forms a sticky substance that could dramatically reduce joint movement, clog arteries, and cloud tissues like the lens of the eye, leading to cataracts (Lafferty et al., 1996, 56). Once glycated proteins are formed, they can cause further damage by interacting with free radicals from other sources (Ricklefs and Finch, 1995, 26). The Lethal Clock A gene called clock-1, which was believed to determine an organism=s lifespan was found in small organisms and a very similar gene has also recently been found in humans (Lafferty et al., 1996, 58). Although it is uncertain whether the clock genes affect how susceptible cells are to infections, or if they control the actual aging process, it is generally agreed upon that these genes have something to do, either directly or indirectly, with aging (Allis et al., 1996, 64). It has been proposed in the clock theory that the demise of brain cells, of which we lose thousands each day, is due to regular, programmed cellular destruction, and not to random *accidents= (Keeton, 1992, 50). As cells divide, the number of divisions that they undergo is monitored and kept track of. After a certain number of divisions, the clock genes are triggered and may produce proteins responsible for cell destruction (Keeton, 1992, 50). Cellular Aging In 1961, a discovery made by Leonard Hayflick showed that normal, diploid cells from such continually Areplaced@ parts of the body as skin, lungs, and bone marrow, divide a limited number of times. Although the cells stop dividing at the point just before DNA synthesis, they do not die. The longer-lived the species, the more divisions the cells undergo. As the age of an individual increases, the number of potential divisions decreases (Ricklefs and Finch, 1995, 29). This discovery was found using fibroblasts, or cells found in the connective tissues throughout the body. The cells were placed in a laboratory dish under sterile conditions and allowed to grow and divide until t...
