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Introduction
Prior studies have found that parents and children have a bidirectional influence on one another’s behavior, in line with transactional models of development (Sameroff, 2009). It is also likely that parents and children affect each other’s physiological functioning. Cortisol is an important physiological marker of stress linked to numerous health outcomes. Research indicates that family members’ cortisol patterns covary over time (Papp, Pendry, & Adam, 2009), 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 examine the direction of effect between parents’ and children’s cortisol patterns across a four-day period, hypothesizing that parent-child cortisol covariation will be bidirectional.
Methods
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 two cortisol indicators: cortisol awakening response (CAR; slope of cortisol between waking and 30 minutes post-wake) and bedtime levels of cortisol. Given the diurnal rhythm of cortisol (daily cortisol levels peak after waking and decline over the day),unhealthy patterns of cortisol include high bedtime levels of cortisol and blunted CAR. We converted cortisol values to nmol/l and log transformed them for analyses. Models estimated cross-lagged paths, including parent-driven paths (parent predicts child cortisol) and child-driven paths (child predicts parent cortisol). Models examined associations between the same cortisol indicator (e.g., parent/child CARs) and different indicators (e.g., bedtime levels/CAR). Models included stability paths, allowing the cross-lagged paths to be estimated while controlling for previous levels. 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.
Results
When controlling for prior levels, higher children’s bedtime cortisol levels were significantly associated with higher parent bedtime cortisol levels the following day (B=.12, p<.001; Figure 1). 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). Higher children’s bedtime cortisol levels were associated with lower parents’ CAR the next morning (B=-.14, p<.001), but not vice versa (B=.06, p=ns). Model fit was acceptable according to RMSEA, NNFI, and CFI.
Conclusions
Parent and child cortisol patterns were associated across days. However, these associations were not bidirectional, as we hypothesized. Instead, they reflect a primarily child driven process of stress transmission in families: child cortisol affected parent cortisol but not vice versa. Interventions to help parents become less physiologically reactive to children’s stress are warranted. We will discuss the unique benefits of daily diary studies with biomarkers as well as possible reasons and processes underlying our findings.
Melissa Lippold, The University of North Carolina at Chapel Hill
Presenting Author
David Almeida, The Pennsylvania State University
Non-Presenting Author
Peter Molenaar, The Pennsylvania State University
Non-Presenting Author
Soomi Lee, University of Southern Florida
Non-Presenting Author
Kelly Chandler, Oregon State University
Non-Presenting Author