# Early Life Adversity, Biological Embedding, and Risk for Developmental Precursors of Mental Disorders

> **NIH NIH R01** · WASHINGTON UNIVERSITY · 2024 · $2,499,658

## Abstract

PROJECT SUMMARY
Early exposure to social disadvantage, specifically family and neighborhood financial disadvantage in utero and
through the first 3 years of life, is a powerful and potentially modifiable environmental determinant of risk for
childhood psychopathology. The ongoing Early Life Adversity and Biological Embedding (eLABE) study launched
in 2017 has aimed to elucidate mechanisms of this risk trajectory and guide preventive interventions. To date,
eLABE has detected powerful associations between prenatal social disadvantage and structural and functional
brain development at birth which are mediated through elevations in maternal cytokines and alterations in the
gut microbiome. These neonatal neurodevelopmental variations have been linked to elevations in markers of
psychopathology risk at age 2 years. Further, decreased caregiver nurturance mediated some aspects of this
relationship, with supportive caregiving mitigating child psychopathology risk. Our central hypothesis is that pro-
inflammatory immune and gut microbiome profiles evident in children exposed to prenatal and early life social
disadvantage induce neuronal effects that negatively impact structural and functional brain development leading
to increased risk for psychopathology. This renewal proposes to build upon the existing data to continue following
our unique and well-characterized sample of 377 children for whom we have assembled a rich, unparalleled
repository including comprehensive measures of social disadvantage (in utero and ages 1, 2, and 3 years) with
early life measures of inflammation, the gut microbiome, and brain development (structural, microstructural, and
functional MRI at birth and ages 2 and 3). In the next phase of eLABE, we propose to follow this sample into
school entry (age 6) and middle childhood (age 8), adding assessments of social disadvantage,
developmental/behavioral, inflammatory marker, multimodal MRI, and caregiver and social support measures at
both timepoints and one additional wave of the gut microbiome at age 6. We will utilize these data to test specific
hypotheses about mechanistic pathways to mental disorders that begin to clearly emerge in early childhood and
school age, and will utilize novel brain metrics to more directly examine the roles of neuroinflammation and
plasticity in this risk pathway. We will also examine the effects of caregiver and family, peer, and school supports
on this risk trajectory, including their role as possible resilience factors, and explore whether there are sensitive
periods for these effects. The results will provide the first systematic and intensive prospective examination of
the relationship of social disadvantage to chronic systemic inflammation, the gut microbiome, and their links to
brain development and behavior related to risk for clinical mental disorders. Critically, by targeting caregiving,
inflammation, and the gut microbiome as key mechanistic pathways, these data will also have tremendous
c...

## Key facts

- **NIH application ID:** 10908635
- **Project number:** 5R01MH113883-07
- **Recipient organization:** WASHINGTON UNIVERSITY
- **Principal Investigator:** JOAN L. LUBY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $2,499,658
- **Award type:** 5
- **Project period:** 2018-05-22 → 2028-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10908635

## Citation

> US National Institutes of Health, RePORTER application 10908635, Early Life Adversity, Biological Embedding, and Risk for Developmental Precursors of Mental Disorders (5R01MH113883-07). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10908635. Licensed CC0.

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