Our understanding of genes and aging has exploded in recent years, due in large part to groundbreaking work done in simpler organisms.

Researchers have identified 19 genes in baker's yeast (Saccharomyces cerevisiae) that are associated with increased longevity, and even more provocatively, have found human versions of two of these genes.³ Further study is ongoing.

Caenorhabditis elegans, a roundworm with a normal 20-day life span, makes an ideal research subject. A single mutation in one of its genes, labeled age-1, increases its average life span by 65% and its maximal life span by 110%. Possessing the protective version of the age-1 gene grants this worm greater resistance to cell damage by toxic free radicals, excess heat or ultraviolet light.^4,5 Among the roundworm genes with human counterparts are daf-2, which encodes an insulin-like receptor and daf-16, which encodes a transcription factor akin to a mammalian protein involved in insulin signaling.

Drosophila melanogaster, a slightly more complex organism than the roundworm, shows evidence of a more complex pattern of heritable longevity. Researchers have identified a gene they have named Methuselah, which increases life span in fruit flies by 35%. The Methuselah gene grants enhanced resistance to stress from heat and oxidative damage. Researchers have noted that long-lived flies have increased stores of glycogen (needed for energy production) and fats, reserves for times when food is scarce or great amounts of energy are required.⁶ Other scientists have identified genetic traits in fruit flies that shorten life span. These genes reduce flies' ability to combat the damage free radicals, the byproducts from the breakdown of oxygen, do to their cells.⁷

As mammals whose biologic systems offer many parallels to those of humans, mice are often studied in aging research. The Ames dwarf mouse is a strain that has an inherited defect in the development of the pituitary gland, which means that this mouse does not secrete growth hormone. The absence of growth hormone results in defective transcription of the gene for an insulin-like growth factor. These genetic changes increase the mouse's life span. In other studies, researchers have found that "knocking out" or deleting a gene labeled p66shc in mice results in greater stress resistance and increased life span. Scientists have also identified genes in mice that shorten life span. One such gene triggers apoptosis, or the process by which cells are programmed to die. This gene was found in cells of the mouse immune system, and mice with these genes are more susceptible to infection and are shorter-lived.⁸