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Soc Sci Med. 2015 Apr;130:16-22. doi: 10.1016/j.socscimed.2015.01.030. Epub 2015 Jan 21.

Childhood and later life stressors and increased inflammatory gene expression at older ages.

Author information

1
Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089, USA. Electronic address: canon@usc.edu.
2
David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
3
Survey Research Center, Institute for Social Research, University of Michigan, Ann Arbor, MI, USA.
4
Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089, USA.

Abstract

Adverse experiences in early life have the ability to "get under the skin" and affect future health. This study examined the relative influence of adversities during childhood and adulthood in accounting for individual differences in pro-inflammatory gene expression in late life. Using a pilot-sample from the Health and Retirement Study (N = 114) aged from 51 to 95, OLS regression models were run to determine the association between a composite score from three proinflammatory gene expression levels (PTGS2, ILIB, and IL8) and 1) childhood trauma, 2) childhood SES, 3) childhood health, 4) adult traumas, and 5) low SES in adulthood. Our results showed that only childhood trauma was found to be associated with increased inflammatory transcription in late life. Furthermore, examination of interaction effects showed that childhood trauma exacerbated the influence of low SES in adulthood on elevated levels of inflammatory gene expression-signifying that having low SES in adulthood was most damaging for persons who had experienced traumatic events during their childhood. Overall our study suggests that traumas experienced during childhood may alter the stress response, leading to more sensitive reactivity throughout the lifespan. As a result, individuals who experienced greater adversity in early life may be at higher risk of late life health outcomes, particularly if adulthood adversity related to SES persists.

KEYWORDS:

Inflammation; Social genomics; Stress

PMID:
25658624
PMCID:
PMC4394113
DOI:
10.1016/j.socscimed.2015.01.030
[Indexed for MEDLINE]
Free PMC Article

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