Abstract
Reduced volumes in brain regions of interest (ROIs), primarily from adult samples, are associated with posttraumatic stress disorder (PTSD). We extended this work to children using data from the Adolescent Brain Cognitive Development (ABCD) Study® (N = 11,848; Mage = 9.92). Structural equation modeling and an elastic-net (EN) machine-learning approach were used to identify potential effects of traumatic events (TEs) on PTSD symptoms (PTSDsx) directly, and indirectly via the volumes 300 subcortical and cortical ROIs. We then estimated the genetic and environmental variation in the phenotypes. TEs were directly associated with PTSDsx (r = 0.92) in children, but their indirect effects (r < 0.0004)—via the volumes of EN-identified subcortical and cortical ROIs—were negligible at this age. Additive genetic factors explained a modest proportion of the variance in TEs (23.4%) and PTSDsx (21.3%), and accounted for most of the variance of EN-identified volumes of four of the five subcortical (52.4–61.8%) three of the nine cortical ROIs (46.4–53.3%) and cerebral white matter in the left hemisphere (57.4%). Environmental factors explained most of the variance in TEs (C = 61.6%, E = 15.1%), PTSDsx (residual-C = 18.4%, residual-E = 21.8%), right lateral ventricle (C = 15.2%, E = 43.1%) and six of the nine EN-identified cortical ROIs (C = 4.0–13.6%, E = 56.7–74.8%). There is negligible evidence that the volumes of brain ROIs are associated with the indirect effects of TEs on PTSDsx at this age. Overall, environmental factors accounted for more of the variation in TEs and PTSDsx. Whereas additive genetic factors accounted for most of the variability in the volumes of a minority of cortical and in most of subcortical ROIs.
Highlights
Exposure to traumatic events (TEs) is common, with approximately 80% of the US population having experienced at least one during their lifetime (Breslau 2009)
The range of λ values that restricted the fit within one standard error (SE) of maximum increase of mean squared error (MSE), identified five subcortical, one global, and nine cortical volumetric regions of interest (ROIs) potentially associating with the indirect effects of TEs on PTSDsx
We demonstrated that the measures of TEs and PTSDsx had low endorsement rates, TEs strongly associate with PTSDsx in children 9–11 years old
Summary
Exposure to traumatic events (TEs) is common, with approximately 80% of the US population having experienced at least one during their lifetime (Breslau 2009). TEs are common during childhood (Farrugia et al 2011) and are necessary but not sufficient risk factors for developing posttraumatic stress disorder (PTSD) and symptoms (PTSDsx) thereof (Cloitre et al 2009). Meeting PTSD diagnosis after experiencing TEs is less common (Breslau 2009; Perkonigg et al 2000; Santiago et al 2013), and the risk varies depending on the type of trauma. Greater risk for developing PTSD is linked to: (i) exposure to TEs during childhood or adolescence as opposed to exclusively during adulthood (Kulkarni et al 2013); and (ii) interpersonal. Behavior Genetics trauma (IPT; e.g., sexual and physical assault; Forbes et al 2012; Thege et al 2017; Weaver and Clum 1995) compared to experiencing accidental TEs (e.g., natural disasters, motor vehicle accident) or witnessing them. Beyond type of trauma experienced, neurobiological (Akiki et al 2017; Cross et al 2017; Herringa 2017) and genetic factors (Nievergelt et al 2019; Nugent et al 2008; Sheerin et al 2017) are associated with risk of PTSD
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