Individual Submission Summary
Share...

Direct link:

Investigation of a developmental pathway from infant anger reactivity to childhood ADHD symptoms: inhibitory control as mediator

Sat, March 23, 2:30 to 4:00pm, Hilton Baltimore, Floor: Level 1, Latrobe

Integrative Statement

Background.
ADHD is a neurodevelopmental disorder with a complex pathogenesis. Individual differences in temperamental reactivity—in particular, anger reactivity (negative emotional responses to frustrating or limiting events)—are predictive of ADHD (e.g., Willoughby, Gottfredson, Stifter, & The Family Life Project Investigators, 2017). However, we know little about how this reactivity-related risk translates into ADHD symptoms (i.e., what are mediators and moderators of this risk?). Using a 9-year multi-method prospective longitudinal design, the goal of this study was to examine the mediating role of poor inhibitory control, one domain of executive functioning deficits that frequently co-occur with ADHD symptoms (Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005), on the relation between infant anger reactivity and childhood ADHD symptoms. Given the transactional relations between temperament and caregiving early in life on child development (Bates & Pettit, 2007), we also examined whether early caregiving moderated the effects of anger reactivity on either inhibitory control or ADHD symptoms in a moderated mediation model.

Methods.
Participants included 291 children (132 male; 159 female) who took part in a larger study of temperament and social-emotional development. Anger reactivity was assessed by observation of facial anger during an arm restraint task at 9 months of age. Caregiving behaviors were observed during a series of semi-structured mother-infant tasks at 9 months of age (higher quality = more sensitive, less intrusive). Inhibitory control was assessed by performance on a go/no-go task at 5 years of age. ADHD symptoms were assessed by parent- and teacher-report questionnaires at 7 and 9 years, respectively.

Results.
Anger reactivity (B = .16, p < .05) and poor inhibitory control (B = -.21, p< .01) were predictive of ADHD symptoms. Caregiving moderated the effects of anger reactivity on inhibitory control (B = .23, p < .01), but not ADHD symptoms (B = .11, p > .05). Simple slope analyses examining the relation between anger reactivity and inhibitory control at lower and higher quality caregiving revealed that anger reactivity was negatively related to inhibitory control at lower-quality caregiving (i.e., -1SD; B = -.32, p < .01), but not significantly related to inhibitory control at higher-quality caregiving (i.e., +1SD; B = .11, p > .05). Results of mediation analyses supported a moderated mediation model, in which the indirect effects of anger reactivity on ADHD symptoms were conditional on quality of caregiving. Inhibitory control mediated the effect of anger reactivity on ADHD symptoms, but only among children exposed to lower-quality caregiving (b = .04, 95% CI [.004, .08]). Effects remained significant controlling for verbal IQ.

Conclusions.
Anger reactivity is predictive of ADHD from infancy, suggesting anger reactivity as an early indicator of ADHD risk. Higher-quality maternal caregiving did not buffer against the direct risk of anger reactivity on ADHD, but did buffer against the indirect risk by reducing the negative effect of anger reactivity on inhibitory control. Thus, in the developmental pathway from anger reactivity to ADHD, more sensitive, less intrusive parenting may support the development of protective mechanisms to remediate ADHD risk.

Authors