ABSTRACT
Sleep duration is a substantial risk factor for several cardiovascular diseases, including atrial fibrillation (AF). Despite much research, the precise nature of the relationship between the amount of sleep and AF remains unclear. This narrative review explores the relationship between AF and sleep duration, looking at genetic, mechanistic, and epidemiological data to explain this association. A U-shaped association (nonlinear relationship or curvilinear association) between sleep duration and AF has been seen, where longer and shorter sleep duration, more or less than seven to eight hours, have been associated with increased AF risk. Multiple mechanisms such as autonomic dysfunction, inflammation, and structural atrial remodeling have been proposed linking sleep disturbances to AF. Moreover, confounding factors such as individual lifestyle, comorbidities, and sleep quality could affect this association. Additionally, the interpretation of study results is further impacted by methodological limitations, including self-reported sleep duration and observational study designs. It is imperative to comprehend the complex relationship between sleep duration and AF to develop effective preventive and therapeutic methods. The main goals of future research should focus on prospective cohort studies with objective sleep metrics, exploring the mechanistic pathways, and comprehensive confounder adjustments that link sleep disturbances to AF. In summary, addressing sleep disturbances may represent one of the novel approaches to AF prevention and management, with potential implications for improving cardiovascular health and reducing AF-related morbidity and mortality.
ABSTRACT
The gut-brain axis (GBA) is a two-way communication system that is influenced by signals from the nervous system, hormones, metabolism, the immune system, and microbes. The GBA may play a key role in gastrointestinal and neurological illnesses. Signaling events from the gut can regulate brain function. As a result, mounting data point to a connection between autoimmune disorders (AIDs), both neuroinflammatory and neurodegenerative diseases, and the GBA. Clinical, epidemiological, and experimental studies have shown that a variety of neurological illnesses are linked to alterations in the intestinal environment, which are suggestive of disease-mediated inter-organ communication between the gut and the brain. This review's objective is to draw attention to the clinical and biological relationship between the gut and the brain, as well as the clinical importance of this relationship for AIDs, neurodegeneration, and neuroinflammation. We also discuss the dysbiosis in the gut microbiota that has been linked to various AIDs, and we make some assumptions about how dietary changes such as prebiotics and probiotics may be able to prevent or treat AIDs by restoring the composition of the gut microbiota and regulating metabolites.