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. 2013 Jul 1;24(7):1089-97.
doi: 10.1177/0956797612464059. Epub 2013 Apr 29.

Loneliness promotes inflammation during acute stress

Lisa M Jaremka  1 , Christopher P Fagundes, Juan Peng, Jeanette M Bennett, Ronald Glaser, William B Malarkey, Janice K Kiecolt-Glaser
Affiliations

Loneliness promotes inflammation during acute stress

Lisa M Jaremka et al. Psychol Sci. .

Abstract

Although evidence suggests that loneliness may increase risk for health problems, the mechanisms responsible are not well understood. Immune dysregulation is one potential pathway: Elevated proinflammatory cytokines such as interleukin-6 (IL-6) increase risk for health problems. In our first study (N = 134), lonelier healthy adults exposed to acute stress exhibited greater synthesis of tumor necrosis factor-alpha (TNF-α) and IL-6 by peripheral blood mononuclear cells (PBMCs) stimulated with lipopolysaccharide (LPS) than their less lonely counterparts. Similarly, in the second study (N = 144), lonelier posttreatment breast-cancer survivors exposed to acute stress exhibited greater synthesis of IL-6 and interleukin-1 beta (IL-1β) by LPS-stimulated PBMCs than their counterparts who felt more socially connected. However, loneliness was unrelated to TNF-α in Study 2, although the result was in the expected direction. Thus, two different populations demonstrated that lonelier participants had more stimulated cytokine production in response to stress than less lonely participants, which reflects a proinflammatory phenotype. These data provide a glimpse into the pathways through which loneliness may affect health.

Keywords: health; inflammation; loneliness; neuroendocrinology; psychoneuroimmunology; stress reactions.

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Conflict of interest statement

All authors declare that there are no financial conflicts of interest.

Figures

Figure 1
Figure 1
Figure 1a and b. To illustrate the relationship between loneliness and inflammation, Study 1 averages of stimulated TNF-α and IL-6 production were graphed for participants 1 standard deviation above and below the mean of loneliness. Sample means were estimated using a model that included loneliness as a continuous measure and are adjusted for SAD, age, and gender.
Figure 2
Figure 2
Figure 2a-c. To illustrate the relationship between loneliness and inflammation, Study 2 averages of stimulated TNF-α, IL-6, and IL-1β production were graphed for participants 1 standard deviation above and below the mean of loneliness. Sample means were estimated using a model that included loneliness as a continuous measure and are adjusted for SAD, age, time since treatment, and comorbidities.
Figure 2
Figure 2
Figure 2a-c. To illustrate the relationship between loneliness and inflammation, Study 2 averages of stimulated TNF-α, IL-6, and IL-1β production were graphed for participants 1 standard deviation above and below the mean of loneliness. Sample means were estimated using a model that included loneliness as a continuous measure and are adjusted for SAD, age, time since treatment, and comorbidities.
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