http://pss.sagepub.com/content/24/7/1089.abstract
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.
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