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People with panic disorder-agoraphobia and their relatives often react anxiously to CO(2)-enriched gas mixtures. Available data are not suited to disentangle genetic from common environmental causes of familial aggregation of CO(2) reactivity, nor provide quantitative estimations of the sources of trait variation. Three-hundred-forty-six twin pairs belonging to the general population-based Norwegian NIPH Mental Health Study underwent self-assessments of anxiety and of DSM-IV panic symptoms after inhalation of a 35%CO(2)-65%O(2) mixture. Two thresholds were employed - at sample's 75th and 90th percentiles of responses - to define provoked panic attacks and to calculate polychoric correlations. Variance components were estimated by structural equation modelling (SEM). For definitions of responses based on the sum of all 13 panic symptoms, SEM could not discriminate between shared environmental versus genetic causes of familial resemblance for provoked attacks. For definitions of responses based on global anxiety, or on the sums of those symptoms (dyspnea, dizziness, palpitations) with highest variance post-CO(2), the best-fitting models indicated additive genetic factors as the sole causes for within-family resemblance. Best-fit heritability estimates ranged from 0.42 to 0.57. Genetic and idiosyncratic environmental factors explain most of individual differences in reactivity to hypercapnia. Within-family similarities for this trait are largely explained by genetic determinants.

In a sample of 398 twin pairs aged 8-17 belonging to the Italian Twin Registry we explored the extent to which physical clumsiness/motor problems covary with a broad spectrum of behavioral problems identified by the Child Behavior Checklist 6-18/DSM oriented scales, and the causes of such covariation. Only Anxiety and Attention Deficit Hyperactivity (ADH) Problems maintained significant correlation with Clumsiness after partialling out the effects of the other problem scales. By the co-twin control method we found no indication of clear, direct causal effect of Clumsiness upon Anxiety or ADH Problems, or vice versa. Twin bivariate analyses showed that the co-occurrence of motor problems and Anxiety/ADH Problems is best explained by genetic factors shared between Clumsiness and the behavioral problems phenotypes.

Heterogeneous life events (LE) precede the onset of-and potentially increase the susceptibility to-panic disorder (PD). It remains unknown whether LE can act as moderators in the context of gene-by-environment interactions (G×E) that alter the susceptibility to PD and the related trait of CO₂ sensitivity, nor it is known whether such moderation may depend on occurrence of events at different epochs in life. In 712 general population twins we analyzed by Maximum Likelihood analyses of ordinal data whether life (major- and stressful) events moderate the genetic risk for PD and CO₂ sensitivity, as indexed by the 35% CO₂ /65% O₂ challenge. For CO₂ sensitivity, best-fitting models encompassed both additive and interactional effects that increased linearly with the cumulative number and severity (SEV) of events in lifetime. By analyzing the moderation effect of cumulative SEV separately for events that had occurred in adulthood (between age 18 and 37) or during childhood-adolescence (before the 18th birthday), we found evidence of G×E only within the childhood-adolescence window of risk, although twins had rated the childhood-adolescence events as significantly (P = 0.001) less severe than those having occurred during adulthood. For PD, all interactional terms could be dropped without significant worsening of the models' fit. Consistently with a diathesis-stress model, LE appear to act as moderators of the genetic variance for CO₂ sensitivity. Childhood-adolescence appears to constitute a sensitive period to the action of events that concur to alter the susceptibility to this panic-related trait.

Although Internalized and Externalized problem behaviors are described as separate phenomena at the psychometric and clinical levels, they frequently co-occur. Only few studies, however, have investigated the causes of such covariation. In a sample of 398 twin pairs aged 8-17 drawn from the general population-based Italian Twin Registry, we applied bivariate genetic analyses to parent-rated CBCL/6-18 Internalization and Externalization scores. Covariation of Internalizing and Externalizing problem behaviors was best explained by genetic and common environmental factors, while the influence of unique environmental factors upon covariance appeared negligible. Odds ratio values showed that a borderline/clinical level of Externalization is a robust predictor of co-existing Internalizing problems in the same child, or within a sibship. Our findings help to approximate individual risks (e.g., in clinical practice, predicting the presence of Internalization in an externalizing child, and vice-versa), and to recognize that several shared environmental and genetic factors can simultaneously affect a child's proneness to suffer from both types of problem behaviors.

Objective: To explore the contributions of genetic and environmental influences to individual variation and covariation of the Child Behavior Checklist (CBCL) DSM-oriented scales (DOS) originally proposed by Achenbach and associates in 2001. Method: A classic twin study of 398 twin pairs ages 8 to 17 years belonging to the population-based Italian Twin Registry, assessed by parents using the CBCL for Ages 6 to 18 (CBCL/6-18). Results: Univariate analyses showed that compared with the classic CBCL/6-18 empirical subscales, the DOS have higher heritability (lowest 0.54 for Anxiety Problems, highest 0.71 for Conduct Problems) and simpler causal structure in that the phenotypic variance was satisfactorily explained by additive genetic and unique environmental factors only. Multivariate analyses showed that the causes of phenotypic correlation among the different DOS can be attributed to one common genetic factor and to two idiosyncratic environmental factors, each loading differently on the Internalizing (Anxiety and Affective Problems) and the Externalizing (Attention-Deficit/Hyperactivity, Oppositional Defiant, and Conduct Problems) CBCL/6-18 DOS. Conclusions: Several common risk factors of both genetic and environmental nature can simultaneously affect a child's proneness to develop the psychopathological signs and symptoms captured by the CBCL/6-18 DOS.