Associations between actigraphy-assessed sleep, inflammatory markers, and insulin resistance in the Midlife Development in the United States (MIDUS) study

Abstract

BACKGROUND: Disturbed sleep has been associated with increased insulin resistance and elevated inflammation. Although there is growing body of evidence that activation of inflammatory pathways plays a crucial role in the development of insulin resistance, the mediational model whereby sleep disturbances influence inflammation that drives insulin resistance has not been fully assessed in general population studies with objectively measured sleep. This study aimed to examine associations between objectively measured sleep, inflammatory markers, and insulin resistance simultaneously and in a mediational analysis, thereby offering insights into the possible causal model.

METHODS: Cross-sectional data collected from 2004 to 2009 during the Midlife Development in the United States II biomarker project were used. The study population included 374 community-based participants (138 men and 236 women) who completed seven nights of wrist actigraphy. Multiple regressions controlling for age and statistically significant variables in univariate regressions were performed to evaluate the associations between actigraphy-assessed sleep measures, inflammatory cytokines, and insulin resistance.

RESULTS: The regression models showed that in women, higher sleep onset latency (SOL) was associated with higher insulin resistance after controlling for age, smoking, obesity, diabetes, depression, and inflammatory cytokines. Higher SOL was also associated with higher interleukin (IL)-6 and C-reactive protein (CRP) levels in women, but no association was found in men. Using mediation models in women, the association between SOL and insulin resistance was partially explained by the indirect effect of inflammatory cytokines.

CONCLUSION: A combination of inflammation and other unidentified pathways may contribute to the relationship between disturbed sleep and glucose homeostasis.