Abstract
A growing literature in human social genomics has begun to analyze how everyday life circumstances influence human gene expression. Social-environmental conditions such as urbanity, low socioeconomic status, social isolation, social threat, and low or unstable social status have been found to associate with differential expression of hundreds of gene transcripts in leukocytes and diseased tissues such as metastatic cancers. In leukocytes, diverse types of social adversity evoke a common conserved transcriptional response to adversity (CTRA) characterized by increased expression of proinflammatory genes and decreased expression of genes involved in innate antiviral responses and antibody synthesis. Mechanistic analyses have mapped the neural “social signal transduction” pathways that stimulate CTRA gene expression in response to social threat and may contribute to social gradients in health. Research has also begun to analyze the functional genomics of optimal health and thriving. Two emerging opportunities now stand to revolutionize our understanding of the everyday life of the human genome: network genomics analyses examining how systems-level capabilities emerge from groups of individual socially sensitive genomes and near-real-time transcriptional biofeedback to empirically optimize individual well-being in the context of the unique genetic, geographic, historical, developmental, and social contexts that jointly shape the transcriptional realization of our innate human genomic potential for thriving.
Highlights
The spectacular adaptive success of Homo sapiens is attributable in large part to our capacity to self-organize into complex social systems or ‘‘metaorganisms’’ [1,2,3]
Social regulation of gene expression has long been observed in animal models of morphological plasticity such as worker bee maturation into guards and scouts, cichlid sex switching, and status-dependent changes in body size, coloring, brain development, immune response, and reproductive capacity [6,7,8,9]
Scientists, policy makers, and the general public have long wondered how such animal dynamics might pertain to everyday human life
Summary
The spectacular adaptive success of Homo sapiens is attributable in large part to our capacity to self-organize into complex social systems or ‘‘metaorganisms’’ [1,2,3]. Following the initial analyses of social isolation, a diverse array of studies has begun to document similar leukocyte transcriptome shifts in other adverse social conditions, including low socioeconomic status (SES) [9,17,18,19,20], chronic stress (e.g., care-giving for a dying spouse) [21,22], bereavement [23], post-traumatic stress disorder (PTSD) [24,25], and cancer diagnosis [26,27] 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]. A key gene involved in mediating these effects shows evidence of recent adaptive variation across human populations [52]
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