From the Outside In

Biological Mechanisms Linking Social and Environmental Exposures to Chronic Disease and to Health Disparities

Susan Bagby, Damali Martin, Stephanie T. Chung, Nishadi Rajapakse

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)S56-S63
JournalAmerican Journal of Public Health
Volume109
Issue numberS1
DOIs
StatePublished - Jan 1 2019

Fingerprint

Environmental Exposure
Chronic Disease
Health
Population
Biological Models
Vulnerable Populations
Hydrocortisone
Public Health
Phenotype
Research

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health

Cite this

From the Outside In : Biological Mechanisms Linking Social and Environmental Exposures to Chronic Disease and to Health Disparities. / Bagby, Susan; Martin, Damali; Chung, Stephanie T.; Rajapakse, Nishadi.

In: American Journal of Public Health, Vol. 109, No. S1, 01.01.2019, p. S56-S63.

Research output: Contribution to journalArticle

@article{0b19cffb33d241aca44702980a113baf,
title = "From the Outside In: Biological Mechanisms Linking Social and Environmental Exposures to Chronic Disease and to Health Disparities",
abstract = "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.",
author = "Susan Bagby and Damali Martin and Chung, {Stephanie T.} and Nishadi Rajapakse",
year = "2019",
month = "1",
day = "1",
doi = "10.2105/AJPH.2018.304864",
language = "English (US)",
volume = "109",
pages = "S56--S63",
journal = "American Journal of Public Health",
issn = "0090-0036",
publisher = "American Public Health Association Inc.",
number = "S1",

}

TY - JOUR

T1 - From the Outside In

T2 - Biological Mechanisms Linking Social and Environmental Exposures to Chronic Disease and to Health Disparities

AU - Bagby, Susan

AU - Martin, Damali

AU - Chung, Stephanie T.

AU - Rajapakse, Nishadi

PY - 2019/1/1

Y1 - 2019/1/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=85060934786&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85060934786&partnerID=8YFLogxK

U2 - 10.2105/AJPH.2018.304864

DO - 10.2105/AJPH.2018.304864

M3 - Article

VL - 109

SP - S56-S63

JO - American Journal of Public Health

JF - American Journal of Public Health

SN - 0090-0036

IS - S1

ER -