Aging and the Aged: II. Life Expectancy and Life Span

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II. LIFE EXPECTANCY AND LIFE SPAN

In the United States in 1900, the average life expectancy (also referred to as longevity) of a newborn baby was 47.7 years—46.4 for males and 49.0 for females. By 1990 the average life expectancy increased to 75.4 years—78.8 for females and 72.0 for males. Why did life expectancy increase so rapidly in the twentieth century, and what are the prospects for increasing it further? Perhaps more important, has the overall health of the population improved or worsened during this transition, and what are the health consequences of further increases in life expectancy?

The measure of life expectancy at birth is a statistic that represents the expected duration of life for babies born during a given time period, usually one calendar year. Calculated from death rates observed at every age, it is based on the critical assumption that the age-specific risks of death observed during a given year will prevail for all babies born in that year, for the remainder of their lives. In contrast, life span is the theoretical upper limit to life that would be observed if everyone in the population adopted ideal lifestyles from birth to death and if external threats to life were eliminated. Some researchers believe that there is no biologically determined life span per se (Carey et al.), but rather a series of time-dependent physiological declines that may eventually be subject to modification.

Life expectancy in the developed nations increased rapidly during the twentieth century because of rapid declines in death rates (usually expressed as the number of deaths per 100,000 population over one year) at younger and middle ages. This transformation in death rates, which has occurred to some extent in every nation, is referred to as the epidemiologic transition (Omran). During this transition, death rates from infectious and parasitic diseases, which tend to kill at younger ages, decline rapidly and the saved population lives to older ages, at which they are exposed to aging-related disorders such as vascular diseases and cancer. Although a small fraction of the population has always survived to older ages, the epidemiologic transition allows over 90 percent of all babies born to survive past the age of sixty-five. The redistribution of death from younger and middle ages to older ages is a general characteristic of the epidemiologic transition, although varying degrees of decline in death rates are experienced by different nations and subgroups of populations within nations.

Mortality Transition Patterns

There are two interesting patterns in the epidemiologic transition of the United States. In 1900 the average life expectancy for women was 2.6 years greater than that of men. By 1990 this difference had increased to 6.8 years. Although the increasing gender gap in longevity is attributable to more rapid declines in death rates for women at every age and for most causes of death, it is unclear why the mortality transition of women has proceeded at a faster pace than that of men. The prevailing explanation for the widening gender gap in life expectancy in the twentieth century is a combination of lifestyle characteristics among men that make them more prone to vascular diseases and cancer, and, with extended longevity, the increased expression of genetic differences.

Another interesting pattern in the U.S. mortality transition is the difference observed in historical trends in longevity between blacks and whites. In the early part of the twentieth century, the expectation of life at birth was lower for blacks than for whites by about ten years because blacks had higher death rates than whites. The difference in death rates between blacks and whites is thought to be due to a combination of biological, social, and environmental factors, but scientific studies to date have not adequately determined the relative importance of these factors. In the later twentieth century the racial gap in longevity was reduced to seven years. This indicates that the mortality transition for blacks was faster than that of whites—particularly for black females. However, it is important to remember that because blacks had considerably higher mortality at most ages than whites early in the century, larger reductions in death rates were required for blacks to close the racial gap in longevity.

An interesting aspect of racial trends in longevity is that at older ages (i.e., at ages seventy and older), the death rates for blacks in 1995 were lower than those of whites. This is caused either by poor data quality, resulting in an underestimation of old-age mortality for blacks, or by selective survival, in which only the most robust segment of the black population survives to older ages. Also interesting is the trend since 1984 toward declining life expectancy for blacks, while life expectancy for the rest of the population continues to increase. This unexpected trend is a direct result of increasing death rates for blacks between the ages of fifteen and forty-four—a product of higher mortality from accidents, homicides, and AIDS.

Extending Life Expectancy

The prospect for increasing life expectancy further is a subject of intense scientific debate. Projections of life expectancy can have a significant influence on anticipated changes in social programs, such as Social Security and Medicare, that are influenced by the future size and health status of the older population. Some scientists have argued that life expectancy at birth for humans cannot practically exceed about eighty-five years (Olshansky et al., 1990). This conclusion is based on the facts that (1) survival up to and beyond the age of 110 is as rare in the early twenty-first century as it has always been; (2) the rapid increase in death rates from aging-related diseases that begins in the second decade of life has not changed in recorded history—instead, death rates have shifted down at comparable rates for most age groups; (3) the reduction in death rates required at every age to increase average life expectancy at birth to eighty-five years is extremely large—in fact, larger than what would occur with the elimination of cancer and heart disease; and (4) life expectancy has been shown to be a demographic statistic that becomes less sensitive to declining death rates as it approaches higher levels. Taken together, these facts point clearly to the difficulty in achieving the reduction in death rates required to increase life expectancy past eighty-five years.

Other researchers have argued that theoretically, average life expectancy at birth could reach 100 years (Manton et al.; Ahlburg and Vaupel). Several conditions are required for this to occur. Under one scenario, everyone in the population would have to adopt an "optimal" risk-factor profile, maintain their physical functioning throughout life, retain the risk-factor status of a thirty-year-old for the duration of life, and respond in the same beneficial way to a fixed regime of risk-factor modifications (Manton et al.). This means that everyone would have to eliminate behaviors such as smoking, drinking, and overeating, and somehow avoid the health problems, such as arthritis and sensory impairments, that now tend to compromise physical functioning in older ages.

In a second scenario, a life expectancy of 100 could be achieved if death rates declined by 2 percent at every age for every year for the next century (Ahlburg and Vaupel). Recent evidence indicates that mortality declines of this magnitude have been rare in the historical record of the United States (Olshansky and Carnes), and that such models lead to death rates that are inconsistent with evolutionary theories about the onset and progression of death rates from aging-related causes (Carnes and Olshansky). It is doubtful that either of these scenarios is practicably achievable, although they do represent laudable goals for healthcare planners.

Effects of Extended Life Expectancy on General Population

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 of aging (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.

The Impact of Science on Life Expectancy

Population aging also has implications in the context of human evolution. Scientists in the field of evolution biology have hypothesized, in nonhuman species, a link between reproduction and the rate of senescence (Finch). Although it is unlikely that the physiological mechanisms regulating human reproduction will be altered intentionally to postpone senescence, it may eventually become possible to manipulate the genome to achieve the same effect. In fact, the mapping of the human genome may eventually reveal these and other aging-related genes that could be manipulated by methods being developed in molecular biology. There is reason to believe that breakthroughs in this area are forthcoming and that by controlling genes that influence diseases of aging, it may become possible to allow more people to survive longer and healthier than is currently the case. Just how much longer and healthier people can survive through manipulating the genome is the subject of intense debate. It may also become possible to achieve increases in longevity by introducing pharmaceuticals that alter the environment in which the genome operates. One example is the effort to introduce into the human diet natural and artificial antioxidants (i.e., substances that reduce the amount of damage caused by the presence of free radicals, products of normal metabolism implicated in the aging process). The result may be a general deceleration of the entire aging process.

If methods of increasing human longevity are realized by manipulating the genome or introducing pharmaceuticals, then a new set of questions will arise: How would such developments influence the age structure of the human population and the social and economic institutions that have been developed under the assumption that human longevity is limited? These may prove to be a much more difficult set of problems than those we face today.

s. jay olshansky (1995)

bibliography revised

SEE ALSO: Autonomy; Death; Future Generations, Reproductive Technologies and Obligations to; Harmful Substances, Legal Control of; Human Dignity; International Health; Justice; Life, Quality of; Natural Law; Population Ethics; Right to Die, Policy and Law; and other Aging and the Aged subentries

BIBLIOGRAPHY

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