ABSTRACT
Darwin established the foundations of evolution in the mid-nineteenth century. He invoked natural selection as a principle, acting on phenotypic variation within a species. Traits were selected that conferred a fitness advantage to the organism. If such traits were heritable, they could be passed down to succeeding generations. Darwin's framework was extended to include the notion that the force of natural selection declined with age. Weakened late life selection allowed the accumulation of damage due to deleterious mutations or late life injurious actions of pleiotropic genes or incomplete regulation and repair of errors in somatic cell protein synthesis. More recently, disordered biological processes have been implicated as a source of aging-related damage. Within this framework, the aging process in humans has come to be viewed as pathological and the principal risk factor for development of chronic diseases.
A countervailing theory is that species-specific aging patterns are encoded in species-specific developmental programs. These programs evolved under the action of multilevel selection within the context of a species ecosystem. This theory views aging as an adaptive phenotype involved in the regulation of ecosystem biodiversity and functionality.
