From the outside in: biological mechanisms linking social and environmental exposures to chronic disease and to health disparities
Open accessAbstract
The ongoing epidemic of chronic diseases involves a spectrum of clinical entities now understood to represent late manifestations of progressive metabolic dysfunction initiated in early life. These diseases disproportionately affect disadvantaged populations, exacerbating health disparities that persist despite public health efforts. Excessive exposure to stressful psychosocial and environmental forces is 1 factor known to contribute to population-level disparities in at-risk settings. Yet increasing evidence reveals that even a single adverse environmental exposure—especially during very early developmental years—can become literally biologically embedded, inducing long-lasting disease-promoting pathways that amplify responses (e.g., cortisol, immune, inflammatory) to all future adverse stressors, thus enhancing their disease-promoting impacts. The same pathways may also interact with ancestrally linked genetic variants to modify chronic disease risk. We address how, in at-risk populations, environmentally activated disease-promoting pathways can contribute to a biologically based disease-susceptible phenotype; this is likely to be uniquely damaging in populations with multiple adverse exposures and is capable of cross-generational transmission. Intended to complement existing models, this biological perspective highlights key research opportunities and life-stage priorities with potential to enhance the reduction of health disparities.
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Biological embedding stands out as the primary mechanism through which susceptibility mediates the impact of SDOH.
“Biological embedding stands out as the primary mechanism through which susceptibility mediates the impact of SDOH”
From Nurse-led approaches to address social determinants of health and advance health equity: A new framework and its implications (2023) · cites this paper as Bagby, Martin, Chung, & Rajapakse, 2019
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- Authors
- Bagby, S. P., Martin, D., Chung, S. T., & Rajapakse, N.
- Affiliations
- National Institutes of Health (US)
- Venue
- American Journal of Public Health
- Publisher
- American Public Health Association
- Published
- 2019-01
- Volume
- 109
- Issue
- S1
- Pages
- S56-S63
- ISSN
- 0090-0036 (ISSN-L)
- 1541-0048
- PMC
- PMC6356139
- OpenAlex
- W2914448975
- Cited by
- 79
- References
- 39
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 13 · 2023: 12 · 2022: 10 · 2021: 8 · 2020: 14 · 2019: 6
- FWCI
- 9.27
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Public Health (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Social Sciences › Health › Health disparities and outcomes
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Health, Environment, Cognitive Aging
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Keywords
- health disparities, chronic disease, environmental exposure, psychosocial stress, developmental origins of health and disease, biological embedding, cortisol, inflammation, immune response, gene-environment interaction, intergenerational transmission, disadvantaged groups
- MeSH terms
- Chronic Disease, Environment, Humans, Longitudinal Studies, Risk Factors, Vulnerable Populations, Racial Groups, Healthcare Disparities
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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