Causal Associations Between Sleep Traits and Low Grip Strength: A Bidirectional Mendelian Randomization Study.

Background: Sleep disorders and low grip strength often co-occur clinically and are geriatric symptoms that cause significant socioeconomic burden. Previous observational studies have found an association between sleep behaviors and grip strength, but the causal relationship remains unclear. Purpose: With the Mendelian randomization (MR) approach, the study aimed to determine the causal association between sleep traits (sleep duration, insomnia, daytime napping, sleep-wake disorders, chronotype) and low grip strength. Methods: The study used genetic variants from the genome-wide association study (GWAS) archived in UK Biobank and FinnGen. We assessed the potential causal relationship between sleep behaviors and grip strength using inverse variance weighting (IVW), weighted median (WM), and MR-Egger. Additionally, we performed sensitivity analyses using Cochran's Q test, MR Egger Intercept test, funnel plots, and leave-one-out method. Results: We found that sleep duration is causally negatively associated with low grip strength (OR = 0.618, 95% CI = 0.424-0.900, P = 0.012). Sleep-wake disorders have a positive association with low grip strength (OR = 1.018, 95% CI = 1.002-1.034, P = 0.029). Reversely, high low grip strength risk was causally associated with increased daytime napping (OR = 1.018, 95% CI = 1.004-1.032, P = 0.011). Conclusion: The study revealed causal associations between sleep duration, sleep-wake disorders, and low grip strength. Understanding their relationship helps in early clinical intervention to improve the life quality of the elderly.

Causal associations of physical activity and leisure sedentary behaviors with age at onset of Huntington's disease: A mendelian randomization study.

BACKGROUND: Huntington's disease (HD) is a neurodegenerative disorder for which effective therapies are currently lacking. Studies suggest that increasing physical activity (PA) and reducing leisure sedentary behavior (LSB) mitigate the progression of HD, but their causal relationship with the age at onset (AAO) of HD remains uncertain. To investigate this, we conducted the Two-sample Mendelian Randomization (MR). METHODS: Exposure were retrieved from the UK BioBank's (UKB) Genome-Wide Association Study (GWAS). PA included accelerometer-based average PA, vigorous PA, self-reported moderate-to-vigorous PA (MVPA), and light do-it-yourself activity. LSB included television (TV) time, computer time, and driving time. Outcome came from the GWAS of the GEM-HD Consortium. We applied several MR methods such as inverse variance weighted (IVW), MR-Egger regression, weighted median (WM) for sensitivity analysis. RESULTS: Increases in light PA (ß = 8.53 years, 95 % CI = 10.64 to 44.09, P = 0.001) and accelerometer-based vigorous PA (ß = 5.18, 95 % CI = 0.92 to 9.43, P = 0.017) delayed AAO of HD, while longer TV time was associated with earlier AAO of HD (ß = -2.88 years, 95 % CI = -4.99 to -0.77, P = 0.007). However, other PA and LSB phenotypes did not significantly affect AAO of HD. CONCLUSION: The study revealed a unidirectional causality between PA, LSB and the AAO of HD. Increasing PA and reducing TV time delay HD onset. Therefore, we recommend increasing physical activity and reducing sedentary behavior to delay the occurrence of motor symptoms for premanifest HD individuals.