Suicide is a major concern among active-duty military personnel. Aggression represents a salient risk factor for suicide among civilians, yet is relatively understudied among military populations. Although several theories posit a relation between aggression and suicide with putative underlying mechanisms of social isolation, access to firearms, and alcohol use, researchers have yet to test these potential mediators. This study uses rich, longitudinal data from the Army Study to Assess Risk and Resilience (STARRS) Pre/Post Deployment Study (PPDS) to examine whether aggression longitudinally predicts suicide attempts and to identify mediators of this association.

Army soldiers (N = 8483) completed assessments 1 month prior to deployment and 1, 2–3, and 9–12 months post-deployment. Participants reported on their physical and verbal aggression, suicide attempts, social network size, firearm ownership, and frequency of alcohol use.

As expected, pre-deployment aggression was significantly associated with suicide attempts at 12-months post-deployment even after controlling for lifetime suicide attempts. Social network size and alcohol use frequency mediated this association, but firearm ownership did not.

Findings further implicate aggression as an important suicide risk factor among military personnel and suggest that social isolation and alcohol use may partially account for this association.

Prior work has indicated both theoretical and empirical overlap between social and physical aggression. The extent to which their covariance can be explained by the same underlying genetic or environmental factors, however, remains unclear. It is also uncertain whether or how the origins of their covariance might vary across sex. The current study sought to fill these gaps in the literature.

We examined maternal and teacher reports of youth physical and social aggression in over 1000 6–10 years old (mean age = 8.02 years) twin pairs from the Michigan State University Twin Registry. We made use of the bivariate correlated factors model to clarify the origins of their association. We further tested both sex difference and no-sex difference versions of that model to determine whether there are sex differences in the association between social and physical aggression, as often assumed.

The covariation between social and physical aggression was due to overlapping genetic factors and common environmental conditions. Specifically, 50–57% of the genetic factors, 74–100% of the shared environmental factors, and 28–40% of the unique environmental factors influencing physical aggression also influenced social aggression according to both mother and teacher reports. These shared etiological factors did not differ across sex.

These findings argue against the common assumption that social aggression is the ‘female version’ of male physical aggression, and instead suggest that social aggression may be best conceptualized as a form of antisocial behavior that shares developmental pathways with other manifestations of externalizing pathology.

Physical aggression (PA) tends to have its onset in infancy and to increase rapidly in frequency. Very little is known about the genetic and environmental etiology of PA development during early childhood. We investigated the temporal pattern of genetic and environmental etiology of PA during this crucial developmental period.

Participants were 667 twin pairs, including 254 monozygotic and 413 dizygotic pairs, from the ongoing longitudinal Quebec Newborn Twin Study. Maternal reports of PA were obtained from three waves of data at 20, 32 and 50 months. These reports were analysed using a biometric Cholesky decomposition and linear latent growth curve model.

The best-fitting Cholesky model revealed developmentally dynamic effects, mostly genetic attenuation and innovation. The contribution of genetic factors at 20 months substantially decreased over time, while new genetic effects appeared later on. The linear latent growth curve model revealed a significant moderate increase in PA from 20 to 50 months. Two separate sets of uncorrelated genetic factors accounted for the variation in initial level and growth rate. Non-shared and shared environments had no effect on the stability, initial status and growth rate in PA.

Genetic factors underlie PA frequency and stability during early childhood; they are also responsible for initial status and growth rate in PA. The contribution of shared environment is modest, and perhaps limited, as it appears only at 50 months. Future research should investigate the complex nature of these dynamic genetic factors through genetic–environment correlation (rGE) and interaction (G × E) analyses.