Social regulation of human gene expression: mechanisms and implications for public health
Open accessAbstract
Recent analyses have discovered broad alterations in the expression of human genes across different social environments. The emerging field of social genomics has begun to identify the types of genes sensitive to social regulation, the biological signaling pathways mediating these effects, and the genetic polymorphisms that modify their individual impact. The human genome appears to have evolved specific “social programs” to adapt molecular physiology to the changing patterns of threat and opportunity ancestrally associated with changing social conditions. In the context of the immune system, this programming now fosters many of the diseases that dominate public health. The embedding of individual genomes within a broader metagenomic network provides a framework for integrating molecular, physiologic, and social perspectives on human health.
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Both physical and psychological processes contribute to the net effect of a given social environment on gene expression, with each mechanism activating some distinct gene modules as well as a conserved generalized response to adverse life circumstances.
“Parallel studies on the transcriptional correlates of social disparities in health subsequently suggested that both physical and psychological processes contribute to the net effect of a given social environment, with each mechanism activating some distinct gene modules as well as a conserved generalized response to adverse life circumstances (Figure 1) [3], [5], [12].”
From Human Social Genomics (2014) · cites this paper as [3]
Across diverse forms of adversity, a common conserved transcriptional response to adversity (CTRA) has emerged, including increased expression of proinflammatory genes and decreased expression of genes involved in Type I interferon innate antiviral responses and IgG antibody synthesis.
“Across these diverse forms of adversity, a common pattern of conserved transcriptional response to adversity (CTRA) has emerged, including increased expression of proinflammatory genes and decreased expression of genes involved in Type I interferon innate antiviral responses and IgG antibody synthesis [3], [5], [28].”
From Human Social Genomics (2014) · cites this paper as [3]
In both leukocytes and tumors, chronic threat and SNS signaling activate tissue-specific transcriptional defense programs that enhance organismic mobility and prime wound healing and antimicrobial responses to tissue injury.
“In both, chronic threat and SNS signaling activate tissue-specific transcriptional defense programs that enhance organismic mobility and prime wound healing and antimicrobial responses to tissue injury [3], [5], [36].”
From Human Social Genomics (2014) · cites this paper as [3]
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The Biosocial Approach to Human Development, Behavior, and Health Across the Life Course
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Self-citationSubjective social status and inflammatory gene expression.
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Contemporaneous Social Environment and the Architecture of Late-Life Gene Expression Profiles
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Longitudinal analyses indicate bidirectional associations between loneliness and health
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Psychological well-being and gene expression in Korean adults: The role of age
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Mindfulness, Health, and Longevity
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Socioeconomic inequalities in molecular risk for chronic diseases observed in young adulthood
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- Authors
- Cole, S. W.
- Affiliations
- Steven W. Cole is with the Division of Hematology-Oncology, School of Medicine, University of California, Los Angeles.
- Venue
- American Journal of Public Health
- Publisher
- American Public Health Association
- Published
- 2013-10
- Volume
- 103
- Issue
- S1
- Pages
- S84-S92
- ISSN
- 0090-0036 (ISSN-L)
- 1541-0048
- PMC
- PMC3786751
- OpenAlex
- W1985096225
- Cited by
- 225
- References
- 81
- Citations by year
- 2026: 11 · 2025: 16 · 2024: 18 · 2023: 21 · 2022: 18 · 2021: 18 · 2020: 20 · 2019: 24 · 2018: 19 · 2017: 19 · 2016: 17 · 2015: 14 · 2014: 9 · 2013: 1
- FWCI
- 6.23
- 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)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG028748, R37AG033590, AG033590, P30AG028748, P30AG017265)
- National Cancer Institute (R01CA116778, CA-116778)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Social Sciences › Health › Health disparities and outcomes
- Keywords
- social genomics, social environment, genetic polymorphism, immune system, disease susceptibility, adaptive evolution, public health implications
- MeSH terms
- Gene Expression Regulation, Humans, Public Health, Social Environment, Signal Transduction, Genome, Human, Evolution, Molecular, Genomics, Gene-Environment Interaction
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