Health Risk of Seclusion Has Physiological Basis


Seclusion can increase the risk of premature death by 14 percent in older adults,  Ethically to a study release Monday that posits a physiological basis for the phenomenon.

The dangers of social isolation have long been known but its effects on the body have not been well understood, the exploer said in the work release in the Proceedings of the National Academy of Sciences/PNAS.

Led by University of Chicago psychologist John Cacioppo, the exploer team had already identified a link between solitude and both a heightened expression of genes involved in inflammation and a diminution in the activity of other genes that play a role in the body’s antiviral responses.

The result is a weakened immune systems that makes a person who lives alone more vulnerable to disease.

In their latest research, the exploer looked at leukocytes, white blood cells that the immune system uses to protect against bacteria and viruses.

They find out the same shift in genetic expression in the white blood cells of people who lived alone and in social isolation.

They also found that seclusion predicted the gene behavior a year or more in advance — and contrariwise that gene expression predicted seclusion measured a year or more later.

Leukocyte gene expression and seclusion appear to have a mutual relationship, suggesting that each can help propagate the other over time.

These results were specific to seclusion and could not be explained by depression, stress or social support.

The researcher then studied rhesus macaques, a highly social primate, and found a similar cellular process linked to their social experience.

“Lonely-like” monkeys had enhanced gene expression involved in inflammation and less gene expression in antiviral stronghold.

Both lonely humans and ‘lonely like’ monkeys showed highest levels of monocytes in their blood.

Other studies showed that the increased production of immature monocytes was amplifying the high inflammation/low antiviral impact in the pool of white blood cells.

The resulting shift in monocyte output may both propagate seclusion and contribute to its associated health risks.