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Loneliness Promotes Inflammation During Acute Stress

Lisa M. Jaremka¹; Christopher P. Fagundes¹; Juan Peng²; Jeanette M. Bennett^1,3; Ronald Glaser^1,4,5,6; William B. Malarkey^1,4,6; Janice K. Kiecolt-Glaser^1,6,7

¹ Institute for Behavioral Medicine Research, The Ohio State University College of Medicine · ² College of Public Health, The Ohio State University College of Medicine · ³ Division of Oral Biology, The Ohio State University College of Dentistry · ⁴ Department of Internal Medicine, The Ohio State University College of Medicine · ⁵ Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University College of Medicine · ⁶ Comprehensive Cancer Center, The Ohio State University College of Medicine · ⁷ Department of Psychiatry, The Ohio State University College of Medicine

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.

DOI

10.1177/0956797612464059

Volume

24 (7)

Pages

1089-1097

Language

en

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