Poster #20 - Differential Effects of Type and Timing of Childhood Adversity on Inflammatory Processes in Adolescence

• In Event: 2-163 - Poster Session 08
  In Poster Session: PS 08 Section - Biological Processes: Psychophysiology

Integrative Statement

There is ample evidence to suggest that early life adversity is associated with systemic inflammation in adulthood. However, previous studies utilizing the cumulative risk approach yielded inconsistent results. Recent studies propose that the unique characteristics of a stressor may differently shape neurobiological pathways, but few studies have examined the effects of different adverse experiences - as well as the timing at which they occur - on inflammatory processes.
Using longitudinal data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we examined associations between different adversities that occurred at three developmental periods – infancy/early childhood (age 0-3), middle childhood (age 4-9) and adolescence (age 12-16), and inflammation at ages 9, 15 and 17. Inflammatory markers at age 9 included C-reactive protein (CRP; N = 5,022) and interleukin-6 (IL-6; N = 5,071), and CRP was measured again at ages 15 (N = 3,426) and 17 (N = 3,208). The sample size differed across analyses based on the different adversities that were included in each model. Adversities that occurred in infancy and childhood were reported by the mother and included economic hardship, abuse, family instability, death of a close figure, neighborhood stress, hospitalizations and maternal depression. At age 16, the teen reported on similar adversities that they experienced since age 12. Additional adversities reported in adolescence include peer-victimization, serious illness experienced by the teen or other family members, parental legal problems, and becoming pregnant or a parent. Gender, body mass index (BMI) and previous CRP levels were controlled for in each analysis.
A series of linear regression analyses revealed that financial difficulties experienced during infancy and early childhood were associated with higher levels of IL-6 at age 9 (ß = .03, p < .05), and with elevated CRP at age 15 (ß = .04, p < .05). Additionally, abuse and family instability experienced in middle childhood predicted elevated IL-6 levels (ß = .04, p < .05; ß = .05, p < .01, respectively). Death of a family member during middle childhood predicted both higher levels of IL-6 (ß = .03, p < .05) and CRP (ß = .03, p < .05) at age 9. Elevated CRP levels at age 15 were also predicted by hospitalizations during early childhood (ß = .04, p < .05) and by experiencing a serious illness in adolescence (ß = .05, p < .05). Finally, family instability experienced during adolescence predicted elevated CRP levels at age 17 (ß = .06, p < .05).
These findings provide further support for the long-lasting effects of early life adversity on inflammatory processes. However, distinct effects are observed based on different types of adversities and the developmental period at which they occur. For instance, while elevated inflammation was predicted by economic hardship experienced in early childhood, it was also predicted by family instability experienced in middle childhood and adolescence. Thus, future studies may benefit from examining the unique features of adverse life events in order to elucidate the mechanisms by which childhood adversity may alter neurobiological pathways and increase risk to disease.

Authors

• Meital Mashash, University of California, Davis
  Presenting Author

• Camelia E. Hostinar, University of California-Davis
  Non-Presenting Author

• LillyBelle K. Deer, UC Davis
  Non-Presenting Author

• Paul Hastings, University of California, Davis
  Non-Presenting Author