Feeling lonelier with reduced social contact in everyday life predicts elevated inflammation.

Trait loneliness robustly predicts heightened inflammation and, in turn, poorer health. Nevertheless, the etiology of loneliness in daily life remains largely unexplored and is an important research direction. The current study examines a source of daily loneliness fluctuation: how daily loneliness increases with reduced social contact, i.e., loneliness reactivity. It further tests how loneliness reactivity relates to inflammation in the 2004-2009 Midlife in the United States study. Adults (N = 159, ages 35-83) completed 8 consecutive nightly telephone interviews in which they self-reported how lonely they felt and whether they spent less time with others than normal that day. Participants separately (M(SD)time_lag = 1.75(15.52) months) provided blood samples assayed for interleukin (IL)-6, C-reactive protein (CRP), and tumor necrosis factor (TNF)-α. Loneliness reactivity slopes were extracted from multilevel models predicting daily loneliness from reduced social contact. Regression models tested associations between these slopes, a signature of reactivity, and inflammatory markers. Reduced social contact predicted higher daily loneliness [B(SE) = 0.20(0.03), p < 0.001], and individuals varied in this loneliness reactivity (Random SD: 0.34). In turn, higher loneliness reactivity predicted higher IL-6 [B(SE) = 0.79(0.39), p = 0.043], CRP [B(SE) = 1.47(0.66), p = 0.027], and TNF-α [B(SE) = 0.47(0.22), p = 0.035]. Findings highlight the importance of examining loneliness in daily life and reactivity as a novel dimension of daily loneliness. Results also suggest that future research should examine health implications of loneliness reactivity to reduced social contact in daily life for novel just-in-time interventions aiming to offset the health risks of loneliness.