Being Mortal: Medicine and What Matters in the End (5 page)

BOOK: Being Mortal: Medicine and What Matters in the End
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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.

Inside skin cells, the mechanisms that clear out waste products slowly break down and the residue coalesces into a clot of gooey yellow-brown pigment known as lipofuscin. These are the age spots we see in skin. When lipofuscin accumulates in sweat glands, the sweat glands cannot function, which helps explain why we become so susceptible to heat stroke and heat exhaustion in old age.

The eyes go for different reasons. The lens is made of crystallin proteins that are tremendously durable, but they change chemically in ways that diminish their elasticity over time—hence the farsightedness that most people develop beginning in their fourth decade. The process also gradually yellows the lens. Even without cataracts (the whitish clouding of the lens that occurs with age, excessive ultraviolet exposure, high cholesterol, diabetes, and cigarette smoking), the amount of light reaching the retina of a healthy sixty-year-old is one-third that of a twenty-year-old.

I spoke to Felix Silverstone, who for twenty-four years was the senior geriatrician at the Parker Jewish Institute, in New York, and who has published more than a hundred studies on aging. There is, he told me, “no single, common cellular mechanism to the aging process.” Our bodies accumulate lipofuscin and oxygen free-radical damage and random DNA mutations and numerous other microcellular problems. The process is gradual and unrelenting.

I asked Silverstone whether gerontologists have discerned any particular, reproducible pathway to aging. “No,” he said. “We just fall apart.”

*   *   *

THIS IS NOT
, to say the least, an appealing prospect. People naturally prefer to avoid the subject of their decrepitude. There have been dozens of bestselling books on aging, but they tend to have titles such as
Younger Next Year
,
The Fountain of Age
,
Ageless
, or—my favorite—
The Sexy Years
. Still, there are costs to averting our eyes from the realities. We put off dealing with the adaptations that we need to make as a society. And we blind ourselves to the opportunities that exist to change the individual experience of aging for the better.

As medical progress has extended our lives, the result has been what’s called the “rectangularization” of survival. Throughout most of human history, a society’s population formed a sort of pyramid: young children represented the largest portion—the base—and each successively older cohort represented a smaller and smaller group. In 1950, children under the age of five were 11 percent of the US population, adults aged forty-five to forty-nine were 6 percent, and those over eighty were 1 percent. Today, we have as many fifty-year-olds as five-year-olds. In thirty years, there will be as many people over eighty as there are under five. The same pattern is emerging throughout the industrialized world.

Few societies have come to grips with the new demography. We cling to the notion of retirement at sixty-five—a reasonable notion when those over sixty-five were a tiny percentage of the population but increasingly untenable as they approach 20 percent. People are putting aside less in savings for old age now than they have at any time since the Great Depression. More than half of the very old now live without a spouse and we have fewer children than ever before, yet we give virtually no thought to how we will live out our later years alone.

Equally worrying, and far less recognized, medicine has been slow to confront the very changes that it has been responsible for—or to apply the knowledge we have about how to make old age better. Although the elderly population is growing rapidly, the number of certified geriatricians the medical profession has put in practice has actually fallen in the United States by 25 percent between 1996 and 2010. Applications to training programs in adult primary care medicine have plummeted, while fields like plastic surgery and radiology receive applications in record numbers. Partly, this has to do with money—incomes in geriatrics and adult primary care are among the lowest in medicine. And partly, whether we admit it or not, a lot of doctors don’t like taking care of the elderly.

“Mainstream doctors are turned off by geriatrics, and that’s because they do not have the faculties to cope with the Old Crock,” Felix Silverstone, the geriatrician, explained to me. “The Old Crock is deaf. The Old Crock has poor vision. The Old Crock’s memory might be somewhat impaired. With the Old Crock, you have to slow down, because he asks you to repeat what you are saying or asking. And the Old Crock doesn’t just have a chief complaint—the Old Crock has fifteen chief complaints. How in the world are you going to cope with all of them? You’re overwhelmed. Besides, he’s had a number of these things for fifty years or so. You’re not going to cure something he’s had for fifty years. He has high blood pressure. He has diabetes. He has arthritis. There’s nothing glamorous about taking care of any of those things.”

There is, however, a skill to it, a developed body of professional expertise. One may not be able to fix such problems, but one can manage them. And until I visited my hospital’s geriatrics clinic and saw the work that the clinicians there do, I did not fully grasp the nature of the expertise involved, or how important it could be for all of us.

*   *   *

THE GERIATRICS CLINIC—OR
, as my hospital calls it, the Center for Older Adult Health (even in a clinic geared to people eighty years or older, patients view words like “geriatrics” or just “elderly” askance)—is only one floor below my surgery clinic. I passed by it almost every day for years, and I can’t remember ever giving it a moment’s thought. One morning, however, I wandered downstairs and, with the permission of the patients, sat in on a few visits with Juergen Bludau, the chief geriatrician.

“What brings you here today?” the doctor asked Jean Gavrilles, his first patient of the morning. She was eighty-five years old, with short, frizzy white hair, oval glasses, a lavender knit shirt, and a sweet, ready smile. Small but sturdy in appearance, she had come in walking steadily, her purse and coat clutched under one arm, her daughter trailing behind her, no support required beyond her mauve orthopedic shoes. She said that her internist had recommended that she come.

About anything in particular? the doctor asked.

The answer, it seemed, was yes and no. The first thing she mentioned was a lower-back pain that she’d had for months, which shot down her leg and sometimes made it difficult to get out of bed or up from a chair. She also had bad arthritis, and she showed us her fingers, which were swollen at the knuckles and bent out to the sides with what’s called a swan-neck deformity. She’d had both knees replaced a decade earlier. She had high blood pressure, “from stress,” she said, before handing Bludau her list of medications. She had glaucoma and needed to have eye exams every four months. She never used to have “bathroom problems,” but lately, she admitted, she’d started wearing a pad. She’d also had surgery for colon cancer and, by the way, she now had a lung nodule that the radiology report said could be a metastasis—a biopsy was recommended.

Bludau asked her to tell him about her life, and it reminded me of the life Alice lived when I first met her at my in-laws’. Gavrilles said that she lived alone, except for her Yorkshire terrier, in a single-family house in the West Roxbury section of Boston. Her husband died of lung cancer twenty-three years ago. She did not drive. She had a son living in the area who did her shopping once a week and checked on her each day—“just to see if I’m still alive,” she joked. Another son and two daughters lived farther away, but they helped as well. Otherwise, she took care of herself quite capably. She did her own cooking and cleaning. She managed her medicines and her bills.

“I have a system,” she said.

She had a high school education, and during World War II she’d worked as a riveter at the Charlestown Navy Yard. She also worked for a time at the Jordan Marsh department store in downtown Boston. But that was a long time ago. She stuck to home now, with her yard and her terrier and her family when they visited.

The doctor asked her about her day in great detail. She usually woke around five or six o’clock, she said—she didn’t seem to need much sleep anymore. She would get out of bed as the back pain allowed, take a shower, and get dressed. Downstairs, she’d take her medicines, feed the dog, and eat breakfast. Bludau asked what she had for breakfast that day. Cereal and a banana, she said. She hated bananas, but she’d heard they were good for her potassium, so she was afraid to stop. After breakfast, she’d take her dog for a little walk in the yard. She did chores—laundry, cleaning, and the like. In the late morning, she took a break to watch
The Price Is Right
. At lunchtime, she had a sandwich and orange juice. If the weather was nice, she’d sit out in the yard afterward. She’d loved working in her garden, but she could no longer do that. The afternoons were slow. She might do some more chores. She might nap or talk on the phone. Eventually, she would make dinner—a salad and maybe a baked potato or a scrambled egg. At night, she watched the Red Sox or the Patriots or college basketball—she loved sports. She usually went to bed at about midnight.

Bludau asked her to sit on the examining table. As she struggled to climb up, her balance teetering on the step, the doctor held her arm. He checked her blood pressure, which was normal. He examined her eyes and ears and had her open her mouth. He listened to her heart and lungs briskly, with his stethoscope. He began to slow down only when he looked at her hands. The nails were neatly trimmed.

BOOK: Being Mortal: Medicine and What Matters in the End
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