Cited by 84Stress Responses and CortisolChild Abuse and TraumaResilience and Mental Health

Testing the biological embedding hypothesis: Is early life adversity associated with a later proinflammatory phenotype?

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Ehrlich, Katherine B., Ross, Kharah M., Chen, Edith, Miller, Gregory E.·2016·Development and Psychopathology

Abstract

Accumulating evidence suggests that the experience of early life adversity is a risk factor for a range of poor outcomes across development, including poor physical health in adulthood. The biological embedding model of early adversity (Miller, Chen, & Parker, 2011) suggests that early adversity might become embedded within immune cells known as monocytes/macrophages, programming them to be overly aggressive to environmental stimuli and insensitive to inhibitory signals, creating a "proinflammatory phenotype" that increases vulnerability to chronic diseases across the life span. We tested this hypothesis in the present study. Adolescent girls (n = 147) had blood drawn every 6 months across a 2.5-year period. To assess inflammatory responses to challenge, their monocytes were stimulated in vitro with a bacterial product, and production of the cytokine interleukin-6 was quantified. Hydrocortisone was added to cultures to assess the cells' sensitivity to glucocorticoids' anti-inflammatory signal. Using cluster analyses, we found that early life adversity was associated with greater odds of displaying a proinflammatory phenotype characterized by relatively larger interleukin-6 responses and relatively less sensitivity to glucocorticoids. In contrast, ongoing social stress was not associated with increasing odds of being categorized in the proinflammatory cluster. These findings suggest that early life adversity increases the probability of developing a proinflammatory phenotype, which, if sustained, could forecast risk for health problems later in life.

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  • A longitudinal study of adolescent girls (n = 147) showed that early life adversity was associated with greater odds of displaying a proinflammatory phenotype, generating low-level non-resolving inflammation (higher levels of IL-6 and decreased sensitivity to cortisol).

    “A longitudinal study of adolescent girls (n = 147) showed that ELA was associated with greater odds of displaying a proinflammatory phenotype, generating low-level non-resolving inflammation (higher levels of IL-6 and decreased sensitivity to cortisol) [117].”

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Authors
Ehrlich, K. B., Ross, K. M., Chen, E., & Miller, G. E.
Affiliations
  • University of Georgia (US)
  • University of California, Los Angeles (US)
  • Northwestern University (US)
Corresponding author
Ehrlich, Katherine B.
Venue
Development and Psychopathology
Published
2016-10-03
Volume
28
Issue
4pt2
Pages
1273-1283
ISSN
  • 0954-5794 (ISSN-L)
  • 1469-2198
OpenAlex
W2528704889
Cited by
84
References
83
Citations by year
2026: 7 · 2025: 6 · 2024: 9 · 2023: 8 · 2022: 8 · 2021: 12 · 2020: 9 · 2019: 11 · 2018: 10 · 2017: 4
FWCI
5.33
Type
journal article
Language
en
Open access
Locations
  • Development and Psychopathology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Canadian Institutes of Health Research (67191)
  • National Institute on Drug Abuse (P30DA027827)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (F32HD076563, R01HD058502)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
  • Social Sciences › Psychology › Clinical Psychology › Resilience and Mental Health
Keywords
childhood adversity, biological embedding, pro-inflammatory phenotype, monocytes, macrophages, interleukin-6, glucocorticoid sensitivity, cortisol, social stress, adolescent girls, inflammation, chronic disease risk
MeSH terms
Adolescent, Female, Humans, Hydrocortisone, Inflammation, Life Change Events, Phenotype, Probability, Risk Factors, Stress, Psychological, Interleukin-6, Epigenesis, Genetic

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