Some theories of aging address what controls these processes and why the controls exist as they do. Other theories of aging address the issues of whether senescence is more programmed than random entropy, thus offering some advantage for a species. For example, senescence may have evolved because without it, a species would accumulate ill-adapted older members. These members would compete with potentially better adapted younger members, slowing the rate at which adaptive mutations are introduced. Theoretically, free radicals, generated during oxidative phosphorylation, can variously modify macromolecules, primarily through oxidation.
Considerable evidence suggests that oxidative damage increases with age.
For example, in older organisms, specific amino acids in specific proteins tend to be oxidized residues, leading to decreases in the specific activity of these proteins. Additionally, specific oxidized derivatives of nucleotides from DNA increase in frequency. Glucose is thought to promote senescence mainly through nonenzymatic attachment to proteins and nucleic acids, through the same process that produces glycated hemoglobin. Glycated protein levels increase with age. Otherwise, there is little direct evidence that glycation has a major role in senescence.