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1. Features Of The Decline
The great mortality decline started in Western and Northern Europe in the middle of the eighteenth century or perhaps earlier, leveled oﬀ for a couple of decades in the mid-nineteenth century, and then continued again. Life expectancy at birth rose from some 35 years to more than 70 years over this period. The development in North America was similar. Typically, mortality began to decline some 50 to 150 years before the industrial revolution and before living standards started to improve monotonically, and some 100 to 150 years before marital fertility started its own long-term decline. Exceptions are England, where the decline in death rates started at about the same time as the industrial revolution during a period of falling real wages, and France, where fertility started declining at about the same time as mortality, and also well before living standards improved. The timing of the great mortality decline is strikingly similar in the countries of Western and Northern Europe despite diﬀerences in economic structure and development. It could also be surprisingly simultaneous in diﬀerent regions in the same country despite large diﬀerences in economic development.
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In countries where we have long historical series of age-speciﬁc mortality rates (England, France, and some others including the Nordic countries), we know that the decline began with a fall in the rates of infant and child mortality. This was due mainly to a reduction in deaths from smallpox, which was a very common childhood disease in the eighteenth century. The increase in life expectancy during this period was due almost entirely to the decline in infant and child mortality.
While infant mortality continued to decline in Sweden throughout the nineteenth century, it leveled oﬀ in England and remained stable until end of the nineteenth century; then dropped rapidly as it did in all other Western countries. Childhood mortality in both countries actually increased in the middle of the nineteenth century before it started a persistent decline. This exempliﬁes two patterns of the historical infant and childhood mortality decline: a northern pattern with declines essentially throughout the nineteenth century and a Western one with a leveling oﬀ during the nineteenth century and a new decline after the 1880s (Perrenoud 1984).
Adult and old age mortality started to decline slowly at the beginning of the nineteenth century, or possibly earlier for England. The decline was generally more pronounced in the latter part of the nineteenth century and accelerated after World War I along with mortality at all other ages. The decline slowed down for adults and the elderly around 1950 but accelerated again in the 1970s.
With the great mortality decline followed a change in the composition of the causes of death, away from pestilence, over receding pandemics, to manmade diseases. Omran (1971), in his theory of epidemiological transition, distinguished between three development patterns: the classical or Western pattern, described above, the accelerated pattern, and the delayed pattern. They are distinguished by diﬀerences in timing and speed. The decline that took 200 years in the West started 150 to 200 years later in the Third World but then took less than 50 years to complete. There are still many countries where the great mortality decline has been delayed and where it remains to reap the gains from low mortality.
2. Explanations Of The Mortality Decline
An understanding of the great mortality decline can be based on two approaches, namely period and cohort explanations. One should also make a distinction between factors that rely almost entirely upon the actions of man and those beyond deliberate human control.
2.1 Period Explanations
A widely accepted multifactorial explanation (United Nations 1953) is based on period factors that depend upon our activities such as public health reforms, advances in medical knowledge, improved personal hygiene, and rising income and standards of living. This type of explanation is consistent with demographic transition theory and with the theory of the epidemiological transition.
The demographic transition theory was once one of the most widely accepted ‘truths’ in social sciences and one of the main pillars of the UN paradigm of how to promote developing countries. It stated that mortality was high and ﬂuctuated strongly before the demographic transition. The transition was said to begin with a decline in the level of mortality and with a dampening of its ﬂuctuations. This was regarded as a consequence of a modernization of the economies (the agricultural and industrial revolutions). A rapid increase in population size would follow because fertility adjusted much later due to a slow response in institutions and norms that inﬂuence fertility (Davis 1945, Notestein 1953).
The idea of a stable level of mortality prior to modernization is a central feature in the theory, but before the mid-eighteenth century the mortality level was far from stable, as was shown for England by Wrigley and Schoﬁeld in their classic book (1981). Similar patterns had been demonstrated by many other scholars as well, but only for individual parishes or institutions, or for smaller regions like southern Sweden (Bengtsson and Oeppen 1993) or northern Italy (Galloway 1994). Since the mortality level prior to the great mortality decline was not stable, it is not appropriate to use it to date the beginning of the demographic transition. Another ﬁnding that questions the demographic transition theory is the long- term movement in fertility in the past. Since such changes took place in the past, one cannot justify the assumption that fertility norms changed slowly and kept fertility high for many decades after the start of the demographic transitions (Bengtsson and Ohlsson 1994).
On a broader front, McKeown (1976) questioned the multifactorial explanation of the great mortality decline. He argued that a single factor, namely better nutrition, could explain almost the entire great mortality decline. His criticism was based on a study of cause-speciﬁc mortality in England and Wales from 1838 to 1947, where he observed that two-thirds of the mortality decline was due to a reduction in infectious diseases. In later work he also analyzed mortality rates and economic development for other countries and further back in time, though not in such detail as for England and Wales.
McKeown argued that medical advances had little inﬂuence on mortality trends before the breakthrough of sulfonamides and antibiotics in the 1930s and 1940s. In earlier periods the only disease that one could cure was diphtheria. Very few deaths, however, were due to diphtheria, and it was already retreating when the antitoxin came in use around 1900. For periods before 1838, McKeown argued that inoculation and vaccination for smallpox had little or no impact on the general mortality decline. Vaccination started in England at the end of the eighteenth century, but it was not widespread until after 1840, at which time it became available at public expense. Others have drawn the same conclusion for Sweden, where inoculation never became widespread. Only about 50,000 individuals were inoculated between 1750 and 1800 (Skold 1997). If inoculation provided total safety against death from smallpox, some 7,500 would have been saved, assuming a fatality rate of 15 percent. This saving should be compared with the 300,000 who died from smallpox in Sweden during this period. Thus, even though inoculation saved some lives and possibly slowed the spread of the disease, it was not a major factor behind the initial mortality decline.
A similar story can be told about vaccination. In all the Nordic countries, the smallpox mortality declined before vaccination started in the ﬁrst years of the nineteenth century and well before vaccination became common in the 1820s. Even though the level of mortality in smallpox was low already when vaccination started, the disease continued to be fatal for many decades. There were outbreaks in Finland and Sweden as late as in the 1880s, most likely because not all children were vaccinated (for an overview of the Nordic countries, see Bengtsson 1992). In England, vaccination did not become widespread until the latter part of the nineteenth century. Thus neither inoculation nor vaccination was of major importance for the initial mortality decline but it is likely that vaccination ensured that the disease never came back once it had essentially been eradicated.
The improvement of personal hygiene may have had some eﬀect on mortality in England and Wales after about 1880, when a decline in intestinal infections coincided with substantial improvements in water supply and sewage control, which must have reduced the incidence of waterborne infections. Since changes in mortality from intestinal infections were only a smaller part of the general mortality decline prior to, say, 1870, the general reduction must have been due mostly to factors other than improved personal hygiene, according to McKeown. For the same reason the type of public health measures discussed above must have had little impact on the great mortality decline prior to 1870 and only a partial eﬀect afterwards. Other public health measures, such as the breastfeeding campaigns that took place in Sweden in the 1830s and later, were not discussed by McKeown. Fridlizius (1984) has argued for Sweden that these campaigns might very well have had an impact on infant mortality, but that they started much later than the decline in mortality. Incidentally, childhood mortality went up somewhat during the period when breastfeeding campaigns started.
Helleiner argued in 1957 that the population of Western Europe must have increased from the mid-eleventh century to the late thirteenth century and from the mid-ﬁfteenth century to the end of the sixteenth century. The population increase observed in the eighteenth century should therefore not be unique except that mortality decline started from a higher level and went on longer than before. Helleiner and others scholars have argued that these changes in mortality were spontaneous (natural), and in 1973 the UN added natural factors as a ﬁfth determinant of the great mortality decline. Later, others like Fridlizius (1984), Perrenoud (1984), and Schoﬁeld (1984) have asserted that a change in the virulence of pathogens initiated the great mortality decline. The basic idea is that the virulence of pathogens changes spontaneously over time. Virulence in an organism is generally understood as its ability to overcome host defenses. At this point it is important to note that some pathogens develop more quickly in a malnourished host while others do not depend on such circumstances to produce very high mortality. (Inﬂuenza epidemics, for example, are neither created nor sustained in malnourished persons, and they never were.)
McKeown’s main argument on this issue, though not proved, is that the initial mortality development during the latter part of the eighteenth century was an integrated part of the great mortality decline, which continued for the next two centuries and therefore cannot be due to a spontaneous reduction in the virulence of pathogens. According to McKeown, what is left is nutrition as an explanation not only for the decline in infectious diseases from the mid-nineteenth century onwards but also for the initial phase. This reasoning is part of his attempts at ﬁnding one explanation for the entire mortality decline.
In criticism, Fogel (1994) noted that McKeown only discussed the nutritional intake, the diet, and not the claims from the body to maintain itself and build up cells. Thus, McKeown only took into account gross nutrition, not net nutrition, and the latter must be more closely related to health and mortality. We will come back to this issue shortly.
While Helleiner regarded the virulence hypothesis as a period explanation outside of man’s control, Kunitz (1986) did not agree. He argued that the disappearance of epidemics, such as plague, typhus, and smallpox, is associated with the growth of stable governments, the expansion and integration of nation states, and the emergence of disciplined armies in the seventeenth and eighteenth centuries. These advancements made it possible to control epidemics by means of isolation and better hygiene. Population growth and loss of regional and local isolation then converted epidemics into relatively more benign childhood diseases. The mortality in the latter diseases varied depending on nutritional status and the availability of adequate nursing, as did mortality in the nonspeciﬁc pneumonia–diarrhea complex, which became relatively more important when epidemic diseases declined. Poverty, crowding, poor sanitation, and hazardous work conditions became more important as determinants of death, particularly in the cities. As a result, the eighteenth century saw a divergence in the life expectancy in the upper and lower classes, according to Kunitz. His empirical evidence for this conclusion is rather weak since it is only based on a comparison of aggregate infant mortality rates in England, France, Sweden, Germany, and Spain, and with rough estimates of the standard of living in these countries at the end of the eighteenth century.
The ﬁrst part of Kunitz’ explanation, namely the control of epidemics by means of isolation and better hygiene, is much in line with Easterlin’s arguments. He argued that technology (in a broad sense) is the main determinant of the great mortality decline (Easterlin 1999). Easterlin argued that that the mortality decline from the beginning of the nineteenth century onwards is not due to economic growth and market developments but to public policy initiatives and new institutions based on new knowledge of disease. This could explain the simultaneous mortality patterns among countries despite diﬀerences in economic development.
2.2 Cohort Explanations
Cohort explanations of the mortality decline refer to features that initially aﬀect only certain young age groups but that may have long-lasting eﬀects for the groups involved. We mainly have improvements in childhood conditions in mind, or even conditions during the fetal stage that have lasting eﬀects on health and on the lifespan. Net nutrition is seen as the main determinant of the development of cells, which is most rapid during the fetal stage and which diminishes gradually until the body is fully developed at an age around 20, or a little later. Net nutrition is what is left for the development of cells after nutritional claims needed for other life-supporting claims and claims to sustain work are accounted for. A low net nutrition could thus either be due to a low nutritional intake or to additional claims coming from diseases. Also, many diseases not only make their own claims on nutrients but also make it more diﬃcult for the body to absorb nutrients in general. This is the case for infectious diseases. If cells and organs do not develop, children may become stunted, become shorter in general and less healthy. Thus we can basically diﬀerentiate between two types of cohort explanations for the mortality decline, namely (a) increased nutritional intake during the fetal stage and/or early years of life, and (b) decreased claims during the fetal stage or early years of life due to a reduction in diseases in the mother or the child.
The importance of early childhood conditions for later life has probably been well-known since time immemorial. The idea is that each generation seems to carry along the same relative mortality from childhood to old age. Both medical and historical research on this matter has expanded rapidly over the last couple of decades (for an overview, see Elo and Preston 1992).
In this connection, the work by Barker (1994 and elsewhere) has been of major importance. He has summarized the medical evidence for the importance of the nutrition of the fetus and newborn infant for the health of the adult. Fogel (1996) has advocated these ideas in historical research perhaps more than anyone else. In addition, Preston and van de Walle (1978) for urban France, and Fridlizius (1989) for Sweden, emphasize the importance of cohort factors for the mortality decline.
Steckel (1983) and Fogel (1996 and previous work) use ﬁnal body height as a measure of net nutrition and health during childhood. Individuals who had well-nourished and healthy mothers and were well- nourished themselves during the fetal stage have a lower risk of death during infancy. If they are well- nourished and healthy their cells and organs develop better and they reach greater heights and live a longer life. Since net nutrition and not gross nutrition determines health there is no direct link between gross nutrition and height. Improvements in health and height may either be a result of better nutrition (better diet), or fewer claims due to diseases. Thus a decline in the prevalence of smallpox, for example, has a positive eﬀect on height and extends the lifespan, everything else being equal. The problem is that it is diﬃcult to evaluate how much of the improvement in health is due to diet and how much is due to lower claims. Calculating diets for premodern populations is a diﬃcult task (Fogel 1996), and it is even more diﬃcult to calculate claims. Still, historical records show similarities between trends in height and gross consumption (Fogel 1994, 1996), indicating that trend in claims has been of minor importance. If that is the case, then McKeown’s focus on gross nutrition can be justiﬁed.
Undernourishment, whether due to a low or badly composed intake, or due to an increased claim because of diseases, may lead to a stunting of height or weight and illness, diseases and mortality later in life instead of increasing mortality in the immediate future. The immediate relationship—i.e., the period link between economy and mortality—is therefore much weaker than what Malthus believed, according to Fogel. The rather weak short-term relationship often found between prices and deaths for many European countries, shown by Lee (1981, 1993), Galloway (1988) and others, supports this interpretation (Fogel 1994). Thus cohort factors matter more to the mortality decline than period ones, according to Fogel.
A warning against an uncritical use of cohortmortality notions is implied in the ﬁndings by Fridlizius (1989), who has shown that the mortality of the Swedish cohorts born in the beginning of the nineteenth century deviated greatly from what would have been anticipated given their mortality at younger ages. He called them deformed cohorts and saw the excess mortality for men as due to high levels of alcoholism during the 1830s and 1840s. Such life-styles lifted their mortality above what would otherwise be their ‘programmed’ level. Other analyses of aggregate cohort mortality data also bring any strong cohort eﬀect of conditions in early life into question.
While Fogel was mainly concerned with chronic malnutrition, we may also note that temporary disturbances in nutrition, in particular during some periods at the fetal stage, may also have long-lasting eﬀects on health, since later improvements cannot always compensate for prior loss (Barker 1994). Therefore, temporary malnutrition due to lack of nutrients or to an increased disease load, whether of mother or of child, may have long-lasting eﬀects on health and lifespan. It has, for example, been shown for Sweden that the disease load in the ﬁrst year of life has a strong impact on mortality from airborne infections and other diseases in later life (Bengtsson and Lindstrom 2000). Consequently, elimination of temporary malnutrition, which is still a major problem in many countries of the world, may cause another long-term cohort decline in mortality.
2.3 Mortality Fluctuations
Another feature of the great mortality decline, as observed by demographers, is that the mortality ﬂuctuations became much smaller in the nineteenth century than they were previously. Its consequences for the balance between the population and the economy in the preindustrial society, and also its eﬀects on the mortality decline, have been controversial. There are two schools of thought, and they have reached very diﬀerent conclusions. According to those who analyze mortality crises (Meuvret 1946, Goubert 1965), the reduction in such crises was a major factor behind the secular decline in mortality. This view gained support during the 1960s and 1970s. Wrigley and Schoﬁeld (1981) showed, however, that the elimination of crises accounted for only a small fraction (about 10 percent) of the secular decline in mortality in their analysis based on a large national sample of English parishes. Many others also obtained similar results (see Ortega Osona 2000 for an overview). This view is now questioned by Ortega Osona, who has found that the conclusion of Wrigley and Schoﬁeld holds true for England but not for Northern Italy and New Castile, where the reduction of the variability in mortality is important for the initial decline in mortality.
Few scholars today will argue that a single factor is the main determinant of the great mortality decline. Of course, it is no coincidence that the greater resources made available by the transformation of our economies in the eighteenth and nineteenth centuries runs parallel with the great mortality decline and with the fertility transition as well. In a millennial perspective, these events took place at about the same time. That is not to say that there is a close relationship between the economy and the great mortality decline. On the contrary, economic growth is not likely to be even a major determinant, neither before the decline nor in its initial stages, and perhaps far less than expected during its later stages. Instead, the causes are multifactorial and vary from the start to the end of the decline.
Parts of the initial decline may very well be the results of pure luck—a spontaneous decline of the aggressiveness of smallpox pathogens that were a part of an old demographic pattern and not a result of a modernization process. The development and compulsory use of vaccine surely prevented the disease’s return. Improvements in nourishment and in the care of mothers and children had long-lasting eﬀects on the lifespan. Advancements in water supply and sanitation, as well as better housing, contributed to the decline from the second part of the eighteenth century onwards. Medical development in the twentieth century prolonged life. The fact that health is determined by net nutrition, intake minus claims, and that claim is due partly to diseases, makes it diﬃcult to evaluate the determinants of the mortality decline. The inﬂuence of conditions in childhood, as well as temporary ones on mortality at older ages, also adds to the complexity. The impact of each individual factor is therefore very diﬃcult to measure and requires a long series of high quality data. Several variables, like the virulence of pathogens and the claims on nutrients due to disease, can at best be estimated indirectly, if at all. The analyses based on highly aggregate longitudinal data have identiﬁed the problems and directed us towards the solutions. It is, however, more doubtful as to whether solutions will be found at that level of analysis. Perhaps the use of longitudinal micro-data will serve as an important complement, as it has in other areas.
Thus the cause of the great mortality decline is multifactorial and the importance of the various factors changes over time. The factors are also involved with each other. For example health is both a cause and a consequence of net nutrition, and this makes it extremely diﬃcult to measure the impacts of each factor. Still it seems very unlikely today that the initial part of the great mortality decline was a result mainly of an increasing standard of living and of intervention by man. From the nineteenth century onwards, we are certain that improved nourishment and various interventions have an impact on the decline. One might therefore argue that the initial decline is not a result of modern developments but rather is a part of an old pattern, where the level of mortality varied. If this pattern would have continued, one could have anticipated an upswing in mortality during the latter part of the eighteenth century, and in fact such an upswing started in several European countries around the middle of the century, although it was only of limited strength. At present, we know that improved nourishment, personal care, and various public health measures mattered. Thus, we may speculate that it was not the initial mortality decline that was a result of the development of modern society, but rather the absent increase. This leads us to a new generalization of the demographic transition, where the pretransition stage is characterized by changing levels of mortality, not controlled by man, and population growth varies as do nuptiality and fertility. From around the middle of the eighteenth century this pattern was broken and man determined levels of mortality as well as fertility.
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