A new study has revealed that loneliness triggers cellular changes that can increase the risk of premature death by 14 percent.
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The study shows that loneliness leads to fight-or-flight stress signalling, which can ultimately affect the production of white blood cells.
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In the study, University of Chicago researchers examined gene expression in leukocytes, cells of the immune system that are involved in protecting the body against bacteria and viruses.
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They found that loneliness predicted future conserved transcriptional response to adversity (CTRA) gene expression measured a year or more later. Interestingly, CTRA gene expression also 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.
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In another study, the team investigated the cellular processes linking social experience to CTRA gene expression in rhesus macaque monkeys. Like the lonely humans, the 'lonely like' monkeys also showed higher CTRA activity and higher levels of the fight-or-flight neurotransmitter, norepinephrine.
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They determined that this monocyte-related CTRA shift had real consequences for health. In a monkey model of viral infection, the impaired antiviral gene expression in 'lonely like' monkeys allowed simian immunodeficiency virus (the monkey version of HIV) to grow faster in both blood and brain.
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Taken together, these findings supported a mechanistic model in which loneliness results in fight-or-flight stress signalling, which increases the production of immature monocytes, leading to up-regulation of inflammatory genes and impaired anti-viral responses.
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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.
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The study is published in the Journal Proceedings of the National Academy of Sciences.
