We cannot retard senescence or reverse its direction,
unless we know the nature of the mechanisms which are
the substratum of duration [basis of longevity].
—Alexis Carrel, Man the Unknown, 1935
In this set of posts, we take an overall view of what we are up against in the way of aging mechanisms. There are two basic types of aging: One is caused by random damage brought about by a large variety of dangerous substances found both outside of our bodies and made in our bodies. The other type of damage is nature’s “planned obsolescence,” wherein we are
subject to natural programs which eventually turn us off. Successful life extensions in experimental animals indicate that animals are subject to these same types of aging damage. So far, most of the life extension successes have involved interfering with the random damage aging, but progress is being made in understanding and intervening in “planned”
aging, as well. In humans, random aging damage is usually the most important up to about 110 years of age, with programmed “planned obsolescence’ becoming very important thereafter.
There are two basic types of aging events:
(1) random (accident), and
(2) planned, as in nature’s “planned obsolescence.” The planned events of aging involve aging clocks, which cause a programmed sequence of alterations and shutdowns to various body systems, resulting in physiological decline as time passes. The reasons for these clock-directed changes are not well understood, although promising theories exist. Well- known examples of aging clocks include menopause and male pattern baldness.
Random aging events result in a cumulative damage which occurs in a sporadic fashion, such as damage caused by ultraviolet light, X-rays, free radicals (chemically reactive entities produced in the body, particularly by the abnormal oxidation of fats, and also encountered in the environment),
aldehydes (a common class of often nasty compounds found both inside and outside of the body), etc. The body has repair mechanisms for damage caused by such entities to DNA (your genetic master blueprint), cell membranes, and other structures. However, these repair systems are not perfect. The rate of repair declines relative to the rate of damage, partly be-
cause of planned events (aging clocks) and partly because damage is not perfectly repaired, leading to further damage, etc. Since the rate of physiological decline with age is only about 1 percent per year, on the average, a small improvement in the ratio of repair to damage can have a significant impact on average species life span (the age most species
members live to) and, perhaps, on maximum species life span (the longest life span reached by a member of a species). Here is a simple hypothetical example: Suppose that one of your vital life support systems is randomly damaged at a rate of 10 percent per year, while your damage repair rate for that system is 9 percent per year. That system will degrade—age—
at 10 percent — 9 percent = I percent per year. Now suppose that you use life extension technologies which slow the damage rate by only 1 part in 10 and speed up the repair by only 1 part in 10. Your damage rate is now about 9 percent per year, but your repair rate is now about 10 percent per
year. You are now repairing your damaged system by 1 percent per year faster than it is being damaged.
Each year, that vital life support system of yours will in some ways be 1 percent better instead of the normal 1 percent worse. Each year, parts of your system become a bit younger rather than a bit older! Note that this remarkable feat has been accomplished by a very small decrease in the damage rate plus a very small increase in the repair rate.
Experiments in animals have shown that it is possible to successfully intervene to reduce damage rates by interfering with the reactions of particular classes of damaging chemicals and to increase activity levels of protective and repair systems. It is even possible to alter the effects of some aging clocks, so that animals’ life spans are extended.
The same aging mechanisms seem to be operating in all animals. The differences between animals’ life spans are due to different relative contributions of all these aging mechanisms. Different species of animals have different levels of and types of protective mechanisms and different time sequences on their aging clocks. Understanding biochemical
differences between long- and short-lived species is one way to find out what enables longer lived animals, such as man, to live such relatively long lives, and to improve our techniques for increasing our life span.
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