Why we age: what science is discovering about the body's journey through life

Abstract

Aging represents a progressive physiological decline that initiates near puberty, characterized in humans by a mortality rate that doubles approximately every eight years. While average life expectancy has increased significantly due to public health improvements, the fundamental rate of biological senescence remains largely constant across historical eras and diverse cultures. Evolutionary biology provides the primary framework for understanding this process; aging is not a programmed self-destruction for species benefit but a consequence of the declining force of natural selection with age. This decline allows late-acting deleterious mutations to accumulate or permits genes with early-life benefits to exert harmful pleiotropic effects in later stages. Proximally, senescence is driven by cumulative cellular damage, particularly through oxidative stress from free radicals and the non-enzymatic browning of proteins via glycation. Comparative zoology reveals that species with lower extrinsic mortality—such as those capable of flight or bearing protective shells—evolve slower aging rates and more robust repair mechanisms. Although caloric restriction consistently extends lifespan in laboratory models, its efficacy in humans remains unverified. Most widely marketed geriatric interventions currently lack empirical evidence of retarding the intrinsic aging process, highlighting the distinction between treating specific age-related diseases and altering the underlying rate of biological decay. – AI-generated abstract.