In the eighteenth and nineteenth centuries, a common form of self-help manual was the so-called home medical companion. In many households, such a volume was kept on the shelf alongside a book consulted only slightly less frequently, the family Bible. Perhaps the best known and certainly the longest-lasting of these home therapy tomes was William Buchan’s Domestic Medicine, published in Edinburgh in 1769 and reprinted in scores of English and American versions. But my favorite of the genre, largely because of its title and the fact that it was the first of its kind produced in the United States, is a monograph written in 1734 by a Tidewater physician named John Tennant, entitled Every Man his own Doctor. This little handbook’s subtitle described the text’s purpose: Prescribing Plain and Easy Means for Persons to cure themselves of all, or most of the Distempers, incident to this Climate, and with very little Charge, the Medicines being chiefly of the Growth and Production of this Country. If we are to assume the job of the body’s maintenance ourselves, we can do no better than to use Tennant’s title as an inspiration, for surely every man and woman can be his or her own doctor, in the sense of being the maintenance person who takes over the responsibility at which nature becomes less adept as the sixth and seventh decades approach. Certainly, the kinds of habits and behaviors that will make such a difference in the quantity and quality of our lives conform in large portion to the criterion of being “Easy Means for Persons to cure themselves of all, or most of the Distempers, incident to this Climate, and with very little Charge.”
In thinking about the ways in which personal behavior may influence the rate and degree of aging, it is useful to have some idea of the machinery itself, and the extent to which the passage of years is likely to affect individual parts of it. Though it has been emphasized that normal aging is not a disease, aging must nevertheless be seen as that long continuum whose eventual culmination is the disease that leads to death. The goal of an optimal lifestyle is to so slow down the process of this gradual change—the journey along the continuum—that reaching the threshold into sickness is long delayed.
Like all other generalized words, “aging”—whether in animals or man—is difficult to define with specificity. Nevertheless, all gerontologists—the scientists who study it—would agree that it is most usefully described as the process by which a healthy individual of any species gradually deteriorates into one that is frail, one whose bodily capacities and reserves are constantly diminishing at an ever-increasing rate, and one who is therefore becoming more and more vulnerable to disease and ultimate death. Though the tone of such a generic description sounds gravely pessimistic, what is actually experienced in the aging of human beings need hardly be so grim. The fact is that so little is yet known about the totality of factors that affect aging in any specific man or woman—not only with respect to organs, tissues, and the entire body, but even on the cellular and molecular level—that it is not at all clear that the progression is as relentless as such a generalized description makes it sound. Quite the contrary: Observations of large cohorts of older men and women provide strong evidence that the course of aging in humans is susceptible to modifying influences, some of which are within the control of each of us.
One of the reasons for the unpredictability in any individual human being is that so little is known about the interrelationships between the inherited genetic contributions to aging and those contributions that are either environmental or the result of what might be called an attitudinal response to the passing years. By this latter is meant that society has traditionally harbored lower physical and mental expectations for people older than sixty. In such an atmosphere of presumed decreased prospects, inactivity and sedentary habits become the norm, leading to a downward spiral of disuse and neglect of the very organ systems whose vibrancy is so necessary if debility and sickness are to be staved off. The consequence is deterioration into such problems as obesity, osteoporosis, hypertension, and chronic symptoms requiring drug therapy. Paradoxically, the very pharmaceuticals meant to mitigate debilitation may have side effects that in themselves lead to further decline. The interdependence of these four factors—normative genetic aging changes, disease, environmental influences, and decreased expectations resulting in inactivity of body and mind—are so complex that it is difficult to know what degree of influence each has as an independent variable. In any given man or woman, one or two of the factors may far outweigh the others. From numerous studies, it has become well known that higher activity levels correlate well with longer life spans. So much for the immutability of aging.
Even the seemingly inevitable normative—and genetically determined—aging deteriorations appear less inevitable when they are closely examined. Such changes are in certain ways susceptible to modification, in response to modifications in our daily lives, and here is how:
The accumulation of errors in the regulation of gene function does lie at the basis of that portion of the aging process that is strictly biological. Some of these errors probably occur because they are predetermined by inherited controlling mechanisms—what might be called a “genetic tape”—that begins to run at conception and ends at death. Others are due to wear-and-tear factors in the environment within and around the cell as well as the environment within and around the entire body—such as diet, ultraviolet radiation, air pollutants, absorbed toxins like nicotine, and, very likely, stress. And, of course, time itself takes a toll. There is the decreasingly efficient removal from within the cell of toxic by-products of the cell’s own metabolism; the cumulative oxidizing damage caused by the infamous free radicals; the occurrence of so-called cross-links between protein molecules that make them less flexible; the progressive collection of the yellow-brown pigment called lipofuscin within cells; the gradual aggregation of clumplike protein material, such as amyloid, in the extra-cellular fluid—and there are others. Such wear and tear affects not only genes, but protein molecules, biochemical interactions, and general cellular and organic function. To varying extents, we have some control over them.
Within each of our approximately seventy-five trillion cells, mechanisms exist to correct these errors as they occur, whether the errors are caused by relentless rolling of the genetic tape or by wear and tear. The longevity of any of us is largely determined by the ability of such cellular corrective mechanisms to counteract the baleful influence of time on our genetic functioning. But these mechanisms decline with age. As noted earlier, some of us are hereditarily better gifted for longevity than others, but all of us could be capable of helping our hereditary predisposition if only we knew how. Some of the “hows” that lie within the ability of all of us are well known. They consist of those lifestyles and environmental factors that maximize the cell’s genetic battle against progressive deterioration. This means that we do have some control even at the level of our deepest biology.
One of the striking findings of research into the aging of the various organ systems of our bodies is the extreme variability between individuals. The brain, the liver, or the immune system, for example, of two people of the same age are often vastly different, with one person seeming much older than the other—much further along the continuum toward disease and death. Much of the difference is due to an inherited ability to recover from the various accumulated injuries to genetic integrity, but some of it is caused by the way an individual has lived his or her life, the environment in which one’s life has been lived, and the attention paid to a healthy lifestyle—the amount of wear and tear, in other words. It is at the cellular and genetic level that we begin to find the way toward increased healthy longevity—but the cellular and genetic are influenced by the factors we encounter every day: diet, exercise, exposure to noxious agents, medications, and the like.
One example of the great individual variability of response to aging is found in the immune system, the body’s complex of mechanisms that not only ward off infection but also play a large role in responding to the various agents that may cause cancer and autoimmune processes like rheumatoid a
rthritis and certain bowel diseases. Though the majority of the elderly have immunity that is 30 to 50 percent less than that of the young or middle-aged, some older people are able to mount an immune response almost as effectively as those much younger. Much of this responsiveness or lack of it is related to a person’s general state of health, including such factors as nutrition, smoking, alcohol consumption, and environmental pollutants. The presence of intercurrent disease—what physicians call comorbidity—is also a factor, as are drugs and other medications used to treat it. So important are such influences that the ability to respond to assaults on the immune system is a good indicator of one’s general state of health. The better shape we are in, the less prone we are to the condition that gerontologists call “immunosenescence”—senility of the immune system. The root sen is derived from the Latin senex, meaning “old man.” No one wants to let his or her immune system become an old man.
Of all the parts of our bodies, the one in which the “let” of the previous sentence is most operative is surely the brain. The new research in neuroscience is demonstrating the remarkable ability of the human brain to influence its own aging. As astonishing as such a statement might at first seem, there is ever-increasing evidence of its validity, based not only on studies of cognition and behavior, but on equally revealing investigations into the structure and functioning of nerve cells, synapses, and the myriad networks of communications between far-flung parts of the central nervous system. Not only that, but the concept of mind—long a notion left for the most part to the ruminations of philosophers—is emerging as the object of scrutiny in the laboratories of our most talented scientists. It is no longer enough to conceive of mind as a function only of the brain; it must be thought of as influenced by the very factors that it has long been recognized to influence, namely, the body and our perceptions of the environment in which we find ourselves. In other words, the reciprocity of communication among the brain, the body, and what has been called “the econiche” in which we are situated determines the vast range of impressions and responses that go into the entirety of mind. As we mature, our exchange with the econiche becomes gradually more sophisticated, and the tree of knowledge and experience arborizes into a vast superstructure containing increasing numbers of reference points upon which incoming new material can adhere; the older brain is a huge and wide-ranging repository of information to which additional information is widely admitted because there are so many more points of entry as time passes and learning continues. In these ways, mind is often able to compensate for any organic capacity to perceive, learn, integrate, and use information that may be lost with advancing years. Brain may age, but mind continues to grow. Used well, an aging brain can become a more useful brain, and often a wiser one.
There can be no doubt that some organic capacity is indeed lost because of aging, but—assuming the absence of neurological or other comorbidity—such losses appear to be less than has long been presumed. There is unquestionably an approximate 5 percent decrease in brain weight and volume every ten years beyond the age of about forty, but some areas are relatively invulnerable to tissue loss. Because so much of the weight and volume loss consists of supporting tissue and the insulation around nerve fibers, rather than the cells’ bodies, the meaning of the 5 percent figure is obscure. What is of realistic importance is not loss of substance in the sense of tissue but loss of substance in the sense of functioning. For this reason, the following discussion focuses on how the aging brain works rather than on which of its parts change in volume.
The fact is that modern methods of counting nerve cells (also called neurons) show no definite evidence of any but perhaps minimal age-related loss, except in the hippocampus—an area involved in emotional expression, learning, and memory—and selected locations in the cortex (the prefrontal and temporal-association areas), and only in certain parts of even these. In other words, the total number of brain cells in healthy older people decreases only slightly. But quality may influence these cells’ effectiveness as much as quantity does. Like all other cells, those of the aging brain have been undergoing damage to proteins and metabolic processes throughout a long lifetime, as well as some slowing of cerebral blood flow. Decreased blood flow results in decreased metabolism of the oxygen and glucose so important in providing for the brain’s enormous energy needs. It is likely that any losses in cognitive function are due to deficiencies in chemical neuro-transmission rather than to any decrease in the number of neurons.
The cumulative result of such processes is lessened function, but the amount of lessening is so variable among individuals that it ranges from inconsequential to clinically troublesome. Among the several reasons why it may be inconsequential is redundancy, by which is meant that there is so much extra brain tissue that loss of some of it is without effect on function or intellectual capacity, since there are plenty of other nerves and fibers left to do the job. In addition, the same message may be transmissible over several distinct neural pathways, so that the loss of one of them merely means that a different course will be used thereafter.
Synapses are the connections between the fibers (called axons and dendrites) that extend from the bodies of nerve cells. Messages are carried across synapses—and therefore from one neuron to another—by means of chemicals called neurotransmitters. The cortex, the brain’s convoluted outer mantle that does our thinking, contains some thirty billion nerve cells, and one million billion synapses by which these nerve cells interconnect with one another in myriad ways. The aging brain may have decreased numbers of synapses in some areas, but this is compensated by such factors as plasticity: the ability of synapses to become stronger and therefore more effective, to proliferate when required by neural activity, to enlarge in size, and to change configuration in response to altered patterns of usage. Loss of synapses in some areas is accompanied by no such loss in others, and is accompanied in some places by an increased number. In this as in so many other ways, the brain is always changing.
This ability to change is also demonstrable in the case of neurotransmitters and the receptors on the surface of nerve cells onto which they attach. While some neurotransmitters and some receptors decrease with age, others increase, with the result that certain cerebral functions may be lessened, certain may be heightened, and certain may remain unaffected. Also, cell loss is at least in part compensated by the production of new cells, as has been discovered only in the past decade. Prior to this discovery, it was believed that no such process was possible in the central nervous system.
The result of the competing and balancing influences of gain and loss manifests itself in how effectively the brain functions in any given individual. The following paragraphs should be considered a general summation of what occurs in normative healthy aging, realizing that variability is so great that far more than a few older men and women continue into extreme old age with minimal or even no demonstrable loss of cerebral ability.
It is true that learning is somewhat slower, and the amount learned with the same effort and exposure lessens, as the later years progress. But the ability to assimilate information and to learn from experience does not change appreciably. Perhaps as important to acquiring new knowledge, attention does not become impaired. Though verbal abilities do not decrease, creative thinking and problem-solving abilities slowly decline. This means that intellectual quickness and on-the-spot reasoning slow; mental agility is the province of the young. As Sir Francis Bacon put it three centuries before brain scanning had become so much as a possibility on the horizon, “Young men are fitter to invent than to judge, fitter for execution than for counsel, and fitter for new projects than for settled business.”
Not only is intellectual quickness impaired with aging but so is reaction time. Aging increases reaction time because the process of cognition—the awareness and instantaneous processing of information—is somewhat slowed, as is the peripheral motor response to stimuli. Ordinarily, these changes are perceptible only under conditions of immediacy, but m
odern living means that immediacy is everywhere, and especially behind the wheel of an automobile going seventy miles an hour in a rainstorm at night. As drivers get into their seventies and beyond, they should choose their traveling times and conditions with increasing circumspection.
The cognitive complaint most often made by or about older men and women is loss of memory. Though long-term memory (and sensory memory too, of smells, tastes, and sounds) is not significantly disrupted—nor is vocabulary and the general store of culture- and education-based information—short-term memory is more likely to become a problem, even under the physiological conditions of healthy aging. And yet, some nonagenarians continue with memory so unimpaired as to be comparable to that of a young adult. Such a circumstance is usually the reflection of a general state of cerebral function that has remained at a high level for all parameters of activity.
At the beginning of this discussion, reference was made to the brain’s ability to influence its own aging. The evidence for this comes from several disparate sources. One source of evidence is the observation that the frequency of Alzheimer’s disease and other dementias appears to be somewhat less in people who have pursued an active intellectual life. Another source of evidence is the discovery in the laboratory of a class of protein substances that have the ability to protect neurons against injury and death, as well as the ability to stimulate the production of new neurons from adult stem cells in the brain. It has been demonstrated in cell culture and in rodents that the production and effectiveness of these protein substances, called neurotrophic (nerve growth) factors, is determined by the amount of activity going on in nearby neural circuits; the more the circuits are used, the more neurotrophic factor is produced. This means not only that lost, damaged, or impaired nerve cells can be replaced, but also that an increased population of new nerve cells may occur in certain locations in the brain. It is now clear that there is a demonstrable biochemical reason—the increase in various neurotrophic factors, which are a result of increased cerebral activity—why using our brains is likely to increase the number and effectiveness of neurons. This evidence substantiates the everyday observation that those who continue to challenge themselves intellectually are likely to be those who maintain the capacity to do so.
The Art of Aging Page 3