Loneliness and inflammation

Loneliness is associated with the inflammatory response. Continue scrolling to read key resources on the relationship between loneliness and inflammation.

 

Hackett et al. (2012)

Loneliness and stress-related inflammatory and neuroendocrine responses in older men and women

Quasi-experimental Study

Primary finding: Greater loneliness was associated with larger IL-6 (p=0.044) and IL-1Ra (p=0.006) responses to psychological stress and higher MCP-1 (p<0.001) levels in women, independently of age, grade of employment, body mass index and smoking status.


Smith et al. (2020)

The association between loneliness, social isolation and inflammation: A systematic review and meta-analysis

Systematic Review and Meta-Analysis

Primary finding: Qualitative syntheses of 14 studies indicated mixed results on the association between loneliness and inflammation, 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.


Eisenberger et al. (2017)

In Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior

Theoretical Review

Primary finding: This review first summarizes evidence that inflammatory processes regulate social behavior, leading to characteristic changes that may help an individual navigate the social environment during times of sickness. Specifically, this review shows that inflammation: (1) increases threat-related neural sensitivity to negative social experiences (eg, rejection, negative social feedback), presumably to enhance sensitivity to threats to well-being or safety in order to avoid them and (2) enhances reward-related neural sensitivity to positive social experiences (eg, viewing close others and receiving positive social feedback), presumably to increase approach-related motivation towards others who might provide support and care during sickness. Next, this review summarizes evidence showing that social behavior also regulates aspects of inflammatory activity, preparing the body for situations in which wounding and infection may be more likely (social isolation).


Moieni et al. (2018)

Effects of inflammation on social processes and implications for health

Theoretical Review

Primary finding: This review summarizes findings in this field, specifically highlighting work that provides support for the idea that inflammation can lead to (1) increases in sensitivity to negative, threatening social experiences and (2) increases in sensitivity to positive, socially rewarding experiences. These diverging sensitivities in response to inflammation may depend on context and be adaptive for recuperation and recovery from illness. This review also discusses the implications of these findings for health and future research, including implications for depression, loneliness, and inflammatory disorders.