Obstructive Sleep Apnea Associated with Higher Odds of Age-Related Macular Degeneration
A systematic review and meta-analysis evaluated the association between obstructive sleep apnea (OSA) and age-related macular degeneration (AMD). The study included observational studies with a total sample size of 3,536,314 adults with and without OSA. The primary outcome was overall AMD risk, with secondary outcomes including neovascular AMD (nAMD), non-neovascular AMD, late AMD with geographic atrophy (GA), and anti-VEGF therapy requirement. Follow-up duration was not reported.
In crude analyses, OSA was associated with higher odds of overall AMD (OR=1.45, 95%CI: 1.13-1.84), neovascular AMD (OR=1.76, 95%CI: 1.06-2.93), and non-neovascular AMD (OR=1.95, 95%CI: 1.04-3.66). However, in subgroups without confounder adjustment and in regression-adjusted analyses, no significant associations were observed. Propensity-score matched studies showed higher odds of AMD (OR=1.92, 95%CI: 1.05-3.52). Adjusted analyses confirmed an association (aOR=1.44, 95%CI: 1.11-1.77), and time-to-event analyses showed increased hazard of AMD (aHR=1.66, 95%CI: 1.13-2.19). Stage-specific analyses for neovascular and non-neovascular AMD were not significant.
Safety and tolerability data were not reported, as the study focused on observational associations rather than interventional outcomes. The review did not report adverse events, serious adverse events, or discontinuations.
Compared to prior landmark studies, this meta-analysis aggregates data from multiple observational studies, providing a broader but less controlled perspective. Previous studies have suggested a link between OSA and AMD, but this analysis highlights the inconsistency when adjusting for confounders.
Key methodological limitations include variability in diagnostic criteria for OSA and AMD, high heterogeneity in several analyses, and reliance on observational data, which precludes causal inference. The certainty of evidence ranges from moderate to very low.
Clinically, these findings suggest that OSA may be a risk factor for AMD, but the association is not robust after adjustment. Clinicians should consider OSA as a potential modifiable risk factor in AMD patients, but further research with rigorous confounder control is needed.
Unanswered questions include whether treatment of OSA reduces AMD risk, the role of intermittent hypoxia in AMD pathogenesis, and the impact of OSA severity on AMD subtypes. Prospective studies with standardized diagnostic criteria are warranted.