Why do we age?

Since ancient times there have always been people dreaming of immortality, but also fantasized about all kinds of tricks. Unfortunately, none of these elixirs and magic techniques have worked. Even in modern society, the average life expectancy has been greatly increased from 30 or 40 years old a few decades ago to 60 or 70 years old now, but the natural life expectancy of people has not been increased. The increase in average life expectancy has been achieved through improved health conditions and medical advances that have reduced premature death, not by delaying aging. In fact, people in their sixties or older today are still, on the whole, as old as people in their sixties or older a thousand years ago. Why do we age until we die? Some say it is a natural law. This is just a different way of putting the question, without giving the real reason. And this “law of nature” is not universally true either. Organisms that reproduce asexually by cell division, such as sea anemones, can die from accidental causes, but they do not die of natural age, and if they are carefully nurtured, they can remain young forever. Death by aging seems to be a characteristic of sexually reproducing organisms. It is also said that dying of old age can prevent the world from becoming more crowded. This is a purposive argument, and to accept it we need to first believe that there are mysterious forces in heaven and earth that make such ingenious arrangements. Death makes the world less crowded, which is an additional meaning of death, but not the cause of death. Some say that aging is genetically programmed. It is true that we now see reports of genes associated with aging, and researchers often say that “programmed cells die”. But this only shows how we age, it does not tell us how aging originates, i.e., where all those “aging genes” come from. Obviously, we need to identify the evolutionary factors of aging to finally answer this question. One theory is that old age and death are the result of natural selection. The death of old age frees up space for offspring to live, saving resources for survival, and the result of natural selection is to leave more offspring, isn’t it? But this seemingly justified argument is actually contrary to the principle of natural selection. The death of the older generation of a group is indeed beneficial to the survival of the offspring as a whole; however, the death of a single individual is not directly beneficial to the survival of its offspring. Natural selection cannot sacrifice the immediate benefit of an individual for the long-term benefit of the group. Natural selection can only work when there is a direct advantage to the individual and its offspring. The great British biologist Holden first pointed out in the 1940s that old age and death are not the result of natural selection, but, on the contrary, are the result of natural selection not working. Natural selection is expressed by the fact that different individuals have different reproductive capacities, so that those genes that act before the individual loses reproductive capacity are selected by natural selection. A lethal gene that is expressed during adolescence is likely to die before the patient leaves offspring, so such a gene would be eliminated by natural selection and would be difficult to pass on and spread. Conversely, a lethal gene that is expressed in secrecy after young adulthood, and whose carrier has already left offspring before the disease, cannot be eliminated by natural selection and will continue to be inherited. As the world goes on, more and more lethal genes expressed only in old age are bound to accumulate in the population and spread out. In every human being there are more or less such lethal genes, and therefore, it is inevitable that they will age and die. For asexually reproducing organisms, on the other hand, they retain the ability to reproduce, and natural selection is always at work, forcing them to remain healthy and therefore not to age. Another British biologist, W.D. Hamilton, developed a mathematical model for this theory of aging in the 1960s. Since the seventies, this model has been confirmed by many experiments. This theory of aging predicts that if we slow down the reproductive period of sexually reproducing organisms, their lifespan will be extended after several generations. One of the experiments was done with fruit flies. Fruit flies grow to about two weeks before they start laying eggs. The researchers threw away all the eggs laid by the young fruit flies and incubated only those laid by older fruit flies (at least six weeks old). After ten generations of this, the resulting fruit flies lived two or three times longer than normal fruit flies, and they appeared more youthful. They are more resistant to starvation, more resistant to desiccation, and more capable of walking and flying. We can imagine that if we were to conduct similar experiments on humans, forcing them to breed late and letting natural selection work without medical techniques to save their offspring from disease, then after ten generations, the natural lifespan of humans would also be significantly longer. Of course, we cannot do such barbaric experiments. To prolong life, we have to find other ways. The traditional way is to believe that “life is exercise” and to do consistent physical exercise. However, although the exercise can enhance the body’s function, improve the quality of life, but failed to show that it can really extend the life of people. Another approach is to control the diet. For example, researchers found that those who eat only seven or eight portions of the life of rats, obviously longer than those who indulge in food life. No one knows whether this approach also applies to humans. Moreover, it would not be attractive to the average person to have to endure hunger for a long time in order to live longer. At the cellular level, aging is caused by the fact that normal cells have a limited number of divisions and can only divide fifty to one hundred times, and only cancer cells can divide indefinitely. Each time a normal somatic cell divides, the sequence of its chromosome ends (telomeres) has to be lost some and its length has to become shorter. At a certain point, the somatic cell will stop dividing. However, sex cells and cancer cells have a telomerase that prevents telomere shortening. We can imagine that if we could use telomerase or other drugs to stop the telomeres of chromosomes from getting shorter, somatic cells could divide indefinitely without aging. But so far no one has been able to demonstrate that the lifespan of an entire individual is extended by this method. This approach, moreover, is highly likely to induce cancer. Cellular activity generates oxidative free radicals. An excess of free radicals may be a contributing factor to aging. There is an enzyme in the body that scavenges free radicals, and fruit flies with higher activity of this enzyme also live longer. We don’t know if this is true for humans. We also do not know of a safe way to scavenge free radicals in the human body. By comparing long-lived individuals to those with normal lifespans, we have identified a number of genes that may have anti-aging functions. However, we do not yet know how these genes work. According to the theory of aging we described above, aging is the result of the expression of many lethal genes that have accumulated over time. These genes, which may number in the hundreds or thousands, are associated with the vast majority of the body’s biochemical functions. To conquer aging, we must first figure out all the mechanisms of aging, which means finding all these genes related to aging and understanding their role. This is a rather difficult task, which may be possible only in the second half of the twenty-first century. Only then will we be able to find a truly effective way to prolong life.