At the Chronicle of Higher Education, Helen Fields examines a recent study, performed by Stephen Cole at the University of California, Los Angeles, and his colleagues which identifies a specific pathway wherein gene-social environment interactions directly impact a patient's health. Using a bioinformatic strategy coupled with an expression responsive array-based method to identify environmentally responsive transcription factors, Cole and his collaborators predicted that a single nucleotide polymorphism, rs1800795, at the human interleukin 6 promoter might play a role in altering human health risk based on stress from social adversity. IL6, which helps to promote the inflammatory response, "is a problem if you make it all the time," leading to chronic inflammation, Fields writes. "It's almost like a generic fertilizer for the diseases that most often kill us," Cole told the Chronicle. "Things like coronary heart disease, the most prevalent kinds of cancer, neurodegenerative diseases, probably Type 2 diabetes as well," are associated with chronic inflammation. By first testing the models' predictions in a cell line exposed to norepinephrine — to induce stress in the cells and, ultimately, to cause GATA-1 transcription factor activation — and then in a colleague's long-term cohort of older adults, Fields reports, the team was able to confirm that those with "the nonmutated sequence were twice as likely to die in the next 10 years." In effect, the rs1800795 mutation appears to protect those who have it. The team's next step, Fields reports, is to examine "whether happiness might balance out stress in the cells." Cole told the Chronicle that the teams' largest remaining question is that "if people cannot or will not give up stress, is there something we can do biologically to help?"
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