Summary: Socially isolated individuals may have an increased risk of physical inflammation in the body. Researchers found social isolation was associated with the presence of C-reactive protein and increased levels of glycoprotein fibrinogen. The link between social isolation and physical inflammation was more common in males.
Source: University of Surrey
Social isolation could be associated with increased inflammation in the body new research from the University of Surrey and Brunel University London has found.
In the largest study of its kind researchers investigated the link between social isolation and loneliness with inflammation in the body. Analyzing 30 previous studies in this area researchers found that social isolation could be linked to increased inflammation in the body.
Inflammation is the body’s way of signaling the immune system to heal and repair damaged tissue, as well as defending itself against viruses and bacteria. Inflammation can eventually start damaging healthy cells, tissues and organs and lead to an increased risk of developing non-communicable diseases such as cardiovascular disease.
Researchers found that social isolation, the objective state of being isolated from other people, was associated with the presence of C-reactive protein, a protein substance released into the bloodstream within hours of a tissue injury, and increased levels of the glycoprotein fibrinogen, which is converted into fibrin-based blood clots.
Interestingly, researchers also identified that the link between social isolation and physical inflammation was more likely to be observed in males than females. Further work is needed to clarify why this might be, but previous work suggests that males and females might respond differently to social stressors.
The link between loneliness and inflammation was less clear-cut with results indicating a possible link between loneliness and the pro inflammatory cytokine IL-6. However, this finding was not consistent across the studies examined. Taken in combination with previous knowledge the researchers propose that it is likely that loneliness changes how the inflammatory system responds to stress rather than directly impacting inflammatory response.
Dr Kimberley Smith, Lecturer in Health Psychology at the University of Surrey, said: “Loneliness and social isolation have been shown to increase our risk of poorer health. Many researchers propose that part of the reason for this is because they influence the body’s inflammatory response.
“The evidence we examined suggests that social isolation may be linked with inflammation, but the results for a direct link between loneliness and inflammation were less convincing. We believe these results are an important first step in helping us to better understand how loneliness and social isolation may be linked with health outcomes.”
Christina Victor, Professor of Gerontology and Public Health at Brunel, added: “Our results suggest loneliness and social isolation are linked with different inflammatory markers. This shows how important it is to distinguish between loneliness and isolation, and that these terms should neither be used interchangeably nor grouped together.”
Funding: This study was published in Neuroscience and Biobehavioural Reviews.
The association between loneliness, social isolation and inflammation: A systematic review and meta-analysis
The review synthesised evidence examining the association between a. loneliness with inflammation and b. social isolation with inflammation in adults aged 16 or older from the general population. From an initial 7,400 articles we identified 14 papers that examined loneliness, and 16 that examined social isolation. Qualitative syntheses indicated mixed results, variable study quality, and methodological heterogeneity. Most studies provided associations for C-reactive protein CRP, fibrinogen and Interleukin-6 IL-6, and these results were synthesised using random-effects meta-analyses. There was no association between loneliness with CRP or fibrinogen, but there was a significant association between loneliness and IL-6 for most-adjusted but not least-adjusted analyses. There was also a significant least-adjusted association between social isolation with CRP and fibrinogen, which remained significant for fibrinogen in most-adjusted analyses. There was no association between social isolation with IL-6. Sensitivity analyses indicated that methodological heterogeneity impacted on results. Results indicate that social isolation and loneliness could be linked with systemic inflammation, but more robust methodology is needed to confirm these associations and unpack mechanisms.