Loneliness or social isolation is a health risk that can increase the risk of chronic illness and premature death. Why? Loneliness leads to fight-or-flight stress signaling, which can ultimately affect the production of white blood cells. Essentially, lonely people had a less effective immune response and more inflammation than non-lonely people. The study was part of the Chicago Health, Aging, and Social Relations Study (CHASRS) and followed 144 people over 10 years. From Science Daily:
Loneliness is more than a feeling: For older adults, perceived social isolation is a major health risk that can increase the risk of premature death by 14 percent.
Now a team of researchers, including U Chicago psychologist and leading loneliness expert John Cacioppo, has released a study shedding new light on how loneliness triggers physiological responses that can ultimately make us sick. The paper.... shows that loneliness leads to fight-or-flight stress signaling, which can ultimately affect the production of white blood cells. The study examined loneliness in both humans and rhesus macaques, a highly social primate species.
Previous research from this group had identified a link between loneliness and a phenomenon they called "conserved transcriptional response to adversity" or CTRA. This response is characterized by an increased expression of genes involved in inflammation and a decreased expression of genes involved in antiviral responses. Essentially, lonely people had a less effective immune response and more inflammation than non-lonely people.
For the current study, the team examined gene expression in leukocytes, cells of the immune system that are involved in protecting the body against bacteria and viruses. As expected, the leukocytes of lonely humans and macaques showed the effects of CTRA--an increased expression of genes involved in inflammation and a decreased expression of genes involved in antiviral responses. But the study also revealed several important new pieces of information about loneliness' effect on the body.
Next, the team investigated the cellular processes linking social experience to CTRA gene expression in rhesus macaque monkeys at the California National Primate Research Center, which had been behaviorally classified as high in perceived social isolation. Like the lonely humans, the "lonely like" monkeys showed higher CTRA activity. They also showed higher levels of the fight-or-flight neurotransmitter, norepinephrine.
Previous research has found that norepinephrine can stimulate blood stem cells in bone marrow to make more of a particular kind of immune cell--an immature monocyte that shows high levels of inflammatory gene expression and low levels of antiviral gene expression. Both lonely humans and "lonely like" monkeys showed higher levels of monocytes in their blood.
Taken together, these findings support a mechanistic model in which loneliness results in fight-or-flight stress signaling, which increases the production of immature monocytes, leading to up-regulation of inflammatory genes and impaired anti-viral responses. The "danger signals" activated in the brain by loneliness ultimately affect the production of white blood cells. The resulting shift in monocyte output may both propagate loneliness and contribute to its associated health risks.