Triumphs of Experience: The Men of the Harvard Grant Study (34 page)

Dementia, like arthritis, is a curse of longevity. Vital aging at ninety is closely dependent upon the preservation of cognitive faculties, and the best way to achieve this is by minimizing the vascular risk factors. Alzheimer’s disease, however, is a special case. It is a major source of health decline after eighty, but, unlike the purely vascular dementias, it seems to be surprisingly independent of the factors that I have been enumerating.

Death before eighty can be avoided to some degree by wise lifestyle choices, but so far the Study has provided no clues as to how to prevent the two greatest and most dreaded sources of total disability after eighty—most cancers and Alzheimer’s disease.

WHAT WAS NOT IMPORTANT

Ancestral longevity.
Lacking lifetime studies of humans, scientists have studied aging in fruit flies. You can breed and study many generations of fruit flies in a year, and their longevity, it appears, depends heavily
upon
genes. Therefore, one of the first variables the Study looked at was ancestral longevity.

The myth that ancestral longevity is passed on is hard to test well; this is because most people are either so old that they no longer remember the exact ages of their grandparents’ deaths, or so young that they don’t yet know when their parents will die. It takes at least a two-generation study to learn from the subjects’ parents the age that the grandparents died, and then to follow the subjects until the last of their parents have died as well. (In the Grant Study, the last parent died in 2002, sixty-five years and three generations after the Study began. The Study men themselves were very unreliable informants about the age of death of their grandparents.)

For the College men, we calculated ancestral longevity by averaging the ages of death of the oldest of the first-degree ancestors (parents and grandparents) on the maternal and paternal sides. As I’ve noted, the longevity of the forty-four men with the longest-lived first-degree ancestors was seven years longer than the longevity of the thirty-six men with the shortest-lived ancestors. That difference was significant, but just barely. Moreover, to my surprise, the average lifespans of the ancestors of the men with the best and worst mental and physical health at eighty were identical.
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In the Inner City sample as well, the longevity of the men’s parents seemed irrelevant to the quality of their own aging at seventy.
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Fruit flies are clearly not always good models for human aging. Obviously, specific genes are very important in predicting the specific illnesses that shorten life, and soon the precise genes that facilitate longevity may be discovered. In the meantime, however, the McArthur twin studies and investigators using the Swedish Twin Registry confirm our finding that variance in longevity cannot simply be attributed to genetic inheritance.
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Psychosomatic stress.
When the Study began, psychosomatic medicine was in high fashion. Hans Selye had shown the world that stress could
kill,
and psychoanalytic theories about the role of emotions in medical illness were all the rage, attributing peptic ulcers to repressed anger or longing for love.
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It would be decades before the medical profession brought itself to accept that the most common cause of duodenal ulcers is a gram-negative bacterium of the genus
Helicobacter.

Besides, many people
do
feel physically sick under stress. They have headaches; they can’t sleep; their stomachs ache; they get itchy; they’re running to the bathroom all the time. This observation suggests an attractive hypothesis, to which in the 1960s I earnestly subscribed: that individuals who experience stress psychosomatically in midlife would suffer poor physical health in old age.
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When I joined the Grant Study in 1966, I was thrilled to be in possession of prospective Study data that I suspected would prove this hypothesis.

A secondary hypothesis in psychosomatics, to which I also subscribed, held that individuals have characteristic “target organs” in which they experience stress.
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This proposition was based on the observation that one person’s place of experiencing somatic symptoms under stress may be quite different from another’s, and it was much emphasized in my residency training. Theoreticians anticipated that the organ affected by stress would be the same one in which signs of psychosomatic illness appear.

A third related hypothesis, one that I felt certain of proving, was the implicit assumption that the development of “psychosomatic” illnesses (for example, colitis, asthma, and hypertension) reflect more psychopathology than the development of “real” illnesses (such as diabetes, myocardial infarction, and osteoarthritis). Indeed, many of the mental health screening tests of the 1950s and ’60s, some of which, like the Minnesota Multiphasic Personality Inventory, are still in use today, use the presence of multiple physiological symptoms under stress as indicators of emotional illness.

In the 1970s I finally analyzed the data to test these three psychosomatic hypotheses so favored by me and other armchair speculators.
My
intention was to demonstrate 1) that psychosomatic illness leads to accelerated aging; 2) that “target organs” for stress (the stomach, the lungs, and so on) are real and remain stable over time; and 3) that psychosomatic illness is a reliable hallmark of mental illness. Longitudinal study proved them all wrong.

(Note that the evidence for this belief system had been derived over the years from retrospective data. Furthermore, the source of the data was patients who presented themselves repeatedly for medical attention—a group likely to have mental health issues.
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The Grant Study, on the other hand, was a prospective study of men who explicitly were
not
patients.)

Over the years, the Study men were systematically asked where in their bodies they experienced emotional stress. Decades of follow-up revealed that this site varied considerably over time.
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The idea of stable target organs (hypothesis II) was not supported.

Nor did the number of physical symptoms under stress before age fifty predict physical health at age seventy-five or at ninety. If you wait a few decades, people often recover from psychosomatic illnesses. And at age eighty, the physical health of the men with multiple apparently psychosomatic illnesses was actually, if insignificantly, better than that of men with none. Hypothesis I was not confirmed either.

Hypothesis III, the supposition that there’s a connection between psychosomatic illness and mental health, didn’t fare any better than the other two. The Study has carefully followed the men’s objective physical health from the age of forty, when it was still very good, up through the present or until their deaths. By fifty, over half of the Study men had required medical treatment for conditions thought by some physicians to be psychosomatic: hypertension, respiratory allergies, ulcer, colitis, and chronic musculoskeletal complaints. Admittedly, these five disorders do not define psychosomatic illness conclusively, but they make a good start. At age forty-seven, after almost thirty
years
of observation, the men were ranked for emotional health. There was no correlation with the number of psychosomatic complaints. The number of psychosomatic illnesses that the men suffered didn’t predict mental health at age sixty or eighty, either. As a faithful believer in psychosomatic medicine, I was profoundly disappointed.

We also found that the childhoods of the men who experienced relatively few physical symptoms under stress and no psychosomatic illnesses were no warmer in blind ratings than those of men cursed with a great deal of psychosomatic symptomatology.
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As I’ve noted, in our first study of aging, premorbid psychopathology did correlate with early onset of chronic (real) physical illness, but only up to the age of fifty-five. We had some middle-aged Study men who frequently visited medical doctors and who took more than five or more sick days a year. They displayed our distinguishing markers for mental health issues—drinking, psychiatric intervention, use of tranquilizers and antidepressants, and so on—and in this they resembled the self-selected populations of the old retrospective studies. In other words, people with mental health issues brought more illnesses of all kinds—real and imagined—to the attention of the medical community.

When in 1970 I first presented these findings at a national psychosomatic meeting, I was met with outrage and disbelief as a traitor to dynamic psychiatry. Today, my findings would be regarded as unremarkable. Over the last forty years, a medical model of psychosomatics has displaced the earlier one, thanks in part to the
Helicobacter
story and the fading influence of psychoanalysis in academic psychiatry. My research life, and the Study’s, spanned both eras.

Cholesterol.
Magazines would lose valuable advertising revenues, and probably readers, if they talked too much about really significant risks to health—like Virginia Slims and wine coolers. But it’s OK to fuss about cholesterol, because the butter and egg lobbies don’t advertise
in
Cosmopolitan.
Moreover, as the TV ads tell us, your cholesterol can be magically lowered by statins, even if you don’t eat less or exercise more. So the war on cholesterol would appear to be a win-win-win situation—for patient, for doctor, and for the pharmaceutical industry.

Countless studies show that the ratio between high- and low-density lipoproteins (HDLs and LDLs) is important and that reducing LDL levels is good for the heart. But in neither the College nor the Inner City sample did average cholesterol levels at age fifty distinguish the men who lived to ninety from those who died before eighty. The estimated age of death of the fifty-eight Grant Study men with cholesterol levels below 206 mg/dl was eighty-three. The estimated age of death of the fifty-seven men with cholesterol levels over 254 mg/dl was eighty-one, which was not a statistically significant difference. This finding has been confirmed by much larger and more representative studies.
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It’s situations like these that persuaded me to include my experiment with the Boston Museum of Science computer—not as entertainment, but as an alert. To understand longevity we need longitudinal images, not snapshots. The more sacred our cows, the more they need longitudinal testing. This is one of the ones we were able to test.

Bleak childhood.
Alas, we cannot choose our families. Without asking permission they endow us with their genes. They also bathe us in their warmth and riches—or parch us with emotional and financial poverty. Many aspects of childhood are important to aging, as I’ve described in
Chapter 4
. But most of them do not predict length of life. Parental social class, stability of parental marriage, parental death in childhood, and IQ (at least in our samples with their two different but limited ranges) were not important to longevity. The men from the
warmest
childhoods lived only a year and a half longer than the men from the bleakest childhoods, a difference that was not statistically significant.

Vital affect and general ease in social relationships.
These were the two personality traits most highly valued by the original Study investigators, and for the Harvard cohort, they correlated highly with good psychosocial adjustment in college and in early adulthood.
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But they, too, failed to predict healthy aging.

CONCLUSION

After seventy-five years of collecting, analyzing, and reanalyzing our data on aging, what have we learned from all this? First, we’ve been reminded again and again that a strong association does not necessarily imply cause. Snow is associated with winter, but snow does not
cause
winter. Heavy smoking is strongly associated with fatal automobile accidents, but not because drivers take their eyes off the road to search for the cigarette lighter. The association is the result of a third factor—alcoholism, which very significantly increases the likelihood both of heavy smoking and of fatal accidents.
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The seventy-year duration of the Grant Study have been invaluable in allowing us to draw lines between causes and associations.

For example, there is a strong association between exercise and physical health, which most of us understand to mean that exercise causes good health.
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But might it not be the other way around? Healthy people enjoy exercise. Among the College sample, exercise at age sixty correlated more highly with health at age fifty-five than with health at eighty. Health at fifty very significantly predicted exercise at eighty, and health at sixty significantly predicted exercise at eighty. In
other
words, health predicted exercise at all ages, but exercise did not predict health in later years.

Admittedly, exercise at age thirty did significantly predict health at fifty-five and sixty, and exercise at sixty predicted health at age seventy through eighty-five, although not significantly. Presumably the exercise mavens must not be written off entirely. But it’s important to keep in mind—as the Museum of Science computer didn’t—that everything affects everything else, and that some things are horses and others are carts. When it comes to physical aging, alcohol abuse and education are looking more and more like horses. And, as
Table 7.3
documents to my sorrow, after thirty years of betting the farm that maturity of defenses (the involuntary coping mechanisms that I’ll discuss in the next chapter), would be the horses that pull us to late-life physical health, longitudinal study has proved me wrong. He who lives by the sword dies by the sword.

Social supports are often assigned a causal role in successful aging. In his classic review of the evidence, however, sociologist James House acknowledged that almost no attention has been paid to social supports as a dependent variable.
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That is, social supports may be the result of the very variables that they are supposed to be causing. In the prolonged prospective view of the Grant Study, social supports at age seventy were strongly associated with the pre-age-fifty protective health factors identified in
Table 7.2
, yet only weakly associated with longevity (
Table 7.3
). In other words, good health predicts good social support better than good social support predicts future health. Indeed, good social supports in old age may be in large part a result of earlier habits that preserve physical health.
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