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Authors: Sherwin B Nuland

BOOK: How We Die
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The microbes of pneumonia lie in wait for the appearance of any added insult that might inhibit further the already-damaged defenses of the aged. Coma is their perfect ally. It takes away every conscious way of resisting their predations, and even destroys so basic a safety device as the cough reflex. Any bit of regurgitation or foreign matter that under ordinary circumstances would be forcefully ejected at the first sign of its invasion of the airway now becomes the vehicle on which the germs ride triumphantly into the respiratory tissues. The microscopic air sacs called alveoli then swell and are destroyed by inflammation. As a result, proper exchange of gases is prevented, and blood oxygen diminishes while carbon dioxide may build up until vital functions can no longer be sustained. When oxygen levels drop below a critical point, the brain manifests it by further cell death, and the heart by fibrillation or arrest. Pneumonia triumphs.
Pneumonia’s blitzkrieg has yet another way to kill—its putrid headquarters in the lung serves as a focus from which the murderous organisms can enter the bloodstream and be dispersed into every organ of the body. Called sepsis or septicemia by doctors and blood poisoning by the rest of the world, this process sets off a series of physiologic events that results in collapse of the integrity of heart, lungs, blood vessels, kidneys and liver, with an ultimate drastic drop in blood pressure to shock levels, followed by death. In sepsis, even the most powerful antibiotics are often no match for the microbes’ overwhelming assault.
Whether the terminal event is pneumonia, heart failure, or the acidosis of uncontrollable diabetes, the salient fact about stroke is that it is always to be found in the company of its friends—the ubiquitous corps of killers of the old. A stroke is simply one part of the wide spectrum of end-stage cerebrovascular disease, which, while it may be hastened by self-abuse, can never be stopped in its determined course. Henry Gardiner, who compiled my 1845 edition of Thomas Browne’s writings, has bound into its appendix a long quotation from Francis Quarles, a seventeenth-century literary figure, who properly said: “It lies in the power of man, either permissively to hasten, or actively to shorten, but not to lengthen or extend the limits of his natural life.” And then in a sublime bit of wisdom, Quarles added, “He only (if any) hath the art to lengthen out his taper, that puts it to the best advantage.” There is no way to deter old age from its grim duty, but a life of accomplishment makes up in quality for what it cannot add in quantity.
Many doctors, especially those who spend much of their time in laboratories, share with statisticians the disbelief in the necessity of death from old age. Reading my account of my Bubbeh’s last days, they will by now undoubtedly have pointed out that pneumonia and other infections become, after all, the second most common identifiable cause of death once people reach the very great age of eighty-five, and atherosclerosis is the first. My grandmother had both, and therefore, they may claim, her mode of death supports their worldview and argues for vigorous intervention to treat the named pathologies in order to prolong life. To me, this is more sophistry than science.
I grant these doctors their perspective, but there is plenty of evidence that life does have its natural, inherent limits. When those limits are reached, the taper of life, even in the absence of any specific disease or accident, simply sputters out.
Fortunately, most bedside doctors who restrict their practice to the care of the aged have come to understand this. The geriatricians are to be applauded for the great contributions they have already made to elucidating the pathologies afflicting those who are slowly being overwhelmed by the defects in their waning senescent powers, but even more so do they deserve our admiration for the compassion they bring to their work. I recently discussed this with my school’s professor of geriatric medicine, Dr. Leo Cooney, who later summarized his viewpoint in two pithy paragraphs of a letter:
Most geriatricians are at the forefront of those who believe in withholding vigorous interventions designed simply to prolong life. It is geriatricians who are constantly challenging nephrologists [kidney specialists] who dialyze very old people, pulmonologists [lung specialists] who intubate people with no quality of life, and even surgeons who seem unable to withhold their scalpels from patients for whom peritonitis would be a merciful mode of death.
We wish to improve the quality of life for older individuals, not to prolong its duration. Thus, we would like to see that older people are independent and lead a dignified life for as long as possible. We work to decrease incontinence, manage confusion, and help families deal with devastating illnesses like Alzheimer’s.
Basically, geriatricians can be viewed as the primary care doctors for elderly people, this generation’s solution to the problem of the absence of the old family doctor who knew his patients as well as he knew their diseases. If a geriatrician is a specialist, his specialty is the entire elderly person. In late 1992, there were only 4,084 certified geriatricians in the United States; at the same time, there were some 17,000 heart specialists.
One might question certain portions of my evidence for saying that the natural limits of an individual’s life permit little tampering. There are in fact some very elaborate studies that have been conducted on aging people who have remained well. In those investigations, age-specific changes in function were evaluated in men and women who had no disease process that could be expected to affect that function. The results are as I have described them—the aging process goes on, regardless of anything else that may be happening. Aging may be said to be both independent and codependent, in the sense that it certainly contributes to disease and may in turn be accelerated by it. But disease or no disease, the body continues to get older.
My disagreement with the viewpoint of many of those laboratory researchers who study the physiology of aging centers around the philosophy of treatment. When it is possible to identify a disease by giving it a name, its ravages become the subject of treatment, with the potential aim of cure. And that, after all, is the real reason a modern scientific doctor becomes a specialist. No matter his stated interest in relieving human suffering and no matter the sincerity of his efforts, the average specialist physician does what he does because he is absorbed by the riddle of disease and longs to conquer it by solving each puzzlement it presents to his inquisitive mind, whether he is a researcher or a clinician. At each end of life, the pediatric and geriatric age groups, patients are fortunate to be guided by one of today’s equivalents of the family doctor.
The diagnosis of disease and the quest for overcoming it with his intellect are the challenges that motivate every specialist who is any good at what he does. He is fascinated with pathology. When faced by the certainty of his own impotence to treat it, the would-be healer too often turns away. If a riddle is by its nature insoluble, it cannot long hold the interest of any but a tiny fraction of the doctors who treat specific organ systems and disease categories. Old age is as insoluble as it is inevitable. By giving scientific names of treatable diseases to its manifestations, too many of the specialists from whom the elderly seek care retain their riddle and their fascination. They also believe they give patients some kind of hope, though in the end the hope must always prove to be unjustified. These days (if I may steal a term from the jargon of the contemporary rialto), it is not politically correct to admit that some people die of old age.
Can there be any doubt that the intrinsic physical processes associated with aging inevitably cause an individual to become progressively more vulnerable to mortality? Can there by any doubt that every year we grow less able to marshal the forces required to fight off the lethal dangers that lurk constantly around us? Can there be any doubt that this growing inability is the result of gradually incremental debilitation in the powers of our tissues and organs? Can there be any doubt that the debilitation is due to a general running down of normal structure and function? Can there be any doubt that a general running down, whether in a motor or a man, will eventually lead to nonfunction? Can there be any doubt that Thomas Jefferson knew what he was talking about?
The understanding expressed by Jefferson is in fact millennia-old. In the oldest extant medical book of China, or anywhere else—the
Huang Ti Nei Ching Su Wen
(
The Yellow Emperor’s Classic of Internal Medicine
), written some 3,500 years ago—the mythical emperor is being instructed about old age by the learned physician Chi Po, who tells him:
When a man grows old his bones become dry and brittle like straw [osteoporosis], his flesh sags and there is much air within his thorax [emphysema], and pains within his stomach [chronic indigestion]; there is an uncomfortable feeling within his heart [angina or the fluttering of a chronic arrhythmia], the nape of his neck and the top of his shoulders are contracted, his body burns with fever [frequent urinary-tract infections], his bones are stripped and laid bare of flesh [loss of lean muscle mass], and his eyes bulge and sag. When then the pulse of the liver [right heart failure] can be seen but the eye can no longer recognize a seam [cataracts], death will strike. The limit of a man’s life can be perceived when a man can no longer overcome his diseases; then his time of death has arrived.
The major question is not
whether
aging leads to debility, the inability to overcome disease, and then death, but
why
individuals age in the first place. The Preacher of
Ecclesiastes
was among the first in the Western tradition to point out that “To every thing there is a season, and a time to every purpose under the heaven: A time to be born, and a time to die,” but the theme is so commonplace as to echo through our literature in every era. Before the Preacher, Homer had written, “The race of men is like the race of leaves. As one generation flourishes, another decays.” And there are good reasons that one generation must give way to the next, as made clear in another of the letters Jefferson wrote to the equally venerable John Adams near the end of his life: “There is a ripeness of time for death, regarding others as well as ourselves, when it is reasonable we should drop off, and make room for another growth. When we have lived our generation out, we should not wish to encroach on another.”
If it is the way of nature that we not “encroach on another” (and simple observation confirms that it is), then nature must of necessity provide some means of certainty that we, like Homer’s leaves, progressively attain a stage at which we “drop off, and make room for another growth,” as gentleman farmer Jefferson put it. Scientists of every stamp have attempted to identify the mechanism by which living things do this, and we still don’t know for certain what it is.
Basically, there are two distinct lines of reasoning to explain the aging process. One emphasizes the continued progressive damage done to cells and organs by the commonplace process of carrying out their normal functions in the ordinary environment of everyday life. This is often called the “wear and tear” theory. The other suggests that aging is due to the existence of a genetically predetermined life span that controls not only the longevity of individual cells but of organs and entire organisms, like ourselves, as well. In descriptions of this latter thesis, the image is often invoked of a “genetic tape” that begins to run at the instant of conception and plays out a sequential program that preordains not only the hour of death (at least in the metaphoric sense) but even the hour at which the death-dealing notes begin to he heard. Carried to its most specific implication, this theory might mean, for example, that the day or week of a cancer’s first cell division has already been determined at the time the same event is happening in the just-fertilized egg.
As used by the proponents of the “wear and tear” theory, the word
environment
may refer to the environment of this planet or the environment within and around the cell itself. It may be that such factors as background irradiation (both solar and industrial), pollutants, microbes, and toxins in the atmosphere slowly result in damage that changes the nature of the genetic information transmitted by cells to their offspring. It may even be that the environment plays no part—the misinformation may result from random errors in transmission. Either way, the accumulated alterations in DNA might then cause the errors in a cell’s function that lead to its death and those obvious changes in the whole organism that manifest themselves as aging. This process of frank cellular death is called by some the “error catastrophe.”
Some of the environmental hazards originate within our tissues and inside the cell. I have already described the constant bombardment that affects the basic nature of molecules, but there are other mechanisms as well. In order to continue in vibrant health, cells must efficiently break down the toxic products of their own metabolism. If there is any degree of escape from this mechanism, the harmful by-products may accumulate and affect not only function but the DNA itself; whether its cause is the environment, random errors in transmission, or toxic products of metabolism, the development of errors in the DNA is thought by many to be a major factor in the aging process.
Although we should not take the fright literature of New Age doom describers too seriously, there is no doubt that some of their shibboleths, such as aldehydes and free radicals of oxygen, demand attention because they may play a role in the damaging and aging of protoplasm if they are not properly degraded into less hazardous substances. A free radical is a molecule whose outer orbit contains an odd number of electrons. Such structures are extremely reactive, because stability can be acquired only by gaining an electron or losing the one that is unpaired. The extreme reactivity of free radicals has made them either the culprit or the hero of numerous biological theories, ranging from the very origins of life on this planet all the way along the spectrum to mechanisms of aging. Some of our more activist would-be extenders of life are convinced that an extra load of beta carotene or vitamin E or C in the diet will rescue our tissues from oxidation by free radicals. Unfortunately, there is as yet no definitive evidence to prove that they are correct.

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