Age-related hearing loss is linked to loneliness and poorer cognitive health, but it remains unclear whether loneliness helps explain associations between hearing difficulties and cognitive performance or dementia, and whether these patterns reflect causal pathways or shared underlying liability. In this preregistered study, we triangulated analyses across multiple data sources spanning approximately 18 years of observational data with 8 sources of molecular genetic information to examine whether loneliness helps explain the association between hearing difficulty and cognitive performance, Alzheimer’s disease dementia, and all-cause dementia, and whether hearing-aid use may buffer this association. In longitudinal parallel-process latent growth curve models (N = 10,375) using nine waves of longitudinal data from the Survey of Health, Ageing and Retirement in Europe (SHARE), poorer hearing was associated with greater loneliness, and greater loneliness was associated with poorer cognitive performance, consistent with partial mediation. In contrast, worsening hearing over time was not clearly associated with increasing loneliness over time. Cumulative hearing-aid use did not appear to alter long-term loneliness trajectories, although current hearing-aid use weakened the concurrent association between poorer hearing and greater loneliness. In genetic analyses, we found little evidence that hearing phenotypes or loneliness had clear total or indirect effects on Alzheimer’s disease dementia or all-cause dementia. Analyses accounting for shared genetic liability with neuroticism provided some evidence linking loneliness with poorer cognitive performance, and colocalization analyses further suggested shared genetic architecture across hearing, loneliness, cognition, and neuroticism-related traits. Overall, the findings support a robust cross-domain association between poorer hearing, greater loneliness, and poorer cognitive performance, while suggesting that long-term change and genetic evidence are more consistent with shared liability than with a single causal pathway.

The authors have declared no competing interest.

David A. Sbarra's contributions to this paper were partially supported by NIH R01AG078361-01.

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Institutional Review Board of the University of Arizona waived ethical approval for this work.

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The analytic code used in this study will be made available upon publication. Data availability is subject to the access policies of the original data sources, including the Survey of Health, Ageing and Retirement in Europe (SHARE) and the GWAS datasets used in the genetic analyses. SHARE data are available to eligible researchers through the data provider's application procedures, and GWAS summary statistics are available from the original studies, consortia, or repositories subject to their respective access policies.