Competing in vain for the attention of someone special or fretting over a mid-term exam may not be healthy. Such stress seems to boost a person’s supply of two proteins that cause inflammation, researchers report January 23 in the Proceedings of the National Academy of Sciences.
These inflammatory triggers have been linked to an increased risk of heart disease, high blood pressure, cancer and depression. The new results add to a growing body of research that links social stress with biological risks.
“We wanted to see how mental states such as optimism, or social relationships such as competition, get under the skin,” says study coauthor Shelley Taylor, a social neuroscientist at the UCLA School of Medicine. She and her colleagues looked at the relationship between day-to-day stress and two proteins that trigger inflammation in the body, called pro-inflammatory cytokines.
The researchers asked 122 young, healthy adults to keep a diary of all positive and negative social interactions for eight days, as well as descriptions of any incidents that involved competition. “We picked young adults with no history of heart disease or inflammation disorders or depression [because] we wanted to look at the biological processes in a population that was healthy,” Taylor says.
Several days later, the scientists swabbed the volunteers’ inner cheeks for fluid samples. Analyses revealed that the people with the most negative social interactions recorded in their diaries, and those who reported stressful competition in work or academic pursuits, had substantially higher levels of one of the inflammatory proteins — TNF receptor 2 — than did those who recorded fewer such incidents. People reporting stressful competition for another’s attention had high concentrations of the other inflammatory protein, interleukin-6.
The volunteers then underwent a stressful 25-minute test in which they did arithmetic calculations in their heads and gave a brief speech in front of strangers. After this test, people who had had the most negative interactions earlier in the week again showed high levels of the inflammatory proteins.
The link between short-term stress and revved-up inflammation could have an evolutionary basis, suggests Nicolas Rohleder, a psychologist at Brandeis University in Waltham, Mass., who wasn’t part of the study team. “As early humans, we had to fight for our lives — fight or flight,” he says. Inflammation has a useful short-term role in fending off pathogens, so triggering inflammation as a response to stress may have been a way the body fended off infections caused by those encounters, which often resulted in some form of injury, he says.
“Humans are not really running away now,” Rohleder says. And nowadays, conflict tends not to end in physical violence. So while an acute reaction to stress might have paid dividends in the Stone Age, he says, stress may often result in chronic inflammation instead.
So reduced stress — and therefore less inflammation — may be one of the mechanisms that links social support with health outcomes, Taylor says. “Relationships are vital to health, like your diet,” she says.