Investigating bidirectional causal relationships between gut microbiota and insomnia
image: Study flowchart. Dutch, Dutch Microbiome Project; GWAS, genome-wide association study; IV, instrumental variable; IVW, inverse variance weighted; MiBioGen, MiBioGen alliance; MR, Mendelian randomisation; MR-PRESSO, MR Pleiotropy RESidual Sum and Outlier; SNP, single-nucleotide polymorphism; WM, weighted median.
Credit: Shangyun Shi, Dongming Liu, Ancha Baranova, Hongbao Cao, Fuquan Zhang.
Insomnia is often treated as a single, uniform sleep disorder. Nevertheless, anyone who has experienced persistent sleeplessness or cared for patients with it recognises that its origins and effects may differ greatly from person to person. Emerging research has increasingly pointed to a surprising contributor outside the brain: the gut, for which a recent genetic study offers compelling evidence that insomnia and the gut microbiome are strongly linked and could influence each other in meaningful ways.
Researchers from China, as well as international collaborators, have recently published a study in General Psychiatry, exploring whether specific gut bacteria play a role in insomnia and whether insomnia, in turn, can alter the gut microbiome. To investigate this aim, they applied Mendelian randomisation, which is a genetic method that uses naturally occurring DNA variants to infer causal relationships rather than relying on simple associations.
The study drew on extensive genetic data from more than 386,000 people with information on insomnia, alongside gut microbiome data from two large international cohorts totaling over 26,000 participants. This approach enabled the team to examine the gut–sleep relationship in both directions while reducing the confounding influence of environmental and lifestyle factors.
Results revealed a complex, bidirectional link, suggesting that disrupted sleep is not merely an outcome of gut imbalance; it can actively drive microbial changes.
On one hand, specific gut bacterial groups were found to increase the risk of insomnia, while others appeared to offer some protective effect. These microbes spanned multiple taxonomic levels, including genera, families, and orders, suggesting that insomnia risk may be influenced by broad patterns of the microbial ecosystem rather than a single pathogenic species. On the other hand, conversely, the analysis showed that insomnia can also reshape the gut microbiota. Among those with a genetic predisposition to insomnia, people showed shifts in the abundance of several microbial taxa, with some taxa increasing and others decreasing.
One notable example was the genus Odoribacter. Using additional statistical tests to confirm the direction of effects, the researchers found strong evidence that Odoribacter both influences and is influenced by insomnia, making it a potential key player in the gut–brain axis.
Overall, the study argues that insomnia should be viewed as more than a disorder rooted solely in the brain. Rather, it reflects a broader physiological interplay, particularly involving communication between the gut and the nervous system. Although the findings are not yet ready for clinical application, they reveal promising new avenues for treatment. If specific microbial patterns contribute to insomnia, future interventions might include targeted probiotics, dietary strategies, or other microbiome‑based approaches tailored to an individual’s biological profile.