Background: Depression and obstructive sleep apnea (OSA) have complex and incompletely understood pathophysiological links. Our study used National Health and Nutrition Examination Survey (NHANES) data from 2005 to 2008 to elucidate their associations.
Methods: Initial assessment employed multivariable logistic regression to quantify links between depressive symptom severity and OSA manifestations in NHANES data. Mendelian randomization (MR) was implemented to establish potential causal pathways connecting depression and OSA pathogenesis.
Results: The NHANES investigation enrolled 5099 individuals. Through multifactorial logistic regression analyses, progressively adjusted models revealed consistent correlations between depressive symptom scores and OSA risk. MR approaches substantiated a statistically significant causative association linking depression with OSA pathogenesis.
Conclusion: This study indicates a firm association between depression and OSA risk. This underscores the necessity for further research into the causal pathways from depression to OSA, identifying potential targets for intervention in this prevalent respiratory condition. In addition, clinical work should focus on the OSA disease in patients with depression symptom, as well as antidepressant and OSA treatment methods, and the possibility of clinical benefit of treatment for these patients with comorbidities.
Background: Despite a strong link between obstructive sleep apnea (OSA) and sleep traits, the shared genetic architecture remains unclear. This study aims to explore the shared genetic basis and bidirectional causal between OSA and sleep traits.
Methods: Using large-scale genome-wide association studies summary statistics for OSA and sleep traits, we employed linkage disequilibrium score regression (LDSR) and MiXeR to examine genetic correlations and quantify polygenic overlaps. The causal association was explored by bidirectional Mendelian randomization. In addition, we identified shared genomic loci through conditional and conjunctional false discovery rate (cond/conjFDR) analysis, followed by annotation to identify shared genes. Finally, we performed enrichment, developmental trajectory, and phenome-wide association study analysis of the shared genes to explore underlying mechanisms.
Results: We found that both LDSR and MiXeR results revealed substantial genetic correlations and polygenic overlaps between OSA and most of sleep traits. MR analysis supported bidirectional causality between OSA and sleep traits such as insomnia and snoring. Subsequent conjFDR analysis pinpointed 168 distinct shared loci, which encompassed 695 unique genes, and these genes are predominantly enriched in the neurodevelopmental and metabolic process pathways. Notably, the expression of 38 shared genes exhibits a significant correlation with both OSA and sleep traits. These shared genes exhibit specific developmental trajectories and demonstrate significant pleiotropic associations with phenotypes such as metabolism, immunity, and brain structure.
Conclusion: This study uncovers the broad pleiotropy of the genetic architecture shared between OSA and sleep traits, highlighting neurodevelopmental and metabolic pathways as the key shared biological underpinnings.
Objective: To examine the associations between physical activity (PA), sleep duration, and cognitive function among middle-aged and older adults, focusing on the mediating and moderating roles of sleep duration.
Methods: Data were derived from the 2020 wave of the China Health and Retirement Longitudinal Study. A cross-sectional design was employed. Multiple linear regression and PROCESS Models 1 and 4 were used to analyze the effects of PA intensity and sleep duration on cognitive function, as well as their interactive relationships.
Results: Sleep duration was a significant positive predictor of cognitive function (B = 0.214, p < 0.001). Moderate- and light-intensity PA were negatively associated with cognitive performance (B = −1.068 and B = −1.401, p < 0.001), whereas vigorous-intensity PA was positively associated (B = 0.546, p < 0.001). Sleep duration buffered the negative effect of moderate-intensity PA on cognition but amplified the detrimental effect of light-intensity activity. Moreover, sleep duration suppressed the positive association between vigorous PA and cognitive function.
Conclusion: PA and sleep duration appear to be associated with cognitive function through interaction and mediation pathways. Optimizing both PA and sleep behaviors may contribute to the preservation of cognitive function.