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The two foremost concepts of aging are the mechanistic free radical theory (FRT) of how we age and the evolutionary antagonistic pleiotropy theory (APT) of why we age. Both date from the late 1950s. The FRT holds that reactive oxygen species (ROS) are the principal contributors to the lifelong cumulative damage suffered by cells, whereas the APT is generally understood as positing that genes that are good for young organisms can take over a population even if they are bad for the old organisms. Recent Advances: Here, we provide a common ground for the two theories by showing how aging can result from the inherent chemical reactivity of many biomolecules, not just ROS, which imposes a fundamental constraint on biological evolution. Chemically reactive metabolites spontaneously modify slowly renewable macromolecules in a continuous way over time; the resulting buildup of damage wrought by the genes coding for enzymes that generate such small molecules eventually masquerades as late-acting pleiotropic effects. In aerobic organisms, ROS are major agents of this damage but they are far from alone.

A Tale of Two Concepts: Harmonizing the Free Radical and Antagonistic Pleiotropy Theories of Aging