Xenology: An Introduction to the Scientific Study of Extraterrestrial Life, Intelligence, and Civilization
© 1975-1979, 2008 Robert A. Freitas Jr. All Rights Reserved.
Robert A. Freitas Jr., Xenology: An Introduction to the Scientific Study of Extraterrestrial Life, Intelligence, and Civilization, First Edition, Xenology Research Institute, Sacramento, CA, 1979; http://www.xenology.info/Xeno.htm
Gerontology is the science of physiological aging and death. Modern researchers have concluded that while no single cause of aging exists, it may soon be possible to sharply reduce or eliminate this process in many Earthly animals -- including man. The prospect of such great advancement in human biotechnology raises the presumption that alien gerontologists -- xenogerontologists-can do at least as well.
Death from old age is no more "natural" or inevitable than smallpox or plague. As the twice Nobel laureate Dr. Linus Pauling asserted more than twenty years ago:
Death is unnatural. Theoretically, man is quite immortal. His body tissues replace themselves. He is a self-repairing machine. And yet, he gets old and dies, and the reasons for this are still a mystery.2647
To paraphrase the venerable Seneca: Old age is a curable disease.
The general consensus among gerontologists today is that there exist within humans identifiable "clocks of aging." These clocks are genetically determined programs which dictate when and how fast we shall age and die. Since such mechanisms appear to be rather common throughout the entire animal kingdom, there is good reason to suspect that ETs should possess something functionally similar. While the mystery of aging has not yet been solved, a tripartite theoretical model with three primary "clocks" has begun to emerge.
The first of these is rather simple: Wear and tear. Medawar, one of the earliest scientists to link genetics with aging, has called this the "broken test tube" theory. Say that we start off with 1000 brand new test tubes in a chemical laboratory. Over time, the number of "survivors" would steadily dwindle. Some tubes with factory flaws (birth defects?) would be thrown out first (die?), while others would break from chance accident or hard usage after a number of years. Eventually the entire population of test tubes will have broken in this manner, and we then may plot a "survival curve" of aging and death for the glassware entities. The analogy to the mortality of living beings is inescapable: Wear and tear does us in.
The second clock of aging is called the Hayflick Factor after UCSF researcher Dr. Leonard Hayflick. In 1961, he discovered that young human cells growing in a culture medium could divide only a limited number of times (roughly 50 generations) before all their descendents aged and died. Cells taken from adults divided even fewer times (about 20) before death ensued.
Hayflick then compared the growth cycles of human cells to those taken from other animals. Not surprisingly, tissues taken from nonhuman creatures differed markedly (between species) as to the total number of generations they could produce before dying. It was also found, however, that animals with longer lifespans also had the longest-lived cells. (See Table 16.1.) Hayflick concluded that cell death in all organisms was an expression of aging at the microscopic level. Aging thus appeared to be a built-in genetic limitation to cellular regeneration and growth.
In the last two decades, Hayflick’s work has been largely verified. Studies of identical twins -- who, like clones, have identical DNA -- show that both individuals generally have about the same lifespan. (This is to be expected if genes control longevity as Hayflick suggests.) In another series of experiments, a number of cultured human cells of various "ages" were placed in cold hibernation at liquid nitrogen temperatures. These were then thawed out, a few at a time, over a period of ten years. Each cell "remembered" its correct "age" and proceeded to divide up to the normal allotment of 50 generations, at which point death set in as usual. In yet another study, nuclei from young cells were transplanted into the protoplasm of old cells. Cells which had already doubled, say, 37 times, which were renucleated with a nucleus from a young cell that had passed through only 10 generations, went on to divide for about 40 more cycles before old age set in.
On the basis of the normal 50 divisions found in human cultured cells, Hayflick calculated that the normal lifespan of man should be about 110-120 years. But we know that only a negligible fraction of the human race ever attains such advanced age. This brings us to the last factor in the tripartite model of aging.
Dr. W. Donner Denckla, a medical researcher at the Roche Institute of Molecular Biology, believes that the third clock of aging is hormonal in nature and resides somewhere in the brain -- most probably in the human endocrine glands. Denckla found, after a detailed study of autopsy data and death records, that most people die because of a failure of one of the two major body systems: The cardiovascular or the immune systems. Death occurs in the former instance from heart stoppage or from an inability of the blood vessels to deliver oxygen and nutrients to vital organs, and in the latter instance from a failure of the body’s immune system to ward off an attack of invading microorganisms.
The thyroid gland, Denckla believes, may be of central importance because its product -- thyroxine -- appears to be the master rate-controlling hormone. Then humans age, they don’t lose the ability to produce thyroxine. Rather, they lose the ability to utilize whatever quantities of the hormone are available.
Denckla suspects that the pituitary may release some kind of blocking hormone -- which he calls the "death hormone" -- that prevents cells from using thyroxine. The diminishing utility of the vital secretion in later life could cause a number of critical imbalances, increased destructive oxidation, chromosomal mutations and heart tissue dysfunction.
Another endocrine gland -- the thymus -- has been implicated in the process of human aging. The thymus is a soft, flattened organ just behind the breast bone in man. Older medical texts say that the function of the gland is unknown, but many modern specialists link it to the production of "T cells" (a variety of lymphocyte or "white cells") under the direction of the pituitary and the hypothalamus.
During life, the thymus changes dramatically in size. At birth it weighs about 12 grams. At puberty it reaches its maximum at 37 grams. Thereafter, it shrinks rapidly until by the age of 40-50 years it has all but disappeared in many people. By age 60 it weighs at most a paltry 6 grams.
According to Dr. Allan Goldstein of the University of Texas Medical Branch, Galveston, the level of thymosin -- the secretion of the thymus gland -- falls off with age in direct proportion to the diminishing size of the organ. As the concentrations of thymosin drop, the failure rate of the human immune system rises markedly. Lymphocytes, our "white cells," become increasingly incompetent. They fail to rid the body of hostile pathogens and mistakenly attack the body’s own cells as if they were foreign invaders. As a result, older organisms are vastly more susceptible to a wide range of potentially lethal diseases.
To test his theory, Goldstein has injected thymosin into children afflicted with severe immune-deficiency diseases. The revitalization of the youngsters’ immune systems was dramatic, but more verification is necessary. The next step will be to try to revitalize aging immune systems in adult humans using similar therapy. If these experiments succeed, immune failure as a cause of death could virtually be eliminated.
Regardless of the exact mechanisms of hormonal control, argues Denckla, the control is there. And it would appear to have great survival value. So far as we know, Earthly species evolve naturally only by mutation, a fairly slow process. To speed it up, more parents must be cycled through the system. The faster the turnover rate in the reproducing population, the more variability will be available quickly from the gene pool. Mortality of individuals thus has selective value because, in the words of one writer, "species survival requires a large enough quantity of individuals in any given generation to ensure that a significant number of them will be the beneficiaries of chance mutations that can be passed along, and a short enough lifespan to permit the necessary turnover."2137
According to modern gerontologists, then, aging is "an absolutely fail-safe killing mechanism without which the species would not survive." Under the general tripartite theory (Figure 16.1), three clocks of aging are simultaneously ticking against us. If one stage of the death process is escaped, others remain:
Stage 1 -- Denckla/Goldstein hormonal imbalances occur which cause the cardiovascular and immune systems ultimately to fail. This is the body’s primary self-destruct mechanism. Typical life expectancy: 30-80 years.
Stage 2 -- The Hayflick cellular aging program causes body cells to cease dividing after a fixed number of generations. It is designed to set a second limit in case the Stage 1 hormonal malfunction is ineffective. This is the body’s secondary self-destruct mechanism. Typical life expectancy: 110-120 years.
Stage 3 -- Medawar’s "broken test tube" wear and tear on body structures. Irreversible genetic deterioration or severe accidental trauma eventually cause senescence and death. This is the body’s last line of defense against immortality, a tertiary backup system. Typical life expectancy: ~1000 years.
Figure 16.1 Human Current (upper) and Future (lower) Mortality
While the tripartite aging model may turn out to be correct for mammalian life on Earth, this is no guarantee that beings of other worlds must be designed in the same way. Still, the basic evolutionary concept of the survival value of death for naturally evolving species should be as valid in alien ecologies as it is on this planet. There is no reason to suspect that extraterrestrial aging mechanisms will be any more or less complicated than our own.
Last updated on 6 December 2008