Loneliness not only feels bad, but it’s also bad for your health.

Subjective social isolation is a known social epidemiological risk factor that has been linked to heart disease, viral infections and cancer.

In addition, loneliness has physical effects on gene regulation and expression, according to DNA microarray analyses of 209 gene transcripts (the first step in synthesizing a protein) out of more than 20,000 in white blood cells of 14 volunteers.

UCLA’s Steve Cole, Jesusa Arevalo, and Caroline Sung collaborated with Robert Rosen of University of Texas and University of Chicago’s Louise Hawkley and John Cacioppo to report that individuals who reported high loneliness on Daniel Russell’s UCLA Loneliness Scale showed different gene expression in circulating leukocytes than volunteers who did not report loneliness.

Lonely individuals were less able to ward off inflammatory responses and viruses, and less able to produce antibodies because controlling genes were under-expressed.
In contrast, lonely individuals were at risk for greater inflammatory responses and more active immune systems  because the related genes were over-expressed.

These volunteers showed “down-regulation” of genes supporting mature B lymphocyte function and type I interferon response, when researchers controlled for effects of circulating cortisol levels, demographic, psychological, health risk, medications, or social network factors.

The social experience of loneliness desensitizes glucocorticoid receptors and reduces cortisol’s immune control and anti-inflammatory effects.

Cole’s team found that loneliness was more dependent on the number of close relationships rather than the total number of acquaintances.
This suggests the importance of cultivating meaningful social relationships for both social support, reciprocity, and for enhanced health.

Cole, and Arevalo collaborated with UCLA colleague Jeffrey Ma and University of North Carolina’s Barbara Fredrickson, Karen Grewen, Kimberly Coffey, Sara Algo, and Ann Firestine to consider the impact of different types of happiness on gene expression in 80 adult volunteers.

They evaluated two types of happiness:

• “Eudaimonic well-being,“ a Socratic ideal based on leading a virtuous life, striving toward a meaningful purpose, pursuing “worthwhile” service, and more fully developing personal capabilities
• “Hedonic well-being,” focused on pleasure, consumption, and enjoyment.

Fredrickson’s team compared leukocyte basal gene expression profiles for volunteers who reported hedonic well-being in contrast to those who reported eudaimonic well-being.
The team also considered negative psychological and behavioral factors.

People with high levels of hedonic well-being showed “up-regulated” pro-inflammatory genes and decreased expression of genes involved in antibody synthesis and type I IFN response in peripheral blood mononuclear cells during stress [conserved transcriptional response to adversity (CTRA)].

In contrast, volunteers with high levels of eudaimonic well-being showed CTRA down-regulation, suggesting less stress on body systems.

Fredrickson and team concluded that “genes can tell the difference” between a purposeful life and a more pleasure-centric life, even when self-reports do not distinguish between these two types of happiness.

These finding suggest the importance of pursuing prosocial purposes and developing meaningful, trust-based relationships with others to experience greatest health and happiness – down to your genes.

-*How have you seen social relationships and mood affect immunity to illness and stress?

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