Probst Christine 303458589 Life Sciences 2 Section E Michelle Kim May 12, 2008 Word Count:
Why do we age and can we stop it? If you take a look at the leading causes of death among Americans, you will notice an interesting pattern. Until the age of 44, the leading cause of death is accidents, mainly motor vehicle. Those between 45 and 64 years old are most affected by cancer and heart disease. Those 65 and older mainly die from heart disease and cancer, but also diseases of the brain and lungs. Also, increasing age marks an exponential increase in mortality, with only 20 deaths per 100,000 for ages 5-14 and 5,071 death per 100,000 in ages 24. The increased risk of mortality and physiologically life-threatening diseases is due to a process that we are all familiar with: aging. We may associate aging with wrinkly skin, frailty, and mental slowness. However, aging is scientifically defined as "an accumulation of random damage do the building blocks of life...that begins early in life and eventually exceeds the body's self repair capabilities" (page 30, course reader). In this paper, we will examine why we age, and whether or not the aging process effectively be slowed. It is important to remember that although aging may increase vulnerability to disease, aging itself is not a disease. The difference is that a disease can be diagnosed based upon a precise series of symptoms, whereas aging causes deterioration of practically all organ systems, including the cardiovascular to the lymph to the nervous. This is mainly due to the fact that aging happens on a cellular level, as mitochondria release free radicals that tend to accumulate with age, causing deleterious effects on alleles of the DNA. Although some organs are more affected than others, given enough time, essentially every organ will not run with the same efficiency as it would without damaged DNA. Therefore, even if scientists could find cures for the top ten diseases that kill older people, aging would continue to occur and people would become more and more vulnerable to the vast array of diseases. Quickly enough, a new disease that was not one of the top ten killers would become a top ten killer if the rest of the diseases were no longer an issue. So, although longevity may be slightly increased, cannot one hope to live several times over. We may initially be baffled the process of aging. We know that some genes increase your risk of cancer, so why haven't these genes been weeded out from natural selection? Surprisingly enough, the answer to this question is natural selection. Aging differs greatly from species to species, and can be explained through the theory of evolution. According to the natural selection, genes that increase the fitness of an organism should be favored and proliferate throughout a community. However, recall that fitness is the ability to reproduce, not health. Therefore, genes that may be responsible for the death of the organism in the post-reproductive period are invisible to
natural selection. This may be an explanation to why death rates due to physiological diseases such as cancer increase sharply at age 45, as this it the age women become infertile. It is possible to control organisms in lab so they are only able to reproduce later in life. Research on the fruitfly Drosophilia melanogaster has shown longevity is greatly increased if mating delayed to later in life, as individuals who suffer from the most accelerated aging die before reproduction. In this case, the genes responsible for delayed aging increase fitness and become visible to natural selection. However, this strategy is unrealistic to use on humans in a real-life setting. No one would be willing to give up the freedom of being parents at a youthful age so that they could possibly increase the longevity of people generations hundreds, if not thousands of years away. Rather than manipulating evolution, many people believe that it is possible to slow aging on an individual basis. Antioxidant consumption, hormone replacement, and caloric restriction have all claimed to slow the process of aging, but none of these techniques have proven a direct influence on aging. However, scientists are hopeful that a further understanding of aging may improve our ability to slow it down. Recent breakthroughs have shown that lowering reactive oxygen species, while increasing the level of poly (ADP-ribose) polymerase can increase longevity of organisms in lab. Perhaps, if we can develop drugs to synthesize these effects in the human cell, we can truly slow the process of aging.