Knocking on Heaven's Door: The Path to a Better Way of Death (21 page)

the newspaper, especially after my divorce, I’d often worked the

holiday for the time-and-a-half overtime pay. But as the four of

us sat in our tippy bentwood chairs around the long oak table my

mother had bleached and refinished—my father and T.J. so quiet,

my mother and I so talkative—I remembered times of grace.

On our last Christmas Eve in Oxford, a young boy in a cap

had come to our door in the snowy twilight, opened his hymnal,

and started singing. I stood behind the leaded glass listening as

my mother whispered
Wait, don’t open the door yet, listen.
I still remember him there, the snow falling in the lamplight on his

cap and his hymnal, his clear, pure voice singing
Silent Night,

and when I opened the door, the sudden stop of his singing.

My mother handed me a silver shilling to give him; he took it,

closed his book, thanked me, and was gone.

I remembered another Christmas Eve, my third in Amer-

ica, the year I turned eleven. It was 1960, John Kennedy had

recently been elected president, and we’d put up our first

Christmas tree in the new Techbuilt overlooking the lake on the

outskirts of Wellesley. I’d spent the day at the house of my best

friend, Janet, whose mother’s alcoholism was well advanced.

There were lots of grown-ups there that day, drinking and smok-

ing and playing guitar in the kitchen. Janet cooked us a lunch of

canned SpaghettiOs, and the adults forgot about us. It began to

snow, and by nightfall the highway that ran the three miles from

Janet’s house to my own was closed.

By then, my closeness to my father was long gone—lost to

our nightly dinner-table arguments and his terrified preoccupa-

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tion with his own work. I thought I would spend the night with

Janet’s family, and nobody would much care. Then my father

called to say he would walk halfway to meet me. It was a long

cold way to go alone, but as I walked through the falling snow,

from street lamp to street lamp along the soft, silent highway,

I was not afraid. It was a beautiful night, and the snow, caught

in the street lamps, sparkled as it whirled and fell. The mem-

ory was precious to me, a reminder of how much my father

loved me. He was there to meet me halfway, and not angry, and

together we walked home.

I put down my napkin, and my mother helped my father

unloop his. We helped T.J. back to his car, said good-bye to him

for what turned out to be the last time, and blew the candles out.

Under the bamboo branch that my mother and I had hung with

baubles, I found, the next morning, a beautifully wrapped pres-

ent. It was a paperback book called
Best Buddhist Writing 2005
.

On the frontispiece, my mother had written out part of a stanza

from a Stephen Mitchell translation of the
Tao Te Ching
that I’d given her years before:

Dearest Katy

The path into the light seems dark,

The path forward seems to go back,

The direct path seems long,

True power seems weak.

True clarity seems obscure . . .

The Tao is nowhere to be found,

Yet it nourishes and completes all things.

Love, Ma.

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Full fathom five thy father lies;

Of his bones are coral made;

Those are pearls that were his eyes:

Nothing of him that doth fade

But doth suffer a sea-change

Into something rich and strange.

—Ariel, in
The Tempest,
William Shakespeare

From the perspective of an electron microscope, the young,

healthy brain is like a net hung with jewels, a complex web of

branching and interconnected nerve cells chattering to each other

through long filaments, playing enormous games of gossip, sucking

up and spitting out neurochemicals, and passing on messages to

their neighbors via tiny charges of electricity. From a greater dis-

tance, the brain could be envisioned as an enormous city, bigger

than Jakarta, composed of clusters of semi-independent neighbor-

hoods, eighty-six billion neurons strong, connected via electro-

chemical freeways, alleys, dirt paths, donkey routes, thoroughfares,

and side streets. When one freeway in the brain collapses, mes-

sages often get through by other pathways. When a neighborhood

specializing, say, in finding words is obliterated by a stroke, cells in other neighborhoods try to pick up part of the work, with varying

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degrees of success. The healthy brain, like the healthy young heart

and body, is full of programmed redundancies, work-arounds, and

backup routes. Neurologists call this resilience “cognitive reserve.”

But at the astonishingly early age of twenty-two, some parts

of the neural city begin to decay, even as others—such as those

involved in bridling impulsivity, thinking through decisions,

regulating emotion, and gaining mastery over complex crafts

like journalism, teaching, or cabinet-making—continue to

elaborate. Each year, scores on standardized tests of short-term

memory, reasoning, reaction time, dexterity, the rapid genera-

tion of new ideas, and speed of learning fall by up to 1 percent.

Great breakthroughs in fields like chemistry, mathematics, and

physics—as in athletics—are usually the work of people in their

late twenties and early thirties. Our brains shrink. Dendritic

spines, the knobby lumps on individual brain cells that act as

contact points between neurons, grow sparse and stubby, like a

tree limb that has been harshly pruned. Synapses fail, and asso-

ciated neural pathways fall into disuse. Arteries thicken, reduc-

ing blood flow. Myelin, the fatty white protective sheath that

surrounds filamental brain cells like insulation, grows as porous

and leaky as an old hose, slowing the speed at which messages

move from one cell to another. Even as we grow more deliber-

ate, emotionally skilled, and patient, we understand what peo-

ple say to us more slowly, and our thinking grows less sharp.

In our fifties, levels of hormones fall noticeably, including

several, like estrogen, androgen, and dopamine, that enhance

memory, mood, and focus. We forget names. We fumble more

with tweezers. We get distracted when too many people talk at

once. For a long time, minor losses of brainpower remain invis-

ible to us and our friends and perceptible only on standardized

tests. Our brains’ multiple work-arounds keep working. The

cunning, wisdom, and accumulated knowledge of middle age

triumph over ignorant and impulsive youth.

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katy butler

The declines accelerate after age sixty. Proteins, badly cop-

ied, fold into odd shapes inside cells and clog things up. Tan-

gles of dead cellular material—a defining biological hallmark

of Alzheimer’s disease but occurring in smaller quantities in

the brains of the sharp-minded as well—block neural highways

like uncollected garbage. Inflammation takes a toll. Shrinkage

occurs in the hippocampus, a seahorse-shaped brain region

deep in the skull that shuttles memories from short-term to

long-term brain storage like a switching station. We take longer

to learn languages and to operate new electronic devices.

The pauses that follow the search for a name grow longer. We

drive more slowly to compensate for our slower reaction times.

We joke about “senior moments.” Minor cellular damage accumu-

lates, and neural work-arounds grow scarcer. Depending on how

broadly the damage is defined, 10 percent to 30 percent of people

over sixty-five exhibit what neurologists call “mild cognitive impair-

ment,” an umbrella term for mental decline that is bad enough to

be worrisome but not yet severely disabling. It includes forgetting

important appointments and conversations, having difficulty mak-

ing decisions, misplacing keys and reading glasses, and paying the

same bills twice. We adapt. We keep stricter appointment books

and follow rigid, easy-to-remember schedules, becoming set in

our ways. Yet we remain, we think, fundamentally ourselves.

What happened to my father between 2005 and 2008—the

final three years of his life, the years that his doctors thought he

would not have lived to see without his pacemaker—was worse

than that.

To the end of his days, he never wandered away from home,

or had to be confined or tied up, or forgot my face or my name,

or drooled, or thought he saw the faces of the dead, or dandled a

baby doll in his arms, or insisted it was time he got dressed and

off to work. He never became blissfully unaware of his decline.

He still remembered the pattern of Hartford’s twisting streets

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and freeway on-ramps, and acted as navigator when Toni took

him there to the eye doctor. He had islets of competence. He

remained, to the end, my dear father Jeff.

But there came a time when the losses mounted beyond what

a human being could bear to watch or to endure. Or should be

forced to by an act of medicine.

His brain cells did not simply lose their dendritic spines, as

occurs in ordinary aging. They died in large enough numbers to

obliterate neural pathways connecting areas of the brain that

took in what he saw and sensed with those designed to form

a plan to do something about it. Dr. Fales, my father’s inter-

nist, came to think of the years that followed as “Jeff’s Ordeal.”

Exactly what he had feared came to pass. “My heart went out to

what your parents went through,” he said to me years later. “Par-

ticularly your mother, because she experienced watching him,

being his partner of so many years.” The age-related degenera-

tion that had earlier slowed my father’s heart and shrunk his

brain moved on to attack his eyes, lungs, bladder, and bowels.

He was collapsing slowly, like an ancient, shored-up house.

In June 2005, my father complained of double vision and was

diagnosed with wet macular degeneration in his right eye, a rogue

overgrowth of blood vessels in the retina that leads to blindness. It

is caused by accumulating DNA glitches that allow the replication

of cells that shouldn’t replicate, a process that occurs throughout

the aging body, leading to funny growths as harmless as skin tags

and as deadly as cancer. The extra blood vessels formed a black

spot at the center of my father’s field of vision. “There is not much

that one can do about it; one just suffers from it with age,” he

wrote to me philosophically. The localized blindness layered itself

upon a sight already globally dimmed by time: proteins in the crys-

talline lenses of our eyes grow stiff and yellowed with age, like a

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katy butler

dirty window. The eye of even a healthy sixty-year-old lets in one

third as much light as the eye of someone of twenty.

Thus my father entered the second-to-last stage of the long

chess match with death that we play with such absorption and

lose with such surprise. Things that should be supple, like

arteries, grow stiff, and things that should be strong, like bones,

grow porous. Some cells die and aren’t replaced. Cartilage and

collagen thin. Calcium is pulled from bones and dumped into

arteries. Surgeons operating on aged hearts can feel them crin-

kle. Bone spurs sprout on femurs and knee joints like knobs

of coral. Some cells undergo destructive metabolic processes

called “browning,” analogous to rusting or slow cooking. Mus-

cles wither with disuse. The ends of our cellular DNA lose a

few last notes of code with every replication, increasing the like-

lihood of cancerous mutations. The longer we live, the more our

brains and bodies are pummeled by what Shakespeare called

“the thousand natural shocks the flesh is heir to.”

What we call aging is the cumulative effect of more than seven

thousand separate degenerative bodily processes, each shaped by

our genes, habits, and environment. Sentinel cells in the blood-

stream devour fewer invading microbes and increase the chances

of succumbing to a flu, bronchitis, urinary tract infection, or pneu-

monia. Even our ability to regulate our body temperature weakens.

Our optimistic, science-worshipping culture wants to medicalize

aging and make it nothing more than a collection of specific dis-

eases that medicine can prevent or fix, one item at a time. But

no matter what deal we make with the devil, nature outwits us.

Dying can be postponed, but aging cannot be cured. Although

brilliant minds hunt for a longevity gene, and life extension Web