Being Mortal: Medicine and What Matters in the End

by Gawande, Atul

  For those who had no interest in moving into such places—Alice Hobson, for instance—it became acceptable and feasible to remain in their own homes, living as they wanted to live, autonomously. That fact remains something to celebrate. There is arguably no better time in history to be old. The lines of power between the generations have been renegotiated, and not in the way it is sometimes believed. The aged did not lose status and control so much as share it. Modernization did not demote the elderly. It demoted the family. It gave people—the young and the old—a way of life with more liberty and control, including the liberty to be less beholden to other generations. The veneration of elders may be gone, but not because it has been replaced by veneration of youth. It’s been replaced by veneration of the independent self.

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  THERE REMAINS ONE problem with this way of living. Our reverence for independence takes no account of the reality of what happens in life: sooner or later, independence will become impossible. Serious illness or infirmity will strike. It is as inevitable as sunset. And then a new question arises: If independence is what we live for, what do we do when it can no longer be sustained?

  In 1992, Alice turned eighty-four. She was in striking health. She’d had to make a transition to false teeth and undergo removal of cataracts in both eyes. That was all. She’d had no major illnesses or hospitalizations. She still went to the gym with her friend Polly and did her own shopping and took care of her house. Jim and Nan offered her the option of turning their basement into an apartment for her. She might find it easier to be there, they said. She wouldn’t hear of it. She had no intention of not living on her own.

  But things began to change. On a mountain vacation with the family, Alice didn’t turn up for lunch. She was found sitting in the wrong cabin, wondering where everyone was. We’d never seen her confused like that before. The family kept a close eye on her for the next few days, but nothing else untoward happened. We all let the matter drop.

  Then Nan, visiting Alice at home one afternoon, noticed black-and-blue bruises up and down her leg. Had she fallen?

  No, Alice said at first. But later she admitted that she’d taken a spill going down the wooden basement stairs. It was just a slip, she insisted. It could have happened to anyone. She’d be more careful next time.

  Soon, however, she had more falls, several of them. No broken bones, but the family was getting worried. So Jim did what all families naturally do nowadays. He had her see a doctor.

  The doctor did some tests. He found that she had thinning bones and recommended calcium. He fiddled with her medications and gave her some new prescriptions. But the truth was he didn’t know what to do. We were not bringing him a fixable problem. Alice was unsteady. Her memory was slipping. The problems were only going to increase. Her independence would not be sustainable for long now. But he had no answers or direction or guidance. He could not even describe what to expect would happen.

  2 • Things Fall Apart

  Medicine and public health have transformed the trajectory of our lives. For all but our most recent history, death was a common, ever-present possibility. It didn’t matter whether you were five or fifty. Every day was a roll of the dice. If you plotted the typical course of a person’s health, it would look like this:

  Life and health would putter along nicely, not a problem in the world. Then illness would hit and the bottom would drop out like a trap door—the way it did for my grandmother Gopikabai Gawande, who’d been perfectly well until the day she was struck by a fatal case of malaria, not even thirty years old, or for Rich Hobson, who had a heart attack on a business trip and then was gone.

  Over the years, with medical progress, the bottom has tended to drop out later and later. The advent of sanitation and other public health measures sharply reduced the likelihood of death from infectious disease, especially in early childhood, and clinical advances dramatically reduced the mortality of childbirth and traumatic injuries. By the middle of the twentieth century, just four out of every hundred people in industrialized countries died before the age of thirty. And in the decades since, medicine found ways to cut the mortality of heart attacks, respiratory illnesses, stroke, and numerous other conditions that threaten in adult life. Eventually, of course, we all die of something. But even then, medicine has pushed the fatal moment of many diseases further outward. People with incurable cancers, for instance, can do remarkably well for a long time after diagnosis. They undergo treatment. Symptoms come under control. They resume regular life. They don’t feel sick. But the disease, while slowed, continues progressing, like a night brigade taking out perimeter defenses. Eventually, it makes itself known, turning up in the lungs, or in the brain, or in the spine, as it did with Joseph Lazaroff. From there, the decline is often relatively rapid, much as in the past. Death occurs later, but the trajectory remains the same. In a matter of months or weeks, the body becomes overwhelmed. That is why, although the diagnosis may have been present for years, death can still come as a surprise. The road that seemed so straight and steady can still disappear, putting a person on a fast and steep slide down.

  The pattern of decline has changed, however, for many chronic illnesses—emphysema, liver disease, and congestive heart failure, for example. Instead of just delaying the moment of the downward drop, our treatments can stretch the descent out until it ends up looking less like a cliff and more like a hilly road down the mountain:

  The road can have vertiginous drops but also long patches of recovered ground: we may not be able to stave off the damage, but we can stave off the death. We have drugs, fluids, surgery, intensive care units to get people through. They enter the hospital looking terrible, and some of what we do can make them look worse. But just when it looks like they’ve breathed their last, they rally. We make it possible for them to make it home—weaker and more impaired, though. They never return to their previous baseline. As illness progresses and organ damage worsens, a person becomes less able to withstand even minor problems. A simple cold can be fatal. The ultimate course is still downward until there finally comes a time when there is no recovery at all.

  The trajectory that medical progress has made possible for many people, though, follows neither of these two patterns. Instead, increasingly large numbers of us get to live out a full life span and die of old age. Old age is not a diagnosis. There is always some final proximate cause that gets written down on the death certificate—respiratory failure, cardiac arrest. But in truth no single disease leads to the end; the culprit is just the accumulated crumbling of one’s bodily systems while medicine carries out its maintenance measures and patch jobs. We reduce the blood pressure here, beat back the osteoporosis there, control this disease, track that one, replace a failed joint, valve, piston, watch the central processing unit gradually give out. The curve of life becomes a long, slow fade:

  The progress of medicine and public health has been an incredible boon—people get to live longer, healthier, more productive lives than ever before. Yet traveling along these altered paths, we regard living in the downhill stretches with a kind of embarrassment. We need help, often for long periods of time, and regard that as a weakness rather than as the new normal and expected state of affairs. We’re always trotting out some story of a ninety-seven-year-old who runs marathons, as if such cases were not miracles of biological luck but reasonable expectations for all. Then, when our bodies fail to live up to this fantasy, we feel as if we somehow have something to apologize for. Those of us in medicine don’t help, for we often regard the patient on the downhill as uninteresting unless he or she has a discrete problem we can fix. In a sense, the advances of modern medicine have given us two revolutions: we’ve undergone a biological transformation of the course of our lives and also a cultural transformation of how we think about that course.

  * * *

  THE STORY OF aging is the story of our parts. Consider the teeth. The hardest substance in the human body is the white enamel of the teeth. With age, it nonetheless wears aw
ay, allowing the softer, darker layers underneath to show through. Meanwhile, the blood supply to the pulp and the roots of the teeth atrophies, and the flow of saliva diminishes; the gums tend to become inflamed and pull away from the teeth, exposing the base, making them unstable and elongating their appearance, especially the lower ones. Experts say they can gauge a person’s age to within five years from the examination of a single tooth—if the person has any teeth left to examine.

  Scrupulous dental care can help avert tooth loss, but growing old gets in the way. Arthritis, tremors, and small strokes, for example, make it difficult to brush and floss, and because nerves become less sensitive with age, people may not realize that they have cavity and gum problems until it’s too late. In the course of a normal lifetime, the muscles of the jaw lose about 40 percent of their mass and the bones of the mandible lose about 20 percent, becoming porous and weak. The ability to chew declines, and people shift to softer foods, which are generally higher in fermentable carbohydrates and more likely to cause cavities. By the age of sixty, people in an industrialized country like the United States have lost, on average, a third of their teeth. After eighty-five, almost 40 percent have no teeth at all.

  Even as our bones and teeth soften, the rest of our body hardens. Blood vessels, joints, the muscle and valves of the heart, and even the lungs pick up substantial deposits of calcium and turn stiff. Under a microscope, the vessels and soft tissues display the same form of calcium that you find in bone. When you reach inside an elderly patient during surgery, the aorta and other major vessels can feel crunchy under your fingers. Research has found that loss of bone density may be an even better predictor of death from atherosclerotic disease than cholesterol levels. As we age, it’s as if the calcium seeps out of our skeletons and into our tissues.

  To maintain the same volume of blood flow through our narrowed and stiffened blood vessels, the heart has to generate increased pressure. As a result, more than half of us develop hypertension by the age of sixty-five. The heart becomes thicker-walled from having to pump against the pressure, and less able to respond to the demands of exertion. The peak output of the heart therefore decreases steadily from the age of thirty. People become gradually less able to run as far or as fast as they used to or to climb a flight of stairs without becoming short of breath.

  As the heart muscle thickens, muscle elsewhere thins. Around age forty, one begins to lose muscle mass and power. By age eighty, one has lost between a quarter and a half of one’s muscle weight.

  You can see all these processes play out just in the hand: 40 percent of the muscle mass of the hand is in the thenar muscles, the muscles of the thumb, and if you look carefully at the palm of an older person, at the base of the thumb, you will notice that the musculature is not bulging but flat. In a plain X-ray, you will see speckles of calcification in the arteries and translucency of the bones, which, from age fifty, lose their density at a rate of nearly 1 percent per year. The hand has twenty-nine joints, each of which is prone to destruction from osteoarthritis, and this will give the joint surfaces a ragged, worn appearance. The joint space collapses. You can see bone touching bone. What the person feels is swelling around the joints, reduced range of motion of the wrist, diminished grip, and pain. The hand also has forty-eight named nerve branches. Deterioration of the cutaneous mechanoreceptors in the pads of the fingers produces loss of sensitivity to touch. Loss of motor neurons produces loss of dexterity. Handwriting degrades. Hand speed and vibration sense decline. Using a standard mobile phone, with its tiny buttons and touch screen display, becomes increasingly unmanageable.

  This is normal. Although the processes can be slowed—diet and physical activity can make a difference—they cannot be stopped. Our functional lung capacity decreases. Our bowels slow down. Our glands stop functioning. Even our brains shrink: at the age of thirty, the brain is a three-pound organ that barely fits inside the skull; by our seventies, gray-matter loss leaves almost an inch of spare room. That’s why elderly people like my grandfather are so much more prone to cerebral bleeding after a blow to the head—the brain actually rattles around inside. The earliest portions to shrink are generally the frontal lobes, which govern judgment and planning, and the hippocampus, where memory is organized. As a consequence, memory and the ability to gather and weigh multiple ideas—to multitask—peaks in midlife and then gradually declines. Processing speeds start decreasing well before age forty (which may be why mathematicians and physicists commonly do their best work in their youth). By age eighty-five, working memory and judgment are sufficiently impaired that 40 percent of us have textbook dementia.

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  WHY WE AGE is the subject of vigorous debate. The classical view is that aging happens because of random wear and tear. The newest view holds that aging is more orderly and genetically programmed. Proponents of this view point out that animals of similar species and exposure to wear and tear have markedly different life spans. The Canada goose has a longevity of 23.5 years; the emperor goose only 6.3 years. Perhaps animals are like plants, with lives that are, to a large extent, internally governed. Certain species of bamboo, for instance, form a dense stand that grows and flourishes for a hundred years, flowers all at once, and then dies.

  The idea that living things shut down instead of wearing down has received substantial support in recent years. Researchers working with the now famous worm C. elegans (twice in one decade, Nobel Prizes went to scientists doing work on the little nematode) were able, by altering a single gene, to produce worms that live more than twice as long and age more slowly. Scientists have since come up with single-gene alterations that increase the life spans of fruit flies, mice, and yeast.

  These findings notwithstanding, the preponderance of the evidence is against the idea that our life spans are programmed into us. Remember that for most of our hundred-thousand-year existence—all but the past couple of hundred years—the average life span of human beings has been thirty years or less. (Research suggests that subjects of the Roman Empire had an average life expectancy of twenty-eight years.) The natural course was to die before old age. Indeed, for most of history, death was a risk at every age of life and had no obvious connection with aging, at all. As Montaigne wrote, observing late-sixteenth-century life, “To die of age is a rare, singular, and extraordinary death, and so much less natural than others: it is the last and extremest kind of dying.” So today, with our average life span in much of the world climbing past eighty years, we are already oddities living well beyond our appointed time. When we study aging what we are trying to understand is not so much a natural process as an unnatural one.

  It turns out that inheritance has surprisingly little influence on longevity. James Vaupel, of the Max Planck Institute for Demographic Research, in Rostock, Germany, notes that only 3 percent of how long you’ll live, compared with the average, is explained by your parents’ longevity; by contrast, up to 90 percent of how tall you are is explained by your parents’ height. Even genetically identical twins vary widely in life span: the typical gap is more than fifteen years.

  If our genes explain less than we imagined, the classical wear-and-tear model may explain more than we knew. Leonid Gavrilov, a researcher at the University of Chicago, argues that human beings fail the way all complex systems fail: randomly and gradually. As engineers have long recognized, simple devices typically do not age. They function reliably until a critical component fails, and the whole thing dies in an instant. A windup toy, for example, works smoothly until a gear rusts or a spring breaks, and then it doesn’t work at all. But complex systems—power plants, say—have to survive and function despite having thousands of critical, potentially fragile components. Engineers therefore design these machines with multiple layers of redundancy: with backup systems, and backup systems for the backup systems. The backups may not be as efficient as the first-line components, but they allow the machine to keep going even as damage accumulates. Gavrilov argues that, within the parameters established by our genes
, that’s exactly how human beings appear to work. We have an extra kidney, an extra lung, an extra gonad, extra teeth. The DNA in our cells is frequently damaged under routine conditions, but our cells have a number of DNA repair systems. If a key gene is permanently damaged, there are usually extra copies of the gene nearby. And, if the entire cell dies, other cells can fill in.

  Nonetheless, as the defects in a complex system increase, the time comes when just one more defect is enough to impair the whole, resulting in the condition known as frailty. It happens to power plants, cars, and large organizations. And it happens to us: eventually, one too many joints are damaged, one too many arteries calcify. There are no more backups. We wear down until we can’t wear down anymore.

  It happens in a bewildering array of ways. Hair grows gray, for instance, simply because we run out of the pigment cells that give hair its color. The natural life cycle of the scalp’s pigment cells is just a few years. We rely on stem cells under the surface to migrate in and replace them. Gradually, however, the stem-cell reservoir is used up. By the age of fifty, as a result, half of the average person’s hairs have gone gray.