Many studies have shown that the insulin pathway is critical to lifespan in all species that have been tested. The key protein in the insulin pathway is Daf16 in C. elegans or Sirt1 in humans. Daf16 and Sirt1 are histone deacetylase enzymes that promote gene silencing by altering chromatin folding. Recently, the insulin pathway has been implicated as central to the ability of caloric restriction to extend lifespan. The telomeric ends of chromosome are also critical to lifespan in C. elegans and the preliferative lifespan of human cells in culture. Lengthening telomeres by expressing telomere binding proteins or telomerase can extend C. elegans lifespan or immortalize human cells. Recent evidence also indicates that oxidative stress, which is largely produced in mitochondria, preferentially damages chromosome ends, which is poorly repaired in cells not expressing telomerase. Based on these and other data, a probabilistic model of aging is presented in which epigenetic changes in chromatin capping and chromatin folding determine the aging and lifespan of cells and organisms. The model elucidates much of the sometimes conflicting results on aging and lifespan.