Prospective associations between stressful life events and inflammation among adolescents with a history of early institutional rearing

• In Event: Pubertal Recalibration in PI Youth: Associations with Physiology, Mental Health, Behavior, and Inflammation

Abstract

Exposure to early adversity is associated with chronic diseases in adults (Brown et al., 2009; Danese et al., 2009; Felitti et al., 1998) and chronic low-grade inflammation in youth (Baumeister, Akhtar, Ciufolini, Pariante, & Mondelli, 2016; Broyles et al., 2012; Ehrlich, Ross, Chen, & Miller, 2016). While these findings algin with the early biological embedding model (Hertzman, 1999; Miller, Chen, & Parker, 2011; Shonkoff, Boyce, & McEwen, 2009), findings in youth have been inconsistent. Following an alternative stress-sensitization hypothesis (Daskalakis, Bagot, Parker, Vinkers, & de Kloet, 2013; Hammen, Henry, & Daley, 2000), we examined whether early institutional rearing sensitizes individuals to stressful events in adolescence engendering chronic low-grade inflammation. We expected that more stressful life events in adolescence would moderate higher levels of inflammation among adolescents with a history of early intuitional rearing. We also expected early foster care intervention to diminish these risks.


Participants are from the Bucharest Early Intervention Project, a randomized trial of foster care as an alternative to institutional care. At baseline (ages 6-31 months), institutionalized children in Romania were randomly assigned to foster care (n=68) or to remain in usual care within institutions (n=68). A group of never-institutionalized children (n=72) was recruited as an in-country comparison sample. At ages 12 and 16, participants reported stressful events using a modified version of Coddington’s Child Life Events Scale (Coddington, 1972). At age 16, a subset of participants (n=127) provided dried blood spots, from which inflammatory markers, Interleukin-6 (IL-6) and C-reactive protein (CRP), were derived. To test our hypothesis, multiple-group regression models were conducted, while adjusting for sex and health behaviors (i.e., body mass index, cigarette smoking, medication, exercise, and body temperature). We used χ2 difference tests to evaluate whether study groups differed in paths of interest (i.e., effect of stressful life events at ages 12 and 16 on inflammation at age 16).

Results revealed significant group differences in the associations between total stressful life events and IL-6, χ2diff (4)= 10.18, p= .038. Among children assigned to care as usual, more stressful events at age 12, but not age 16, were associated with higher levels of IL-6 (Table 1A; Figure 1). In the same group of adolescents, stressful events at age 16 were associated with higher levels of CRP, though these effects attenuated after adjusting for covariates (Table1B). In contrast, these associations were not observed in the foster care or never-institutionalized groups.

These findings support the stress-sensitization hypothesis. They suggest that heightened inflammation following stress exposure is one pathway through which early neglect could compromise physical health. In contrast, early family care might buffer against these risks.

Authors

• Alva Tang, University of Texas at Dallas
  Presenting Author

• Mark Wade, University of Toronto
  Non-Presenting Author

• Nathan A Fox, University of Maryland - College Park
  Non-Presenting Author

• Charles A. Nelson, Harvard Medical School
  Non-Presenting Author

• Charles H Zeanah, Tulane University
  Non-Presenting Author

• Natalie Slopen, University of Maryland - College Park
  Non-Presenting Author