Clinical Brown Bag

Stefanie Mayer, Clinical Doctoral Student

Thursday, March 21, 2013, 12:00 pm – 1:00 pm
3021  East Hall

Event Information

Background: Dysregulation in Hypothalamic-Pituitary-Adrenal (HPA) axis response to stress is associated with a wide range of internalizing and externalizing problem behaviors in children and adults, through unclear mechanisms. Clarifying mechanisms requires a more nuanced understanding of this stress system. Researchers have identified cognitive and contextual factors that drive individual and group differences in HPA response to stress. Yet, the way cognition and context interact to impact stress reactivity is poorly understood. The current study investigated whether the impact of a cognitive factor - effortful control (EC) - on cortisol reactivity is moderated by type of stress context (frustration vs. a fear task). Method: Sixty-four participants were recruited from families that participated in a NIMH-funded longitudinal study (Olson, Sameroff, Kerr, Lopez, & Wellman, 2005). Laboratory and mother-rated EC was measured at age 3; at age 6 children were randomly assigned to one of two stress protocols to elicit frustration (n = 31; undoable task) or fear (n = 33; exposure to fake snake). A total of 17 saliva samples were collected.

Results: We used a modified growth curve modeling framework to examine the impact of cognition and stress context on cortisol reactivity to the two stress protocols. Both laboratory EC (EC-lab) and mother-rated EC (EC-mom) interacted with stress context in predicting cortisol peak levels (p < .05, p = .05, respectively) as well as slope to peak (both ps < .05). Separate models were also conducted for each stress context. In the frustration context, children with higher levels of effortful control – both EC-lab and EC-mom- showed decreased cortisol peak values (both ps < .01) and a flatter slope to peak (both ps < .01). In the fear context, children with higher levels of EC-lab showed increased cortisol peak levels (p < .05) and a steeper slope towards peak (p < .05). Results for EC-mom produced a similar pattern in the fear context, but failed to reach significance (ps > .05).

Discussion: Individual differences in neuroendocrine stress responses may be due to interactions between cognitive skills and stressor type. Our study demonstrated that early individual differences in EC (measured at age 3) modulated children`s stress responses at age 6 depending on the type of stressor. While high EC predicted reduced cortisol response during frustration, it predicted heightened stress response to fear. It is likely that different components of EC, such as emotion regulation and attention, interact with the stress context. A better understanding of this complex interplay may help us tailoring stress intervention techniques by targeting specific cognitions that are particularly salient in modulating stress reactivity in a given context. Ultimately, these efforts will help us better understand the role of stress in disease and develop improved methods for modulating its negative effects.