Old age must be resisted
and its deficiencies supplied.
—Cicero
We know that as we grow older, our chances of continued survival decline. How does aging kill us? The answers to this question lead directly to the big payoff—how to slow or partially reverse these deadly processes.
The accumulated result of the unrepaired or imperfectly repaired damage done by all the different aging mechanisms is what we call aging. The probability of dying doubles about every eight years after puberty (the Gompertz law): Although we know a fair amount about a number of aging mechanisms, we don’t yet know how much each mechanism contributes to
the final result: the individual aging rate of each person. Research is now being done by us and many others which we hope will be able to shed some light on this problem.
There are two basic classes of aging mechanisms, random damage and genetically programmed obsolescence. Most people die of random age-related damage, such as cancer escaping control by a deteriorating immune system or a coronary thrombosis from an arterial blood clot caused by inhibition of the formation of your natural clot-preventing hormone PGI,
(also called prostacyclin) by organic peroxides produced by free radicals. (These things are explained in later chapters.) If these random damage events were eliminated or perfectly repaired, you could live a healthy life to the end of your genetically determined life span, probably around 110 to 120 years.
At this time, it is thought that aging clocks, particularly those located in the brain, would rather suddenly shut off some of your vital systems. We know more about the causes and “cures” for random aging damage than for the programmed aging. Maximum possible life span seems to be determined by
the programmed aging, whereas average life span is determined by random aging damage. Nevertheless, if we could remain healthy and active until 110 or 120 years of age, that would be a tremendous improvement over our present pattern of aging, which is dominated by random damage and progressive loss of functions.
There is some evidence that there are programmed aging clocks in the testes, ovaries, pituitary, and hypothalamus which measure accumulated random damage and are triggered when this damage reaches a critical level. Perhaps this is how-antioxidants, which are effective against many random damage mechanisms, have been able to increase measurably
the maximum life span of a few species. In any case, the time that you “buy” by reducing the rate of random damage is time which scientists are using to attack the problem of genetically programmed aging. Remember that the difference between the average human life span of 73 years and the maximum potential life span (limited by genetic programs ) of
110 to 120 years is 40 years. Forty years ago, we did not know what DNA—the program blueprints—did or how it worked.
Since knowledge in this area is doubling every 5 to 10 years, this potential for at least an extra 40 years gained from the control of random damage means a knowledge increase of 16 to 256 times over what we know now. Fortunately, when you are buying time, you don’t have to buy it all at once.
A phenomenon characteristic of aging populations is the reduced speed or degree of the body’s biochemical adaptation in response to changes in the environment. This problem has been extensively studied by Dr. Richard D. Adelman. An older animal’s greatly increased risk of death may be largely
explainable in terms of this particular physiological change due to aging. For example, following administration of glucose to two-month-old Sprague-Dawley rats after a 72-hour- fast there is an increase of activity of hepatic glucokinase (a sugar-processing liver enzyme) by several fold. The time required for aged rats (24 months old) to increase this enzyme’s
activity to the same level is three times as long.
Life is a state of dynamic equilibrium (movement and change combined with balance), rather like walking a tightrope. Your continued life requires that your body manufacture tens of thousands of chemicals in the right amounts, at the right places, and at appropriate times. Accumulated damage at the cellular level (regardless of cause) will interfere with this balancing act. Finally a stress comes along (an infection, a mutation causing cancer, or simply exertion from shoveling snow) that you could have handled easily in your youth—but now it pushes you too far from your living dynamic equilibrium, and you fall off the tightrope of life into your
grave.
The response of enzyme systems in different tissues of several animal species to environmental stimuli have been studied by Adelman. He found that there are four basic types of responses (as depicted in the graphs):
- The old animal is slower in altering its enzyme level,
but eventually this reaches a young adult level. - The old animal increases its enzyme activity at the
same rate as the young adult animal, but the old animal’s enzyme level cannot reach the high final level of the young animal. - The old animal’s enzyme activity responds more slowly and cannot reach the high level of the young adult.
- The time course and level of activity of both old and young are very similar. (Only in this case has the enzyme system been little affected by aging.)
Enzyme activity levels depend on a large number of control systems. Delayed enzymatic adaptation could, for example, be due to impairment of regulation of enzyme synthesis. And this, in turn, could be due to several factors. One of the mechanisms of impaired liver enzyme adaptation during aging, as suggested by Adelman, is changes in availability and/or potency of one or more hormones involved. Adelman has found in old rats that seven slightly different versions of insulin were produced, only one of which had the pharmacological activity of the young rat insulin, but all of which could
take up chemical sites normally occupied by the single correct insulin molecule. The common clinical laboratory hormone-measuring tests cannot distinguish between closely related but not equally functional molecules.
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