Child / Adolescent - Anxiety
Allison A. Morra, B.S.
Graduate Student
Miami University
Oxford, Ohio
Anne E. Kalomiris, Ph.D.
Staff Psychologist
Cincinnati Children's Hospital
Cincinnati, Ohio
Robin D. Thomas, Ph.D.
Professor
Miami University
Oxford, Ohio
Elizabeth J. Kiel, Ph.D.
Professor
Miami University
Oxford, Ohio
Understanding developmental and environmental risk factors for anxiety is paramount to better identify risk and potential early intervention targets. Parent-report remains a standard for assessing anxiety symptoms in early childhood. Error-related negativity (ERN), an event related potential evident in EEG recording when making a mistake, can serve as a neural indicator of anxiety unaffected by reporting biases (Meyer, 2017). Anxiety can be heritable, but environmental factors may also predict anxiety and ERN (Barlow, 2000). Parenting is one key environmental factor, as overprotective parenting behaviors have been correlated with more anxiety and larger ERN in children (Kessel et al., 2019). Differential susceptibility theory, however, says that people vary in their reactivity to environmental factors (Ellis et al., 2011); susceptible children may be more impacted by overprotection. We test this theory by examining how markers of susceptibility, such as cortisol reactivity or inhibited temperament (Gunnar & Quevedo, 2007; Kagan, et al., 1984), moderate the relation between overprotection and anxiety/ERN. We predict that the relation between overprotection and anxiety/ERN will occur only, or most strongly, for children at high levels of cortisol reactivity and inhibited temperament.
Children (n = 149; 40% female; 85% White, 93.8% not Hispanic) and their mothers (92.3% White, 96.4% not Hispanic) participated in laboratory visits at child ages 1 and 2 years for assessment of inhibited temperament (Fox et al., 2001), cortisol reactivity (area under the curve with respect to increase, AUCi; Pruessner et al., 2003), and overprotection (Buss, 2011; New Friends Vignette, McShane and Hastings, 2009). Dyads (n = 89) returned to the laboratory at early school age (M= 64.80 months, SD= 4.02) to assess anxiety symptoms (Preschool Anxiety Scale, Spence, 2001) and complete an EEG (Flanker task, Brooker & Buss, 2014). All data are collected and cleaned, except for ERN, which is being processed.
The first models tested whether susceptibility (inhibited temperament and AUCi in separate models) moderated the relation from overprotection (self-reported and observed in separate models) to mother-reported anxiety symptoms. With complete cases (n = 86), a marginal interaction emerged between observed overprotection and inhibited temperament (b = 1.63, SE = 0.94, t = 1.74, p = .086): the relation between overprotection and anxiety became increasingly positive at higher values of inhibited temperament. The interaction remained similarly sized (b = 1.43, SE = 0.87) when tested using multiple imputation to handle missing values. Additional regression models predicting ERN will be analyzed by the date of the conference.
Thus far, results are consistent with a diathesis-stress, rather than differential susceptibility, model of anxiety risk. In other words, an environment characterized by low overprotection does not confer benefits for inhibited toddlers more than uninhibited toddlers, but high overprotection is uniquely predictive of anxiety for more inhibited toddlers. Thus, reducing overprotection during child anxiety intervention may be expected to bring inhibited children’s functioning to the same level as their uninhibited peers.