Aging and Life Span

Many scientists have hypothesized that some genes may control aspects of aging separate from the development of disease. These hypotheses are based on experimental studies of non-human organisms and the observation that longevity in humans appears to run in families. Studies of yeast and roundworm have identified over ten genes in each that are associated with longevity and aging, and more recent studies have suggested similar genes exist in the fruit fly. The exact function of these genes is unknown, but one or more may help slow down the metabolic rate. Studies in mice have shown that reducing metabolism by reducing food intake can increase life span. Finally, shortening of the telomeres decreases longevity in some model organisms.

Finding similar genes in humans is more complicated, since scientists cannot experimentally control genes to test their effects on longevity in Life span is determined partly by genetics: These grandchildren are more likely to live longer based on the long life span of their grandparents. humans. Therefore, genetic studies of human longevity require a more observational approach. One study design is to examine large numbers of long-lived individuals such as centenarians and see what factors they have in common, such as lifestyle, medical history, and genetics.

Studies of centenarians have suggested that variants in multiple genes, including the human leukocyte antigen (HLA) genes of the immune system, apolipoprotein E (APOE), angiotensin-converting enzyme (ACE), plasminogen activating inhibitor 1 (PAI-1), and p53, are associated with living past age ninety. Forms of several of these genes, such as APOE, ACE, and p53, are associated with increased risk of developing Alzheimer's disease, cardiovascular disease, and cancer, respectively. The association of these genes with longevity may be due to these disease associations, or it may be due to their direct influence on extending the human life span. Regardless, genes clearly influence aging and longevity, whether it is by influencing the development of life span-shortening diseases, or by positively influencing longevity independently of causing disease.