Cited by 42Genetic Associations and EpidemiologyHealth disparities and outcomesRace, Genetics, and Society

Genetic Differential Sensitivity to Social Environments: Implications for Research

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Mitchell, Colter, McLanahan, Sara, Brooks-Gunn, Jeanne, Garfinkel, Irwin, Hobcraft, John, Notterman, Daniel·2013·American Journal of Public Health

Abstract

Researchers have proposed a genetic differential sensitivity to social environmental (GDSE) model positing that individuals with certain genetic makeups are more sensitive to favorable and unfavorable environmental influences than those without these genetic makeups. We discuss several issues facing researchers who want to use GDSE to examine health: (1) the need for greater theorizing about the social environment to properly understand the size and direction of environmental influences; (2) the potential for combining multiple genetic markers to measure an individual’s genetic sensitivity to environmental influence; (3) how this model and exogenous shocks deal with gene–environment correlations; (4) implications of this model for public health and prevention; and (5) how life course and developmental theories may be used to inform GDSE research.

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  • This finding implies a genetically encoded differential sensitivity to the environment using telomere length as the biomarker.

    “This finding implies a genetically encoded differential sensitivity to the environment using TL as the biomarker (13-15).”
  • Specific gene variants moderate the association between the social environment and children's health and well-being.

    “A growing body of research shows that specific gene variants moderate the association between the social environment and children's health and well-being (13-15).”

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Research works printed but not linked: 2

  1. [53]Baltes PB Lindenberger U Staudinger UM Damon W Lerner RM Life span theory in developmental psychology. Handbook of Child Psychology Theoretical Models of Human Development 2006 1 569 664 Wiley New York, NY 6th ed.
  2. [64]Addison JT Urie Bronfenbrenner. Hum Ecol 1992 20 2 16 20

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Authors
Mitchell, C., McLanahan, S., Brooks-Gunn, J., Garfinkel, I., Hobcraft, J., & Notterman, D.
Affiliations
  • Princeton University (US)
  • Colter Mitchell is with the Survey Research Center and Population Studies Center, University of Michigan, Ann Arbor, MI. Sara McLanahan is with the Department of Sociology and Woodrow Wilson School of Public and International Affairs, Princeton University, Princeton, NJ. Jeanne Brooks-Gunn is with the Teachers College and the College of Physicians and Surgeons, Columbia University, New York, NY. Irwin Garfinkel is with the School of Social Work, Columbia University. John Hobcraft is with the Department...
Venue
American Journal of Public Health
Published
2013-10
Volume
103
Issue
S1
Pages
S102-S110
ISSN
  • 0090-0036 (ISSN-L)
  • 1541-0048
OpenAlex
W2016835929
Cited by
42
References
60
Citations by year
2026: 1 · 2025: 2 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 2 · 2019: 4 · 2018: 4 · 2017: 4 · 2016: 7 · 2015: 4 · 2014: 2 · 2013: 2
FWCI
3.28
Type
journal article
Language
en
Open access
Locations
  • American Journal of Public Health (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
Funders
Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD039135, R01HD076592, R24HD058486, R01HD036916, R01HD040421)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
  • Social Sciences › Health › Health disparities and outcomes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Race, Genetics, and Society
Keywords
gene-environment interaction, gene-environment correlation, genetic markers, social environment, external shocks, life course perspective, developmental theory, public health prevention, health outcomes
MeSH terms
Genetic Markers, Humans, Models, Biological, Primary Prevention, Social Environment, Genetic Predisposition to Disease, Genetic Research, Gene-Environment Interaction

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