Several lines of evidence have led to the notion that biological aging occurs as a result of changes in the information-containing molecules either at the genetic or epigenetic level. The error theory, the redundant message theory, the codon restriction theory, and the transcriptional event theory represent the major current conceptualizations of biological aging as held by most gerontologists. The finding that cultured normal human and animal cells undergo a finite number of population doublings in vitro has provided new insights into age changes at the cellular level. The number of mitotic events that cultured normal animal cells can undergo appears to be inversely related to the age of the donor. A direct proportionality exists, however, between the mean maximum life-span of a species and the number of population doublings that their cultured embryonic cells will undergo. The several biochemical decrements known to occur prior to the cessation of mitotic activity in vitro are thought to herald those manifestations of senescence seen in the whole animal. Yet to be explained is how those cell classes such as the germ plasm and continuously propagable cancer cells escape from the inevitability of biological aging.