Pro-Inflammatory Diets and Sleep Disturbances in Hyperlipidemia: Exploring the Connections

In adults with hyperlipidemia, higher scores on the Dietary Inflammatory Index (DII) are associated with a greater prevalence of clinician-diagnosed sleep disorders. Clinically, this link highlights body mass index (BMI) and neuro-metabolic mechanisms as plausible mediators between pro-inflammatory diets and sleep impairment.

A cross-sectional NHANES analysis included 13,195 adults with hyperlipidemia and compared DII (exposure) with self-reported physician-diagnosed sleep disorders (outcome), adjusting for demographic, lifestyle, and clinical covariates: age, sex, race/ethnicity, smoking, alcohol, physical activity, WBC, HbA1c, hypertension, diabetes, CHD, stroke, COPD, education, and poverty–income ratio.

After adjustment, each 1-unit increase in DII corresponded to a 5.7% higher prevalence of sleep disorders (adjusted OR 1.057; 95% CI 1.012–1.105), and participants in the highest DII quartile had roughly 30% higher odds versus the lowest quartile (adjusted OR 1.295; 95% CI 1.039–1.614). Overall, the study demonstrates a modest but statistically significant association between pro-inflammatory diet and sleep disturbance in this hyperlipidemic cohort.

BMI mediation (26.07%) accounted for approximately one quarter of the DII–sleep association, indicating partial mediation rather than full causality. That magnitude suggests diet-induced adiposity explains a meaningful fraction of the effect; the remaining association is compatible with systemic inflammation progressing to neuroinflammation and altered hypothalamic and neurotransmitter control of sleep. Metabolic dysregulation may further disturb circadian regulation and sleep architecture. Together, these pathways form a biologically coherent link between dietary inflammatory potential and sleep disturbance among patients with hyperlipidemia.

Adults with hyperlipidemia—especially those with higher BMI and those under age 60—appear most affected, indicating dietary inflammatory potential is one modifiable factor within a broader risk profile.

Randomized or longitudinal studies are required to determine whether lowering DII improves sleep outcomes in this population.