LONELINESS can increase the risk of premature death by 14 per cent in older adults, according to a study that suggests 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 researchers said in the work published in the Proceedings of the National Academy of Sciences/PNAS.
Led by University of Chicago psychologist John Cacioppo, the researchers had previously identified a link between solitude and both a heightened expression of genes involved in inflammation and a decrease in the activity of other genes that play a role in the body’s antiviral responses.
The result is a weakened immune system that makes a person who lives alone more vulnerable to illness.
The researchers looked at leukocytes, white blood cells that the immune system uses to protect against bacteria and viruses.
They found the same shift in genetic expression in the white blood cells of people who lived alone and in social isolation. They found that loneliness predicted the gene behaviour a year or more in advance, and conversely that gene expression predicted loneliness measured a year or more later.
“Leukocyte gene expression and loneliness appear to have a reciprocal relationship, suggesting that each can help propagate the other over time,” the researchers said.
The results were specific to loneliness and could not be explained by depression or stress, they said.
The investigators then studied rhesus macaques, a highly social primate.
“Lonely-like” monkeys had increased gene expression involved in inflammation and less gene expression in antiviral defences. They were also found to have higher levels of noreprinephrine, a “fight-or-flight” neurotransmitter that stimulates the production of immature monocytes, a white blood cell with high inflammation/low antiviral defence gene expression.
Both lonely humans and ‘lonely like’ monkeys showed higher levels of monocytes.
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