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Are Modern Environments Really Bad for Us Revisiting the Demographic and Epidemiologic Transitions.

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YEARBOOK OF PHYSICAL ANTHROPOLOGY 48:96–117 (2005)
Are Modern Environments Really Bad for Us?:
Revisiting the Demographic and Epidemiologic
Transitions
Timothy B. Gage*
Department of Anthropology and Department of Epidemiology, University at Albany-SUNY, Albany,
New York 12222, and Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio,
Texas 78284
KEY WORDS
demographic transition; epidemiologic transition; mortality; cause of death
ABSTRACT
It is a common assumption that agriculture and modernization have been detrimental for human
health. The theoretical argument is that humans are
adapted to hunter-gatherer lifestyles, and that the agricultural and \modern" environments are novel and hence
likely to be detrimental. In particular, changes in nutrition, and population size and distribution with the adoption of agriculture, are considered to increase the risk of
infectious disease mortality. Similarly, changes due to
modern lifestyles, notably changes in nutrition, smoking,
exercise, and stress, are thought to be associated with an
increased risk of degenerative disease mortality in the
industrial environment. This paper reviews the available
literature on the history and prehistory of total mortality
(the demographic transition) and cause of death (the epidemiologic transition), and finds that neither agriculture
nor modernization is associated with increases in mortality, i.e., declines in health. First, mortality does not appear
to have increased during the transition to agriculture, or
during the early phases of the industrial revolution.
Clearly, infectious diseases have declined with modernization. Second, the empirical data, when uncorrected for
INTRODUCTION
Evolutionary medicine was first proposed as a unified
discipline in the early 1990s (Nesse and Williams, 1994). A
basic tenet of the discipline is that both infectious agents
and human hosts are subject to evolutionary processes,
which have largely been ignored in the mainstream literature. A case in point is the classic work of McKeown
(1976), concerning the decline in infectious disease mortality over the past 150 years. He dismissed any role that the
evolution of virulence might have played in this decline,
largely on the basis that there were few data to demonstrate such changes (McKeown, 1976). Evolutionary medicine has advanced on several fronts: advances in molecular biology have documented the phylogeny and age of
some human pathogens (Holmes, 1999, 2004; Van Blerkom,
2003), advances in evolutionary ecology have revolutionized the concept of host/parasite coevolution and shown
that the evolution of virulence is considerably more complex than previously thought (Antia et al., 2003; Bull,
1994; Ebert, 1999), and anthropology has contributed evidence concerning human evolution and changing lifestyles
throughout human history (Cohen, 1989; Cohen and
Armelagos, 1984; Eaton et al., 1988; Strassmann and Dunbar, 1999). One of the predominant themes of evolutionary
thinking and evolutionary medicine in particular is that
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WILEY-LISS, INC.
misclassification of cause of death, do suggest an increase
in degenerative disease mortality, at least until the mid
20th century, when these causes of death clearly began to
decline. All studies that correct for misclassification of
cause of death, however, find that the general decline in
degenerative disease mortality began much earlier, perhaps as early as the 1850s in the developed countries. This
is about the same time that infectious disease mortality
began to decline in these countries. The exception is neoplasms, which increased with modernization until quite
recently. Part of the increase in neoplasms may be attributable to increases in smoking during the course of modernization. Nevertheless, the overall risk of degenerative
disease mortality appears to have declined with modernization. The fact that the decline in the risk of infectious
disease mortality, and the decline in risk of degenerative
disease mortality, are largely coordinated suggests that
the causes of both declines may be related. Historical trends
in morbidity, and potential causes of the decline in infectious and degenerative disease mortality, are briefly considered. Yrbk Phys Anthropol 48:96–117, 2005.
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2005 Wiley-Liss, Inc.
when organisms are introduced to novel environments,
the health of the organism declines (Nesse and Williams,
1999; Stearns, 1999).
The view that novel environments are detrimental to
health is widely held in biological anthropology, and pervades biological anthropology’s contributions to evolutionary medicine (Cohen, 1989; Cohen and Armelagos,
1984; Eaton and Eaton, 1999; Eaton et al., 1988; Strassmann and Dunbar, 1999). For example, it is argued that
the development of agriculture, a novel environment for
hunter-gatherers, negatively affected human health
(Cohen, 1989; Cohen and Armelagos, 1984). The theoretical basis of this argument is twofold: first, that agriculture changed the diet, leading to poorer nutrition (Eaton
et al., 1988); and second, that increases in population
density and distribution changed the ecology of infectious agents, leading to increased disease loads (Fenner,
*Correspondence to: Timothy B. Gage, Department of Anthropology, AS 114, University at Albany-SUNY, Albany, NY 12222.
E-mail: tbg97@albany.edu
DOI 10.1002/ajpa.20353
Published online in Wiley InterScience
(www.interscience.wiley.com).
ARE MODERN ENVIRONMENTS REALLY BAD FOR US?
1970). The empirical evidence, on the other hand, is contested. Some argued that the skeletal data indicate a
deterioration in health (Cohen and Armelagos, 1984;
Barrett et al., 1998). Others argued that the interpretation of the data by these investigators was flawed and
that the data could just as easily represent a period of improvement in health (Gage, 2000; Strassmann and Dunbar,
1999; Wood et al., 1992). Similarly, modern/industrialized/
Westernized/cosmopolitan environments (i.e., another novel
human environment) are also considered to negatively
influence health, although everyone agrees that longevity
has dramatically increased due to the decline in infectious
disease mortality. Again, the theoretical basis for this
argument is changes in diet, and changes in exercise levels. These changes in diet and exercise are widely considered to \promote the development" (Eaton and Eaton,
1999) of deaths due to the \diseases of affluence" (Eaton
and Eaton, 1999), \diseases of civilization" (Eaton and
Eaton, 1999), and \degenerative and manmade diseases"
(Omran, 1977), particularly the \epidemic" (Barker, 1989,
1999; Maynard Smith et al., 1999) of cardiovascular disease. The empirical evidence, however, is again contested.
There is increasing evidence that the degenerative diseases as a group, and cardiovascular disease in particular,
have declined over the last century (Gage, 1993, 1994;
Preston, 1976), despite the emergence of novel modern
environments and lifestyles. Perhaps modernization is not
as bad for health as some suggest.
The aim of this paper is to review the empirical evidence concerning historical trends in mortality and cause
of death. The trends with respect to the advent of agriculture are briefly examined. However, the main focus of this
paper concerns the last 100–150 years in the currently
modernized/industrialized/Westernized/cosmopolitan countries. The primary intent is to provide an empirical basis
for evaluating how modernization, industrialization, Westernization, and cosmopolitan lifestyles may have influenced health. Modernization, industrialization, Westernization, and cosmopolitan have not been well-defined
terms. For the purposes of this paper, these terms will be
defined loosely as the secular trends observed in countries
that are generally agreed upon as modern, industrial,
Western, cosmopolitan countries, e.g., Western Europe
and United States. For brevity, the terms modern and
modernization will be used when referring to these societies and processes. \Health" will be defined as expectation of life or age-standardized death rates. As expectation
of life increases and age-standardized death rates decline,
\health" improves. Mortality is, of course, only one possible definition of health. Morbidity is also an important
component of health, although considerably less is known
about morbidity. The specific aims are to empirically document the demographic transition, i.e., trends in total mortality, and the epidemiologic transition, i.e., trends in
cause of death, and to briefly examine secular trends in
morbidity. Finally, the paper concludes with a short review
of the vast literature concerning why infectious causes of
death declined, and a short discussion of some hypotheses
as to why degenerative causes of death declined.
SOURCES OF EVIDENCE
Documenting secular trends in mortality and morbidity would seem to be a relatively simple task. However,
this has not proven to be so. The earliest nation to begin
collecting mortality data was Finland in 1722, followed
shortly thereafter by the remaining Scandinavian coun-
97
tries. The other European countries did not follow suit
until later, well after 1800 (Vallin, 1991). Data from the
rest of the world’s nations are available much later or
not at all. A second source of data is from family reconstitution studies. This consists of linking birth, marriage,
and death records from liturgical or other records. These
data are best developed for England and Wales (Wrigley
and Schofield, 1981), and are available from 1541 or so.
Data from prehistoric periods are only available from
skeletal and other archaeological evidence. Consequently,
the history of mortality is of necessity biased in favor of
the Western European experience, and limited to a relatively small number of data sets.
The mortality data to illustrate this paper, and the
basis for many of the papers reviewed here, come primarily from four sources. The life tables for Sweden are available from the Human Mortality Database (2004; revised
as of January 6, 2005) for each year from 1751–2003, and
are unabridged. Information on age-standardized trends
in cause of death in the United States from 1900–1998 is
available from the Center for Disease Control (CDC)/
National Center for Health Statistics (NCHS) National
Vital Statistics Systems. Life tables decremented by cause
of death for an international sample are taken from
Preston et al. (1972). Archaeological data concerning mortality are adapted from Gage (1988, 2000) and Lovejoy
(1977).
Perhaps the most important data set for the historic
period is the sample by Preston et al. (1972). They compiled and examined cause of death in 165 populations of
each sex, representing 43 countries. The vast majority of
these countries were European or of European extraction, e.g., Canada and the United States. However, a few
non-European countries with adequate cause-of-death
data were included: Chile, Colombia, Costa Rica, El Salvador, Guatemala, Japan, Mexico, Panama, Taiwan, Trinidad and Tobago, and Venezuela. England and Wales
represent the longest series of life tables by cause of
death, and are available in Preston et al. (1972), from
1861–1964. England and Wales was the first country to
keep cause-of-death records. All causes of death in this
data set are classified into 12 categories, based on the
International Classification of Diseases, (World Health
Organization, 1955). The categories that are of concern
here are defined in Table 1. These causes of death can
be loosely classified into five primarily infectious and
three primarily degenerative disease categories, plus an
unknown cause of death category. However, the standard
classification conventions are not designed to distinguish
infectious from noninfectious disease, at least for the
broader categories reported here. Consequently, the division into infectious and degenerative deaths is not completely accurate. For example, rheumatic fever is classified as a cardiovascular disease by the ICD (World
Health Organization, 1955). Thus some infectious disease is included in the three categories assumed to represent degenerative causes of death. These problems are
minor, and are not considered to detrimentally affect
general conclusions (Preston, 1976).
It is standard procedure with demography to question
the observed empirical trends in demographic data to
determine if the patterns observed could be a result of \bad
data." The manner in which demographic data are collected, even by modern nations, is prone to error. National
data collection systems and/or liturgical records may not
collect information on the entire population (by age, region,
economic, social, and/or religious status) consistently over
98
T.B. GAGE
TABLE 1. Classification of deaths by cause1
Title
Infectious causes of death
Respiratory tuberculosis
Other infectious and
parasitic diseases
Definitions
B1
B2–17
Respiratory tuberculosis
Tuberculoses (other forms), syphilis, typhoid, cholera,
dysentery, scarlet fever, diphtheria, whooping cough,
meningococcal infections, plague, polio, smallpox, measles,
typhus, malaria, and all other infectious diseases
Influenza, pneumonia, and bronchitis
Influenza, pneumonia,
and bronchitis
Diarrhea
B30–32
Certain diseases of infancy
B42–44
Degenerative causes of death
Neoplasms
Cardiovascular
Certain degenerative diseases
Miscellaneous causes of death
Other and unknown
causes of death
1
ICD7 codes
B36
Gastritis, duodinitis, enteritis, and colitis (except
diarrhea of newborn)
Birth injuries, infections of newborn, and other
diseases due to infancy and immaturity
B18–19
B22, B24–29 A85, A86
Malignant and benign
Vascular lesions, rheumatic fever and heart disease,
arteriosclerosis, other diseases of heart, hypertension,
and diseases of arteries and circulatory system
Nephritis, nephrosis, cirrhosis of liver, ulcers of stomach
and duodenum, and diabetes
B20, B33, B37, B38
B46, B21, B23, B34, B35, B39, B41
All other diseases (except diseases of arteries, A85, and
other diseases of circulatory system, A86), anemias,
nonmeningococcal meningitis, appendicitis, intestinal
obstruction and hernia, hyperplasia of prostate, and
congenital malformations
Adapted and abridged from Preston et al. (1972).
time. Perhaps the most problematic issue for our purposes
is that diagnoses of cause of death and morbidity have
improved over time. Thus, observed trends in mortality
could be due to improvements in data collection and diagnosis rather than true secular trends in mortality.
There are also technical issues with respect to documenting trends in mortality. Crude death rates are generally not useful, because mortality varies with age, and
hence changes in age structure influence mortality estimates. As a result, mortality trends are usually presented
as expectations of life at birth, or as age-standardized
death rates to control for changes/differences in the age
structure of populations compared. Expectation of life at
birth is an estimate of the average number of years a person just born can expect to live, based on a life table. It is
the same as mean age at death in a stationary population.
Age-standardized death rates are estimated by multiplying (for each age) the age-specific death rates estimated
for a population by an arbitrary \standard" age structure
(typically an observed age structure of one of the populations examined), and then summing the age-specific
results. By holding the standard age structure constant in
comparisons across populations and across time periods,
changes in age structure are controlled. However, different
standard age structures will still lead to slightly different
dynamics in age-standardized death rates (due to heterogeneity in mortality among the ages). Consequently, agestandardized death rates are more difficult to interpret
than expectation of life. Thus, expectation of life is preferred for total mortality. Studies of cause of death have
traditionally used age-standardized death rates. Methods
of estimating the effects of a specific cause of death on
expectation of life are available, but are more difficult to
calculate. Only one study reported below used the impact
on expectation of life of specific causes of death. A third
metric, cumulative (lifetime) hazard rates from 0–80 years
of age, is also occasionally used. This is essentially a sum
of age-specific death rates. It can be thought of as the total
risk a person would live through if he or she survived to
age 80. Alternatively, it can be thought of as an age-standardized death rate where the standard age structure has
equal numbers of individuals at each age 0–80. This measure, like expectation of life, is consistent (because the
standard age structure is always the same), and can also
be easily applied to cause of death.
THE DEMOGRAPHIC TRANSITION
Thompson (1929) first proposed the theory of the demographic transition. The \theory" of the demographic transition is a descriptive model of secular declines in mortality, fertility, and consequent population growth that
occurred following the industrial revolution. Only the
trends in mortality will be considered here. Like all models, the demographic transition is a simplification of the
facts. The transition is typically described as occurring in
several discrete stages, but in fact, each phase trends into
the next, so in reality these phases are not completely discrete. Further, the demographic transition did not occur
throughout the world, within Europe, or even in geographically different areas of the same country simultaneously.
Much has been written about rural and urban differentials
in mortality (Woods, 1991, 2000; Wrigley and Schofield,
1981). In particular, urbanization may have slowed (or
stalled) the rate of decline in mortality in England and
Wales (Woods, 2000). Recently, large differentials (larger
than rural-urban contrasts) were identified among rural
areas of England and Wales (Dobson, 1997). Apparently,
local conditions are important with respect to the details
and exact timing of the demographic transition. Nevertheless, there are common characteristics and general trends
with respect to secular changes in mortality stages in all
of the various subdivisions of the population (Vallin, 1991).
These general trends occurring over the course of modernization are presented here.
ARE MODERN ENVIRONMENTS REALLY BAD FOR US?
Fig. 1. Secular decline in mortality, as reflected by increasing
life expectancy. Yearly estimates for 1751–2003 are from Sweden.
Data source, Human Mortality Database, January 6, 2005.
Observed secular trends in total mortality
Stage I of the demographic transition is largely preindustrial, and is characterized by high mortality and fertility, with stationary or slow population growth. Detailed
examinations of this period indicate that \normal" mortality was punctuated by large fluctuations in mortality (crisis mortality) from one year to the next (Fig. 1). Prior to
the second phase of the transition, which began ca. 1850
in Sweden (Fig. 1), crisis mortality began to decline in frequency and amplitude. However, crisis mortality continued into the 20th century, particularly with respect to
influenza, which due to its biology has remained an epidemic disease (Potter, 2002). Perhaps the 1918–1919 influenza pandemic marked the end of the crisis mortality era.
Early on, crisis mortality was not coordinated geographically and/or temporally (Woods, 2000). However, crises
became more geographically and temporally synchronized
after the turn of the 20th century (Fig. 3.2 in Vallin, 1991),
ending with the aforementioned worldwide influenza pandemic of 1918–1919. Presumably, this globalization of the
human infectious disease environment reflects improvements in transportation with modernization.
Stages II and III of the demographic transition are characterized by declining \normal" mortality (Vallin, 1991).
Stage III of the demographic transition involves the
decline in fertility, which does not concern us here, and
continued (stage II) declines in mortality. In any event,
stage II–III declines in mortality began in some European
countries such as Sweden and England and Wales in the
mid 1800s (Figs. 1, 2). It began in less developed countries
worldwide about 1920, e.g., Chile (Fig. 2). Stage II–III
declines in mortality appear to have been completed
around World War II in the developed nations, but continue in less developed countries. However, the process in
less developed countries has been accelerated. Thus, worldwide mortality appears to be converging on low mortality
rates (Fig. 2) (Wilson, 2001).
Stage IV is characterized by the low mortality observed
in developed countries after World War II (Vallin, 1991).
Nevertheless, mortality continues to decline, albeit more
slowly. The slowing of the decline is thought to be due to
the fact that infant, childhood, and young adult mortality
have reached a minimum and will not decline further. Most
99
of the recent declines have occurred among the elderly.
Age-specific declines are discussed in more detail below.
Prehistoric mortality tends to be similar to, or higher
than that observed during the historic stage I period.
Expectation of life derived from prehistoric life tables
ranges from about 18–25 years (Gage, 2000), slightly
below the underlying expectation of life of about 35 years
experienced in Sweden in the late 1750s (Fig. 1). The
highest recorded prehistoric expectations of life are 35
years, reported for the Mediterranean (Acsadi and Nemeskeri, 1970). It is possible that underestimation of age
at death might cause an underestimation of expectation
of life in these prehistoric life tables. Better methods of
aging skeletal data are needed and are actively being
researched (Hoppa and Vaupel, 2002). However, omission
of infant skeletons due to poorer preservation and other
taphonomic issues tend to overestimate expectation of
life in prehistoric life tables. Thus there is no good evidence suggesting a large increase or decline of mortality
just prior to or during the early industrial revolution.
Similarly, there is no convincing empirical evidence that
mortality increased with the agricultural revolution. Mean
expectations of life for a sample of prehistoric life tables
classified by mode of production indicate that hunter-gatherers had a mean expectation of life of 21.6 years (standard
deviation, 2.1), compared with horticulturalists with a
mean of 21.2 years (standard deviation, 3.9) and agriculturalists with a mean of 24.9 (standard deviation, 8.5).
Although agriculturalists have the higher mean expectation of life (lowest mortality), none of the differences are
statistically significant (Gage, 2000). The view that health
deteriorated with the agricultural revolution is based on
the finding that most longitudinal series of life tables from
the same localities indicate a decline in expectation of life
with agriculture, particularly the Neolithic. Further, there
is an increase in skeletal lesions across the archaeological
series (Barrett et al., 1998; Cohen and Armelagos, 1984).
The problem with these observations is that if population
growth accelerated with the agricultural revolution, as was
also argued by Cohen and Armelagos (1984), then estimates of mean age at death and expectation of life are necessarily biased downward for agricultural populations compared to hunter-gatherers (Gage, 2000; Gage et al., 1989;
Moore et al., 1975; Strassmann and Dunbar, 1999; Wood
et al., 1992). Further, the increases in skeletal lesions can
be interpreted as representing improvements in mortality
(Wood et al., 1992) as justifiably as declines in health
(Cohen and Armelagos, 1984). Overall, the empirical evidence does not support the argument that the agricultural
revolution is associated with a decline in health (Gage,
2000; Strassmann and Dunbar, 1999; Wood et al., 1992). In
fact, the prehistoric empirical evidence suggests high levels
of mortality similar to, or slightly higher than mortality for
stage 1 of the demographic transition (Gage, 2000).
Observed secular trends in age-specific
total mortality
As total mortality declines during the historic period,
risk declines at all ages. This is reflected in the construction of the model life tables of Coale et al. (1983). The
age-specific mortality curves at lower expectations of life
(higher levels of mortality) nest inside and above the
age-specific mortality curves at higher expectations of
life (lower levels of mortality) (Fig. 3A). Lee and Carter
(1992) proposed a formal relationship between differences in level of mortality (expectation of life) and differen-
100
T.B. GAGE
Fig. 2. Secular decline in mortality measured as expectation of life at 10-year intervals for developed nation (England and
Wales) and developing nation (Chile). Data source is Preston et al. (1972). Figure reprinted from Gage (2000).
ces in age-specific risk of death. They hypothesized that
mortality declines are a constant function of the log of
risk, i.e., age-specific mortality curves displayed on a log
of risk scale should be equidistantly apart at all ages.
Whether the hypothesis of Lee and Carter (1992) is precisely correct or not, secular declines in mortality have
occurred at all ages, and the largest are for those ages
with the highest risk (Figs. 3, 4).
In Sweden, age-specific mortality was relatively constant
until about 1851 (Fig. 3). It is possible that childhood mortality declined between 1801–1851. However, in other
respects, the curves are remarkably similar until 1851.
Based on absolute measures of risk (Fig. 3A), as opposed to
log of risk, infant and childhood mortality declined moderately, and adult mortality dropped significantly, between
1851–1901. From 1901–1951, infant mortality declined significantly, while childhood through elderly mortality continued to decline. From 1951–2001, infant mortality continued
to decline, but the largest declines occurred at ages of 50
years and above. Currently, there is little room for infant
mortality to decline further. Future declines must occur
among the elderly or not at all. Overall, infant and elderly
mortality declined the most. The picture of the decline looks
rather different when graphed as a log of risk, the standard
convention for presenting age-specific mortality graphically
(Fig. 3B). In this case, mortality appears to decline the most
in the childhood and young adult years. Log of risk measures the decline in mortality in terms of relative decline in
risk. For example, an age group that declined from a risk of
0.2 to 0.1, i.e., by a factor of 0.5, is considered to have
declined by the same amount as an age group that declined
from a risk of 0.8 to 0.4, also by a factor of 0.5. On the other
hand, the decline in absolute risk is 0.1 and 0.4, respectively. The childhood ages experienced the largest relative
decline. However, infants and the elderly experienced the
largest absolute declines in mortality. With respect to the
effects of modernization on health, absolute risk would
appear to be the more informative metric.
The age patterns of risk of mortality for earlier (prehistoric) periods depend on archaeological data. Care must be
taken when interpreting these results. However, a comparison of the Libben life table (Lovejoy et al., 1977, as
smoothed by Gage, 1988) with Sweden in 1751 indicates
characteristic differences between archaeological life tables
and national life tables (Gage, 1988, 2000) (Fig. 4A,B).
These suggest similar levels of mortality until age 5 years,
after which mortality is significantly higher in the paleodemographic life table. The higher mortality at ages
greater than 5 years, of course, reflects differences in
expectation of life between the two life tables (approximately 38 years for Sweden, and 20 years for Libben). As
mentioned above, the surprisingly low mortality in the
Libben life table at the youngest ages is typically thought
to be a result of poor preservation of infant remains. However, if this is true, then the expectation of life of 20 years
is an overestimate, and the Libben mortality was high
indeed, all other things being equal. The high mortalities
at the oldest ages (rapid rate of aging) characteristic of
paleodemographic life tables (Gage, 1988, 2000) are often
attributed to misspecification of age. Howell (1982) argued
that the Libben life table is critically flawed, because the
implied age structure does not resemble observed age
structures, even among contemporary hunter-gatherers.
However, \high" mortality begins well before 20 years of
age, at which age, estimation of age should be relatively
accurate. Further, what is particularly interesting about
Figure 4B is that above age 5 years, the difference
between the Libben and Swedish life tables is relatively
constant using the log of risk metric, i.e., the hypothesis of
Lee and Carter (1992) appears to hold at ages above 5
years (Fig. 4B). Mortality may increase slightly more rapidly than in the hypothesis of Lee and Carter (1992) at
older ages in the Libben life table (due to age misestimation?), but not radically. Thus the relationship between
level of mortality and age-specific risk of death, thought to
hold for contemporary populations, appears to hold for this
ARE MODERN ENVIRONMENTS REALLY BAD FOR US?
101
Fig. 3. Age-specific mortality rates for Sweden, 1751, 1801, 1851, 1901, 1951, and 2001, indicating secular changes in contribution of different ages to decline in mortality. A: Data on absolute scale. B: Same data, based on log of mortality. Data source,
Human Mortality Database, January 6, 2005.
paleodemographic/early historic comparison. Perhaps the
Libben life table is not as flawed as is generally assumed.
A second view of the association of historical declines
in mortality with declines in age-specific risk is provided
by Gage (1993, 1994). This method uses a competing
hazard model (a kind of parametric mixture model) that
divides mortality into three competing components, simi-
lar to the named causes of death (Fig. 5). In particular,
the Siler Model (1979) divides risk of death into immature mortality (which declines with age), residual mortality (which is constant with respect to age), and senescent mortality (which increases with age). The immature
and senescent components represent \endogenous" mortality, while the residual component represents \exoge-
102
T.B. GAGE
Fig. 4. Age-specific mortality rates for Sweden, 1751, and Libben, a North American Late Woodland population (hunter-gatherer) ca. 800–1100 AD. A: Data on absolute scale. B: Same data, based on log of mortality. Data sources, Sweden (Human Mortality
Database 6 January 2005); Libben life table reported by Lovejoy et al. (1977), smoothed by Gage (1988).
ARE MODERN ENVIRONMENTS REALLY BAD FOR US?
103
enza pandemic (Gage, 1993, and below). The decline in
residual (exogenous) mortality is theoretically consistent
with stage I declines in crisis mortality (epidemic mortality). From 1890–1920, both immature and senescent
mortality declined rapidly. From 1920 onward, immature
and residual (exogenous) mortality declined, although
more slowly than during previous periods. Exogenous
mortality became immeasurably small after 1951. Senescent mortality increased a little between 1921–1931, and
a reasonable amount between 1931–1941, before declining. Thus stage II–III mortality declines include all
three components, while stage IV declines are limited to
immature and senescent risks. The point is that, in general, mortality has declined at all ages over the course of
the demographic transition. Senescent mortality did not
decline monotonically, but still declined substantially.
Summary: demographic transition
Fig. 5. Graphical depiction of model of age-specific mortality
(Siler 1979). Model is sum of three components of mortality.
Area \a" is immature component representing decline in mortality immediately following birth, area \b" is senescent component, representing increase in mortality with age, and bottommost area \c" is residual component representing age-independent, exogenous risks. From Gage (1991).
nous" mortality, as defined in the evolution of life-history
literature (Stearns, 1992).
Gage (1994) examined the cumulative (lifetime) risk of
mortality at ages 0–80 with respect to expectation of life
in the sample by Preston et al. (1972) of cause-specific
life tables (Fig. 6). Cumulative or lifetime risk is the
sum total (integral) of risks at each age experienced by
someone who lives, in this case, to the age of 80. For
example, cumulative immature risk is the area labeled
\a" in Figure 5. Total cumulative risk would equal the
sum of areas a–c in Figure 5. Altogether, about 50% of
the decline in total cumulative risk of death across this
sample is due to declines in senescent mortality. A little
more than 25% of the decline in the cumulative hazard
is due to declines in immature mortality. The remaining
25% declines as a constant across all ages. This suggests
that the risks of senescent mortality have declined more
than any other component of mortality. Of course, this
decline is spread across a larger number of age categories than is immature mortality. The figures vary
slightly by sex. Females tend to have slightly higher residual and slightly lower senescent mortality than males,
given identical expectations of life. This difference is
thought to be largely due to maternal mortality (Gage
1994), which occurs in the residual component of female
life tables. Since expectation of life is fixed (controlled
for) in these analyses, senescent or immature mortality
must compensate. In this case, it is senescent mortality
that compensates. Immature mortality is relatively equal
in male and female life tables of the same expectation of
life. Keep in mind that this analysis gives equal weight
to every age up to age 80, whereas conventional measures, such as expectation of life and age-standardized
death rates, tend to give greater weight to younger than
older ages, as described above.
Gage (1993) presented a similar analysis of the historical trends in England and Wales from 1861–1964 (Fig. 7).
Exogenous mortality is the first component to decline, with
rapid declines from 1871–1891. During this period, senescent mortality increases, probably due to the 1890 influ-
Does the historical decline in mortality mean that \modernization" has been good for human health? Clearly, total
mortality has experienced a secular decline over the last
300 years in the developed nations. Mortality prior to the
historic period is consistent with or perhaps slightly
higher than mortality (lower expectation of life) during
stage I of the demographic transition. There is no evidence
that mortality increased during the early phases of the
industrial period, only beginning to decline in the later
phases of the demographic transition (Fig. 1). If this is the
definition of improved health, then modernization and
modern lifestyles have clearly benefited health overall. On
the other hand, no one argues that the decline in infectious
disease mortality accompanied modernization, and that in
this regard health has improved.
The argument that modernization is bad for health typically concerns the secular trends in degenerative diseases,
e.g., cancers, cardiovascular diseases, or diabetes. It is
clear from the evidence presented above that as mortality
declined, the risk of death declined at all ages, including
among the elderly, where the degenerative diseases are
concentrated. However, these declines among the elderly
could be due to infectious diseases of the elderly such as
influenza, pneumonia, and bronchitis. Consequently, the
risk of degenerative disease mortality may have declined,
remained the same, or even increased. It is the assumption
that degenerative causes of death increased with modernization that has given rise to the concept that modern lifestyles are bad for health. Below, I review our knowledge of
the secular trends in cause of death.
THE EPIDEMIOLOGIC TRANSITION
Trends in cause-specific mortality are even harder to
document and interpret than trends in overall mortality.
England and Wales was the first country to formally
record cause of death, beginning in 1830. Very little
empirical information on cause of death is available prior
to 1830 in any population. As with total mortality, there
are difficulties in examining secular trends in cause of
death. First, there have been changes in the conventions
for reporting diseases, which affect the enumeration of
cause of death. The International Classification of Diseases (ICD) is currently in its tenth revision. The transition from one revision of the ICD to the next is often not
completely consistent. For example, beginning with the
eighth revision of the ICD, cardiovascular-renal disease
was categorized with general cardiovascular deaths, whereas
in previous revisions, cardiovascular-renal disease was
104
T.B. GAGE
Fig. 6. Decline in component-specific mortality as total mortality declines in sample of Preston et al. (1972).
Results presented here statistically
control for period (i.e., calendar year)
effects. From Gage (1994).
not included in general cardiovascular deaths. Consequently, some data adjustment is usually necessary to
compile consistent data sets across time. These, however,
are intentional adjustments in classification of cause of
death. There has also been a secular improvement in
classification of cause of death, as medical doctors and
examiners become better trained and more knowledgeable at diagnosing cause of death. It should be pointed
out that classification in the late 20th century was still
far from perfect (Manton and Stallard, 1984), although
earlier periods were far worse. Finally, application of
the ICD classification conventions is also thought to vary
(culturally) among nations (Preston, 1976). However,
even if the underlying data are accurate, there remain
technical difficulties in interpretation. It is as important
with cause-of-death data as with total mortality that
methods account for age-specific risks of death.
A larger proportion of individuals die of degenerative
diseases today than in the past. This does not necessarily
mean that the risk of degenerative death has increased.
The reduction or elimination of one cause of death will, all
other things being equal, increase the number and proportion of deaths attributed to the causes that remain. However, the age-specific risk of the remaining causes may not
have increased. Individuals may simply survive longer
and die at an older age.
Originally, the epidemiologic transition was defined in
terms of the rank ordering of deaths by cause (Omran,
1977). Omran (1977) showed that degenerative diseases
replaced infectious diseases as the most common causes
of death over the last few centuries. The CDC still
reports the rank order of common causes of death. Such
information has important applications. For example,
research dollars might be allocated on the basis of frequency of causes of death. On the other hand, to show
that modernization is bad for health, i.e., that modernization exacerbates the degenerative causes of death, it
is necessary to demonstrate that the risk of degenerative
disease mortality increased with modernization. Consequently, the description of the epidemiologic transition
presented below is based on changes in risk of degenerative disease mortality. In particular, it is argued that the
empirical evidence suggests that the risk of degenerative
death overall has declined with modernization. However,
the decline in infectious disease mortality was larger
than the decline in degenerative disease mortality. Hence
degenerative diseases have become more common than
infectious diseases as causes of death with modernization,
even though both types of cause have declined.
Epidemiologic transition: 1861–1964
The age-standardized observed secular trends in total
infectious, total degenerative, and other and unknown
causes of death for England and Wales 1861–1964 are
shown in Figure 8. Overall, infectious diseases decline,
while degenerative diseases increase slightly. The category of deaths named \other and unknown diseases"
also declines. Although other and unknown diseases do
include inborn errors of metabolism, this category consists predominantly of diseases assigned to causes of
death such as \senility," which have no modern counterpart in the ICD. Hence this category represents predominantly misclassified deaths (Table 1). These misclassified
ARE MODERN ENVIRONMENTS REALLY BAD FOR US?
105
Fig. 7. Decline in component-specific mortality of Siler (1979) in England and Wales, 1861–1964. Data source, Preston et al.
(1972). From Gage (1993).
Fig. 8. Decline in total infectious, degenerative, and other and unknown causes of mortality (as defined in Table 1) for England
and Wales, 1861–1964. Data source, Preston et al. (1972).
deaths decline as classification procedures improve, shifting deaths to other named categories. Thus the trends in
the named causes of death are biased. The declines in
other and unknown diseases are about half as large as the
decline in named infectious diseases, and much larger
than the observed increases in degenerative diseases.
Thus the observed secular increase in degenerative disease
mortality could be due to improvements in diagnosis of
cause of death. Degenerative diseases could have increased, remained the same, or even declined.
All of the infectious disease categories clearly decline
(Fig. 9). However, the trends in degenerative diseases are
less consistent (Fig. 10). Neoplasms fluctuate, but appear
to increase. Cardiovascular deaths fluctuate over time,
and may also increase slightly. Note that in England and
Wales, neoplasms exceed cardiovascular mortality. This
106
T.B. GAGE
Fig. 9. Decline in named infectious, and other and unknown vauses of mortality (as defined in Table 1) for England and Wales,
1861–1964. Data source, Preston et al. (1972).
Fig. 10. Decline in named degenerative, and other and unknown causes of mortality (as defined in Table 1) for England and
Wales, 1861–1964. Data source, Preston et al. (1972).
differs from the United States, where cardiovascular
deaths traditionally exceed neoplasms, possibly due to cultural differences in the application of the ICD classification conventions (Preston, 1976). The remaining degenerative diseases increase and then decline. The highs and
lows in neoplasms and cardiovascular deaths follow the
same trends as the infectious-category influenza, pneumonia, and bronchitis (Fig. 9). Excess deaths due to other
causes of death are often correlated with influenza epidemics (Azambuja and Duncan, 2002; Davenport, 1976;
Lancaster, 1990). One possible explanation for the excess
mortality is that the risk of neoplasm and cardiovascular
disease mortality increases in individuals with influenza
due to the added stress. Consequently, an excess of neoplasm and cardiovascular disease deaths is likely during
an influenza epidemic, depleting the number of individuals
particularly susceptible to neoplasms and cardiovascular
disease deaths. This would then be followed by a period of
lower-than-expected neoplasm and cardiovascular disease
deaths, while the population of susceptibles increases once
again. The high neoplasm and cardiovascular death rates
for England and Wales in 1891 are associated directly with
the influenza epidemic that spans the 1890s, while the relatively low neoplasm and cardiovascular death rates
reported in 1921 occurred a year or so after the end of the
1918–1919 influenza pandemic. This might explain the
fluctuations in neoplasm and cardiovascular disease
deaths from 1861–1964. Taken together, however, the
observed trends in the named degenerative diseases tend
to increase over time, at least until the mid-1950s.
107
ARE MODERN ENVIRONMENTS REALLY BAD FOR US?
Based on observations such as in Figures 8–10, shifts
in cause-of-death structure are described by a second
descriptive model, the \epidemiologic transition" which
accompanied the \demographic transition" (Omran,
1977). Omran (1977) called stage I of the demographic
transition \the age of pestilence and famine." This
period was characterized by high rates of infectious diseases occurring in periodic epidemics (exogenous or crisis
mortality). This was followed by the \age of receding
pandemics" (stages II–III of the demographic transition).
During this period, infectious diseases changed from epidemic to endemic diseases (hence the reduction in exogenous or crisis mortality), and began to decline as causes
of death, but remained endemic childhood diseases. The
final stage (IV) is called the \age of degenerative and
manmade diseases." As infectious diseases declined in
frequency, degenerative diseases, particularly cardiovascular diseases and neoplasms, emerged as the most common causes of death. This occurred in the 1920s in England and Wales (subject to the age structure used to
standardize the data; Fig. 8). Omran (1977) was careful
not to argue that the risk of degenerative diseases
increased, but only that the proportion of deaths due
to degenerative causes eventually exceeded infectious
causes (despite his use of the description \age of degenerative and manmade diseases"). Since other and unknown
diseases declined more than degenerative diseases
increased, it is not reasonable to conclude that the risk of
degenerative diseases must have increased. The emergence of degenerative diseases as the most common cause
of death could have occurred if the risk of degenerative diseases increased, declined, or remained the same, as long
as infectious causes declined faster then degenerative
causes.
Epidemiologic transition 1861–1964: controlling
for misclassification
Three attempts have been made to statistically correct
for misclassification of cause of death, and to clarify the
secular trends in degenerative causes of death during the
later part of the 19th and early part of the 20th centuries.
The first was a statistical analysis conducted by Preston
(1976), based on the international life-table database published in Preston et al. (1972), as described above (Table 1).
Gage (1994) reexamined these same data using the Siler
Model to further focus the analysis. Finally, Gage (1993)
studied the trends in England and Wales using the Siler
Model (1979) and additional decremented life tables, but
based on the sample by Preston et al. (1972). All three
studies are consistent in concluding that the risk of cardiovascular disease, and of certain degenerative diseases,
declined, while neoplasms increased with modernization
(1861–1964). Total degenerative disease (the sum of cardiovascular disease, neoplasms, and certain degenerative diseases) appears to have declined.
Preston (1976) was the first to examine changes in the
cause-of-death structure across the demographic transition statistically. He regressed all cause-standardized
death rates on each cause-specific standardized death
rate. Thus a positive regression coefficient (slope) indicates that the ith cause declines as all-cause mortality
declines. A negative coefficient indicates that the ith
cause increases as mortality declines. The regressions
were conducted so that the slopes of the regression represent the proportion of total decline due to that cause.
The results are summarized in Table 2. In general, the
TABLE 2. Regression of specific causes of death on overall
death rate, all standardized for age structure1
Slope (correcting for
misclassification)
Causes of death
Males
Females
Respiratory tuberculosis
Other infections and parasitic
diseases
Neoplasms
Cardiovascular
0.1188
0.1458
0.1059
0.1398
0.0569
0.0316
(0.2390)
0.2831
0.0245
0.0179
(0.2456)
0.2434
0.1050
0.0206
0.0447
0.1041
0.0165
0.0422
0.0197
0.0041
0.3307
0.9998
Influenza, pneumonia,
and bronchitis
Diarrhea
Certain degenerative diseases
Certain diseases of infancy
Maternal
Violence
Other and unknown
Sum
0.0232
0.3475
1.0002
1
Slopes may be interpreted as % change due to cause. Positive
regression coefficient (slope) indicates that ith cause declines as
all-cause mortality declines. Negative coefficient indicates that ith
cause increases as mortality declines. Preston (1976) only
reported actual value of corrected slope for cardiovascular deaths.
Adapted from Preston (1976).
coefficients are positive, with several exceptions. The
exceptions are neoplasms in both sexes and cardiovascular disease in males, indicating that these categories of
death increased as mortality declined. The category of
certain degenerative diseases, on the other hand, declines
in both sexes. Influenza, pneumonia, and bronchitis are
the largest named contributors to the decline in mortality
(about 25% of the total decline). However, the category of
other and unknown causes of death accounts for an even
larger proportion of the decline (about 34%). It is unlikely
that poorly diagnosed causes of death declined faster than
named and (hopefully) properly diagnosed causes of
death. More likely, diagnosis improved with the epidemiologic transition, and much of the decline in other and
unknown causes of death is due to improvements in classifying these causes of death, rather than the elimination of deaths whose causes were not well-recognized at
the time. Thus the rates of decline in the named categories may be underestimated, while the rates of increase
may be overestimated.
Preston (1976) reexamined the data by regressing allcause standardized death rates, and other and unknown
standardized death rates, on each of the named causespecific standardized death rates. This controls for misclassification of cause of death, provided that the negative correlations between the standardized death rate for
a named cause and the standardized death rate for other
and unknown causes of death across countries in the
international sample are a result of misclassification of
cause of death. The corrected coefficients for neoplasms
indicate that this cause increases as overall mortality
falls in both sexes. On the other hand, the corrected coefficients for cardiovascular disease are positive, indicating
that cardiovascular mortality declines in both sexes as
mortality declines. In fact, the slopes suggest that about
24% of the decline in all-cause mortality is due to
declines in cardiovascular disease mortality. If this is
correct, than the decline in cardiovascular mortality over
the course of the demographic and epidemiologic transitions rivals the impact of influenza, pneumonia, and
108
T.B. GAGE
TABLE 3. Sign and significance of regression coefficients for regressions of component-and-cause-specific deaths
on total deaths, all standardized for age structure, based on the Siler Model1
Trend in cause of death as
mortality declines2
Cause of death
Males
All causes combined
Immature
Residual
Senescent
Respiratory tuberculosis
Residual
Senescent
Other infectious and parasitic diseases
Immature
Residual
Senescent
Certain diseases of infancy
Immature
Residual
Influenza, pneumonia, and bronchitis
Immature
Residual
Senescent
Diarrhea
Immature
Residual
Senescent
Neoplasms
Immature
+
Senescent
+
Cardiovascular disease
Immature
0
Residual
Senescent
Certain degenerative diseases
Immature
Senescent
Females
Misclassification of
cause of death
Period effect
R2
+
0
94.5%
64.3%
73.7%
+
73.2%
47.1%
0
0
0
+
89.2%
83.5%
36.6%
0
0
0
0
71.9%
38.4%
0
0
&
+
0
90.5%
72.9%
74.3%
0
0
0
+
0
0
79.4%
53.0%
59.6%
0
&
0
39.8%
58.6%
0
0
&
0
0
29.8%
17.7%
39.9%
0
&
+
0
31.9%
10.1%
0
0
0
0
0
+
+
1
, Cause of death declines as mortality declines or period increases; +, cause of death increases as mortality declines or period
increases; 0, coefficient not significant; &, cause of death with significant numbers of misclassified deaths. Adapted from Gage (1994).
2
Corrected for misclassification and period effects.
bronchitis as the single largest named cause of general
decline in international mortality (Preston, 1976).
Gage (1994) reanalyzed the same data using the Siler
Model (Fig. 5), which divides deaths into three categories:
immature, residual, and senescent. The sample by Preston
et al. (1972) includes total life tables and cause-eliminated
life tables, i.e., a series of life tables, one for each cause of
death, from which that particular cause of death is mathematically eliminated from the population. Fitting the Siler
Model to each of the total and cause-eliminated life tables
in the database of Preston et al. (1972) allows the proportion of deaths of each cause, including other and unknown
causes, to be subdivided into the three components. Gage
(1994) then conducted regression analyses similar to the
analysis of Preston (1976) reported above, but separately
on each component of the Siler Model. There are two
advantages to this procedure. First, the analysis is based
on the cumulative risk of death, i.e., on the hazard, as
opposed to age-standardized death rates, which vary
depending on the standard. A second advantage of the
component-specific methodology is that \immature" other
and unknown causes are regressed on the named \immature" causes of death, and \senescent" other and unknown
causes are regressed on the named \senescent" causes of
death, etc. This focuses the use of other and unknown
causes as a correction for misclassification of deaths. The
assumption is that senescent other and unknown causes
are likely to be misclassified senescent deaths, i.e., one of
the named causes of senescent death, as opposed to one
of the named causes of immature or residual death. Consequently, the statistical correction for misclassification
of cause of death is likely to be more accurate. Finally,
Gage (1994) included a third independent variable, period
(the year the life table refers to), to control for period
effects.
The results presented in Table 3 are similar to those of
Preston (1976). Not surprisingly, all of the infectious diseases decline. Only influenza, pneumonia, and bronchitis
appear to be significantly misclassified among infectious
causes of death. Infectious diseases also show the only large
period effects. In general, infectious disease mortality tends
to decline in the residual component and increase in the
immature component. In the senescent component, period
increases in respiratory tuberculosis and other infectious
and parasitic diseases are balanced by period declines in influenza, pneumonia, and bronchitis. These secular changes
in component-specific infectious disease mortality support
the hypothesis by Fenner (1970) that increased urbanization and population growth result in a shift from epidemic
(exogenous, i.e., residual component causes) to endemic diseases affecting the very young and elderly.
The analysis of degenerative diseases also supports the
results of Preston (1976). All three degenerative disease
categories are significantly misclassified. Degenerative dis-
ARE MODERN ENVIRONMENTS REALLY BAD FOR US?
109
Fig. 11. Decline in cause-specific total degenerative mortality as mortality declines in sample of Preston et al. (1972), while statistically controlling for misclassification of causes of death and period effects. Decline in senescent degenerative mortality is very
similar. Adapted from Gage (1994). Total degenerative mortality, represents the sum of cardiovascular, neoplasms, and certain
degenerative deaths.
eases occur in all three components of the Siler Model,
but the vast majority of degenerative deaths occur in the
senescent component, i.e., deaths in other components of
the Siler Model are generally several orders of magnitude smaller (Gage, 1991, 1994). Consequently, the
period effects on immature degenerative mortality are
very small. Further, the period effects of the three
degenerative cause-of-death categories tend to cancel
each other out. Corrected for misclassification, senescent
and total neoplasms increase in both males and females
as mortality declines. On the other hand, corrected senescent cardiovascular and certain degenerative disease
mortality all decline (Fig. 11). Interestingly, males benefited more from the decline in infectious disease mortality and less from degenerative diseases than females,
although female mortality fell more, overall (Gage,
1994). In general, these results support those of Preston
(1976). Corrected for misclassification of cause of death,
neoplasms increased, while cardiovascular and certain
degenerative deaths declined. The declines in cardiovascular and certain degenerative diseases outweigh the increase in neoplasms, so total degenerative deaths decline
as overall mortality declines.
Gage (1993) also examined the decline in cause-specific
mortality in England and Wales from 1861–1964, using
the Siler Model. Here, statistical corrections for misclassification of cause of death are not possible, because there is
only a single longitudinal series (statistical correction for
misclassification of cause of death relies on comparisons
across countries with different classification efficiencies).
The trends for total component-specific mortality were
presented earlier (Fig. 7). Overall, senescent mortality
declined between 1861–1964. However, some senescent
deaths are likely to be due to the infectious diseases that
occur in the senescent component (Gage, 1991), i.e., influenza, pneumonia, bronchitis, and respiratory tuberculosis.
Figure 12 shows the trends in total senescent mortality
and senescent mortality with influenza, pneumonia, bronchitis, and respiratory tuberculosis eliminated. In this latter case, the peaks in senescent mortality are notably
reduced. Nevertheless, the remaining degenerative diseases increase until the 1890s and then decline. The
increase in degenerative diseases until 1890 is at least
partly due to the excess mortality resulting from the influenza epidemic of the 1890s (Azambuja and Duncan, 2002;
Davenport, 1976; Lancaster, 1990). On the other hand, the
1921 low in degenerative disease mortality is probably due
to excess degenerative diseases deaths associated with the
1918–1919 influenza pandemic, which occurred 2 years or
so before 1921, as discussed above. If a line is fitted to senescent degenerative deaths, mortality due to this cause
declines. The total risk of senescent degenerative mortality (age-specific senescent risk summed or integrated
across 0–80 years of age) in 1861 was 4.07, which declined
to 3.79 in 1964. Assuming that all misclassified deaths in
the senescent component are degenerative deaths (as
110
T.B. GAGE
Fig. 12. Decline in senescent mortality in England and Wales 1861–1964, with and without infectious senescent causes of death
decremented. Straight line is regression fitted to senescent degenerative disease mortality (i.e., senescent mortality with senescent
infectious diseases decremented). From Gage (1993).
opposed to infectious causes of death) and that no infectious causes remain after decrementing influenza, pneumonia, bronchitis, and respiratory tuberculosis, the result
suggests that degenerative diseases as a group have declined since the 1860s, and dramatically since the 1890s.
Epidemiologic transition: last half of the
20th century
While errors in classification of cause of death are a
serious problem for earlier periods, they are less likely
to bias results during the latter half of the 20th century.
Thus the observed trends are more likely to reflect real
trends in mortality. In October 1978, the National Heart,
Lung and Blood Institute of the National Institutes of
Health sponsored a conference to consider the surprising
finding that the risk of coronary heart disease mortality
was declining (Havlik and Feinleib, 1979; National Center for Health Statistics (NCHS), 1978). The attendees
were charged with the following question: \What preventative, curative, environmental, or other factors contributed to this recent decline, especially to the dramatic
turnaround for ischemic heart disease?" Clearly the
observation that the most common cause of death in the
United States was declining caught the US public health
services off guard. The observed trends of a number of
degenerative diseases for the US during the 20th century
are presented in Figure 13. These data clearly show the
\rise and fall of ischemic heart disease" (Stallones, 1980),
and of cardiovascular mortality more generally, which
peaked in the US in the late 1940s or early 1950s. This
phenomenon is now internationally established, e.g., in
Poland (Zatonski et al., 1998), the Nordic countries (Martelin, 1987), most of Central Europe (Mesle, 2004), various
other European countries (Vallin and Mesle, 2004), and
Japan (Yanagishita and Guralnick, 1988). In fact, the trend
is not limited to cardiovascular mortality. Barker (1989)
discussed a number of diseases that rose and then fell in
the 20th century. The etiology of some of these, like polio, is
well-established (Fenner, 1970); others, like heart disease,
are not well-established. In the late 1990s, even neoplasms
began to decline in the US (Fig. 13). If the recent rates of
decline in neoplasms and cardiovascular deaths continue
at present rates, neoplasms will soon outrank cardiovascular deaths as the most common cause of death in the US.
While Figure 13 only considers the most common degenerative diseases, it is clear, given the dramatic declines in
heart disease, that overall degenerative disease mortality
has declined since the 1940s.
The decline in cancer began in Japan in the 1960s,
much earlier then the decline in other regions of the world
(Gersten and Wimoth, 2002). This is in part because of the
unusual cause structure of cancers in Japan. Much of the
decline in Japan was due to stomach and cervical cancers,
which are largely attributed to infectious agents (Doll and
Peto, 2001). Liver and lung cancers have increased and
continue to increase, probably due to shifts in alcohol consumption and smoking. All of these trends appear to be
heavily influenced by the involvement in World War II
and subsequent economic development. However, the
trends reflect a transition from cancers with a large infectious component of risk to cancers with a large behavioral
component of risk (Gersten and Wimoth, 2002). Similar
trends were observed in other industrialized countries
(Becker, 1998; National Cancer Institute, 1999), although
in general, the decline in infectious cancers must have
been smaller than, and outweighed by, increases in those
cancers associated with behavioral risk factors, since overall, cancers appear to have increased as a group at least
until recently, e.g., the US (the trends in neoplasms, Fig. 13).
How large an effect has the decline in cardiovascular
disease had on the mortality of industrialized nations?
White (1999) examined the two cause-of-death categories
that changed the most during the 20th century in the US:
respiratory tuberculosis and cardiovascular mortality.
Respiratory tuberculosis was considered throughout the
ARE MODERN ENVIRONMENTS REALLY BAD FOR US?
111
Fig. 13. \Rise" and fall of some degenerative diseases and influenza (cause responsible for largest decline in named infectious
disease) in US male population from 1900–1998 (registration states, 1900–1932; US, 1933–1998). Age standardized to US 2000 age
distribution. Data source: CDC/NCHS, National Vital Statistics System, Mortality, unpublished table HIST293.
20th century, while cardiovascular disease was examined
from 1940 rather than 1900 due to the likelihood of errors
in classification in prior periods. In addition, White (1999)
included cardiovascular-renal diseases as general cardiovascular deaths up until the Eighth Revision of the International Classification of Diseases, which formalized this
relationship in 1969. Measured as expectation of life, the
decline in respiratory tuberculosis since 1900 has contributed an additional 5.3 years to expectation of life. On the
other hand, since 1940, the decline in cardiovascular mortality has increased expectation of life by 6.4 years. This is
also reflected in the number of deaths averted by the
declines in these same diseases, estimated to be 26,003 for
respiratory tuberculosis during 1900–2000, and 26,333 for
cardiovascular disease during 1940–2000 (White, 1999). A
similar comparison between the decline in influenza mortality (the cause that declines the most in the sample of
Preston et al., 1972) and degenerative diseases for the US
is presented in Figure 13.
If cardiovascular mortality was declining before 1940,
as suggested by the analyses of Preston (1976) and Gage
(1993, 1994), then the decline in cardiovascular mortality of the last 100–150 years exceeds the decline in any
other named cause of death, as defined in Table 1. In
any event, even if the declines in cardiovascular disease
mortality before 1940 are ignored, cardiovascular mortality is the largest single cause of the historical decline in
mortality in the US during the 20th century.
Epidemiologic transition, age-specific: last
half of the 20th century
Salomon and Murray (2002) conducted an analysis of
relative trends in the cause structure of mortality since
1950, using the Global Burden of Disease 1990 study sample. This consists of 58 countries, mostly European, and
mostly developed for the period 1950–1990 (Murray and
Lopez, 1996). However, a number of less developed countries are also included. For analysis, causes of death were
divided into three groups: group 1, infectious diseases;
group 2, noncommunicable diseases (including neoplasms,
cardiovascular disease, and diabetes mellitus, i.e., degenerative diseases); and group 3, accidents and violence.
Analysis differs from previous studies in that the transition is examined by age and sex and confined to composition of cause of death (as opposed to absolute changes in
level of mortality), as Omran (1977) originally intended.
Unfortunately, the results are voluminous and cannot be
presented here (Salomon and Murray, 2002). However,
their conclusions are as follows. First, their analysis confirms the general principles of the epidemiologic transition, a shift from predominantly infectious disease mortality to predominantly noninfectious and accidental deaths.
Second, as infant mortality declines, infant mortality
shifts from infectious to noninfectious causes of death,
with few or no accidental deaths. Third, children over age
1 year experience shifts from predominantly infectious
deaths to an equal mix of noninfectious and accidental
deaths. Accidental deaths are more common in males than
in females. Fourth, young adults (15–44 years) differ by
sex. In males, declining mortality is associated with a shift
from accidents to noncommunicable diseases, although
this trend is ameliorated by an increased standard of living. As mortality declines among females, there is at first
a trend toward noncommunicable diseases, followed by a
trend toward accidental deaths. Higher standards of living
are again associated with higher accidental deaths.
Finally, males and females over age 50 show almost no
change in composition in cause of death as mortality
declines during the latter half of the 20th century. Thus,
since the 1950s, all causes have declined approximately
equally in the population over 50 years of age.
112
T.B. GAGE
Summary: epidemiologic transition
The history of secular trends in cause of death depends
on whether it is expressed as the proportional structure of
cause of death (Omran, 1977) or as trends in the risk of
cause of death. To answer the question of whether modernization is bad for health, it is the latter definition that
must be employed. The studies presented above suggest
that during the historical decline in mortality in England
and Wales, the US, and other modernized countries, the
risk of both infectious and degenerative causes of death
declined. Clearly, infectious diseases began to decline in
the 1850s. Corrected for misclassification of cause of death,
cardiovascular death rates and certain degenerative disease death rates may have begun to decline at approximately the same time as infectious diseases, but clearly
declined after 1900. This decline is visible without correction for misclassification of cause of death after the 1940s.
Cardiovascular deaths probably account for more of the
general decline in mortality than any other single cause of
death. Neoplasms, corrected for misclassification of cause
of death, increased until late in the 20th century, and only
recently began to decline.
With the exception of neoplasms, these results suggest
that we are in the second stage of a simple two-stage
epidemiologic transition: 1) the age of pestilence and
famine, and 2) the age of declining infectious and degenerative diseases. A future third stage might consist
largely of accidental deaths (Rogers and Hackenberg,
1987), or possibly a return of infectious disease mortality
(Barrett et al., 1998). Most other amendments to the epidemiologic transition involved adding additional stages
to the model (Olshansky and Ault, 1986; Rogers and
Hackenberg, 1987; Vallin and Mesle, 2004; WolleswinkelVan-Den-Bosch et al., 1997). These additions are due to
the view that degenerative diseases increased prior to
declining, as shown in Figure 13. However, as presented
above, these increases appear to be largely due to misclassification of cause of death. It is likely that the
decline in degenerative diseases began prior to 1940.
DEGENERATIVE DISEASE MORBIDITY
If mortality, including overall degenerative disease
mortality, has declined, why has morbidity increased? Or
has morbidity increased? Mortality is only one way to
define health. Health may also be defined as the incidence or prevalence of morbidity. While incidence, prevalence, and mortality are all related with \health" and
with each other, they need not be consistent. A relatively
simple model of the relationship of morbidity and mortality due to degenerative diseases in the presence of
competing causes of death, where morbidity is a clearly
recognizable dichotomous trait, is presented in Figure
14. The model proposes that there is a pool of healthy
individuals who are depleted in two ways. Individuals
from the healthy pool become morbid due to degenerative cause A at a specific rate, which may or may not be
dependent on age and or period effects. For example,
blood pressure is thought to increase with age, so high
blood pressure morbidity increases with age. The rate of
transition from healthy to morbid state A is commonly
called the incidence of the morbid state (number of new
cases). There is then a rate at which morbid individuals
die of cause A, e.g., the rate at which individuals with
high blood pressure have cardiovascular accidents resulting in death. Of course, healthy individuals may also die
Fig. 14. Graphical depiction of relationship of cause-specific
morbidity and mortality. Prevalence of morbid condition A is
function of rate at which healthy individuals become morbid
(incidence), and rapidity at which individuals morbid with cause
A die (of cause A or any other competing cause).
of cause A without entering the morbid state, or enter
the morbid state so briefly that it is not clinically recognized. The prevalence of morbid state A (number of contemporary cases) is then a function of the incidence of
morbidity and the mortality rate of morbid individuals
due to cause A, and the mortality of morbid individuals
due to other competing causes. Clearly, the higher the
incidence and the longer the survival of morbid individuals (whatever the cause of death), the higher the prevalence of morbidity. A low prevalence of morbidity due to
cause A does not necessarily mean that there is a low incidence or low mortality rate due to cause A. In fact, all
other things being equal, the higher the mortality of morbid individuals, the lower the prevalence of morbidity!
A second problem with respect to documenting incidence
and prevalence concerns secular changes in the recognition of morbid conditions. Just as the diagnosis of cause of
death has improved over time, the diagnosis of morbid conditions has also improved. With respect to morbid conditions, the issues are even more complex than when considering cause of death. Unlike death, morbidity may be more
or less severe. Severity may influence diagnoses, and/or
the definition of disease threshold may change, both of
which could artificially influence secular trends in morbidity. It is also possible for a population to experience simultaneously a real increase in prevalence and a decrease in
severity of morbidity, or vice versa. Below, I briefly examine the literature concerning trends in morbidity, with particular reference to degenerative diseases.
Morbidity during the last half of the 20th century
Studies of the change in prevalence of various degenerative diseases over the last 20 or 30 years generally conclude that the prevalence of most degenerative conditions
is increasing (Crimmins, 2004; Crimmins and Saito, 2000;
Cutler and Richardson, 1997; Manton et al., 1995).
These include the prevalence of neoplasms, cardiovascular diseases, diabetes, and arthritis. The increases in
prevalence are due to the faster decline in degenerative
ARE MODERN ENVIRONMENTS REALLY BAD FOR US?
disease mortality than declines in incidence, at least in
community-based studies where incidence can be estimated (Burke et al., 1989; Demirovic et al., 1993; Hunimk
et al., 1997; McGovern et al., 1992, 1996). Stroke follows a
similar pattern, but here incidence may have increased
(Crimmins and Saito, 2000). The average number of morbid diseases reported by individuals also increased,
because people survive diseases that once would have been
fatal. Thus older people display more morbid diseases, but
less disability than in the past. Severity of morbidity has
declined (Crimmins, 2004).
Morbidity during the first half of the 20th century
Information on degenerative morbidity prior to 1960 is
not common, even in modern countries. The results presented below are largely taken from the Early Indicators
Project, under the general direction of Robert Fogel
(Costa, 2000; Fogel, 2005). Estimates of prevalence of
degenerative morbidity are available from Costa (2000),
who compared morbidity rates among Civil War veterans
examined in 1900–1910 and men matched for age from
National Health and Nutrition Examination Survey
(NHANES) from 1971–1975. She reported declines in
prevalence of a number of degenerative conditions
including valvular heart disease, which declined from
19.2% to 1.7%, and arteriosclerosis, which declined from
1.9% to 0.9% among 50–64-year-olds. In older cohorts
(60–74-year-olds), valvular heart disease declined from
26.9% to 3.6%, and arteriosclerosis from 8.2% to 2.3%.
Costa (2000) also reported declines in a number of nonfatal
conditions such as joint and back problems, irregular
pulse, or heart murmur and trills. In general, the prevalence of morbid degenerative conditions may have declined
from the turn of the 20th century to the early 1970s.
Additionally, Costa (2000) estimated the survival (person-years surviving) of individuals with specific morbid
conditions for the Civil War and NHANES (1971–1975)
cohorts. The only significantly shorter life spans for the
Civil War vs. NHANES cohorts were reported for the
total samples of both age groups and 60–74-year-olds
with joint problems. Among the remaining morbid conditions examined, life spans tended to be shorter in the
Civil War cohort, but not significantly so. Thus survival
times with a morbid condition may have increased
slightly between 1900–1971, but have not increased significantly. This would suggest (not surprisingly) that the
declines in prevalence are not due to shorter survival of
morbid individuals in the later cohorts.
Finally, Fogel (2005) reported age at onset of several
degenerative conditions for men born between 1830–1845
and 1918–1927. The age of onset of all conditions examined increased in the younger cohort. For example, average age at onset (diagnosis) for heart disease was 55.9
years for the 1830–1845 cohort, and 65.7 years for the
1918–1927 cohort. Similar results were reported for neoplasma, with age at onset of 59.0 years for the early cohort,
and 66.6 years for the recent cohort. This suggests that
the incidence of these causes of morbidity declined from
the beginning to the end of the 20th century. Given that
diagnoses of many of these morbid conditions were likely
to be underestimated, particularly in the earlier cohort,
these declines in incidence are likely to be underestimates.
Morbidity during the prehistoric period
It is commonly reported that degenerative mortality
prevalence is low in traditional anthropological popula-
113
tions. The empirical basis for this conclusion is that degenerative disease risk factors (e.g., high blood pressure, high
cholesterol, adverse lipoprotein profiles, and obesity) are
absent from these populations (Eaton et al., 1988). As a
result, it is often assumed that degenerative causes of
death are low in these populations. However, as noted
above, the prevalence of morbidity and mortality are, all
other things being equal, negatively correlated.
Cause of death is almost never available for anthropological populations, since the number of deaths observed
by anthropologists in the field is small, because anthropologists are not necessarily well-qualified to pronounce
cause of death, and because the mere presence of an
anthropologist suggests that the population’s mortality
structure may be influenced by contemporary national
populations. Consequently, the assumption that degenerative causes of death are absent in these populations is premature. The evidence that the prevalence of degenerative
disease morbidity is low in traditional populations is better
substantiated (Eaton et al., 1988). If it is assumed that
these traditional populations have a low prevalence of
degenerative disease, and that historical industrializing
populations (ca. late 1800s) had a high prevalence, then
either the incidence of degenerative morbidity increased
at some time prior to the 1850s, the survival of individuals
with degenerative disease morbidity improved, and/or general mortality declined and longevity improved. The only
evidence currently available is that general mortality
appears to have declined (Fig. 1). A better understanding
of these issues requires additional information.
Summary: morbidity
A simple parsimonious explanation for trends in mortality, incidence, prevalence, and survival over the 20th century is that the incidence of degenerative morbid conditions declined throughout the first half of the 20th century,
and that survival with morbid conditions remained
approximately constant until perhaps midcentury, and
then increased in the latter part of the 20th century. As a
result of these trends, prevalence declined until the mid20th century and then began to increase, as survival with
morbidity improved.
WHY DID INFECTIOUS DISEASE
MORTALITY DECLINE?
A large body of research has attempted to identify
exactly why infectious diseases declined with modernization. Despite (or because of) this intensive research, the
cause of the historical decline in infectious disease mortality remains controversial and largely unexplained (Hinde,
2003; Woods, 2000). In his classic exposé on the decline in
infectious disease mortality, McKeown (1976) proposed
four potential causes of the decline: 1) evolution of hostparasite interactions, 2) improvements in sanitation, 3)
improvements in modern medicine (defined as effective
chemotherapy or vaccination), and 4) improvements in
nutrition and standard of living. McKeown (1976) concluded, after eliminating \all other possible causes" (a–c),
that the cause of the decline must be improved nutrition,
despite any hard evidence for or against this conclusion.
This analysis suffers from several problems (Hinde, 2003;
Szreter, 1989; Woods, 2000). First, his arguments against
host-parasite interactions were based on the notion that
host and parasite evolve to accommodate one another, and
that evolution is slow. Recent studies in the ecological literature argue that the evolution of host-parasite interac-
114
T.B. GAGE
tions is considerably more complex, and that parasite evolution can occur more rapidly (Bull, 1994; Ebert, 1999)
than McKeown (1976) assumed. Second, it was argued
that sanitation may have been considerably more effective
than McKeown (1976) supposed (Cutler and Miller, 2005;
Szreter, 1989; Woods, 1991, 2000), although McKeown
(1976) did acknowledge the contribution of sanitation.
Third, the view of McKeown (1976) that improved nutrition (standard of living) was responsible for the decline is
not supported by current data (Floud et al., 1990; Fogel
et al., 1982; Livi-Bacci, 2000; Woods, 2000; Wrigley and
Schofield, 1981). Only the argument by McKeown (1976)
that effective chemotherapy was not responsible for the
decline in infectious disease mortality remains largely
uncontested. Finally, the argument by McKeown (1976)
that these four causes represent all possible causes of the
decline in infectious disease mortality is not convincing.
Clearly, germ theory (medicine defined more broadly), general education, and the implications of behavioral intervention (e.g., washing one’s hands) might have some effect
on infectious disease mortality (Cutler and Miller, 2005;
Ewald, 2000; Preston and Haines, 1991; Schofield and
Reher, 1991; Woods, 2000). The problem with the current
state of the critique of the hypothesis of McKeown (1976)
is that if his standard-of-living argument is incorrect, then
what explains the decline in airborne diseases (e.g., tuberculosis, influenza, or pneumonia), which were among the
largest infectious disease categories contributing to the
historical decline in mortality (Hinde, 2003)? My point
here is not to argue for or against any of the various
hypotheses concerning the decline in infectious disease
mortality with modernization, but simply to point out that
a convincing and comprehensive explanation of the decline
in infectious disease mortality is still not available.
WHY DID DEGENERATIVE DISEASE
MORTALITY DECLINE?
The fact that many of the degenerative diseases declined
historically does not necessarily mean that the risk factors
listed by Eaton and Eaton (1999), Eaton et al. (1988), and
others do not contribute to the etiology of degenerative
mortality. It is likely that cigarette smoking, which has
increased with modernization, contributed to the rise of
neoplasms (Crimmins, 2004; Gersten and Wimoth, 2002).
Further, cigarette smoking, poor nutrition, lack of exercise, and obesity also appear to be risk factors for cardiovascular disease. However, if the historical decline in
degenerative disease is correct, then what is it about modern environments and lifestyles that overcame these wellknown adverse risk factors of modern life and resulted in
an overall decline in degenerative disease mortality?
Listed below are some possible causes of the decline in
degenerative mortality, along with some brief comments
on each potential cause:
1.
2.
3.
4.
Changes in lifestyles;
Improvements in modern medicine;
Direct interactions with infectious diseases;
Indirect interactions with infectious disease mortality;
and
5. Degenerative diseases are infectious diseases.
The 1978 National Institutes of Health symposium concerning the unexpected declines in ischemic heart disease,
observed post-1940, concluded that improvements in life-
style (e.g., nutrition, exercise) and improvements in modern medicine reduced the risk or delayed the onset of cardiovascular disease (Havlik and Feinleib, 1979; National
Center for Health Statistics (NCHS), 1978; Olshansky and
Ault, 1986). However, it seems unlikely that the changes
in lifestyles in question, which began to be recommended
in the 1950s and 1960s, and/or modern medicine (e.g.,
blood pressure medicines, introduced even later) could
explain the long-term decline in cardiovascular and certain degenerative disease mortality observed during the
first half of the 20th century. They might help explain the
continuing declines in degenerative disease mortality in
the last half of the 20th century.
The infectious diseases pandemics, particularly respiratory diseases pandemics, are traditionally associated with
excess degenerative disease mortality (Azambuja and
Duncan, 2002; Davenport, 1976; Lancaster, 1990). Perhaps
the additional stress of these infectious diseases contributed to degenerative mortality, which declined as infectious causes of death declined. This is possible, but the
precise mechanisms remain to be determined. If respiratory diseases simply reduced the survival of individuals
with degenerative disease morbidity (consistent with the
data presented above), then the decline in respiratory diseases could potentially cause the prevalence of degenerative disease morbidity to increase. However, the prevalence of degenerative disease morbidity does not appear to
have increased until late in the 20th century, well after
the respiratory diseases declined as causes of death.
Indirect interactions with infectious disease mortality
could take several forms, such as early life effects (Fogel,
2005) or the fetal origins hypothesis (Barker, 1999; Godfrey and Barker, 2000). Costa (2000) and Fogel (2005)
argued that exposure to infectious disease and/or the
impact of infectious disease on nutritional status early
in life could be a risk factor for developing degenerative
disease later in life. Alternatively, infectious disease and/
or nutritional status of the mother could influence fetal
development and predispose an infant to degenerative disease later in life (Barker, 1999; Godfrey and Barker, 2000).
In either case, infectious disease has an indirect interaction with subsequent degenerative disease, i.e., the incidence of degenerative disease.
Finally, there is the possibility that some degenerative
diseases are in fact due to infectious agents (Ewald, 2000).
There is currently clear evidence that some cancers are
infectious (Doll and Peto, 2001), and both Chlamydia
pneumoniae and Porphyromonas gingivalis are potentially
implicated in the etiology of cardiovascular disease (Grayston, 2000; Patel et al., 1995).
Like the historical decline in infectious disease mortality, the mechanisms and causes of the historical decline in
degenerative causes of death remain to be determined.
WHY HAS HUMAN MORTALITY DECLINED IN
THE FACE OF NOVEL ENVIRONMENTS?
Evolutionary theorists typically postulate that novel
changes in the environment will be detrimental to organisms in these environments. Within biological anthropology, for example, it is argued that humans are \adapted"
to the hunter-gatherer environment and not to the agricultural and \built" industrial environments which are
\novel" (Eaton and Eaton, 1999; Eaton et al., 1988; Nesse
and Williams, 1999). Clearly, however, humans have benefited from the general changes in modern human environments by a general reduction in mortality. Further, it is
ARE MODERN ENVIRONMENTS REALLY BAD FOR US?
not even clear that mortality increased with the adoption
of agriculture. Of course, some factors, such as smoking,
probably have not contributed to this improvement in
health, and there may be other negative factors as well
(Eaton and Eaton, 1999; Eaton et al., 1988). On the whole,
however, during the last several centuries mortality has
declined, although, as discussed above, it is not exactly
clear why.
How can these improvements in health in the face of
novel environments be reconciled with evolutionary
theory? One solution is to consider the improved health
an example of \genotype by environmental correlation."
Genotype by environmental correlation occurs when and
if organisms with specific genotypes seek out genotypically compatible environments (Stearns, 1992). Similarly,
why cannot humans \build" environments that are on
the whole compatible with human biology? After all,
modernization includes the development of sanitation
systems, public health systems, effective chemotherepy,
etc. Of course, there are likely to be constraints on what
can be \built," and consequently some aspects of the
\built" environment may be detrimental, but the overall
affect need not be negative.
CONCLUSIONS
The demographic history of the human population has
proven difficult to establish, because the available empirical evidence is incomplete. Since the evidence tends to
improve with time, secular improvements in data collection have been interpreted as secular trends in mortality
or health. It is the thesis of this paper that degenerative
and infectious diseases have declined over the course of
modernization. The widely held view that modern lifestyles are bad for human degenerative health is largely
due to secular improvements in data collection rather
then a true deterioration in health.
1. Barring occasional pandemics, total mortality has
declined since the 1850s in the developed regions of
the world, and since the 1920s in many of the less
developed regions of the world. There is no indication
that mortality prior to the beginning of the industrial
revolution was significantly lower than the mortality
observed from the 1750s to 1850s in Sweden. Clearly,
overall modernization/industrialization has been associated with improvements in human health.
2. There is no doubt that infectious diseases declined
with modernization, despite increases in population
size and urbanization, which exacerbate infectious
causes of death (Fenner, 1970). Exactly what aspects
of modern environments and modern lifestyles are
responsible for the decline in infectious disease mortality remain controversial.
3. Degenerative diseases as a whole have also declined
with modernization and industrialization. The commonly held concept that degenerative diseases increased until the mid-20th century is based on trends
in cause of death that are uncorrected for misclassification of cause of death. Whenever methods of correcting
for misclassification of cause of death are employed,
degenerative diseases as a group appear to decline.
They begin to decline in the uncorrected data after the
1940s or 1950s. It is likely that cardiovascular mortality has declined more than any of the other major infectious disease categories, such as respiratory tuberculosis (responsible for the largest proportion of the infec-
115
tious disease decline in England and Wales and the US)
or influenza, pneumonia, and bronchitis (responsible for
the largest proportion of the decline in infectious disease
mortality internationally). The exception here is neoplasms, which appear to increase as a cause of death
until recently in most modernized/industrialized countries. This could be due in part to cigarette smoking, a
behavior correlated with modernization. Exactly what
aspects of modern environments and modern lifestyles
are responsible for the decline in degenerative disease
mortality prior to the 1950s are largely unstudied.
4. Mortality is not the only possible definition of health;
morbidity can also be considered. However, due to the
relationship of morbidity and mortality, morbidity
may increase while mortality declines, and vice versa.
Historical information on morbidity is even more
incomplete than on mortality. However, it appears
that the prevalence of morbidity declined during the
early part of the 20th century but began to increase in
the latter part of the 20th century. This increase could
be due to better survivorship of morbid individuals due
to recent improvements in medical treatment.
5. The field of evolutionary medicine, among others, has
argued that the \novel" environmental conditions
experienced by modern/industrialized humans should
be detrimental to health, since we are \adapted" to a
hunter-gatherer lifestyle. This is not an evolutionarily
necessary conclusion. Given that modern environments are at least partly \built" by humans, the
effects might be considered a \genotype by environment correlation," which are often positive.
ACKNOWLEDGMENTS
I thank Sara Stinson, Paul Leslie, Tom Brutsaert, Janet
Padiak, and two anonymous reviewers for comments on
the manuscript, and Lynne Shultis for help in preparing
the figures.
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