Excess body weight, including overweight and obesity, is one of the major factors influencing human health, and plays an important role in the global burden of disease.
Objective
People with poor sleep quality have higher risk of cardiovascular disease (CVD), and one potential mechanism of CVD is chronic inflammation. The aim of this study was to investigate the role of dietary inflammation in the relationship between sleep quality and CVD risk.
Methods
This study involved 5594 participants from the National Health and Nutrition Examination Survey (NHANES) in 2005–2008. Sleep quality, dietary inflammation, and 10-year CVD risk were evaluated via the Pittsburgh Sleep Quality Index (PSQI), the Energy-adjusted Dietary Inflammatory Index (E-DII), and the Framingham Risk Score (FRS), respectively. We used generalized additive model (GAM) and mediation analysis to investigate the relationship among sleep quality, 10-year CVD risk, and E-DII.
Results
PSQI had a non-linear relationship with 10-year CVD risk (
P
< 0.001). Meanwhile, among the participants with poor sleep quality, PSQI was positively associated with increased 10-year CVD risk (
P
< 0.001) and E-DII (
P
< 0.001). Furthermore, the association between sleep quality and CVD risk was partially mediated by E-DII, and the mediated proportion was 14.6%, and the mediating effect of E-DII varied in different gender and age groups. However, in the subjects with good sleep quality, the association among PSQI, E-DII, and 10-year CVD risk was not existed.
Conclusion
Ten-year CVD risk could be reduced by controlling the intake of inflammatory food, especially for whom with sleep disorders. In general, the reduction of inflammatory diet could weaken the effect of sleep disorders on the CVD risk.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Background: Dietary inflammatory index (DII) was associated with Type 2 diabetes mellitus and cognitive function impairment (CFI). Objective: The aim of this study was to explore whether the associations among DII, glycohemoglobin (HbA1c), and CFI were similar in the participants with or without diabetes. Methods: A total of 1,198 participants aged 60 and over from the National Health and Nutrition Examination Survey (NHANES) in 2011–2014 were involved in this study, dividing into subgroups as diabetes and non-diabetes for further analysis. Results: We found that participants with pro-inflammatory diet had higher proportion of CFI patients (p < 0.05). Pro-inflammatory diet and HbA1c were positively associated with the risk of CFI; participants with pro-inflammatory diet was 1.479 times on occurrence of CFI compared with anti-inflammatory diet group. The interaction between inflammatory diet and HbA1c was positive on the risk of CFI and was negative on the CERAD-immediate and CERAD-delayed, respectively. Among the participants without diabetes, the associations of Energy-adjusted DII (E-DII) with Animal Fluency test and Digit Symbol Substitution Test (DSST) were partially mediated by HbA1c, and the mediated proportion was 5.8% and 6.6%, respectively. However, there was no such mediation effect in the diabetes patients. Conclusion: In elderly participants without diabetes, there was an interaction between inflammatory diet and HbA1c on the association with CFI, especially for the dimension of CERAD-immediate and CERAD-delayed. Besides, the associations of E-DII with Animal Fluency test and DSST were partially mediated by HbA1c. For diabetic patients, HbA1c, rather than the inflammatory diet has a positive effect on the CFI risk.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.