The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
Childhood and later life stressors and increased inflammatory gene expression at older ages
Open accessAbstract
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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“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
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“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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Epigenetic programming by maternal behavior
Weaver, I. C. G., Cervoni, N., Champagne, F. A., D'Alessio, A. C., Sharma, S., Seckl, J. R., Dymov, S., Szyf, M., & Meaney, M. J. (2004) · Nature Neuroscience · doi:10.1038/nn1276 · Cited by 6,177
Effect of In Utero and Early-Life Conditions on Adult Health and Disease
Gluckman, P. D., Hanson, M. A., Cooper, C., & Thornburg, K. L. (2008) · New England Journal of Medicine · doi:10.1056/nejmra0708473 · Cited by 3,898
Mechanisms underlying inflammation in neurodegeneration
Glass, C. K., Saijo, K., Winner, B., Marchetto, M. C., & Gage, F. H. (2010) · Cell · doi:10.1016/j.cell.2010.02.016 · Cited by 3,580
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Brain on stress: how the social environment gets under the skin
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Reciprocal regulation of the neural and innate immune systems
Irwin, M. R., & Cole, S. W. (2011) · Nature Reviews Immunology · doi:10.1038/nri3042 · Cited by 910 · cited 2×
“…responses to stress can up-regulate inflammation by enhancing the transcription of pro-inflammatory genes such as interleukin-1 beta (IL1B), interleukin-6 (IL6), interleukin-8 (IL8), cyclooxygenase 2 (COX2/PTGS2) and tumor necrosis factor alpha (TNF) (Cole et al., 2013; Irwin & Cole, 2011).”
BackgroundSelf-citation
Research works printed but not linked: 2
- Miller, 2009, Low early-life social class leaves a biological residue manifested by decreased glucocorticoid and increased proinflammatory signaling, Proc. Natl. Acad. Sci. U. S. A., 106, 14716, 10.1073/pnas.0902971106 · DOI · Paper page
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Cited by
Sorted by citations
More than a feeling: A unified view of stress measurement for population science
Epel, E. S., Crosswell, A. D., Mayer, S. E., Prather, A. A., Slavich, G. M., Puterman, E., & Mendes, W. B. (2018) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2018.03.001 · Cited by 1,077
“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.”
BackgroundCytokine Research in Depression: Principles, Challenges, and Open Questions
Himmerich, H., Patsalos, O., Lichtblau, N., Ibrahim, M. A. A., & Dalton, B. (2019) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2019.00030 · Cited by 313
Loneliness, eudaimonia, and the human conserved transcriptional response to adversity
Cole, S. W., Levine, M. E., Arevalo, J. M. G., Ma, J., Weir, D. R., & Crimmins, E. M. (2015) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2015.07.001 · Cited by 238
Self-citationPrenatal stress and epigenetics
Cao-Lei, L., de Rooij, S. R., King, S., Matthews, S. G., Metz, G. A. S., Roseboom, T. J., & Szyf, M. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.05.016 · Cited by 253
Close social relationships correlate with human gut microbiota composition
Dill‐McFarland, K. A., Tang, Z.-Z., Kemis, J. H., Kerby, R. L., Chen, G., Palloni, A., Sorenson, T., Rey, F. E., & Herd, P. (2019) · Scientific Reports · doi:10.1038/s41598-018-37298-9 · Cited by 246
Metadata
- 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.
- Venue
- Social Science & Medicine
- Publisher
- Elsevier BV
- Published
- 2015-04
- Volume
- 130
- Pages
- 16-22
- ISSN
- 0277-9536 (ISSN-L)
- 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
- 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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