Though loneliness has often been defined by the amount of social interaction a person experiences, a recent study led by scientists at UCLA sheds new light on how loneliness may be linked to the most basic internal processes of our biology.
“It’s our first glimpse into the whole picture of how social factors regulate genomic function to influence human health,” said Steve Cole, an associate professor at the David Geffen School of Medicine and lead researcher for the study.
The study is the first of its kind to use DNA microarrays, chips that contain collections of genetic probes, to analyze differences in gene activity between lonely and non-lonely people. In the study, Cole used the UCLA Loneliness Scale, a widely used psychological survey developed in the 1970s, to assess levels of social isolation and to classify people as lonely or non-lonely.
The researchers found that changes in the gene expression of the cells were not a function of the number of relationships or amount of interaction a person had but rather were related to how the person perceived the quality of the relationships that he or she possessed.
Though people may have a lot of social contact, Cole said, they may still experience loneliness if they do not feel close to those they interact with.
“It’s about how you evaluate your network of social relationships,” said Daniel Russell, a human development professor at Iowa State University and a co-author of the UCLA Loneliness Scale. “Is (your network) meeting your needs? What you want or don’t want is the critical issue.”
Previous studies conducted over the last two decades showed a relationship between being socially isolated and having an increased risk for certain diseases such as heart disease, viral infections and some cancers, as well as death. But before now, researchers did not know exactly what kind of biology was responsible for the different health outcomes, Cole said.
“All of a sudden, a very specific cellular mechanism has been posited,” said John Cacioppo, professor and director of the Center for Cognitive and Social Neuroscience at the University of Chicago.
“Before, genetic processes were thought to be uninfluenced by social processes except for over thousands of years by selection of genes. (Cole’s) advances were critical in putting it together and saying what processes were modulated by social perception.”
Cole and his colleagues took white blood cells, cells of the immune system that defend the body against diseases and drive the inflammation response, from a group of subjects and used microarrays to analyze the gene activity of these cells.
About half of the subjects in the study were classified as consistently lonely, scoring in the top 15 percent of the loneliness scale, while the rest were classified as non-lonely, scoring in the lowest 15 percent of the scale.
Using the microarrays, Cole and his team identified a set of 209 genes that were expressed in different amounts in the two groups.
In the lonely group, the researchers found more activity in the genes responsible for inflammation and less activity in two key protective gene sets: those involved in the production of antibodies ““ molecules that the immune system uses to protect a person against foreign pathogens ““ and those involved in antiviral responses.
“It’s a portrait of an immune system that is doing too much bad stuff ““ too much inflammation signaling and not enough protective things, at least in terms of defending you against infections,” Cole said.
The researchers also found that the receptors of a class of hormones called glucocorticoids on the white blood cells of lonely people were less sensitive than the receptors on the cells of non-lonely people.
People who are lonely may perceive the world as a more threatening and uncertain place, which leads to more physiological stress responses that desensitize these receptors, Cole said. The body normally generates glucocorticoids to suppress inflammation, but in people who were lonely, the body’s response was not regulated normally.
The research provides molecular context for developing treatments for people who suffer from chronic loneliness.
“Our hypothesis is that, instead of changing these people’s personality, we might be able to change their biology in ways that keep them healthy,” Cole said.
Doctors may want to treat people who are chronically lonely with anti-inflammatory agents to protect them against cardiovascular disease, for example, or to use drugs to regulate their bodies’ responses to stress from social interaction, Cole said.
Future research will focus on the effects of psychological versus biological interventions in lonely people.
“A big part of where our research is going is how do we intervene,” Cole said. “Do we change the loneliness or keep it and change the biology?”
The study indicates that there are mechanisms at the most basic levels of our bodies that drive us to interact and form relationships.
“We characterize ourselves as individualistic, but some of our research is saying that that’s not actually what human nature wants,” Cacioppo said. “We are designed to connect. It’s an enduring picture of human nature.”