Physics of the Future: How Science Will Shape Human Destiny and Our Daily Lives by the Year 2100
always hot in the back.
As Nobel laureate Richard Feynman once said, “ There is nothing in biology yet found that indicates the inevitability of death. This suggests to me that it is not at all inevitable and that it is only a matter of time before biologists discover what it is that is causing us the trouble and that this terrible universal disease or temporariness of the human’s body will be cured.”
The second law can also be seen by the action of the female sex hormone estrogen, which keeps women young and vibrant until they hit menopause, when aging accelerates and the death rate increases. Estrogen is like putting high-octane fuel into a sports car. The car performs beautifully but at the price of causing more wear and tear on the engine. For women, this cellular wear and tear might be manifested in breast cancer. In fact, injections of estrogen are known to accelerate the growth of breast cancer. So the price women pay for youth and vigor before menopause is possibly an increase in total entropy, in this case, breast cancer. (There have been scores of theories proposed to explain the recent rise in breast cancer rates, which are still quite controversial. One theory says that this is in part related to the total number of menstrual cycles a woman has. Throughout ancient history, after puberty women were more or less constantly pregnant until they hit menopause, and then they died soon afterward. This meant they had few menstrual cycles, low levels of estrogen, and hence, possibly, a relatively low level of breast cancer. Today, young girls reach puberty earlier, have many menstrual cycles, bear an average of only 1.5 children, live past menopause, and hence have considerably more exposure to estrogen, leading to a possible rise in the occurrence of breast cancer.)
Recently, a series of tantalizing clues has been discovered about genes and aging. First, researchers have shown that it is possible to breed generations of animals that live longer than normal. In particular, yeast cells, nematode worms, and fruit flies can be bred in the laboratory to live longer than normal. The scientific world was stunned when Michael Rose of the University of California at Irvine announced that he was able to increase the life span of fruit flies by 70 percent by selective breeding. His “super-flies,” or Methuselah flies, were found to have higher quantities of the antioxidant superoxide dismutase (SOD), which can slow down the damage caused by free radicals. In 1991, Thomas Johnson of the University of Colorado at Boulder isolated a gene, which he dubbed age-1, that seems to be responsible for aging in nematodes and increases their life spans by 110 percent.“ If something like age-1 exists in humans, we might really be able to do something spectacular,” he noted.
Scientists have now isolated a number of genes (age-1, age-2, daf-2) that control and regulate the aging process in lower organisms, but these genes have counterparts in humans as well. In fact, one scientist remarked that changing the life span of yeast cells was almost like flicking on a light switch. When one activated a certain gene, the cells lived longer. When you deactivated it, they lived shorter lives.
Breeding yeast cells to live longer is simple compared to the onerous task of breeding humans, who live so long that testing is almost impossible. But isolating the genes responsible for aging could accelerate in the future, especially when all of us have our genomes on a CD-ROM. By then, scientists will have a tremendous database of billions of genes that can be analyzed by computers. Scientists will be able to scan millions of genomes of two groups of people, the young and the old. By comparing the two sets, one can then identify where aging takes place at the genetic level. A preliminary scan of these genes has already isolated about sixty genes on which aging seems to be concentrated.
For example, scientists know that longevity tends to run somewhat in families. People who live long tend to have parents who also lived long. The effect is not dramatic, but it can be measured. Scientists who analyze identical twins who were separated at birth can also see this at the genetic level. But our life expectancy is not 100 percent determined by our genes. Scientists who have studied this believe that our life expectancy is only 35 percent determined by our genes. So in the future, when everyone has their own $100 personal genome, one may be able
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