Can Healthy Longevity Be Achieved Despite Accelerated Biological Aging in Inflammatory Rheumatic Diseases? A Geroscience-Based Hypothesis

Inflammatory rheumatic diseases (IRDs) are increasingly recognized as disorders of accelerated biological aging, characterized by chronic inflammation, immunosenescence, cellular senescence, and progressive loss of physiological resilience. These processes contribute to frailty, multimorbidity, functional decline, and reduced life expectancy, raising an important question: Can healthy longevity be achieved despite accelerated biological aging in patients with IRDs? I hypothesize that accelerated biological aging in IRDs is not an inevitable or irreversible consequence of chronic immune-mediated inflammation but rather a dynamic and potentially modifiable process. Early disease control, combined with precision geromedicine strategies, including lifestyle optimization, preservation of intrinsic capacity, candidate geroprotective interventions, and emerging gerotherapeutics, may attenuate biological aging trajectories and promote healthy longevity. This hypothesis can be evaluated through longitudinal studies integrating biological aging clocks, biomarkers of immunosenescence and cellular senescence, assessments of intrinsic and vitality capacity, and patient-centered functional outcomes. Rather than defining therapeutic success solely by disease remission, this framework proposes that preservation of healthspan should become an equally important treatment goal. By introducing healthy longevity as a therapeutic objective in rheumatology, this hypothesis aims to stimulate translational research at the interface of geroscience and rheumatology and to provide a conceptual framework for developing interventions that target biological aging alongside immune-mediated disease.