How We Die (10 page)
Authors: Sherwin B Nuland
There are simple clinical explanations for the many things I saw during my grandmother’s declining years, but somehow they seem unsatisfactory even now. It is all very well to speak of such causative factors as decreased circulation to the brain or senescent degeneration in cerebral cells so subtle that electron microscopy is needed to demonstrate it—there is a certain intellectual detachment to be found in the stark biological description of the death of that very tissue that once enabled a nonagenarian to think clear and sometimes audacious thoughts. The researches of physiologists might here be cited, as well as the work of endocrinologists, psychoneuroimmunologists, and the rapidly evolving modern breed of gerontologists, to explain everything that was unfolding before my adolescent eyes. But that actual seeing is what demands attention, the seeing of a process in the midst of which all of us constantly live. Surrounded by it though we may be, there is for each of us that something within that turns the face of consciousness away from the reality of our own concomitant aging. Something within us will not accept the immediacy of awareness that, even as we bear witness to it in the obviously old, our own bodies are simultaneously and subtly undergoing the same inexorable process that will lead eventually to senescence and death.
And so my grandmother’s brain cells had long before this time begun to die, even as mine are dying today, and yours. But because she was much older than I am just now, and because she was withdrawing from the stimulation of the world around her, her decreased number of brain cells and their decreased responsiveness led to very obvious changes in her behavior. Like all old people, she became increasingly forgetful and was annoyed when reminded of it. Always known for the forthrightness of her dealings with people, she grew overtly irritable and impatient with those few outside our immediate family with whom she still came into contact, and she seemed to rouse herself by offending even those who had in years past looked to her for guidance. Then the time came when she began to sit silently even in company. Eventually, she spoke only when she absolutely had to, distantly and with little emotion.
What was most evident, but only in retrospect, I confess, was the slow drawing away from life. When I was a small boy, and even into my early teens, my grandmother prayed in the synagogue on the High Holy Days. As difficult as the five-block pilgrimage became, she would somehow manage it, negotiating cracked areas in the Bronx pavement with her worn prayer book held very snugly under one armpit lest she sin by letting it fall to the ground. I would take her there. How I regret every murmur of complaint, how I wish I was not sometimes—no, not sometimes, but often—ashamed of being seen with this black-kerchiefed, shuffling remnant of a shtetl culture that was all but gone even as she stubbornly refused to join it in the grave. Everyone else’s grandparents seemed so much younger, they spoke English, and they were independent—mine was a reminder not only of the lost world of Eastern European Jewry but of my own turbulent conflict about the load of emotional detritus I nowadays euphemistically call my heritage.
With her free hand, Bubbeh would hold tightly onto my arm, sometimes gripping the cloth of my sleeve as I guided her with agonizing slowness through the streets, then down the stairs into the synagogue’s vestry (our family prayed in the cheap seats, and could barely afford even those), and then to her chair amidst other ladies we called elderly, but very few of them nearly as foreign or as careworn as she. A few moments later, I would leave her there, her head already bowed over the old tearstained book she had prayed from since girlhood. Its words were printed in both Hebrew and Yiddish, but she prayed from the Yiddish side of the page because it was the only language she knew. Through the long ritual of those holiday services, she quietly murmured the words that became with each passing year more laborious to read, and finally impossible. About five years before her death, Bubbeh could no longer make the long walk to the synagogue, even with both grandsons to help her. Relying largely on her still-intact long-term memory, she recited the liturgy at home, sitting by the open window as she had done every Saturday morning during all the years I knew her. After a few years, even that became too much. She could barely see the sentences and her memory for the prayers learned in her youth was giving out. Finally, she stopped praying altogether.
By the time Bubbeh stopped praying, she had stopped virtually everything else as well. Her food intake had become minimal—she spent most of each day seated quietly at her window, and she spoke sometimes of death. And yet she had no disease. I’m sure some eager physician might have pointed out her chronic cardiac failure and added to it the probability that there was an element of atherosclerosis, and perhaps he would have prescribed some digitalis. To me, that would have been like dignifying the degeneration of her joints by calling it osteoarthritis. Of course it was arthritis, and of course she was in chronic failure, but only because her pinions and springs were giving way under the weight of the years. She had never been sick a day in her life.
The government statisticians and the scientific clinicians insist that proper names must be applied to sluggish circulation and an antique heart. I have no quarrel with that, so long as they do not also insist that assigning a name to a natural biological state means
a priori
that it is a disease. Like the nerve cell, the muscle cell of the heart is one of those that cannot reproduce—as it gets older, it simply wears out and dies. The biological processes that throughout life have been making replacement parts for dying structures within each cell can no longer do their job. The mechanism by which a newly generated piece of cell membrane or intracellular structure can take the place of a section dead of too much use finally becomes inoperative. After a lifetime of regenerating spare parts, the nerve and muscle cells’ capacity of rejuvenation gradually shuts down. The tactic of continuous renewal within each heart-muscle cell is then defeated by the overwhelming strategy through which aging is achieving its ultimate objective of destruction. One after another, like my grandmother’s teeth, the cardiac muscle cells cease to live—the heart loses strength. The same process takes place in the brain and the rest of the central nervous system. Even the immune system is not immune to aging.
a priori
that it is a disease. Like the nerve cell, the muscle cell of the heart is one of those that cannot reproduce—as it gets older, it simply wears out and dies. The biological processes that throughout life have been making replacement parts for dying structures within each cell can no longer do their job. The mechanism by which a newly generated piece of cell membrane or intracellular structure can take the place of a section dead of too much use finally becomes inoperative. After a lifetime of regenerating spare parts, the nerve and muscle cells’ capacity of rejuvenation gradually shuts down. The tactic of continuous renewal within each heart-muscle cell is then defeated by the overwhelming strategy through which aging is achieving its ultimate objective of destruction. One after another, like my grandmother’s teeth, the cardiac muscle cells cease to live—the heart loses strength. The same process takes place in the brain and the rest of the central nervous system. Even the immune system is not immune to aging.
Changes that are at first only biochemical and intracellular become manifest in the function of entire organs. There is a gradual decrease in the cardiac output while at rest, and when the heart is stressed by exercise or emotion, its ability to increase is less than required by the needs of arms, lungs, and every other structure of the body. The maximal rate attainable by a perfectly healthy heart falls by one beat every year, a figure’ so reliable that it can be determined by subtracting age from 220. If you are fifty years old, it is unlikely that your heart can manage much more than 170 beats per minute, even under the most extreme conditions of emotion or exercise. These are only some of the ways in which the aging and stiffening myocardium loses its ability to adapt to the challenges presented to it by everyday life.
The rapidity of circulation slows down. The left ventricle takes longer to fill and longer to relax after a contraction; each heartbeat pushes out less blood than it did a year earlier, and even a smaller fraction of its content. Perhaps in an attempt to compensate, the blood pressure tends to rise somewhat. Between the ages of sixty and eighty, it increases by 20 millimeters of mercury. One-third of people over the age of sixty-five have hypertension.
Not only the muscle of the heart but also its conduction system dies out as the decades pass. By the age of seventy-five, the sinoatrial node may have lost as much as 90 percent of its cells; the bundle of His contains fewer than half of its original fibers. There are related electrocardiographic changes that go along with all of this loss of muscle and nerve tissue, and they can easily be identified on the inked tracing.
As the pump ages, its inner lining and valves thicken. Calcifications appear in the valves and muscle; the color of the myocardium changes somewhat as a yellow-brown pigment called lipofuscin is deposited in its tissues. Like the face of a weather-beaten old man, a heart looks its age. It acts its age as well. There is no need to invoke a disease to explain its failure. Cardiac failure is ten times as common in people older than seventy-five than in those between forty-five and sixty-five years of age. That is precisely the reason I could so easily indent the tissues of my grandmother’s skin, and it was unquestionably the source of her easy shortness of breath. It is probably also the reason that the most common symptom of a heart attack in elderly patients is severe failure, rather than the classic picture of unremitting chest pain.
Not only the heart itself but the blood vessels, too, are affected by the passing years. The walls of the arteries thicken. Like the person in whom they dwell, they lose their elasticity; they can no longer constrict and dilate with the enthusiasm of youth, and so it is more difficult for the body’s regulatory mechanisms to control the amount of blood going to muscles and organs to satisfy their ever-changing needs. Moreover, atherosclerosis continues on its inexorable way with each passing year. Even without the cholesterol-rich obesity or the cigarettes or diabetes that make it appear at a younger stage, the arterial walls gradually narrow as more and more atheroma accumulates with the prolonged contact of decade upon decade of coursing blood.
Before long, every organ is getting less nourishment than it needs to do the job intended for it by nature. Total blood flow to the kidney, for example, decreases by 10 percent for every decade after the age of forty. Actually, only some of that organ’s decline is caused by the lessened cardiac output and narrowed vessels, but those factors worsen the effect of certain aging changes within the kidney itself. For example, between the ages of forty and eighty, the normal kidney loses some 20 percent of its weight and develops areas of scarring within its substance. Thickening of the tiny blood vessels that are inside the kidney further decreases blood flow and results in destruction of the organ’s filtering units, which are, of course, the crux of its ability to clear the urine of impurities. In time, some 50 percent of the filtering units will die.
The changes in its structure decrease the kidney’s effectiveness. With increasing age, it loses its ability not only to get rid of excess sodium but even to retain it in the body when needed. The result is an instability of the aged person’s salt and water volume, tending to increase the possibility of either heart failure on the one hand or dehydration on the other. This is one of the main reasons that cardiologists treating the elderly have so much difficulty treading the narrow frontier between the Scylla of sodium overload and failure and the Charybdis of parched old tissues.
The result of all of these inadequacies is an increased propensity of the kidney to default in its responsibilities. Even when it does not fail outright but merely falters, it recovers more slowly than a younger organ, and is more prone to let its host down altogether under severe stress—death from kidney failure is a common pathway of exit when an aged person is weakened by some other pathology, such as late-stage cancer or liver disease. The blood’s impurities build up; the other organs, particularly the brain, are poisoned; and death from so-called uremia is inevitable, often preceded by a variable period of coma. The terminal event in uremic patients is most commonly an irregularity of cardiac rhythm (an arrhythmia) caused by the kidney’s inability to rid the blood of excess potassium. Victims of kidney failure usually slide into it imperceptibly, then are suddenly dead in a flash of cardiac instability. Only rarely are there any last words or deathbed reconciliations.
Although the kidney is the most significant part of the urinary tract to develop changes with age, the bladder, too, is affected. The bladder is essentially a thick balloon whose wall is made of flexible muscle. As it ages, the balloon loses its distensibility and can no longer hold as much urine as before. Old people need to urinate more frequently, and this is the reason my grandmother got up once or twice each night to grapple in the dark with her coffee can.
Aging also affects the finely tuned coordination between the bladder muscle and the shutter mechanism whose function is to keep urine from leaking out. The result is the occasional incontinence of the aged, which in some people becomes a major problem, especially if complicated by infection, prostate trouble, mental confusion, or medication. Disturbances of the bladder’s emptying capacity are often a major factor in producing urinary-tract infections, a dangerous enemy of the debilitated elderly.
Like the muscle of the heart, brain cells are unable to reproduce. They survive decade after decade because their various structural components are always being replaced as they wear out, like so many ultramicroscopic carburetors and plugs. Though cell biologists use more abstruse terminology than do mechanics (words like
organelle
and
enzyme
and
mitochondrium
), these entities nonetheless require just as efficient a replacement mechanism as do their more familiar automotive analogues. Like the body itself and like each of its organs, every cell has the equivalents of pinions and wheels and springs. When the mechanism to exchange the aging parts for new wears out, the nerve or muscle cell can no longer survive the constant destruction of components that goes on within it.
organelle
and
enzyme
and
mitochondrium
), these entities nonetheless require just as efficient a replacement mechanism as do their more familiar automotive analogues. Like the body itself and like each of its organs, every cell has the equivalents of pinions and wheels and springs. When the mechanism to exchange the aging parts for new wears out, the nerve or muscle cell can no longer survive the constant destruction of components that goes on within it.
That parts-replacement mechanism requires the participation of certain molecular structures within the cell. But the molecules in biological systems have a finite life span. Beyond that prescribed period, their constant collisions against one another change their character enough so that they can no longer generate new spare parts. By the process of wear and tear, they reach the limits of their longevity, thus limiting the longevity of the brain cell they serve. This is the biochemical process that scientists call cellular aging. The cell gradually dies and its fellows do the same. When enough of them are gone, the brain begins to show its age.
Other books
Once a Rake (Drake's Rakes) by Eileen Dreyer
Thunderball by Ian Fleming
Love Beyond Sight by Rebecca Royce
Sanibel Sizzle - Vampire Werewolf Menage by Talyn Scott
El castillo en el bosque by Mailer Norman
Forsaking Gray (The Colloway Brothers Book 1) by Kreig, K.L.
Under the Dragon's Tail by Maureen Jennings
The Journal of Best Practices by David Finch
Outcasts of Velrune by Isaac Crowe
UNSTOPPABLE (Siri's Saga Book 2) by Klide, Jessika
