There are other mechanisms that the laboratory data suggest also may be involved in regulating the aging rate. Perhaps the most persuasive is the cell senescence/telomere theory. Except for stem cells, body cells either divide very rarely (i.e., nerve cells, muscle cells) or divide either continuously (i.e., blood cells, skin cells) or when stimulated (i.e., liver cells). Those cells that divide seem to have an upper limit on the number of divisions they can undergo. There is some evidence that the telomerase enzyme may play a still not quite understood role in regulating this process. The failure to maintain cell numbers in different tissues probably underlies some aspects of age-related loss of function. The operative part of the cell senescence theory may not be the actual number of divisions cells undergo but the probability that nondividing senescent cells alter their SAGE pattern from one that inhibits oxidative damage and permits division to one that permits oxidative damage and inhibits both cell repair and cell division. If this is the case, one could merge the cell senescence/telomerase theory, the oxidative damage theory, and the metabolic change theory into a single general aging theory based on harmful changes in gene expression that shift the cell from a "youthful" preventive stance to an "older" damage-permitting stance. Such a general theory of aging is reasonable although still under construction, and a persuasive data-based account of it can be found in Fossel.
However, the fact that researchers have accomplished successful interventions into the aging process in the absence of a complete understanding suggests that total comprehension is dispensable: It is desirable but not required. How can this be? The evolutionary considerations discussed above make clear that organisms usually are geared toward reproduction as opposed to repair. This means that any population of animals will contain very few, if any, individuals that are optimally configured for repair. Most, if not all, individuals will have one or more physiological processes that are less than optimal. Tweaking any one of them—oxidative stress resistance, metabolic change, for example—will have the effect of making that organism better in that one respect. Other physiological processes not directly affected by the intervention will show no change or a secondary and dependent change induced by the initial perturbation. The animal will have some measurable improvement in at least one of the several aging processes that operate in its body and as a result will age more slowly and live healthier and longer.
This is in effect what has been done with the flies, worms, and mice. The very specific interventions used appear to have brought about a global effect on the organism. The animals live longer despite the researchers' ignorance about exactly what kind of a control cascade brought this about.
An interesting implication comes out of this observation. The more complex an organism is, the greater the number it will possess of different regulatory and control processes that affect aging mechanisms. More complex organisms, which are organized in a hierarchical modular manner, should have more potential sites where intervention could take place. In principle, mammalian aging should be subject to alteration by more interventions than will work in flies and worms (see de Grey et al.). The greater role that cell division, for example, plays in mammalian aging relative to the invertebrates and the probable relationship between cell division and altered gene expression patterns bolster this point. However, having a greater number of potential drug targets is not an unmitigated blessing. The trade-off is that the mammalian interventions probably need to be very biologically specific in order to be effective. There have been interventions that work in flies and worms but so far have failed in mice, possibly because they were not specific enough to coax the mammalian regulatory systems into altering the organism's SAGE patterns. It is likely that deciphering these specificities will constitute much of the research necessary for the development of a successful mammalian pharmaceutical intervention.
The gap between the predicted and actual effects of extended longevity on human society is likely to be huge. All the writing in the world will not define the texture of that future society. Many people would not go forward without detailed knowledge of the consequences. In the twentieth century people faced the question of whether society should permit human flight. It is necessary to ask if people really wish the Wright brothers had failed (or, worse, that their success was suppressed) and that this was still a flightless society.
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