Is aging a product of evolutionary selection, providing an advantage to a species, or is it the result of a lack of selection pressure on late-life health? The mainstream view suggests that aging is a consequence of declining systems due to the prioritization of early reproduction in evolution. This leads to maladapted systems causing aging, known as antagonistic pleiotropy.
While most researchers support the idea of aging as a result of evolutionary processes, there is a growing interest in the concept of quasi-programmed aging. One such viewpoint is the hyperfunction theory, which proposes that aging is a result of developmental programs continuing past their intended duration, leading to damage and diseases.
Evolutionary theory rules out programmed aging but predicts a quasi-program for aging where the developmental program remains active, causing hyperfunction and detrimental effects. Could targeting the TOR pathway, associated with cell senescence and organism aging, help slow down aging and prevent age-related diseases?
Research in yeast, animals, and humans suggests that interventions targeting the TOR pathway, such as caloric restriction and rapamycin, can extend lifespan and prevent age-related diseases. Clinical evidence supports the potential of rapamycin in combating various age-related conditions.
As lifespan extends, new factors contributing to aging, like reactive oxygen species and stem cell exhaustion, may become more prominent. Exploring quasi-programmed senescence could provide valuable insights into aging processes.
Link: https://doi.org/10.4161/cc.5.18.3288
