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BACKGROUND: In man, many different events implying childhood separation from caregivers/unstable parental environment are associated with heightened risk for panic disorder in adulthood. Twin data show that the occurrence of such events in childhood contributes to explaining the covariation between separation anxiety disorder, panic, and the related psychobiological trait of CO(2) hypersensitivity. We hypothesized that early interference with infant-mother interaction could moderate the interspecific trait of response to CO(2) through genetic control of sensitivity to the environment. METHODOLOGY: Having spent the first 24 hours after birth with their biological mother, outbred NMRI mice were cross-fostered to adoptive mothers for the following 4 post-natal days. They were successively compared to normally-reared individuals for: number of ultrasonic vocalizations during isolation, respiratory physiology responses to normal air (20%O(2)), CO(2)-enriched air (6% CO(2)), hypoxic air (10%O(2)), and avoidance of CO(2)-enriched environments. RESULTS: Cross-fostered pups showed significantly more ultrasonic vocalizations, more pronounced hyperventilatory responses (larger tidal volume and minute volume increments) to CO(2)-enriched air and heightened aversion towards CO(2)-enriched environments, than normally-reared individuals. Enhanced tidal volume increment response to 6%CO(2) was present at 16-20, and 75-90 postnatal days, implying the trait's stability. Quantitative genetic analyses of unrelated individuals, sibs and half-sibs, showed that the genetic variance for tidal volume increment during 6%CO(2) breathing was significantly higher (Bartlett Ç = 8.3, p = 0.004) among the cross-fostered than the normally-reared individuals, yielding heritability of 0.37 and 0.21 respectively. These results support a stress-diathesis model whereby the genetic influences underlying the response to 6%CO(2) increase their contribution in the presence of an environmental adversity. Maternal grooming/licking behaviour, and corticosterone basal levels were similar among cross-fostered and normally-reared individuals.

For unknown reasons the inhalation of CO2-enriched air mixtures evokes acute panic-like symptoms in people with panic disorder and in their unaffected relatives. This study was set to determine whether, and to what extent, CO2-induced acute anxiety and panic disorder share the same genetic and environmental determinants. Cholesky structural equation models were used to decompose into genetic and environmental elements the correlation between self-assessed anxiety post-35%CO2–65%O2 inhalation and interview-based DSM-IV lifetime diagnoses of panic disorder in 346 young adult twin pairs of the Norwegian Institute of Health Panel, 12% of whom had been invited to take part into the CO2 study on the basis of self-reported symptoms of anxiety gathered 4–7 years before the provocation challenge. A full model corrected for the partially selective ascertainment showed that the phenotypic correlation between post-CO2 anxiety and DSM-IV panic was largely due to additive genetic influences, while shared and unique environmental agents concurred to explain a relatively minor proportion of the correlation between these two traits. According to the best-fitting model the genetic correlation between post-CO2 anxiety and panic was 0.81 (0.50–0.98); a common genetic factor was sufficient to explain the traits' covariation and a further, specific genetic factor was necessary to account for the residual phenotypic variance. The genetic determinants that lead to overreact to a hypercapnic stimulus coincide at a considerable extent with those that influence liability to naturally occurring panic. Environmental factors provide a modest—or no—contribution to the covariation of CO2-provoked anxiety with naturally occurring panic. © 2007 Wiley-Liss, Inc.

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.