Testing the biological embedding hypothesis: Is early life adversity associated with a later proinflammatory phenotype?
Open accessAbstract
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].”
From Separating the Signal from the Noise: How Psychiatric Diagnoses Can Help Discern Food Addiction from Dietary Restraint (2020) · cites this paper as [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
- Publisher
- Cambridge University Press (CUP)
- Published
- 2016-10-03
- Volume
- 28
- Issue
- 4pt2
- Pages
- 1273-1283
- ISSN
- 0954-5794 (ISSN-L)
- 1469-2198
- PMC
- PMC5475361
- 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
- green
- www.ncbi.nlm.nih.gov
- 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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