Evidence map›Paper›PMID 27691981›Full record

ArticleDevelopment and psychopathology2016

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

Katherine B Ehrlich, Kharah M Ross, Edith Chen, Gregory E Miller

Open access · greenAbstract read
In one paragraph

Article in Development and psychopathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Wild capuchin monkeys as a model system for investigating the social and ecological determinants of ageing.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
  12. Article
  13. Article
  14. Long-Term Impact of Childhood Adversity on the Gut Microbiome of Nursing Students.International journal of environmental research and public health · 2024
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Katherine B EhrlichUniversity of Georgia.
Kharah M RossUniversity of California at Los Angeles.
Edith ChenNorthwestern University.
Gregory E MillerNorthwestern University.
University of California, Los Angeles · US

Funding

Vulnerability to Drug Use & HIV: Advancing Prevention for Rural African AmericansP30DA027827 · NIDA · UNIVERSITY OF GEORGIA · PI BRODY, GENE H. · 2009 to 2018
$10.2M
Biological Embedding of Early-Life SESR01HD058502 · NICHD · UNIVERSITY OF BRITISH COLUMBIA · PI MILLER, GREGORY EVAN · 2009 to 2013
$1.3M
Adolescent Social Relationships and Immune, Endocrine, and Metabolic ProcessesF32HD076563 · NICHD · NORTHWESTERN UNIVERSITY · PI EHRLICH, KATHERINE BABCOCK · 2013 to 2014
$99k
CIHR 67191NICHD NIH HHS F32 HD076563NICHD NIH HHS R01 HD058502NIDA NIH HHS P30 DA027827
6 · The paper itself

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.

Indexed as

Life Change EventsPhenotypeAdolescentEpigenesis, GeneticFemaleHumansHydrocortisoneInflammationInterleukin-6ProbabilityRisk FactorsStress, PsychologicalHydrocortisoneIL6 protein, humanInterleukin-6

Identifiers

PMID27691981
PMCPMC5475361
OpenAlexW2528704889

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.