Observing historical trends in mortality, and anticipating future improvements, raises the question of how the overall health of the population is influenced by these trends. From a historical perspective, there is little doubt that the thirty-year increase in life expectancy in the twentieth century was a result of trading one set of diseases and causes of death for another. The epidemiologic transition allowed much larger proportions of each birth cohort to survive to older ages, something that had never before been experienced by the human population. There is little doubt this was a worthwhile trade. Now that the focus of modern medicine is to attack the causes of death that were traded for earlier in the century, we are faced with the same sort of question: What do we get in return for reducing the risk of death from vascular diseases and cancer? This is a particularly interesting question, since successful efforts to reduce the death rate from fatal diseases will produce much smaller gains in life expectancy than those achieved in the twentieth century, when primarily the younger population was saved from early death.
This question of how future declines in old-age mortality will influence the health status of the population is also an area of intense scientific debate. The debate is framed around what is generally referred to as the expansion versus compression of morbidity hypotheses. Those who follow the compression-of-morbidity hypothesis believe that improved lifestyles and advances in medical technology will postpone the onset of disease to older ages, thus compressing the period of disease and disability into a shorter time before death (Fries). With this hypothesis the critical assumption is that both fatal diseases, and nonfatal but highly disabling age-dependent diseases, will simultaneously be postponed and compressed against a biologically fixed and immutable upper limit to life.
The expansion-of-morbidity hypothesis, however, points out that factors that are known to reduce the risk of death from fatal diseases do not alter the age at onset or progression of the most debilitating diseases of old age, such as Alzheimer's disease and hearing and vision loss. Further reductions in old-age mortality from present levels are therefore hypothesized to allow much larger segments of the population to survive to the oldest ages (over eighty-five), where the risk of age-related disabling diseases is particularly high and currently immutable (Verbrugge; Olshansky et al., 1991). The empirical data used to test these competing hypotheses indicate that morbidity and disability may in fact be declining for those under the age of eighty-five, but after that age the risk of disability and its duration appear to be increasing. However, it is not yet possible to draw definitive conclusions about these hypotheses because of deficiencies in the available data.
Is it possible to extend the human life span beyond early twenty-first century practical limits and achieve an increase in the duration of healthy life among the older population? Answers to these questions may be found in work under way in molecular biology. Based on a current understanding of the process of senescence, extending the human life span would require slowing down the aging rate itself. There is no definitive evidence at this time to indicate that the life span of humans can be modified by any means. However, there is suggestive evidence to indicate that dietary restriction could postpone many of the physiological decrements associated with aging—including those associated with both fatal and nonfatal diseases ofaging (Weindruch and Walford). Although it is not practical to expect that human experiments will be conducted on the longevity benefits associated with dietary restriction, or that enough people will actually restrict their diets to influence national statistics, research in this area may eventually reveal the underlying physiological mechanisms that link dietary restriction to increased longevity. In this way it may eventually become possible to imitate the effects of dietary restriction without actually altering diet.
Scientists debate these issues on scientific grounds, but there are important moral issues close to the surface in the discussions. For example, we know that a lower life expectancy observed among subgroups of the population is linked to poverty and minority status. If we are interested in preventing premature death, then social conditions may be a more direct target than efforts to manipulate the basic rate of aging. Also, the definition of "premature death" is no longer obvious, and raises questions about the value of length of life compared with quality of life when extreme longevity is also associated with the expression of frailty and disability.
Since societies do not have homogeneous views on these competing values, whose values should prevail? Further, societies almost always provide public support for infirm elderly people. How shall we value policies in the context of increasing life expectancy when many other social goods and needs are unfulfilled? This question is stated most clearly in the intergenerational equity debate. That is, should we be donating so much of our resources to the old when so many children live in poverty, when public schools are so needy? Some would argue that increasing longevity is a triumph of modern society, and if we work hard enough on prevention, we can eliminate old-age disability. But even for those who believe this is theoretically possible, it does not seem likely in the foreseeable future. Finally, the push toward increasing life expectancy raises fundamental resource-allocation questions for those concerned about the problems posed by global population growth. For example, it is inescapable that in the long run (i.e., beyond the middle of the twenty-first century), gains in longevity beyond those already expected will accelerate growth rates that, even at early twenty-first century rates of increase, will inevitably lead to a doubling of the size of the human population by the year 2050.
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