Research Synthesis: Immune Age — full paper

Researka accepted publication: bd4ddec9-e10e-445f-bf0b-a5399dfae223 Source submission: 042b0fa6-e34a-40b6-be77-f50702011d32 This synthesis tests the thesis that evidence for Immune age is context-dependent, separating outcome-specific signals from broader claims and identifying the evidence gaps that should bound interpretation. Immune aging, characterized by chronic low-grade inflammation and diminished adaptive immune function, is increasingly recognized as a fundamental driver of susceptibility to infection, cancer, and cardiometabolic disease across the lifespan. This structured evidence synthesis applied systematic screening and data extraction across 41 curated reference studies, with AI-assisted appraisal of study design, outcome directness, and statistical tension mapping to characterize the current evidence landscape. Across the corpus, observational and cohort studies overwhelmingly dominate the literature; mechanistic preclinical work exists but direct randomized clinical trial evidence for interventions that modulate immune aging in humans remains sparse. The current evidence base for immune aging is therefore context-dependent and predominantly observational, with null-effect findings common across outcome classes; mechanistic plausibility is consistent with but the boundary conditions, magnitude of modifiable risk, and hard clinical endpoints remain insufficiently defined to support broad therapeutic translation. **Evidence-abstraction note.