How it went to pieces all at once,
All at once, and nothing first,
Just as bubbles do when they burst.
The wonderful one-horse shay is the perfect image of an optimistic hope about aging: a long, healthy existence followed by an abrupt end of life, with no decline. The one-horse shay image also suggests that life has a built-in “warranty expiration” date. But where does this limit on longevity come from? Is it possible to extend life beyond what we know? The living organism with the longest individual life span is the bristlecone pine tree found in California, more than 4,500 years old, with no end in sight.
The maximum human life span appears to be around 120 years. In fact, we have no valid records of anyone living much beyond that length. There have been claims of people living to the advanced age of 150 or even longer. Some claims have persuaded the National Enquirer, and others even convinced a scientist at Harvard Medical School. But whatever the Enquirer or Harvard scientist wanted to believe, there has never been proof of such longevity. Quite the contrary. Despite the fact that we have millions upon millions of verified birth records in the 20th century, until recently, there were no proven cases at all of any human being living beyond age 120. Then, in 1995, a Frenchwoman named Jeanne Louise Calment did just that, before dying in 1997 at the documented age of 122 (Robine, 1998). Madame Calment actually remembered seeing Vincent van Gogh as a child!
Some scientists argue that even the idea of maximum life span is based only on empirical observation. With biological breakthroughs in the future, might we someday surpass that limit? Indeed, optimists ask, why settle for the one-horse shay?
On the face of it, prolonging the human life span sounds good. But is it feasible? Will it make our lives better? One cartoon in The New Yorker shows a middle-aged man at a bar complaining to his companion: “See, the problem with doing things to prolong your life is that all the extra years come at the end, when you’re old” (Mankoff, 1994). Another cartoon depicts two nursing home residents in wheelchairs confiding to each other: “Just think. If we hadn’t given up smoking, we’d have missed all this.”
These cartoons point to the fact that often the consequences of biophysical aging appear well before reaching maximum life span. Some observers believe that the proper aim of medicine should therefore be to intervene, perhaps even to slow down the rate of aging, so that more and more of us can remain healthy up to the very end of life. At that point, the body would simply “fall apart” all at once, like the wonderful one-horse shay (Avorn, 1984). This view, mentioned earlier, is known as the compression of morbidity, an idea developed and promoted by James Fries (1988, 2004).
The compression-of-morbidity hypothesis looks forward to greater numbers of people who postpone the age of onset of chronic infirmity (Brooks, 1996). In other words, we would aim for a healthy old age, followed by rapid decline and death. Sickness or morbidity would be compressed into the last few years or months of life. But things don’t always work out that way. We may succeed in postponing deaths from heart disease, cancer, or stroke. But what happens if we live long enough to get other diseases? The same preventive measures can have, as an unintended result, increased rates for chronic conditions such as dementia, diabetes, hip fracture, and arthritis (Roush, 1996). Many observers worry that as increasing numbers of people live to advanced ages, the challenge of compressing morbidity will become more and more difficult. One study of mortality did find some evidence that survival curves became more rectangular—that is, deaths became concentrated around a point later in life (Nusselder & Mackenbach, 1996), and a comprehensive review of over 30 years of research suggested that disability levels decreased every year from 1982 to 2004 (Fries et al., 2011), but other studies have found the opposite. Investigators such as Eileen M. Crimmins and Hiram Beltrán-Sánchez (2011) have found that the length of life with disease and limited mobility had increased between 1998 and 2008, a trend that does not support the idea of compression of morbidity. In addition, there is increasing evidence of social inequalities in longevity and the potential for experiencing a healthy old age; gender, ethnicity, and socioeconomic status are interconnected factors to consider in the compression-of-morbidity discussion (Olshansky et al., 2012).
It is important to distinguish here between life expectancy and maximum life span. Life expectancy, or expected years of life from birth (or any other age), has mostly risen, but life span, which is defined as the maximum possible length of life, has evidently not changed at all. As mentioned earlier, to the best of our knowledge, no human being has ever lived beyond 120 years or so. The causes of maximum life span and of aging itself still remain unknown. Biological evidence suggests that maximum life span is genetically determined, and therefore fixed, for each species. Another important idea related to life expectancy and aging is referred to as disability-free or active life expectancy, the number of years an individual can expect to live beyond age 65 without significant functional impairment due to disability or chronic illness (Cherlin, 2010; World Health Organization, 2015).
With this concept of life span limit in mind, compression-of-morbidity is attractive because delaying dysfunction would enhance the quality of life, extend life expectancy, and reduce health care costs (Butler, 1995). A compression-of-morbidity strategy would move life expectancy closer to the hypothetical upper bound of maximum life span. Instead of expecting to live only to age 85, people who reach 65 could expect to become centenarians, yet in good health nearly to the end of life (Fries et al., 2011).
Such a gain in active life expectancy—or health span—would have dramatic consequences for our society. To judge whether this strategy for compression of morbidity is feasible, we need to examine in more detail what is involved in normal aging. We need to understand what is known about the biology of aging and what may be discovered in the future.
The Process of Biological Aging
In favorable conditions, a human being can live to around a hundred years old: A few live a bit longer than that, but not many and not for much more. Why is that? We don’t live to be a thousand years old, and, unlike some species, we don’t live only a few months. Why is that? Why a hundred years and not a few months or many centuries? This is a basic question about the process of biological aging.
Normal biophysical aging, also called senescence, can be defined as an underlying time-dependent biological process that, although not itself a disease, involves functional loss and susceptibility to disease and death. One way to measure susceptibility to death is to look at death rates. For contemporary humans, these rates double every 8 years. This pattern is known as Gompertz law (Kowald, 2002). In other words, a 38-year-old is about twice as likely to die as a 30-year-old, a 46-year-old is four times more likely to die than a 30-year-old, and so on. At any given age, there is an important gender difference: Although men and women age at the same rate, women at every age are less biologically fragile than men—contrary to what our cultural stereotypes might suggest. However, as we will discuss later in this book, there are disparities between women and men when it comes to patterns of chronic illness, disability, and active life expectancy.
Studies of different species of organisms show that aging is almost universal, but the causes of aging are complex. For instance, among animals whose body mass and metabolism are comparable, the rate of aging varies greatly (Olshansky & Carnes, 2002). Consider the differences in maximum life span among some familiar animal species shown in Exhibit 1.
The rate of aging can be correlated, in a general way, with the amount of time it takes for the mortality rate of a species to double. The doubling time is around 8 years for humans today, but only 10 days for a fruit fly and 3 months for a mouse. In rough terms, we can say that a mouse ages at around 25 times the rate of a human being.
What accounts for these clear differences in rates of aging and life span across species? Comparative anatomy—the study of the structure of different species—generates some insights into this question. For example, among mammals and other vertebrates, an increase in relative brain size is positively related to an increased life span. Other factors correlated with life span are lifetime metabolic activity, body size, body temperature,