Trajectories of behavioral inhibition as a function of genetic and environmental risk for psychopathology

• In Event: Poster Session 08
  In Poster Session: PS 08 Topic - Developmental Psychopathology

Abstract

Behavioral inhibition (BI) is a temperament profile characterized by shy, fearful, and hypervigilant behaviors in novel social situations (Kagan et al., 1984). Stability and continuity of high BI through childhood predicts higher rates of multiple anxiety disorders and increased risk for social anxiety in adolescence (Biederman et al., 1992; Chronis-Tuscano et al., 2009). However, not every child with high BI progresses on a trajectory towards anxiety, which highlights the potential role of risk and protective factors in canalizing pathways for these children. Little is known about why some children maintain versus change their rank-order stability from early to middle childhood. Developmental studies of BI have examined parental psychopathology (Stevenson-Hinde et al., 2013) as one risk factor, and report that BI tendencies may be reinforced in the presence of parental anxiety and depression, leading to higher risk for anxiety in these children. However, most of these studies have investigated parent risk factors in genetically-related families, making it impossible to disentangle rearing environmental risk from genetic risks that may contribute to the stability of BI. As genetically-informed studies indicate that BI and its stability and change are genetically influenced (Smith et al., 2012), failure to use a genetically-informed design is a critical limitation. The present study leveraged data from a longitudinal adoption study to investigate how genetic and environmental risk for psychopathology influence BI trajectories and contribute to stability patterns.
The sample included 340 families from the Early Growth and Development Study. Children’s median age at adoption was 2 days (SD = 13 days), 43% were female, and 58% were white (Leve et al., 2019). Child BI was observed at 18 and 27 months (Stranger task), 4.5 years (Scary mask), and 7 years (Speech task). Birth parent (BP) risk for psychopathology was indexed based on symptom and diagnosis count, age of onset, and proportion of first-degree relatives with a diagnosis (Marceau et al., 2015). Adoptive parent (AP) Internalizing was indexed by adoptive mothers’ and fathers’ reports on the Beck Anxiety and Depression Inventories (Beck &Steer, 1993). AP externalizing was indexed by adoptive parents’ reports on substance use from the Composite International Diagnostic Interview (Kessler et al., 1998) and the Antisocial Action scale (Levenson et al., 1995). Reports were averaged across mothers and fathers to index family-wise internalizing and externalizing risk.
Latent growth modeling showed that BI trajectories were more stable (Fig 1) for infants with higher BI at 18 months (β= -0.07, p = .01). BP psychopathology risk interacted only with AP internalizing risk to predict BI trajectories (β= 0.06, p = .02). Simple-slopes analysis (Fig 2) indicated that at low levels of AP internalizing, BI trajectories were not significantly different across levels of genetic risk. In contrast, at higher levels of AP internalizing, children with higher genetic risk for psychopathology showed an exacerbated increase in BI over time, compared to children with low genetic risk. We discuss these findings in light of the specific effect of parents’ internalizing but not externalizing tendencies on BI stability and continuity.

Authors

• Berenice Anaya, Pennsylvania State University, University Park
  Presenting Author

• Koraly Elisa Perez-Edgar, Pennsylvania State University, University Park
  Non-Presenting Author

• Leslie D. Leve, University of Oregon
  Non-Presenting Author

• Jody M. Ganiban, George Washington University
  Non-Presenting Author

• Daniel S. Shaw, University of Pittsburgh
  Non-Presenting Author

• David Reiss, Yale University
  Non-Presenting Author

• Misaki N. Natsuaki, University of California - Riverside
  Non-Presenting Author

• Jenae M Neiderhiser, Pennsylvania State University, University Park
  Non-Presenting Author