Could Inflammation Create Loneliness?
New research reveals fascinating links between inflammation and loneliness.
Posted Dec 09, 2019
It’s a painful paradox: We struggle with epidemic levels of loneliness on a planet inhabited by almost 8 billion other people.
Loneliness and social isolation are major health concerns, with scientific research linking them to an increased risk of heart disease, dementia, and even dying early. These consequences are increasingly relevant, with nearly half of respondents in a recent survey of 20,000 Americans reporting they feel lonely always or sometimes.
The issue also extends far beyond America’s borders. In 2018, the United Kingdom appointed a “minister for loneliness.” A 2019 survey from Australia revealed that half of Australians feel lonely for at least one day a week.
Loneliness is a serious, pervasive problem, and we desperately need actionable solutions and a better understanding of its causes. Since loneliness is seen as a lack of meaningful social interactions, interventions are largely what we might expect. These include the creation of opportunities for social contact, as well as attempts to improve social skills, enhance social support, and address maladaptive social cognition.
However, these efforts to remedy the problem, though helpful, generally ignore a central question: What is it within us that actually creates feelings of loneliness? One fascinating hypothesis: Loneliness could be generated, in part, by inflammation.
When we speak about disease, inflammation is well understood to be a major player. In recent years, we have started to understand that its effects extend far further than we originally expected. In fact, we can now appreciate that inflammation actually affects our thoughts, our mood, and our behavior. Perhaps most notable is the research demonstrating how inflammation contributes to and may actually cause depression.
If inflammation alters our thoughts, and subsequently, our actions, it opens the door to breakthroughs in fields ranging from psychology to immunology to economics. And as it pertains to loneliness, we now have substantial evidence for the idea that inflammation may indeed be a contributor.
As a starting point, though the data have been mixed, loneliness has been linked to higher levels of measured inflammation. For example, a recent study of over 900 middle-aged adults found that, on average, inflammatory markers were significantly more elevated in lonelier people. More social support and social integration were linked to lower levels of inflammation in a 2018 meta-analysis of over 73,000 people.
Of course, this is only an association. And there's certainly more data suggesting that loneliness causes inflammation than the other way around. So, for a more concrete understanding of whether inflammation could generate feelings of loneliness, we’d need to see experiments where inflammation was induced, and outcomes of loneliness recorded. As it turns out, these types of tests have indeed been carried out.
Researchers are able to create inflammation in study participants by giving them either endotoxin (a part of a bacteria) or a vaccination. They can then compare the results of these interventions with those from people who get a placebo shot filled with saline water.
In one of these studies, scientists at UCLA administered either an inflammatory challenge (endotoxin) or placebo to healthy volunteers. They found that people who received the inflammatory challenge had higher levels of inflammation in their blood afterward. More importantly, they also reported higher levels of perceived social disconnection.
These results indicate that when inflammation is increased, people seem to feel more disconnected from others. As it turns out, the link may be even more concerning. Inflammation may sabotage our ability to connect with other people.
In a 2018 study, one group of volunteers was injected with an inflammation-inducing vaccine, while the control group received a placebo. Next, both groups tried to determine the emotions of others by looking at photos of people’s eyes. The group that received the vaccination showed higher levels of inflammation in their blood, and they also had a harder time reading the emotions of others, suggesting that inflammation could damage our social intelligence.
Inflammation also appears to make us more sensitive to social threats. In a 2012 study, people were given endotoxin or a placebo, then had their brains imaged while they were exposed to socially threatening images. Those who received the inflammation-inducing shot showed greater activation of one of the brain’s emotional response hubs (the amygdala) in response to socially threatening images.
Unfortunately, those of us who are prone to loneliness may face a double hit. Data suggest that people who are more sensitive to social disconnection display an increased inflammatory response when faced with an inflammatory challenge, while additionally increasing expression of genes related to inflammation.
Additional research suggests that women might be particularly vulnerable to inflammation-induced symptoms of loneliness. A 2015 study showed that after getting an endotoxin injection, women displayed increased feelings of social disconnection compared to males who had received the same shot.
Though the research is preliminary, the connection between inflammation and loneliness may provide us significant insight into the pathogenesis of the experience of loneliness. It also suggests we could consider intervening on loneliness by targeting inflammation (for example, through dietary modification or stress reduction) in addition to the more traditional aforementioned strategies, like increasing social skills and social integration.
It's clear we need more evidence before we can draw any concrete conclusions. However, it’s worth considering that if loneliness is in part driven by inflammation, then America could be exporting the experience of loneliness throughout the world in the form of pro-inflammatory Western-pattern diets and lifestyles that promote inflammation through chronic stress.