Childhood adversity and inflammatory processes in youth: A prospective study

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• 作者：Natalie Slopen^a ; ^b ; ^c ; ^{nslopen@hsph.harvard.edu} ; Laura D. Kubzansky^b ; ¹ ; Katie A. McLaughlin^a ; ^d ; ^e ; ² ; Karestan C. Koenen^f ; ³
• 关键词：Children ; Adolescents ; Inflammation ; C-reactive protein ; Interleukin-6 ; Acute stress ; Stressful life events ; Prospective cohort ; Avon Longitudinal Study of Parents and Children (ALSPAC)
• 刊名：Psychoneuroendocrinology
• 出版年：2013
• 出版时间：February, 2013
• 年：2013
• 卷：38
• 期：2
• 页码：188-200
• 全文大小：404 K

文摘

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Summary

Background

Retrospective studies show that childhood adversity is associated with systemic inflammation in adulthood. Few prospective studies have examined whether childhood adversity influences inflammation in an observable manner during childhood or adolescence and if these effects are sustained over time.

Methods

Using longitudinal data from the Avon Longitudinal Study of Parents and Children, we examined associations between acute adverse events at seven time points prior to age 8 and inflammation at ages 10 and 15. Inflammatory markers at age 10 included interleukin-6 (IL-6; N = 4655) and C-reactive protein (CRP; N = 4647), and CRP was measured again at age 15 (N = 3286). We further evaluated whether body mass index (BMI), depression, or cigarette smoking mediated associations between adverse events and inflammation.

Results

Adverse events in middle childhood (occurring between ages 6 to 8), as well as cumulative adversity from birth to 8 years, were associated with higher levels of IL-6 and CRP at age 10. Adverse events reported in early childhood (1.5 years) or middle childhood, and cumulative adversity from birth through 8 years predicted increased levels of CRP at age 15, and these associations persisted after adjustment for CRP at age 10. Some, but not all, of these associations were mediated by BMI.

Conclusions

This study documents that exposure to adverse events prior to age 8 is associated with elevated inflammation at age 10 and in mid-adolescence. These findings provide prospective evidence for a biological mechanism by which early experiences may shape long-term health. Future studies with earlier assessments of inflammation are necessary in order to elucidate potential sensitive periods and mechanisms that link childhood adversity to later disease vulnerability.