Cortisol is an important physiological marker of stress, which has been linked to a range of health outcomes. Unhealthy patterns of cortisol are associated with an increased risk for physical health problems, such as cancer and diabetes, as well as poor mental health. This study examined how parent and child cortisol patterns are linked across days. According to transactional models, parents and children likely have a bidirectional influence on one another. Yet, little is known about the extent to which parents and children affect each other’s physiological functioning, including cortisol. Research indicates that family members’ cortisol patterns covary over time, but the direction of effect is unclear (i.e., whether parents affect their child’s cortisol, if children affect their parent’s cortisol, or both). In this study, we test the direction of effect between parents’ and children’s cortisol patterns across a four-day period. We hypothesize there will be bidirectional linkages between parent and child cortisol.
This study used a sample of 311 parent-child dyads in an eight-day daily diary study as part of the Work, Family, and Health Study. Cortisol was collected on four study days and included the cortisol awakening response (CAR; slope of cortisol between waking and 30 minutes post-wake) and bedtime levels of cortisol. Cortisol exhibits a diurnal rhythm, where cortisol levels peak after waking and decline over the day. Therefore unhealthy patterns of cortisol include high bedtime levels of cortisol and blunted CAR. Cross-lagged models estimated parent-driven paths (parent cortisol predicts child cortisol) and child-driven paths (child cortisol predicts parent cortisol). Models controlled for previous levels of cortisol (e.g., stability paths). Nested models were used to test whether model paths could be constrained to be equal across days. Control variables include child age, gender, time of cortisol sample, medication use, daily stressors, and race.
Higher children’s bedtime cortisol levels were significantly associated with higher parent bedtime cortisol levels the following day (B=.12, p<.001). By contrast, parents’ bedtime cortisol levels were not associated with children’s bedtime cortisol levels (B=.04, p = ns). Steeper children’s CAR was significantly associated with steeper parents’ CAR the following day (B= .08, p<.05), but parents’ CAR was not associated with children’s CAR (B = -.03, p = ns). Model fit was acceptable according to RMSEA, NNFI, and CFI.
Contrary to our hypothesis, parent and child cortisol patterns did not have bidirectional associations. Child cortisol predicted parent cortisol but not vice versa, supporting a child-driven model of stress transmission. Thus, children may have strong influences on their parents’ physiological stress system. Interventions that help parents reduce their physiological reactivity to children’s stress are warranted. The discussion will focus on underlying processes and intervention strategies.