The Conglomerate Theory of Aging: A Unified Model of Metal, AGE, and ALE Accumulation

The primary drivers of age-related decline remain incompletely understood despite progress in characterizing damage mechanisms. We propose the Conglomerate Theory of Aging, which identifies four key products of damage from multiple reactive species as primary contributors to biological aging: metal bioaccumulation, advanced glycation end products (AGEs), advanced lipoxidation end products (ALEs), and persistent metal‑AGE/ALE hybrid complexes. Acting in concert, these components establish self‑reinforcing cycles that accelerate damage accumulation and functional decline. The theory integrates insights from biochemistry, pathology, and clinical observations, linking these molecular entities to multiple telomere(definition) attrition, cellular senescence(definition))." style="text-decoration:underline dotted; text-underline-offset:2px; cursor:help;">hallmarks of aging(definition), including genomic instability, loss of proteostasis(definition), and chronic inflammation. By reframing aging as the outcome of autocatalytic, mutually amplifying damage pathways, the Conglomerate Theory accommodates both stochastic insults and their systemic consequences. This framework also yields testable predictions for intervention, recommending multipronged therapeutic approaches such as metal chelation, antiglycation, and antilipoxidation therapies applied in combination. Such strategies aim to disrupt synergistic damage loops more effectively than single‑target interventions. The Conglomerate Theory thus provides a unified conceptual model for understanding aging mechanisms and guiding the development of broad‑spectrum interventions to extend lifespan.