Longevity: Risky Shift in Population Structure?

Abstract

The idea that multiple-stress resistance may serve as a means to expand the individual lifespan has been coined by Parsons (1995) and since then often has been put forward and supported by experimental data (i.e., Cypser and Johnson 2002; Sharabi-Schwager et al. 2009), which led to the development of the “stress resistance” theory of aging. Indeed, long-lived individuals often have increased resistance against a variety of stresses throughout life (Kirkwood et al. 2000; Kirkwood and Austad 2000). Genes underlying the stress response may therefore have the ability to affect lifespan. The progress in modern genetic techniques has allowed researchers to test this idea. The general stress response involves the expression of stress proteins such as chaperones and antioxidative proteins, downregulation of genes involved in energy metabolism, and the release of protective substances (Murphy et al. 2003). Do these same changes in expression patterns have the ability to mitigate aging and prolong lifespan? It appears that parts of this response indeed are also associated with extended longevity, whereas some elements are not due to their high cost or long-term deleterious consequences.