Gordon Irlam

Why we age is an enduring mystery. This manuscript proposes aging is microevolutionarily opposed, but macroevolutionarily favored. Such a conflict between microevolution and macroevolution is highly unusual since traits that are harmful to the organism are usually harmful to the survival of the species. In the case of aging, however, a shorter lifespan makes a species better able to adapt to a changing environment. Conversely, species that age more slowly, and thus live longer, are less adaptable and more likely to go extinct. Drawing on what is known of aging in vertebrates, pathways of aging are identified that agree with this theory. These pathways involve mitochondrial ROS production causing telomeric DNA damage, which leads to cellular senescence, the senescence-associated secretory phenotype, epithelial-mesenchymal transition, thymic involution, and age-related diseases. The resulting framework is capable of explaining the seeming intentionality of many age-related diseases, and offers a high level theoretical framework for better understanding them.