Researchers in China have identified significant alterations in the gut microbiome and fecal metabolome of patients with age-related cataract (ARC), adding further evidence to the emerging concept of a “gut–eye axis” in ocular disease. The findings, published in Scientific Reports, suggest that microbiome-driven inflammatory and metabolic changes could contribute to cataract pathogenesis.
Age-related cataract remains the leading cause of blindness worldwide, affecting an estimated 95 million people. While aging is the dominant risk factor, systemic contributors such as metabolism, oxidative stress, and inflammation are increasingly recognized as important drivers of lens degeneration. Yet the mechanisms linking these systemic factors to cataract formation remain poorly understood.
To investigate whether intestinal dysbiosis may play a role, researchers from Chongqing Medical University, China, analyzed stool samples from 30 patients with ARC and 30 healthy controls using 16S rDNA sequencing, untargeted metabolomics, and targeted short-chain fatty acid (SCFA) profiling.
Although overall microbial diversity did not differ significantly between groups, patients with cataract showed a markedly more dysbiotic microbiome profile.
The metabolic consequences of these microbial shifts were also substantial. ARC patients demonstrated distinct fecal metabolomic signatures, particularly involving disruptions in glycerophospholipid and choline metabolism pathways associated with cell membrane integrity and inflammatory signaling. Researchers identified 430 metabolites that differed between cataract patients and controls, with lipid metabolites comprising the majority of significant changes.
Most notably, levels of key anti-inflammatory SCFAs – acetate, propionate, and butyrate – were significantly reduced in ARC patients. These metabolites positively correlated with the abundance of beneficial SCFA-producing bacteria, suggesting that microbial depletion directly contributed to impaired fermentation activity.
The study authors propose that this combination of altered lipid metabolism and reduced SCFA signaling may promote chronic systemic inflammation and oxidative stress, ultimately accelerating lens opacification. Reduced butyrate availability, they note, may weaken intestinal barrier integrity and permit dissemination of inflammatory mediators capable of damaging lens proteins.
The study also raises the possibility that stool-based microbial or metabolic biomarkers could eventually aid non-invasive cataract risk assessment. The researchers suggest that microbiome-targeted interventions – including dietary fiber supplementation, probiotics, or other approaches aimed at restoring SCFA production – may represent future preventive or therapeutic strategies.
Still, the study authors caution that the work remains exploratory. The cohort was relatively small, the cataract group was modestly older than controls, and the cross-sectional design prevented conclusions about causality. Nonetheless, the study represents one of the first integrated multi-omics investigations of the gut microbiome in ARC and provides further support for the growing view that ocular diseases may be influenced by systemic microbial and metabolic health.
