Thu Nov 23 2023

Social isolation, loneliness, and inflammation: A multi-cohort investigation in early and mid-adulthood

Background: A meta-analysis reveals a 25–30% increased risk of mortality associated with social isolation, loneliness, and living alone (Holt-Lunstad et al., 2015). According to Cacioppo et al. (2006), loneliness, a negative emotional state stemming from perceived social relationship deficiencies, may adaptively respond to social disconnection, preparing individuals for unsafe environments without family and friends’ support. This hypothesis posits that loneliness could alter immune functioning, potentially boosting an individual’s infection-fighting capacity following injury.

Methods: The study involved three cohorts: TRIAGE, Dunedin, and Environmental Risk Longitudinal Twin. Researchers assessed social isolation and loneliness via factors such as living alone and childhood isolation. They measured inflammation using markers like CRP, IL-6, and suPAR, which indicate systemic inflammation.

Results: The study answered 4 questions:

  • Is living alone associated with inflammation in acutely admitted medical patients?

In the TRIAGE Study, acutely admitted medical patients who were living alone had significantly higher median levels of CRP (5.8 mg/L vs. 4.8 mg/L), IL-6 (9.3 pg/mL vs. 7.3 pg/mL), and suPAR (5.2 ng/mL vs. 4.2 ng/mL) compared with patients who were not living by themselves.

  • Is childhood social isolation longitudinally associated with inflammation in adulthood?

Participants who had experienced childhood social isolation or age-38 loneliness had higher CRP, IL-6, and suPAR at age 45, after controlling for sex (and age by design). The associations between childhood social isolation or age-38 loneliness with elevated age-45 suPAR held after controlling for childhood SES, and age-45 BMI, smoking, concurrent depression, and anti-inflammatory medication. In contrast to suPAR, childhood social isolation or age-38 loneliness were not significantly associated with age-45 CRP or IL-6 levels when controlling for age-45 BMI and smoking or further for additional covariates.

  • Is adult loneliness cross-sectionally associated with inflammation?

After controlling for sex, participants who were lonelier at age 45 had higher suPAR levels at age 45, but not CRP or IL-6. The association with suPAR remained significant after controlling for childhood SES, and age-45 BMI, smoking, and concurrent depression. Further controlling for use of anti-inflammatory medication did not change any of the results.

  • Do social isolation and loneliness have a multiplicative effect?

No significant social isolation × loneliness interactions were observed for the three inflammation markers, in either the Dunedin or the E-Risk samples.

Conclusions

This study explored how social isolation and loneliness affect inflammation across different age groups and cohorts. Findings show a stronger link between social isolation and inflammation than loneliness. Childhood social isolation’s impact on inflammation becomes clearer in mid-adulthood. The study suggests suPAR as a reliable indicator of inflammation due to social isolation.

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