Developmental Pathways from Prenatal Substance Exposure to Reactive Aggression.

• In Event: Multisystem Stress Activity and Subtypes of Aggression in Three Developmental Periods.

Abstract

Few studies have examined etiological pathways from prenatal substance exposure to adolescent reactive aggression (i.e., hostile, angry, and often impulsive response to a perceived provocation; Eisner & Malti, 2016). The objective was to examine pathways from prenatal substance exposure to reactive aggression in adolescence via early childhood developmental processes in a higher risk sample experiencing a multitude of stressors (e.g., context of socioeconomic adversity, maternal substance use, and violence exposure) who primarily self-identified as Black or Mixed Race. Importantly, the autonomic nervous system (ANS) has been implicated in the development of aggression. The pattern of functioning across the sympathetic (SNS) and parasympathetic (PNS) branches (e.g., coactivation, coinhibition, or reciprocal activation; Berntson et al., 1991; 1994) of the ANS may be particularly relevant for the development of aggression. As such, the role of the coordination of the ANS was examined in predicting adolescent reactive aggression. We tested a conceptual model for the association between prenatal substance exposure and reactive aggression in early adolescence via three major developmental processes in early childhood: child autonomic reactivity, harsh parenting, and exposure to violence.

The sample included 216 mother-child dyads (106 biologically male children) from a prospective study of prenatal cocaine and other substance exposure (116 cocaine-exposed, 100 non-cocaine exposed). Autonomic reactivity was recorded during frustration tasks at 13 and 48-months and at early school age of approximately 60 months (i.e., at least 3 months after children began kindergarten). RSA reactivity was assessed at 13, 48, and 60 months, and SCL was assessed at 60 months. Maternal harshness was assessed using lab-based behavioral observations during a free-play task at child age of 7, 13, 24, 36 and 48 months. Violence exposure was assessed using mother report at 1, 7, 13, 18, 24, 36, 48, and 60 months. In kindergarten, teacher reports and school observations of externalizing behavior were obtained. In early adolescence (M = 13.26 years, SD = .82), adolescent self-report of reactive relational and physical aggression (α > .74) was obtained.

Structural equation modeling was used to test the conceptual model using Mplus (see Figure 1). Results supported paths from violence exposure across early childhood and early school age to school age autonomic reactivity and early adolescent reactive aggression. There was also a significant interaction effect of SNS and PNS reactivity on adolescent reactive aggression, with sympathetic arousal and parasympathetic suppression at early school age associated with higher reactive relational and reactive physical aggression in adolescence (see Figure 2).

Maternal substance use was also associated with a cascade of risk and similar paths to reactive aggression were found for both relational and physical aggression. Violence exposure and a pattern of SNS activation with PNS withdrawal were associated with both forms of reactive aggression in early adolescence. The different patterns of RSA and SCL coupling predicted lower and higher levels of reactive aggression, which highlight the importance of examining the coordination of the branches of the ANS.

Authors

• Stephanie Godleski, Rochester Institute of Technology
  Presenting Author

• Pamela Schuetze, State University of New York Buffalo State University

• Rina Das Eiden, The Pennsylvania State Univeristy

• Amanda Nickerson, State University of New York at Buffalo (SUNY Buffalo)

• Jamie M. Ostrov, State University of New York at Buffalo (SUNY Buffalo)