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

Levine, M.E.; Cole, S.W.; Weir, D.R.; Crimmins, E.M.

doi:10.1016/j.socscimed.2015.01.030

Cited by 106Child Abuse and TraumaHealth disparities and outcomesStress Responses and Cortisol

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

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Levine, M.E., Cole, S.W., Weir, D.R., Crimmins, E.M.·2015·Social Science & Medicine

DOI 10.1016/j.socscimed.2015.01.030PMC PMC4394113

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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.

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In the Health and Retirement Study, childhood adversity had a significant effect on proinflammatory gene expression.
“When broken down by life period, childhood adversity had a significant effect on proinflammatory gene expression (Levine et al., 2015), as well as telomere length (Puterman et al., 2016), both potential mechanisms of disease development.”
From More than a feeling: A unified view of stress measurement for population science (2018) · cites this paper as Levine et al., 2015
The Results section reports a significant association between childhood trauma and proinflammatory gene expression in a Health and Retirement Study pilot sample. It found no significant association for childhood socioeconomic status or health, so the broader term “childhood adversity” overstates the finding; the observational analysis also establishes an association, not a causal effect. Page numbers were not supplied in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measured
Acute or chronic stress can lead to an increased production of pro-inflammatory cytokines.
“A risk factor like acute or chronic stress could, for example, lead to an increased production of pro-inflammatory cytokines (115, 138–140)”
From Cytokine Research in Depression: Principles, Challenges, and Open Questions (2019) · cites this paper as [140]

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Authors: Levine, M. E., Cole, S. W., Weir, D. R., & Crimmins, E. M.
Affiliations: University of Southern California (US)
University of California, Los Angeles (US)
University of Michigan (US)
Corresponding author: Levine, M.E.
ORCID: Levine, M.E.
Cole, S.W.
Weir, D.R.
Crimmins, E.M.
Venue: Social Science & Medicine
Publisher: Elsevier BV
Published: 2015-04
Volume: 130
Pages: 16-22
ISSN: 0277-9536 (ISSN-L)
DOI: 10.1016/j.socscimed.2015.01.030
PMC: PMC4394113
OpenAlex: W2004931363
Cited by: 106
References: 46
Citations by year: 2026: 6 · 2025: 5 · 2024: 8 · 2023: 7 · 2022: 6 · 2021: 14 · 2020: 17 · 2019: 9 · 2018: 6 · 2017: 11 · 2016: 11 · 2015: 6
FWCI: 14.05
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Social Science & Medicine (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Funders: National Institute on Aging (R24AG037898, P30AG017265, U01AG009740, T32AG000037)
Topics: Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
Social Sciences › Health › Health disparities and outcomes
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords: childhood adversity, childhood trauma, adult socioeconomic status, inflammatory gene expression, pro-inflammatory genes, cyclooxygenase-2, interleukin-8, IL1B, late-life health, gene-environment interaction, aging
MeSH terms: Adolescent, Age Factors, Aged, Aged, 80 and over, Female, Health Status, Health Surveys, Humans, Life Change Events, Male, Middle Aged, Obesity, RNA, Sex Factors, Smoking, Socioeconomic Factors, Stress, Psychological, Body Mass Index, Interleukin-8, Racial Groups, Cyclooxygenase 2, Interleukin-1beta

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

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