Send to

Choose Destination
Dev Psychopathol. 2011 Feb;23(1):101-14. doi: 10.1017/S0954579410000672.

The interactive effect of marital conflict and stress reactivity on externalizing and internalizing symptoms: the role of laboratory stressors.

Author information

School of Education, Stanford University, 485 Lasuen Mall, Stanford, CA 94305-3096, USA.


Growing evidence supports the biological sensitivity to context theory, which posits that physiologically reactive children, as indexed by autonomic nervous system (ANS) reactivity to laboratory stressors, are more susceptible to both negative and positive environmental influences than their low reactive peers. High biological sensitivity is a risk factor for behavioral and health problems in the context of high adversity, whereas in contexts of low adversity it has been found to promote positive adaptation. However, several studies have shown the opposite effect, finding that children who exhibited high ANS reactivity in response to interpersonal stressors were buffered from the deleterious effects of marital conflict, whereas children who showed low ANS reactivity were more vulnerable to high levels of marital conflict. Using an ethnically diverse sample of 260 kindergartners (130 girls, 130 boys), the current study investigated whether the interaction effect of marital conflict and the two branches of ANS reactivity on children's externalizing and internalizing symptoms differs with the nature of the laboratory challenge task used to measure children's stress response. As hypothesized, results indicate that the interaction between ANS reactivity and marital conflict significantly predicted children's behavior problems, but the direction of the effect varied with the nature of the challenge task (i.e., interpersonal or cognitive). This study illustrates the importance of considering the effect of laboratory stimuli when assessing whether children's ANS reactivity moderates the effects of adversity exposure on adaptation.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Cambridge University Press
Loading ...
Support Center