Being lonely may fuel inflammation in the body, which, in turn, seems to increase the activity of inflammation-linked genes, researchers from the University of Chicago and elsewhere report in the Proceedings of the National Academy of Sciences.
Chicago's John Cacioppo and his colleagues conducted transcriptome surveys of peripheral blood mononuclear cells collected over time from 141 people from the Chicago Health, Aging, and Social Relations Study. Chronically lonely people, they found, had upregulated proinflammatory and downregulated type I interferon activity and antibody synthesis.
In a macaque model of social isolation, Cacioppo and his colleagues confirmed this finding and uncovered selective up-regulation of the CD14++/CD16− classical monocyte transcriptome as well as functional glucocorticoid desensitization, downregulation of Type I and II interferons, and impaired response to SIV infection.
This response also predicted subsequent episodes of perceived social isolation, indicating a "reciprocal interaction between inflammatory biology and social perception," the researchers add.
"There are things we can do to get out of a depressed or lonely state, but they're not easy," first author Steven Cole from the University of California, Los Angeles, tells NPR. "Part of the reason is because these negative psychological states develop some kind of molecular momentum."