Senescence or aging is defined as the progressive decline of homeostasis that occurs after the reproductive phase of life is complete, leading to an increasing risk of disease or death. Kirkwood3 has advanced the concept of “disposable soma,” in which aging, rather than being programmed and determined by selected genes, results from the stochastic interaction between injury and repair, as the result of the energy devoted by an individual to maintain organ integrity and protect DNA against oxidative injury. In this model, the failure of organ/cell maintenance/repair results from the integrated action among genes, environment, and intrinsic defects of the organism. Underlying the aging process is a lifelong, bottom-up accumulation of molecular damage. Kirkwood3 also makes the point that cellular defects often cause inflammatory reactions, which can themselves exacerbate existing damage, so that inflammatory and antiinflammatory factors can play a part in shaping the outcomes of the aging process. Thus, aging-associated inflammation/structural change is the results of failure of reactive oxygen species (ROS) elimination, failure of repair of damaged DNA, and telomere shortening, as shown below.