Loneliness is commonly regarded as a social phenomenon in which individual personality differences contribute to its severity. Some people enjoy solitude, for example, because they never feel lonely, while people with high degrees of loneliness have shorter life expectancies than people who never feel lonely.
There may be more to it than that. Recent research shows that the gene expression in the immune cells of people with chronically high levels of loneliness is different than people who do not feel lonely. Even more telling, some genes were underexpressed in the same subjects, including those in antibody production.
Using the UCLA Loneliness Scale on 14 people with available DNA microarrays, the researchers found 6 respondents who met the criteria for lonely. They surveyed the activity of all known human genes in their white blood cells and found 209 gene transcripts that were different for the lonely and not lonely group - 78 were overexpressed and 131 were underexpressed.
Louise Hawkley, Ph.D., is Research Scientist at the Center for Cognitive & Social Neuroscience in the Department of Psychology at the University of Chicago and co-author on a few papers about this topic. Since this was the first time genome-wide transcriptional activity could be matched to social factors, I asked a few follow-up questions.
Hank: Is epinephrine the culprit ( so, a hormonal imbalance that could be treated to ease the loneliness ) or a by-product?
Hawkley: We have no evidence that epinephrine "causes" loneliness, and for that matter, no evidence that loneliness "causes" epinephrine increases (at least not yet). We do, however, have evidence of an association between loneliness and epinephrine that marks heightened fight-or-flight (i.e., sympathetic nervous system) activity.
Why might this be? We know that lonely individuals live in a heightened state of stress: lonely individuals, young and older, perceive life's daily challenges as more stressful and threatening than do nonlonely individuals, even when, objectively speaking, the challenges are comparable in both groups.
To the extent lonely individuals show greater stress-related deployment of the fight-or-flight response, they are more prone to higher levels of circulating epinephrine, a neurohormone that acts on the heart and the blood vessels to accelerate heart rate and alter arterial constriction in ways that could, over time, contributed to atherosclerosis and hypertension.
Hank: There was apparently distinction in adrenal gland output in lonely patients but what other cellular issues did you uncover that may be involved?
Hawkley: We're actively pursuing a variety of cellular and other mechanisms that may contribute to different rates of decline in physiological functioning between lonely and nonlonely individuals. For example, we are or will be examining group differences in gene transcription regulation, cellular aging (e.g., telomerase levels, telomere length), and endothelial cell responses to increased blood flow.
More generally, inflammatory processes are of interest to us, and this represents a broad physiological realm that ranges from molecular to cellular to organismic.
With a generation of Baby Boomers approaching retirement, a 'loneliness' molecule that has greater impact with age and is enhanced by stress and other factors is a high priority for research.
It will be interesting to see where the search for biomarkers that can reduce the impact of loneliness on health takes us in the future.
Louise C. Hawkley, John T. Cacioppo (2007)
"Aging and Loneliness: Downhill Quickly?"
Current Directions in Psychological Science 16 (4), 187–191.
Steve W. Cole, Louise C Hawkley, Jesusa M Arevalo, Caroline Y Sung, Robert M Rose and John T Cacioppo (2007) "Social Regulation of Gene Expression in Humans: Glucocorticoid Resistance in the Leukocyte Transcriptome", Genome Biology 2007, 8:R189doi:10.1186/gb-2007-8-9-r189