Copyright 1997 by
The Cerontological Society of America
The Cerontologist
Vol. 37, No. 2, 200-207
This article is about the few humans who reach very old ages — here called ''longevity
outliers." They are a distinct group, with lower mortality rates than most of the population.
Centenarians are human longevity outliers. They are more resistant to causes of death such as
heart disease and cancer than those who die at younger ages. Inheritance of life span, the
present condition of centenarians, and their causes of death are considered. The maximum
human life span in the future will be affected, at least marginally, as more longevity outliers
survive to challenge today's maximum of 121 years.
Key Words: Age 85 + , Causes of death, Circulatory diseases, Cancer, Longevity, Life span
Centenarians: Human Longevity Outliers
David W. E. Smith, MD 1
What is different about the relatively few humans
who become very old? First of all, they live longer
than most people in their cohorts, who predecease
them. They survive a variety of causes of death to
which most of their contemporaries succumb at
younger ages. For very old people in the United
States today, this included surviving infancy at a time
when the infant mortality rate was about 15% of
those born (15-20 times the contemporary infant
mortality rate in the United States), the infectious
diseases of childhood, the accidental deaths of adolescent and young adult life, the influenza pandemic
of 1918-1919, and tuberculosis, which was the most
common cause of young adult death early in this
century. They lived through a time when medical
practice did not have much to offer. For males it also
included surviving two world wars, and for females it
included surviving child bearing at a time when the
maternal mortality rate was nearly 100 times what it is
today. More recently it included living through the
heart disease, cancer, strokes, and pneumonia
which occur in adult life and continue into elderly
ages with mortality rates that increase with age.
The present article is based on the model of selection for survival, a model that has been described
before (e.g., Olshansky, 1995). In this model the
members of a population are selected for survival on
the basis of resistance to common causes of death.
The present article considers some characteristics
that allow the long survival of a few individuals.
How long must a human live to be considered one
of the very old survivors who are the subject of this
article? People 85 and over are now considered to be
the oldest old; however, according to modern standards, 85 is not particularly old. It is predicted that
20.7% of males and 40.2% of females born in 1990 will
live to be 85 (National Center for Health Statistics,
1994), and given the experience with life expectan-
1
Address correspondence to David W. E. Smith, MD, Department of
Pathology and Buehler Center on Aging, Northwestern University School of
Medicine, 750 North Lake Shore Drive, Suite 601, Chicago, IL 60611-2611.
200
cies in this century, these percentages will almost
certainly be exceeded (Smith, 1993). The mean life
expectancy today of women at age 65 is another
twenty years. Half of the women who are 65 today
will survive to 85.
According to the 1990 Census (Bureau of the Census, 1992), which is based on respondent-reported
age, there were 3.1 million people age 85 and over in
the United States, including slightly more than one
million 90 and over, 213,000 95 and over, 37,000 100
and over, and 6,259 who were 105 and over. There is
probably a tendency to exaggerate the ages of very
old people (Smith, 1993), and census counts of centenarians in the U.S. in the recent past have been
badly discredited. The census count of 1960 indicated 10,400 centenarians. The preferred estimate,
however, based on forward survival and population
reconstruction studies was 3,300. There were 106,000
people counted as 100 and over in the 1970 Census;
however, the age question was marked in error in
many census questionnaires because of easily misunderstood instructions. It is estimated that the actual number of centenarians was about 4,800. There
were 32,000 centenarians counted in 1980, but it is
estimated that there were actually about 15,000 (Metropolitan Life, 1987; Rosenwaike, 1985; Siegel & Passel, 1976). The census count for 1990 of 37,000 centenarians, however, is not considered to be as much in
error. Preliminary estimates are that the actual number was about 30,000. If the revised census estimates
are accepted, then note that the number of centenarians doubled in the ten years between 1980 and 1990.
The over-85 population grew by 40% during this
period. The U.S. population of all ages grew 10%.
Centenarians as Longevity Outliers
The mortality rates of many kinds of animals increase exponentially with age. The mortality rate
doubles within a time interval that does not change
through much of the life span, but which varies for
different species and populations. This is shown for
people in the United States in 1990 in Figure 1. It is a
The Gerontologist
plot of age against log mortality rate from ages 40-45
to 100 + . The exponentially increasing mortality rate
with age appears as a straight line in this plot. The
exponential relationship of mortality rate to age was
first described for humans by the Nineteenth Century English actuary Benjamin Gompertz. The mortality rate doubles with approximately each eight years
of age for humans in developed countries, from
post-adolescence to about age 85 (Finch, Pike, and
Whitten, 1990), as shown in the figure.
The two points in the figure corresponding to the
highest ages indicate an increase in the doubling
time of the mortality rate as age 100 is approached.
The mortality rate increases more slowly around age
100. There are studies of mortality rates past age 100.
One by Riggs and Millecchia (1992), based on death
certificates of the 9 million people who died at 85 and
over in the U.S. between 1956 and 1987 showed that
mortality rates after age 85 had a progressively longer
doubling time. The mortality rate reached a plateau
by 95, and by age 100 and over it actually decreased
with age. There was much scatter in rates beyond 110
because the number living to those ages was very
small. Data for males and females were similar, with
the changes in mortality rates for females occurring
at slightly older ages. In a study of English and Welsh
people who reached 100 in the 1960's, Barrett (1985)
found that mortality rates of males decreased with
age beyond 100. They continued to increase for females past 100, but with a progressively longer doubling time. In yet another study based on death
certificates of people reaching 100 in several developed countries, Kannisto (1988) found that mortality
rates continued to increase for both sexes past 100,
but the rate of increase of mortality rates slowed.
Kannisto doubted the United States data because
they showed an improbably large number of very old
people. This would result in mortality rates that were
erroneously low.
There is a study by Horiuchi and Coale (1990) of
populations of several developed countries that
shows that the mortality rate acceleration for females
slows after about age 75. This initially small slowing
effect is easily overlooked in plots like the one shown
in Figure 1.
The above-cited studies all found that very old
individuals have lower mortality rates than would
have been predicted for their ages if the model of
mortality rate that increases with the same doubling
time applied to the end of the human life span.
Consequently, there are more very old people than
would be predicted from the model.
We have coined the term 'longevity outliers" for
individuals who live to an age when the doubling
time of the mortality rate becomes longer (Smith,
1994) — to age 100 and beyond for the purposes of
the present article. The use of the statistical term
"outliers" in this case does not imply any percentile
of the starting population or any number of standard
deviations from the mean life span. It simply denotes
the occasional individual who lives for an unusually
long time for his or her population. There are analogous individuals among other species that live long
for their populations and must be considered longevity outliers (Smith, 1994). There is no model of
survivorship that accommodates all of the longevity
outliers (Wilson, 1994).
According to our concept, populations are heterogeneous to the end, with not just two kinds of individuals (i.e., outliers and non-outliers), but with a
large variety of individuals with many mortality rates
and a variety of mechanisms of resistance to causes
of death.
Explanation of the Relationship of Mortality Rate
to Age
5.000
Mortality rates that increase exponentially with age
are consistent with multi-hit mechanisms leading to
death (Strehler & Mildvan, 1960). For humans, hits
are deleterious events that advance the pathogenesis
of fatal diseases, which commonly have several
steps. The chance of accumulating the needed number of hits increases exponentially with time. Hits
result from both exogenous and endogenous risks.
There are thresholds, with multiple hits necessary
before a recognizable fatal disease appears. Some
individuals have resistance to hits that is endogenous
and commonly genetic, and some exogenous hits
can be avoided. Hits accumulate over time, and prolonged exposure to risk factors increases the number
of hits.
2.000
40
50
AGE
Causes of Human Death and Resistance to Them
Figure 1. Plot of age against log mortality rate. United States
data, 1990. This plot gives a straight line as the mortality rate
increases exponentially with age. Note that the final two points of
this plot do not fall on the straight line, but fall beneath it,
indicating that the mortality rate is no longer increasing exponential at the oldest ages. Sources: National Center for Health Statistics (1994); Bureau of the Census (1992).
Vol. 37, No. 2,1997
Diseases of the Circulatory System. — Diseases of
the circulatory system, which include ischemic heart
disease (heart attacks) and cerebrovascular disease
(strokes), are the most common causes of human
death in the United States. Most of those who prede201
cease centenarians die of these diseases. Longitudinal studies have clearly identified elevated blood
cholesterol and other lipids, certain patterns of lipoproteins (proteins that bind lipids) in the blood,
elevated blood pressure, male sex, diabetes mellitus,
and smoking as major risk factors in circulatory diseases. Other risk factors include sedentary lifestyle
and obesity (Hazard, 1987; Kannel & Brand, 1985).
As longitudinal studies show, the risk factors and
the hits they produce are predictive of circulatory
diseases during middle adult life, and most people
with substantial risks die well before the century
mark is reached. For example, mean blood cholesterol levels are higher in populations 50 years old
than those 70 and older, because most of those with
higher cholesterol values at age 50 are dead 20 years
later. In midlife, resistance to circulatory diseases is
related to genetically determined endogenous factors such as cholesterol metabolism and the avoidance of external risks such as smoking and dietary
excess.
Circulatory diseases are multi-hit diseases. Ischemic heart disease is based on atherosclerosis — it is
the development of lipid-containing lesions on the
inner surfaces of artery walls that progressively enlarge and obstruct the arteries. There are usually
multiple, independently developing atheromas, and
ischemic heart disease also involves artery obstruction by thrombosis.
The extent to which these same risk factors predispose to circulatory diseases late in life is a matter of
controversy (Hazard, 1987; Kannel & Brand, 1985).
There are a few individuals at advanced ages with
cholesterol levels as high as 50% above recommended values (Theiszen, Hixsom, Nagengast,
Wilson, & McManus, 1990). Survival to advanced
ages with high lipid values is sometimes familial. In
such individuals, resistance to circulatory diseases
must be based on something other than the inheritance of a healthy blood lipid pattern.
Diastolic blood pressure, like cholesterol values,
reaches its peak in middle adult life and plateaus.
Longitudinal studies indicate that most of those with
elevated blood pressure die at relatively young ages.
Systolic blood pressure continues to rise throughout
the human life span, and constitutes an increasing
risk with age (Kannel & Brand, 1985). Blood pressure
has inherited aspects.
Smoking is a voluntary behavioral risk factor in
circulatory diseases. It is also a risk factor for cancer,
and will be discussed below, under that heading.
Age-stratified mortality rates from diseases of the
circulatory system for most age groups have decreased during the last 25 to 30 years, to about half
their 1960 levels (Feinleib, 1984; Levy, 1984). Most of
this decrease has been attributed to lifestyle changes
— healthier diets, reduced smoking, and more exercise. An increasing proportion of the decrease is
attributed to interventions such as drugs that reduce
blood pressure and cholesterol levels and procedures such as coronary bypass surgery and cardiac
pacemaker implantation. The exposure to hits for
circulatory diseases is reduced compared to the past.
202
More people survive to the century mark because
they do not develop fatal diseases at younger ages.
Interestingly, the mortality rates for all circulatory
diseases combined and for ischemic heart disease
fell less for older than younger age groups and
scarcely fell at all for the open-ended age group of
100 and over.
Hits accumulate with time, and even those with
non-elevated blood pressure and cholesterol values
have exponentially increasing mortality rates from
circulatory diseases with age. The circulatory disease
mortality rate doubles faster than the mortality rate
from all causes. Consequently, circulatory diseases
constitute a progressively increasing percentage of
causes of death. In the end, despite the resistance to
causes of death that allowed centenarians to reach
their advanced age, circulatory diseases are indicated on death certificates as their most common
cause of death. Sixty-three percent of centenarians
were certified as dying from circulatory diseases in
1990. Resistance is only relative.
Cancer. — Mortality rates from all cancers combined and from cancer of most sites increase with
age to advanced ages — commonly the 80's or 90's,
and decline at greater ages, as shown in Figure 2.
These findings are based on vital statistics and census
data for 1990 (Smith, 1996). Decreases in rates of
cancer incidence are seen at slightly younger ages
(Miller et al., 1993), consistent with declining cancer
mortality rates at older ages. Cancer mortality rates
increase with age more slowly than mortality from all
causes or from circulatory diseases, and cancer
deaths are a progressively decreasing percentage of
total deaths with age. Nearly 40% of deaths at age 5069, but only 4% of deaths of centenarians, were
attributed to cancer in 1990. Mortality rates from
cancer of centenarians are commonly about half of
mortality rates at peak ages, as shown in Figure 2.
Breast cancer is an exception, with mortality rates
that continue to increase with age past age 100.
Biomedical science is beginning to identify alleles
that represent gene mutations that are commonly
associated with eventual cancer occurrence, and
there are other alleles that are associated with cancer
resistance. Some of the genes probably control steps
in the process of carcinogenesis (Vogelstein & Kinzer, 1993). The alleles may be inherited or may develop in single cells as somatic mutations. Family
history is sometimes predictive of eventual cancer
development, and there are exogenous risks like
smoking and occupational exposure to carcinogens
that are predictive.
Cancer results from a series of changes in a single
cell, and the multistage process of carcinogenesis is a
basis for the age-relatedness of cancer incidence and
mortality through most of the life span (Vogelstein &
Kinzer, 1993). The agents and conditions that facilitate the passage through these stages are the hits that
lead to cancer development.
The author's interpretation of decreasing mortality
rates for most kinds of cancer at advanced ages is that
The Gerontologist
2000
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50
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1
'
1
'
1
1
100
90
70
80
AGE
60
1
110
so
400
-*- COLON CAMCfll
- o - I R E A I T CANCCR. FEMALE
50
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60
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70
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80
AGE
1
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90
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100
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110
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100
110
Figure 2. Age plotted against log mortality rates from cancer. United States data, 1990. Plots are for all malignant neoplasms combined
(panel A) and cancer of several sites (panels B through D). Mortality rates generally peak before age 95. Sources: Center for Health
Statistics (1994); Bureau of the Census (1992); Smith (1996).
for most people, very old smokers must be resistant
to circulatory diseases by some mechanism. For most
people, however, resistance to death from smokingrelated diseases is based on the avoidance of risk
through choice of a nonsmoking lifestyle. The agerelatedness of mortality rates from cancer of most
sites cannot be related to a known risk factor like
smoking and lung cancer.
Unlike age-stratified mortality rates from circulatory diseases, the mortality rates from all kinds of
cancer combined have not decreased during the last
30 years.
survivors to these ages are relatively resistant to
cancer (Smith, 1996).
The decreasing death rate from lung cancer after
age 80-85 (see Figure 2) can be explained by tobacco
smoking carcinogenesis. Most smokers start at
young ages, and if the mean latent period between
starting smoking and death from lung cancer is about
40 or 50 years, it is not surprising that most smokers
are dead by 70, and that the mortality rate of lung
cancer peaks at 80-84. A few very old smokers who
did not die of lung cancer have been described,
including some centenarians (Pessah-Rasmussen et
al., 1990). Perhaps they were resistant to some aspect
of smoking carcinogenesis. These people also did
not die of circulatory diseases at younger ages. Although smoking is a risk factor in circulatory diseases
Vol. 37, No. 2,1997
Resistance to Other Causes of Death
Longevity outliers must survive all the causes of
death they encounter. The individual who is resistant
203
to cancer but who dies of another cause at a relatively
young age does not become a longevity outlier.
Causes of death include accidents, to which resistance may be more luck and care than anything else.
Causes of death have changed throughout history,
and the genes needed for resistance have changed.
For example, constitutional resistance to tuberculosis
was very important in the survival of today's centenarians when they were young, but because of public
health measures and the effective treatment of most
cases of tuberculosis, resistance to tuberculosis is
much less important to survival in the U.S. today.
There are fewer hits contributing to mortality than in
the past, and this trend will probably continue.
Causes of Death in Other Species
The consideration of comparative causes of death
is introduced here only to point out that ischemic
heart disease, cerebrovascular disease, and cancer of
many sites are largely unique as causes of death of
the human species. Other animals have other causes
of death (Smith, 1994), and longevity outliers of those
species must be resistant to different causes of death
than human outliers. For example, laboratory rodents commonly die of kidney failure, which is rarely
a cause of human death, in large part because of the
great functional reserve of the human kidneys. On
the other hand, most nonhuman species are resistant to human causes of death.
Inheritance of Maximum Life Span
Maximum life spans are inherited species characteristics. There are relatively long- and short-lived
species, with humans having the longest maximum
life span of any warm-blooded animal (Smith, 1993).
Within species there are more or less genetically
homogeneous strains that have characteristic
longevities. It has been argued that maximum species life span is not a valid concept, because the
maximum that is observed is a function of population
size (Gavrilov & Gavrilova, 1991). The larger the population, the longer the maximum life span that is
likely to be observed. Still, the maximum life spans
for species appear to approach limits (Finch & Pike,
1996). It must be conceded that the maximum life
span of humans will be longer than that of horses,
which will be longer than that of dogs, which will be
longer than that of mice, however large the populations that are eventually observed.
The evolution of the long human maximum life
span from the much shorter life span of a small
primate ancestor to more than a century is problematic. It is unknown what genes control the maximum
potential human survival or what forces of natural
selection resulted in their establishment as a species
characteristic, although there are some ideas (Smith,
1995a).
It is generally believed that the human life span has
strong hereditary components. ("If ye would live
long, choose well thy ancestors.") The best human
evidence for inheritance of the life span is families in
which some members die at young ages from spe204
cific genetic diseases or diseases that have hereditary
aspects. This kind of inheritance of life span has been
jokingly called "shortivity" (Editorial, 1987). The occurrence of ischemic heart disease in families is a
good example of the inheritance of shortivity (Goldbourt & Neufeld, 1986). Evidence for inheritance of
long life in humans is not impressive. The examination of family histories, insurance records, and the
longevities of both the parents and the children of
long lived individuals suggests a contribution of inheritance, but it is not large — about 10% of the
observed life span (Murphy, 1978). Part of the problem with these data is the changing causes of death
during recent history, as discussed above. Perhaps,
as succeeding generations die of the same cause,
evidence for the inheritance of long life will become
more impressive.
The Maximum Human Life Span
The longest human life span on record is presently
121 years. The record holder, Jeanne Calment, is still
living in France as of January, 1997. There is extensive
documentation of her age and her continuity of identity (Allard, 1993). Her birthday is in February. There
are records of a few other people who died between
110 and 120 years old that are generally accepted. A
few people are reported each year on death certificates (National Center for Health Statistics, 1994) and
in the popular press as achieving greater ages, but
these reports are not generally believed because
there is inadequate evidence of age. There were
probably a few centenarians even in the distant past,
but people surviving into their 70's and older were
considered to be very old at that time (Smith, 1993). If
some credence is given to accounts of centenarians
in earlier societies, then it appears that the maximum
human life span has increased much less than mean
life expectancies in developed countries. There were
more hits to be survived in the past to live 100 years,
but occasionally people survived them.
A quotation from the Bible seems apt in view of the
present record of human longevity. "And the Lord
said, My spirit shall not always strive in man, for he
also is flesh, yet his days shall be numbered at an
hundred and twenty years" (Genesis 6:3).
The Condition of Human Longevity Outliers
Much has been claimed recently in the popular
press and some scientific literature about the wonderful condition of those who reach 100. They have
outlived their contemporaries because of their "hardiness" and "robustness," and allegedly, they live
on in their good condition. This is usually not true.
National population data show that people at age 100
have a mean life expectancy between one and two
years (Barrett, 1985; Kannisto, 1988; Riggs & Millecchia, 1992). The probability of dying within a finite
period plateaus or decreases after age 100, but it is
very great. People who have reached 100 have a 1020% chance of living to 105 and less than a 1% chance
of living to 110. A more realistic view of centenarians
is that although they are longevity outliers, they are a
The Gerontologist
very heterogeneous group. Some reach 100 in a
moribund condition, with minutes, hours, or days to
live, and others will live a few more years.
In a study by Franke (1985) of 575 Germans at 100
years of age, the ratio of females to males was 4.0.
Twenty-nine percent were described as "Rustigen"
— robust, based largely on cardiovascular criteria.
The ratio of females to males in this category was 1.6.
There was an intermediate category of people severely restricted in activity, described as "housebound." This group contained 48% of the centenarians and had a female to male ratio of 2.4. Finally,
there was a category described as "bedfast" that was
23% of the total, with a ratio of females to males of
5.0. The data support the widespread belief that
although about four times more females as males
survive to 100, the male centenarians, on the average, are in better condition. Other authors have also
stated that only about a third of centenarians are in
good condition (Sansoni et al., 1993).
In considering mental function, there is a convergence of "normal aging" and dementia as age 100 is
approached. Psychometric norms lead one to expect
less and less with age (Schaie, 1989). Some orientation as to identity and situation and the preservation
of some social skills are common in centenarians,
but one does not expect much cognitive function by
age 100. Few of the centenarians fulfill the psychometric criteria for dementia of the Alzheimer's type,
but mental function is usually poor (Powell, 1994).
Neuropathologists also have a sliding scale, with
normal aging converging on the pathology of dementing conditions at advanced ages. Amyloid is
usual in the brains of centenarians, but its abundance does not correlate well with the psychometric
characteristics of dementia of the Alzheimer's type.
The correlation is better with neurofibrillary tangles,
which are more variable in their occurrence in centenarian brains. There are also vascular lesions and
atrophic changes that increase with age and are common in the brains of centenarians (Berg, McKeel,
Miller, Baty, & Morris, 1993; Delaere, Fayet, Duyckaerts, & Hauw, 1993).
Dementia, like circulatory diseases and cancer,
increases in incidence with age. Demented centenarians can be regarded as longevity outliers, because
they lived so long. Although their ages of onset of
dementia are not tabulated, these people survived
death at younger ages, which was the lot of most
people who developed dementing conditions.
Causes of Death of Longevity Outliers:
Death Certificates: True Senescence
What are the causes of death of longevity outliers?
As described above, 63% of death certificates of centenarians dying in 1990 indicated diseases of the circulatory system as the underlying causes of death, including about 10% who died of cerebrovascular
diseases. Four percent of deaths were attributed to
cancer, and about 10% were attributed to pneumonia.
In some cases the causes of death of centenarian
decedents were recognizable diseases, with clinical
evidence for the diagnoses. In other cases a cause of
Vol. 37, No. 2,1997
death was entered on the death certificate without
much evidence or by a physician without much
knowledge of the case. Most of the entries in the
International Classification of Diseases (ICD; World
Health Organization, 1977), which provides the
choice of entries that must appear on death certificates, are more useful for the cases of younger people. The younger patient is less likely to die in a
nursing home, the process that terminates in death is
more often recognizable, and the concept of a single
underlying cause of death may have more validity.
Terminally the heart stops beating, and this may
result in the attribution of some deaths to circulatory
diseases. Heart failure (ICD #428) is used to describe
5% of deaths of centenarians. The most common
attribution of circulatory diseases is acute or chronic
ischemic heart disease (ICD #410-414). Other diagnoses that might appear to be especially appropriate
for centenarians are little used, including senile and
presenile psychosis (ICD #290), 1 % of deaths; senility
without psychosis (ICD #797), 1 % ; and nonspecific
signs and symptoms (ICD #780-796, 798-799), 2%.
Autopsies were performed on only 1.9% of decedents 85 and over in 1990, and surely an even smaller
percentage of centenarians was autopsied. There are
several studies indicating substantial disagreement
between death certificate entries and autopsy findings of old people (Smith, 1993). Even autopsy does
not always ensue the finding of a cause of death. In a
study of 200 consecutive autopsies of decedents 85
and over, but including no centenarians, a cause of
death could not be found in 26% (Kohn, 1982). Lesions such as patches of pneumonia and aspirated
gastric contents were found in the lungs of some of
these people, but it is stated that these lesions would
not constitute causes of death in younger elderly
people. It was concluded that these old people are
more vulnerable to challenges than younger people,
because they are less able to compensate for or
survive the challenges. It is argued here that a characteristic of true senescence is the inability to maintain
homeostasis in the face of minor challenges. There is
no death certificate entry corresponding to failure to
maintain homeostasis. Heart failure, especially with a
history of heart disease, may describe failure to
maintain homeostasis, but, as stated above, it is not
commonly used in death certificates of centenarians.
Pneumonia (ICD #480-486) and septicemia (ICD
#038) can be consistent with the terminal breakdown
of homeostasis if the body cannot defend against
invasion by microorganisms. Dying of pneumonia as
the underlying cause of death is probably much less
common than dying with pneumonia, with the pneumonia representing the terminal event in some other
disease process.
The Future
It is widely agreed that the number and percentage
in the population of centenarians will increase. Recall that the number of centenarians doubled and the
number of people 85 and over increased 40% between 1980 and 1990. Future increases in numbers of
very old people will depend on public health and
205
medical advances that continue to reduce death
rates of those at younger ages. Elimination or postponement of one or more of the hits that contribute
to the exponentially increasing mortality rate with
age will allow more people to survive to greater ages.
Decreases of mortality rates from diseases of the
circulatory system during the last 30 years have been
described above, and there are reasons to expect this
trend to continue.
Predictions have been made of numbers of centenarians in the United States in the future. Predictions
for the year 2080 range from 1-2 million centenarians
(Metropolitan Life, 1987; Wade, 1989) to as many as
ten times that number (Vaupel & Gowan, 1986) if the
present growth rate of the centenarian population
continues.
Will two thirds or more of these people be sick,
bedfast, or demented, or will centenarians of the
future be in better condition? Will fewer hits result in
less morbidity as well as longer life span for an
increased number of longevity outliers?
What will happen to the maximum human life span
as it is known today, as perhaps 100 times more
people than today survive past the century mark, and
more people approach today's maximum of 121
years, to challenge that record? Although the maximum human life span may be approaching a limit,
the record will certainly be broken, at least marginally, based on the increased number of longevity
outliers in the future. On the other hand, is it possible that the American society of the future will be less
supportive of very elderly people than it is today, so
that the numbers of longevity outliers will not be as
great as predicted (Smith, 1995b).
References
Allard, M. (1993). About an exceptional duration of human life: The case of
J.C. The Gerontologist, 33 (Special Issue), 335.
Barrett, J. C. (1985). The mortality of centenarians in England and Wales,
Archives of Gerontology and Geriatrics, 4, 211-218.
Berg, L , McKeel, D. W., Miller, J. P., Baty, J., & Morris, J. C. (1993).
Neuropathological indexes of Alzheimer's disease in demented and
nondemented persons aged 80 years and older. Archives of Neurology,
50, 349-358.
Bureau of the Census. (1992). 7990 Census of Population, General Population Characteristics, Vol. CP-1-1. Washington, DC: U.S. Department of
Commerce.
Delaere, P., Fayet, C , Duyckaerts, C , & Hauw, J-J. (1993). A4 deposits are
constant in the brain of the oldest old: An immunocytochemical study
of 20 French centenarians. Neurobiology of Aging, 14, 191-194.
Editorial. (1987). Made to last. Lancet, II, 835-836.
Feinleib, M. (1984). The magnitude and nature of the decrease in coronary
heart disease mortality rate. American journal of Cardiology, 54,
(Suppl., August 27), 2C-6C.
Finch, C. E., Pike, C , & Whitten, M. (1990). Slow mortality rate accelerations
during aging in some animals approximate that in humans. Science, 249,
902-905.
Finch, C. E., & Pike, M. C. (19%). Maximum life span predictions from the
Gompertz mortality model, journal of Gerontology: Biological Sciences, 51A, B183-B194.
Franke, H. (1985). Kardiovasculare Befunde bei Uberhundertjahrigan.
Zeitschrift fur Kardiologie, 74, (Suppl.), 55-63.
Cabrilov, L. A., & Cavrilova, N. S. (1991). Biology of Life Span: A Quantitative Approach. New York: Harwood Academic.
206
Goldbourt, U., & Neufeld, H. N. (1986). Genetic aspects of arteriosclerosis.
Arteriosclerosis, 6, 357-377.
Hazard, W. R. (1987). Aging, lipoprotein metabolism, and atherosclerosis:
A clinical conundrum. In S. R. Bates & C. L. Gangloff (Eds.) Atherogenesis and Aging. New York: Springer-Verlag.
Horiuchi, S., & Coale, A. L. (1990). Age patterns of mortality for older
women: An analysis using the age-specific rate of mortality change with
age. Mathematical Population Studies, 2, 245-267.
Kannel, W. B., & Brand, F. N. (1985). Cardivascular risk factors in the elderly.
In R. Andres, E. L. Bierman, & W. E. Hazard (Eds.), Principles of Geriatric
Medicine. New York: McGraw-Hill.
Kannisto, V. (1988). On the survival of centenarians and the span of life.
Population Studies, 42, 389-406.
Kohn, R. B. (1982). Cause of death in very old people. Journal of the
American Medical Association, 257, 2793-2797.
Levy, R. I. (1984). Causes of the decrease in cardiovascular mortality.
American Journal of Cardiology, 54, (Suppl., August 27), 7C-13C.
Metropolitan Life. (1987). Profile of centenarians. Statistical Bulletin, 680),
2-9.
Miller, B. A., Ries, L. A. G., Hankey, B. F., Kosary, C. L., Harras, A., DeVesa,
S. S., & Edwards, B. K. (Eds.). (1993). SEER Cancer Statistical Review,
1973-1990 (Pub. No. 93-2789). Bethesda, MD: National Institutes of
Health.
Murphy, E. A. (1978). Genetics of longevity in man. In E. L. Schneider (Ed.),
The Genetics of Aging. New York: Plenum Press.
National Center for Health Statistics. (1994). Vital Statistics of the United
States, 1990, Vol. II, Part A. Washington, DC: U.S. Public Health Service.
Olshansky, S. J. (1995). Introduction: New developments in mortality. The
Gerontologist, 35, 583-587.
Pessah-Rasmussen, H., Jemtorp, P., Stavenow, I., Elmstahl, S., Hansen, F.,
Sidegard, J., Galvad, H., Brattstrom, L., & Hamfelt, A. (1990). Eightyyear-old men without cardiovascular disease in the community of
Malmo. Journal of Internal Medicine, 228, 17-22.
Powell, A. L. (1994). Senile dementia of extreme aging: A common disorder
of centenarians. Dementia, 5,106-109.
Riggs, J. E., & Millecchia, D. (1992). Mortality among the elderly in the U.S.,
1956-1987: Demonstration of the upper boundary to Gompertzian
mortality. Mechanisms of Ageing and Development, 62, 191-199.
Rosenwaike, I. (1985). The Extreme Aged in America: Portrait of an Expanding Population. Westport, CT: Greenwood Press.
Sansoni, P., Cossarizza, A., Brianti, V., Fagnoni, F., Snelli, G., Monti, D.,
Marcato, A., Passeri, G., Ortolani, C , Forti, E., Fagiolo, U., Passeri, M.,
and Franceschi, C. (1993). The immune system in healthy aging. Blood,
82, 2767-2773.
Schaie, K. W. (1989). The hazards of cognitive aging. The Gerontologist, 29,
484-493.
Siegel, J. S., & Passel, S. (1976). New estimates of the number of centenarians in the United States. Journal of the American Association of Actuaries, 71, 559-566.
Smith, D. W. E. (1993). Human Longevity. Oxford and New York: Oxford
University Press.
Smith, D. W. E. (1994). The tails of survival curves. BioEssays, 76, 907-911.
Smith, D. W. E. (1995a). Evolution of longevity in mammals. Mechanisms of
Ageing and Development, 81, 51-60.
Smith, D. W. E. (1995b). Why do we live so long? Omega, 31,143-150.
Smith, D. W. E. (1996). Cancer mortality at very old ages. Cancer, 77,
1367-1372.
Strehler, B. L., & Mildvan, A. S. (1960). General theory of mortality and
aging. Science, 132,14-21.
Thieszen, S. L., Hixsom, J. E., Nagengast, D. J., Wilson, J. L., & McManus, B.
M. (1990). Lipid phenotypes, apolipoprotein genotypes, and cardiovascular risk in nonagenerians. Atherosclerosis, 83, 137-146.
Vaupel, J. W., & Gowan, A. E. (1986). Passage to Methuselah: Some demographic consequences of continued progress against mortality. American Journal of Public Health, 76, 430-433.
Vogelstein, B., & Kinzer, K. W. (1993). The multistep nature of cancer.
Trends in Genetics, 9,139-141.
Wade, A. (1989). Actuarial Studies: Social Security Area Population, Projections 1989. Washington, DC: U.S. Department of Health and Human
Services, Social Security Administration.
Wilson, D. L. (1994). The analysis of survival (mortality) data: Fitting Gompertz, Weibull, and logistic functions. Mechanisms of Ageing and Development, 74,15-33.
World Health Organization. (1977). Manual of the Statistical Classification
of Diseases, 9th Rev. Geneva: The United Nations.
Received January 31, 1996
Accepted August 25, 1996
The Gerontologist
UNTIE THE ELDERLY®
A program that strives to ensure the persons' basic human rights of freedom
and autonomy through the elimination ofphysical and chemical restraints.
Sponsored by The Kendal® Corporation,
a not-for-profit organization whose mission is to establish and operate communities and services for older people in
accordance with the principles of the Religious Society of Friends (Quakers).
Program Offerings:
Are staff in your facility
• struggling with comprehension of the regulations on restraint usage, including the use of bed rails?
• trying to deal with resident behavior challenges?
• seeking alternatives to chemical and physical restraints?
If so, we would like to offer our assistance. Since 1988, Untie the Elderly*has been in the forefront of restraint
elimination and has conducted several hundred presentations across the country and in Canada. Feedback has indicated
that our most effective resource has been our full-day workshop; here significant personal interactions take place, and
the specific needs of each organization are addressed. Our program offerings include:
E "Untie the Elderly*," a step-by-step program on the elimination of physical restraints.
E "Freedom from ALL Restraints: Physical and Chemical," a workshop that paves the way to a restraint free
environment.
E "Restraint Removal in Acute Care Settings," a step-by-step program addressing the unique challenges facing
hospitals in the elimination of restraints.
E "Chemical Restraints: How to Avoid Inappropriate Use of Mood Altering Medications" details the intent of the
chemical restraint regulations and the approaches to compliance.
E "Helping the Caregiver Untie the Elderly," a program for nursing assistants focusing on how to deal with
challenging situations and how to individualize care through creativity.
Resource Materials:
Resource Manual, Fourth Edition - $55.00
A 289-page publication that covers Adverse Effects, Legal Issues, Change Process (including algorithms on
Falls, Abusive Behavior and Wandering), Alternatives, Acute Care and Research
Untie the Elderly Videotape - $120.00
Three-part video that can be viewed as separate modules: Philosophy of Restraint Free Care, the Change
Process, and Environmental and Programmatic Alternatives to Care.
Algorithms - $10 each or $25 for the set of three
Care maps that assess Falls, Abusive Behavior and Wandering Behavior.
Resource Reference Library Bibliography - $10.00
Bibliography from 25-topics library; i.e., Alternatives, Environment, Risk Management.
Everyone Wins! Quality Care Without Restraints Core Library - $164.95
An eight-tape video library with printed material that covers: 1) The New Resident, 2) Up and About:
Minimizing the Risk of Fall Injuries, 3) Working With Residents Who Wander, 4) Getting Hit, Grabbed, and
Threatened: What it Means, What to do, 5) Staying Restraint-Free Evenings, Nights, and Weekends, 6) Now
That the Restraints Are Off, What Do We Do?, 7) The Management Perspective, and 8) The Family Guide to
Restraint-Free Care
The Physician's Role in Restraint-Free Care - $21.95
Surveying a Restraint-Free Nursing Facility - $27.50
The Family Guide to Restraint-Free Care - $19.95 (The only piece of the Core Library that is sold separately.)
Note: Prices include shipping and handling.
For additional information, or to order, call or write:
Mary Scharf
The Kendal* Corporation
P. O. Box 100, Kennett Square, PA 19348
Phone: 610-388-5580
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