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Background: Few factor analyses and no network analyses have examined the structure of DSM phobic fears or tested the specificity of the relationship between panic disorder and agoraphobic fears. Methods: Histories of 21 lifetime phobic fears, coded as four-level ordinal variables (no fear to fear with major interference) were assessed at personal interview in 7514 adults from the Virginia Twin Registry. We estimated Gaussian Graphical Models on individual phobic fears; compared network structures of women and men using the Network Comparison Test; used community detection to determine the number and nature of groups in which phobic fears hang together; and validated the anticipated specific relationship between panic disorder and agoraphobia. Results: All networks were densely and positively inter-connected; networks of women and men were structurally similar. Our most frequent and stable solution identified four phobic clusters: (i) blood-injection, (ii) social-agoraphobia, (iii) situational, and (iv) animal-disease. Fear of public restrooms and of diseases clustered with animal and not, respectively, social and blood-injury phobias. When added to the network, the three strongest connections with lifetime panic disorder were all agoraphobic fears: being in crowds, going out of the house alone, and being in open spaces Conclusions: Using network analyses applied to a large epidemiologic twin sample, we broadly validated the DSM-IV typography but did not entirely support the distinction of agoraphobic and social phobic fears or the DSM placements for fears of public restrooms and diseases. We found strong support for the specificity of the relationship between panic disorder and agoraphobic fears. [ABSTRACT FROM AUTHOR]

Background: Vulnerability to depression can be measured in different ways. We here examine how genetic risk factors are inter-related for lifetime major depression (MD), self-report current depressive symptoms and the personality trait Neuroticism. Method: We obtained data from three population-based adult twin samples (Virginia n = 4672, Australia #1 n = 3598 and Australia #2 n = 1878) to which we fitted a common factor model where risk for 'broadly defined depression' was indexed by (i) lifetime MD assessed at personal interview, (ii) depressive symptoms, and (iii) neuroticism. We examined the proportion of genetic risk for MD deriving from the common factor v. specific to MD in each sample and then analyzed them jointly. Structural equation modeling was conducted in Mx. Results: The best fit models in all samples included additive genetic and unique environmental effects. The proportion of genetic effects unique to lifetime MD and not shared with the broad depression common factor in the three samples were estimated as 77, 61, and 65%, respectively. A cross-sample mega-analysis model fit well and estimated that 65% of the genetic risk for MD was unique. Conclusion: A large proportion of genetic risk factors for lifetime MD was not, in the samples studied, captured by a common factor for broadly defined depression utilizing MD and self-report measures of current depressive symptoms and Neuroticism. The genetic substrate for MD may reflect neurobiological processes underlying the episodic nature of its cognitive, motor and neurovegetative manifestations, which are not well indexed by current depressive symptom and neuroticism. [ABSTRACT FROM AUTHOR]

Background. The nature of the relationship between depressive vulnerability (DV) and acute adversity in the etiology of major depression (MD) remains poorly understood. Method. Stressful life events (SLEs) and MD onsets in the last year were assessed at four waves in cohort 1 (females) and at two waves in cohort 2 (males and females) from the Virginia Adult Twin Study. Structural equation modeling was conducted in Mplus. Results. In cohort 1, DV was strongly indexed by depressive episodes over the four waves (paths from +0.72 to 0.79) and predicted by SLEs in the month of their occurrence (+0.31 to 0.36). Wave-specific DV was associated both with stable DV (+0.29 to 0.33) and by forward transmission of DV from the preceding wave (+0.33 to 0.36). SLEs were predicted by stable DV (+0.29) and from SLEs in the preceding month (+0.06). As the cohort aged, MD onsets were better indexed by DV and more poorly predicted by SLEs. Parameter estimates were similar in males and females from cohort 2. In individuals with prior depressive episodes, the association between MD onset and SLEs was weakened while the prediction of SLEs from DV was substantially strengthened. We found no evidence for 'reverse causation' from MD episodes to SLEs. Conclusion. The interrelationship between DV and acute adversity in the etiology of MD is complex and temporally dynamic. DV impacts on MD risk both directly and indirectly through selection into high stress environments. Over time, depressive episodes become more autonomous. Both DV and SLEs transmit forward over time and therefore form clear targets for intervention. [ABSTRACT FROM AUTHOR]

BackgroundAlthough prior genetic studies of interview-assessed fears and phobias have shown that genetic factors predispose individuals to fears and phobias, they have been restricted to the DSM-III to DSM-IV aggregated subtypes of phobias rather than to individual fearful and phobic stimuli.MethodWe examined the lifetime history of fears and/or phobias in response to 21 individual phobic stimuli in 4067 personally interviewed twins from same-sex pairs from the Virginia Adult Twin Study of Psychiatric and Substance Abuse Disorders (VATSPSUD). We performed multivariate statistical analyses using Mx and Mplus.ResultsThe best-fitting model for the 21 phobic stimuli included four genetic factors (agora-social-acrophobia, animal phobia, blood-injection-illness phobia and claustrophobia) and three environmental factors (agora-social-hospital phobia, animal phobia, and situational phobia).ConclusionsThis study provides the first view of the architecture of genetic and environmental risk factors for phobic disorders and their subtypes. The genetic factors of the phobias support the DSM-IV and DSM-5 constructs of animal and blood-injection-injury phobias but do not support the separation of agoraphobia from social phobia. The results also do not show a coherent genetic factor for the DSM-IV and DSM-5 situational phobia. Finally, the patterns of co-morbidity across individual fears and phobias produced by genetic and environmental influences differ appreciably. [ABSTRACT FROM AUTHOR]