results in a subsequent attenuation of trigeminal nociception, mediated by protonic activation of TRPV(1) and ASIC channels. A potential central mechanism for this attenuation is discussed. The antihyperalgesic effects of intranasal CO(2) application might be useful for the treatment of trigeminal pain states.