In a small population of patients, researchers surveyed more than 20,000 genes using DNA microarrays to compare how the genes of lonely and nonlonely individuals express themselves in molecular processes and, ultimately, in personal health. They found that gene expression is different at 209 sites in chronically lonely people and that many of those changes fit a pattern of elevated immune activation, inflammation, and depressed response to infection. “We now have a molecular framework for understanding the relationship between social experience and physical health,” explains the study’s lead author, Steve Cole of UCLA.
The study found that loneliness desensitizes the glucocorticoid receptors, cutting off the immune control and anti-inflammatory effects of cortisol, a stress-related hormone that also helps regulate the conversion of carbohydrates to energy. The depressed cortisol response concurs with the known effects of loneliness and provides a potential target for treatment.