About This Weblog

This weblog is a personal project to bring together (online, in real time) my thoughts on global-imbalances, demography, fertility and economic growth. Eventually the posts will all form one continuous block which can be read sequentially. In the meantime it is a 'work in progress' with bits of me serving as 'gum and chickenwire' to hold together a bunch of arguments from and links to the pertinent papers.

I hope the outcome will be readable and useful to someone.

Introduction

We are getting older.

This commonplace is both self-evident - individually we are always that little bit older, each and every day - and surprising - Niger is getting older, Mali is getting older, Somalia is getting older. This is surprising since these are, effectively, among the youngest societies on earth (Niger 15.8 Mali median age 16.35, Somalia median age 17.59). Everyone is aware that Japan is getting older, everyone is aware that Germany is getting older (these are currently the two oldest societies on the planet), but Niger, Mali and Somalia!


In fact, apart from 18 'demographic outliers' as identified in the 2005 United Nations Human Development Report, each and every country on the planet is getting older. Nor is this societal 'ageing' a recent phenomenon, it starts from virually the outset of what has become known as the demographic transition - something which began in many European societies in the late 18th and early 19th centuries. The transition begins with a sudden and sustained drop in mortality, the society becomes 'suddenly young' and after this it is continuous ageing all the way.

So if this work is about ageing, its starting point is that this ageing is not a new or recent phenomenon (the 'discovery of ageing' is of course more recent, but that is another story). The end point? Well there is no end point, as life expectancy continues to push ever onwards and upwards we will all be living longer, and to date there does not seem to be any special biological limit to this process. That is the good news.

The bad news comes with the how. Following the sharp mortality decline which characterises the onset of the demographic transition ageing commences, but historically it has done so at a relatively slow rate. The difficult part of the ageing process as it affects us today is that now proceeding more rapidly, with the evidence suggesting that those societies which began the transition later are ageing even more rapidly. Countries like China and Brazil have experienced sharp declines in their birth rates accompanied by rapid increases in life expectancy. This means that the median age at historically unprecedented rates, and that these societies run the risk of becoming 'old' before they become 'rich'.

The ageing process is also associated in the contemporary world with sizeable changes in the age structure of the population, changes, which given our existing customary boundaries between the ages of work and retirement, are likely to produce a significant increase in elderly dependency ratios across all the OECD countries.

There are however solutions available to address the problems which this rapid ageing will produce. In part it will be the objective of this book to describe and explain the changes which are taking place around us, and in part the aim will be to explain and justify the changes we need to make if contemporary 'ageing' is to become not a threat but a boon and a challenge.

The provisional structure of the book is as follows:

Chap I Nasty Brutish and Short?
Chap II The Second Stage?
Chap III The Discovery of Age Structure
Chap IV The Mysteries of Growth
Chap V The Life Cycle
Chap VI Asymetric Shocks
Chap VI Global Imbalances
Chap VII Remedying the Global Imbalances

Nasty Brutish and Short I

Nasty Brutish and Short









The 21st century will doubtless bear witness to a great many new and strange phenomena, but somewhere high up on the list of things which are going to define the coming century will surely be the fact that most countries experienced a substantial and sustained ageing in their populations as the century progressed. This phenomenon of population ageing, which has now become something of a commonplace for us, is in fact the result of a twofold process, a general decline in birth rates, and a generalised and substantial increase in the levels of life expectancy.



In the developed world birth rates have long been falling, and are now either hovering around ( one or two countries like the United States and Ireland) or significantly below (the rest of the OECD member states) replacement level. Since there is no consensually agreed theory among demographers which explains why fertility rates have fallen so low the future trajectory of fertility is hard to foresee, but in the immediate future it is clear that for many countries below replacement levels of fertility are likely to remain the norm, and the big question - the billion dollar one in fertility theory terms - is really 'just how low can you go'?





Side by side with this most developing countries are, and will continue for some time to be, in the process of seeing their fertility levels fall steadily (and even dramatically) from TFRs which are initially in the high to moderate band, first to replacement, then to below replacement, and finally to lowest-low fertility and beyond. The case of Iran is instructive here. Having dropped from around 5 to just under 3 between 1989 and 1996, Iran's total fertility rate has continued to decline rapidly, and in the early years of this century dropped below replacement level. data from results from the 2000 Demographic and Health Survey (DHS) for Iran revealed a decline of 32 percent in the TFR between 1996 and 2000, from nearly 3 to around 2 children per woman. The data also shows that reduced fertility is not simply an urban phenomenon but is occurring throughout the country, with some of the most dramatic declines being in the rural areas, where the 1996-2000 decline was some 31% when compared with only an 18% decline in the urban areas (Abbasi-Shavazi, 2002). Data from the Italian statistical agency ISTAT reveal a similar picture with TFRs in the North rising steadily from 1.05 in 1995 to 1.34 in 2005 while in some rural regions fertility fell to very low levels ( Sardinia 1.07, and Molise and Basilicata 1.14, see ISTAT 2006).. Data for East Germany reveal a similar pattern, in that the TFR rapidly converged towards and then went below the already low level of the former Federal Republic. Thus if convergence is taking place (see Wilson, 2001) it is both between and within countries and towards intitially lowest-low fevels of TFR.





At the time of writing some 71 countries (or 43% of the global population) have fertility rates which are in the 2.1 to 5.0 TFR band. These countries are classified by the United Nations as 'intermediate fertility' ones (UN, 2002). Essentially all those countries where TFRs have already fallen below 5-0 may conveniently be described as having initiated their demographic transition, and as such these countries are experiencing steady and sustained fertility declines. It is reasonable to expect that between now and 2050 they will all enter the below replacement fertility group, with the vast majority entering sooner rather than later. As and when they do so they will steadily swell the ranks of the 44 countries who already 'enjoy' this status.



The consequences of such generalised low fertility are not hard to imagine: populations will gradually start to decline and in an increasing number of countries. At the same time our populations will become older, and even a quick glance at any of our garden variety news sources will nowadays normally suffice to find some reference or other to long-term population projections which show truly daunting ageing figures. If, for example, fertility rates in the developed world remain, as they are today, well below replacement, and if we continue to experience improvements in life expectancy at the current rate, then half the population of today's industrialised countries is projected to be over 60 by the time we enter the last quarter of the 21st century. Of course just how 'old' 60 will actually be by the time we get there is an issue in and of itself, and one which forms a significant part of the 'meaty content' of the present ageing debate.





At the same time many developing countries, such as, for example, China, may well find themselves ageing in an especially dramatic fashion, since fertility rates in the third world have been falling very rapidly (UN, 2002) and longevity rates are also rising equally dramatically. So, if the current distribution between working and retirement ages is maintained, in less than two decades China will find itself facing an old-age dependency burden similar to the one which can be found in the older Western European countries today.





The 'ageing phenomenon' itself, of course, willl come as no surprise at all to anyone who has a smattering of knowledge about standard demographic theory, since progressive ageing could arguably be considered to be one of the 'stylised facts' associated with the process which has come to be known as the demographic transition. Now the term demographic transition has normally been used to describe the transition from a demographic regime based on high birth rates, high infant and child mortality rates and low life expectancy to a regime more typified by falling birth, infant and child mortality rates, together with steadily increasing life expectancy. This process has often been thought to occur as a core part of the economic development and modernisation process which carries a country from the condition of being a pre-industrial society to one of being an industrial and then a post-industrial one (Easterlin, 1995, 1983 Caldwell, 1982).





What Is The Demographic Transition?





From the end of World War II and until at least the 1980s, there was probably no research issue that was either mentioned more frequently or debated more passionately in demographic literature than the theories and explanations adavnced in relation to the phenomenon which has become known as the demographic transition.



Transition theory has, right from the start, been characterised by a penchant for a phasal typology, and the original formulation of the theory was no exception to this rule, being presented as it was in terms of a three stage demographic evolution from a regime of high birth and death rates - "a high balance" - to one of low birth and death rates - "a low balance". An intermediate stage of high rates of natural population increase was thought to result from a tendency towards faster declines in death rates than in birth rates. Early pioneers of the theory like Warren Thompson and Frank Notestein, in addition to presenting the basic classification system, also suggested a list of major correlates and causes of fertility decline. These included decreased infant and child mortality, the spread of urbanization, increased costs of raising children, rising parental aspirations, increases in literacy, rises in women's status, a rise in individualism, a decline in religiosity and changes in other cultural factors. Many of these factors have often been included under that wide umbrella which has become known as the modernization processes.



According to the original version of the standard theory, after years of - more or less - homeostatic population drift (often termed the 'Malthusian era'), the start of the transition itself is normally thought to be marked by a sharp and sustained decline in mortality, and in particular by a decline in infant and child mortality. This mortality decline in and of itself produces a large and significant drop in the median age of the society concerned. After this it is, in one sense, up-hill all the way, since normally societies tend to embark on a continuing ageing process, an ageing process which has to date no known end-point. In this sense both the fertility decline associated with the initial or 'first' transition and the more recent one which sees the arrival of below replacement fertility - a process which some have ventured to call the second demographic transition - are intimately related, since the underlying 'driving factors' are undoubedly the same and the whole process is, in its core, an ageing one.



This alone should alert us to at least one difficulty: is it really adviseable to use the expression 'ageing society' in relation to our contemporary developed societies, since if collective ageing is associated with declining fertility and increasing life expectancy, then our societies have long been ageing ones, as indeed they will continue so to be for as far ahead as we can see.



Are There Really Two (Or Should That Be Three) Transitions?



As has been suggested there are those who in addition to breaking the demographic transition down into stages would also break it down into 'transitions'. Insofar as some theorists have gone on to use the expression 'second transition' (Lesthaeghe, 1995, Van de Kaa, 1987) they have normally done so in order to break the entire fertility transition down into two component parts, one which sees fertility decline from its earlier 'higher' pre-modern steady state to the modern, industrial-age near-replacement level, and a second, posterior, transition during which fertility drops from replacement level to one which is substantially below replacement (and in many cases falling as far as what some - Kohler et al, 2002 - have termed 'lowest-low fertility' which they define as lying in the sub-1.3 Total Fertility Rate range). As has previously been argued, there is no sound theoretical or empirical basis to justify making such a radical distinction between a first and a second transition, nonetheless since this terminology is widely used, it will continue to be applied here as a convenient shorthand for describing that package of social and other life course changes which are conventionally associated with the arrival of below replacement fertility.









Stylised Facts Concerning the Modern Demographic Transition





1/. As has been said the key differences between the two 'transitions' (the early pre-industrial transition and the later post-industrial one) is that while in the first case the fertility decline was accompanied by a sharp and continuing drop in infant and child mortality, in the second one it is old-age mortality which declines alongside the continuing fertility decline and it is the life-expectancy of the older-old which rises. This process is sometimes described as the rectangularisation of mortality in reference to the way in which the age-related mortality curve changes during the different stages of the transition, moving as it does from a U shape towards a rectangle as mortality gets gradually compressed at both extremes. The combined impact of the two phases of the transition then is that - after an initial "mortality shock" - all societies enter a process of seemingly continuous ageing. One noteable contemporary consequence of this is the fact that today there are only 18 countries - themselves considered to 'demographic outliers' by the United Nations (and identified as such in the 2005 edition of their Human Development Report) - which are not actually ageing.



So this is the first stylised fact: the demographic transition is a transition from a society with a relatively stationary age structure, and relatively static life expectancy, to one with a gradual and continuous increase in life expectancy and a steadily rising median age. In short, the transitional/post-transition society is an ageing one.







2/. In global terms it is undoubtedly true to say that the twentieth century was the century of life expectancy, since during its course average life expectancy at birth more than doubled - rising from an average of around 30 in 1900 to some 65 years by the end of the century (Riley, 2001). It may well be possible to say the same of the century to come too, since if present trends continue the planetary average life expectancy is projected to further rise to around 81 by the end of the 21st century (Lee, 2003). There is still no consensually agreed explanation for why life expectancy has been increasing in this way. Indeed there is some dispute as to whether in some cases it will now actually begin to decline (the case of obesity in the United States would be but one well-known example of a counter case, declining male life expectancy in Russia would be another, and the Aids epidemic in Africa another (Olshansky et al, 2005, Brainerd and Cutler, 2004, Pelletier, 2004). At the same time there is still no agreement among scholars about whether - as for example James Fries believed (Fries, 1980) - human lifespans have a more or less fixed upper limit or whether a phenomenon known as 'negative senesence' may not be at work (Vaupel et al, 2004). The key question is, as the cohorts which have had heavy disease loads and nutritional deficiencies in their early years pass through their life courses, and life expectancy pushes up towards the previous 'higher limits' whether subsequent cohorts will still exhibit the same upward trend in expectancies. Such uncertaintly not withstanding, and amidst so many potential areas of dispute, one factor does seem to be evident:: the process of increasing life expectancy has been closely associated with increased levels of education and with growing health awareness. In particular almost all studies of the topic highlight the fact that life expectancy and level of education have a strong positive correlation. So significant has the relation between increased life expectancy, increased education and economic growth been across in almost all countries that have experienced a fertility decline, an industrial revolution, and a modern process of economic growth that Columbia University economist Xavier Sali i Martin concluded a recent review of the last 15 years of new growth research with the conclusion that "life expectancy is one of the variables most robustly correlated with growth" (Sali i Martin, 2002). Since as Sam Preston has demonstrated life expectancy is itself correlated with education levels, it is possible that we have here in outline form one important part of the transition transmission mechansism (Preston, 1996)..



Equally the twenty-first century is almost certainly going to be the century when low fertility (meaning by this below replacement fertility) becomes the global norm since as it runs its course the vast majority of our planets population will enter below replacement level fertility regimes. In this sense something important is happening as we are almost certainly fast approaching a turning point in terms of population dynamics, and it is highly probable that global population will peak later in the century, possibly during the last quarter century (UN, 2002).



This then is the the second 'stylised fact' of the transition: the post-transition society has two core characteristics, declining fertility and increasing life-expectency. In fact it is perfectly possible that these two components are themselves interconnected, and this is a possibility which will be extensively explored in the subsequent sections of this book.



3/. The third 'stylised fact' is that while all societies age during the transition, not all age at an equal rate. Differences between societies are evident in terms of the relative rates of fertility decline and the relative rates of increase in life expectancy. Both of these differ substantially from one society to another, and clarifying the factors which lie behind such differences in transition rates and timing is undoubtedly one of the outstanding challenges still facing demographic research.





4/. Another trend has been that those societies who entered the transition earlier generally passed through it at a slower pace, while those who have started their transition later - and in particular in the most recent cases of the drop below replacement fertility - it seems that the process has accelerated considerably (UN, 2002). Indeed it is normally true to say that the later the entrant, the more rapid the subsequent fertility decline and the shorter the generational timescale required to reach the higher life expectancies associated with economic development would seem to be an increasingly valid generalisation. There is possibly an acceleration principle in operation here.



5/. A closer examination of declining fertility quickly brings us face to face with what might be called the fifth stylised fact: about the transition and this is that the fertility transition is normally accompanied by (and in fact often the result of) a steady and continuous increase in woman's mean age at first birth (WMAFB).This state of affairs was often less than evident, since at certain key points in the transition WMAFBs have fallen rather than rising (in England in the late eigtheenth century, during the industrial age following what became known as the second industrial revolution, and more recently after WWII in the context of the so-called 'baby boom' phenomenon). Indeed in the 'second', below replacement, transition this lowering of the MAFB process plays a predominant role, with changes in final parities having a relatively secondary overall importance (Sobotka, 2004). Developed fertility regimes now seem to be characterised by steadily rising MAFBs, and there seems little realistic likelihood that this situation will reverse.





6/ Finally, the increase in WMAFB is normally closely correlated with a steady rise in female education levels, female participation rates in employment and in the number of years of education and training required before entering first employment.. (Elaborate).





Was Life Really So Nasty and Brutish Before the Transition?





Safely armed with the above list of basic 'facts' we are now perhaps in a better position to understand some of the principal characteristics of the demographic transition process itself, but before moving forward to explore this, it may be worth pausing to think a little about life before the transition, life in the pre-transitional society, what was that actually like? How can it best be defined and understood? Was it really, as some have suggested, 'nasty brutish and short'? And if it was so, was this always and everywhere? This question is certainly worth asking ourselves since according to what seems (among economists at least) to be the most widely accepted version our pre-transition reality:



"Until the early 18th century, global population size was relatively static and the lives of the vast majority of people were nasty, brutish, and short.” (Bloom et al 2002).



Or, in the words of Berkeley demographer Ronald Lee (Lee, 2003):



"Before the start of the demographic transition, life was short, births were many, growth was slow and the population was young."



At this point, of course, all the roads lead us back to the work of the very Reverend Thomas Malthus for whom, it will be recalled, slow population growth was no accident. For Malthus population in the long run was held in relatively stable equilibrium with a slowly growing economy by a combination of what he termed 'positive' and 'preventive' checks.



The basis of Malthus's argument is straightforward enough, and really only depends on two fairly simple postulates. The first of these is the evident reality that humans need to eat and thus need food, the production of which in historical societies increases only slowly with time. And secondly there is the idea that 'nature itself' has ordained a passion between the sexes which remains constant through time. This latter 'instinctive urge' should, Malthus thought, lead to a steady stream of children coming continuously online. Since our resource supply can only be improved gradually not all of these children can be be maintained, and herein lies the source of what he termed the positive check.





Now Malthus himself has often been read as suggesting that populations are maintained virtually on the edge of starvation. In fact this is not necessarily the case, either according to the Malthus theory, or in reality. In hunter gatherer societies, for example, it has been estimated that violent deaths, often in warfare, accounted for around 30% of male adult mortality (Coleman 1986). Thus Malthus' mechanism might rather work due to the fact that the increase in population creates additional mortality issues, and one of these is the fact that the increase leads people to take more risks, such as moving farther afield to hunt etc, and in this way the level of 'population attrition' might well turn out to be greater.



Also there is the fact that Malthus himself believed that the greatest mortality problem associated with a limited food supply occured as a result of the fact that those who are under-nourished are more likely to die of infection, especially during epidemics. With more young to fend for, and less nutrition per capita, infants and young children are surely more vulnerable to even the simplest of health insults. This view is really not that far from the opinions of most modern epidemiological theorists and a brief look at the data for death from diahorrea in some third world countries today lamentably still offers a clear and simple illustration of the continuing operation of the process Malthus described.



We don't then need to read Malthus over-simplistically and indeed in some senses his argument here is surprisingly modern: as the Caldwells note, his argument on child nutrition and susceptibility to infection is not at all incompatible with the 20th ventury work of writers like Thomas McKeown and Robert Fogel (Caldwell, and Caldwell, 2003). As I have said Malthus's positive checks were really what we would nowadays call resource constraints: increasing population would inevitably find itself pushing against an agricultural output which was simply unable to keep pace (in a non Boserupian technological environment), and the resulting "misery" and undernourishment leads to a mortality rise which serves, in the long run, to counterbalance the increase itself.





Malthus's preventive checks, on the other hand, were not natural but social in character. They were constituted by socially evolved mechanisms designed to constrain fertility such as, for example, delayed marriage, protracted lactation or pre-modern forms of contraception (although it is important to note that Malthus himself was completely unaware of the possible importance of factors like lactation, or the fact that our reproductive biology may contain its own feedback components which are internalised in what has now become known as 'natural fertility' control: see Henry,1961 Ellison, 2001).





In the case of pre-industrial Europe, as well as in pre-modern foraging societies, Malthus was, in a certain sense, right: population was normally held in a kind of weak equilibrium with its resource environment via a combination of positive and preventive checks. In saying this we need to be cautious in just how we interpret the expression 'weak equilibrium. Robert Fogel, in his Nobel acceptance speech (Fogel, 1993) makes just this point:







"(My) analysis.....points to the misleading nature of the concept of subsistence as Malthus originally used it and as it is still widely used today. Subsistence is not located at the edge of a nutritional cliff, beyond which lies demographic disaster. The evidence outlined in (this) paper implies that rather than one level of subsistence, there are numerous levels at which a population and a food supply can be in equilibrium, in the sense that they can be indefinitely sustained. However, some levels will have smaller people and higher “normal” (non-crisis) mortality than others".





In other words according to the levels of height and the lengths of life-expectancy which are selected-for there are not one, but several, available population subsistence equilibria, and the situation is far from being a deterministic one. Factors well beyond the simple availabilty of the food supply have been at work, and many of these factors were 'natural' in origin (climate, disease) while many of the adaptive responses which evolved in conjunction with these natural ones were social in character (delaying childbirth, increasing terms of lactation).



Nevertheless, equilibrium, in some very general sense, was normally attained. To put this in another way, the resource/population process was a homeostatic one in the very long run. Population tended to osscilate around some general equlibrium level (allowing for height and life expectancy differentials) until weather, disease or political disturbance knocked population strongly away from this equilibrium. At this point the combination of positive and preventive checks would serve as some form of pre-modern 'automatic stabiliser', and the population 'carrying load' would eventually once more be brought back towards its long run equilibrium trend (allowing here for some very gradual forms of social learning and technological change). As as result, for the best part of 10,000 years global population size was remarkably stable, and growth in absolute numbers was slow. (Lee, 1987, 1997; Lee and Anderson, 2002),



However it is important to note that while there is plenty of evidence to suggest the existence of such a clear long-term trend, there is also plenty to support the idea that sizeable fluctuations around the trend occured, and that life expectancy in Europe, for example, varied significantly during the centuries preceding the industrial revolution.





Malthus himself, (like Cantillon before him) was an astute observer of the social customs of his times, and he was far from unaware of the wide variety of social institutions and practices - such as age of marriage, the percentage of women marrying, extra-marital fertility, or contraceptive practices - which had evolved and which served to mediate the operation of what some would call our 'naked biological' reproductive potential in determining the number of children per woman actually born.



In fact Malthus himself was well aware that in Western Europe prior to 1800 the key 'preventive check' in operation was what we now call the European marriage pattern. This expression is normally used to describe marriage customs which seem to have been widely practised during a long period of historic time across a substantial part of Europe, and in particular across that part of Europe which lies to the west of an imaginary frontier running from St. Petersburg to Trieste. The pattern has been found to have been in operation to varying degrees from the late middle ages onwards, and it was still to be found operating in some parts of rural Europe as late as the early twentieth century. The high point of its operation, however, is undoubtedly to be found during the seventeenth century.(Clark, 2005)





Malthus himself devoted a large part of Book II of his Essay to describing the marriage system in Western Europe and how it was characterised by late marriage. According to Malthus, the majority of European men and women delayed marriage until they had the economic resources necessary to support their families at their desired standard of living. In this sense many of the modern explanations for the birth postponment process which is thought to characterise the 'second' transition are not necessarily 'un-Malthusian', although it is important to note and understand the importance of the fact that while, during the Malthusian regime, first birth ages fluctuate and adjust to maintain a given standard of living, in the post-Malthusian regime the rise in first birth ages is secular, and associated with a steadily improving standard of living.



Malthus in fact believed that such delayed marriages prevented individuals from experiencing a substantial reduction in their standard of living on marriage and at the same time prevented the population from growing rapidly enough for positive checks and generalised misery to come into play . In particular Malthus noted that delayed marriage was especially widespread in Norway, Switzerland, and England (1986/1803, Vol. 2:238). He also believed that marriage rates in England were so low that a substantial fraction of English biological reproductive capacity was not being used (1986/1803, Vol. 2:239). Malthus in fact says:



“In a review of the checks to population in the different states of modern Europe, it appears that the positive checks to population have prevailed less, and the preventive checks more, than in ancient times, and in the more uncultivated parts of the world. The destruction occasioned by war has unquestionably abated…And although in the earlier periods of the history of modern Europe, plagues, famines, and mortal epidemics were not infrequent, yet, as civilization and improvement have advanced, both their frequency and their mortality have been greatly reduced, and in some countries they are now almost unknown. This diminution of the positive checks to population, as it has been certainly much greater in proportion than the actual increase of food and population, must necessarily have been accompanied by an increasing operation of the preventive checks; and probably it may be said with truth that, in almost all the more improved countries of modern

Europe, the principal check which at present keeps the population down to the level of the actual means of subsistence is the prudential restraint on marriage” (Malthus, 1986/1830:254).





While Malthus did not actually produce a systematic theory to explain delayed marriage, all the elements for such a theory were already present in his writings. As a true child of his times Malthus naturally believed that the aspirations for a respectable standard of living which he felt lead to the delay were based on foresight, and the ability to defer gratification, and these he argued were associated with the higher levels of civilization then to be found in Europe as compared with the majority of the rest of the world.



Thus he attempted to ground the operation of the mechanisms to delay or forego marriage on the psychologically based aspirations of individual women and men. The search for a reasonable (socially determined) standard of living was the central underpinning to the decision to delay marriage, and this constituted the first element in Malthus's system. Postponing marriage, according to Malthus, requires an unwillingness to be patient with pain and misfortune. Whereas expectations and acceptance of future suffering might lead to early marriage, the hope of enjoying life would cause people to postpone marriage (Malthus, 1986/1803, Vol. 2:59). The hope of bettering one’s self and the fear of misery and being without the necessities of life would be motivations to emphasize the preventive check (Malthus, l986/l803, Vol. 3:453-454).



If the first Malthusian element was hope, the second was foresight, the ability to forsee the difficulties that would inevitably attend an early marriage coupled with the rearing of numerous children (Malthus, 1986/1798: 99). Foresight, according to Malthus, requires the ability to look around one and recognize the distress and poverty that normally becomes the lot of those with large families and insufficient means. It requires a certain awareness of the difficulties associated with trying to rear and support children without first being firmly established economically (Malthus, 1986/1803,Vol. 2:14).



And beyond hope and foresight there lies gratification and our ability to defer it. Delayed marriage, according to Malthus, requires an ability to postpone the immediate comforts and satisfactions which might be thought to be offered by marriage with the expectation of receiving even greater benefits at some unspecified point in the future. By delaying gratification, individuals could assure for themselves and their children the resources for respectability and happiness. The comforts and conveniences of life were even possible with delayed marriage (Malthus, 1986/1830: 251-252).



Not everyone, of course, agreed with Malthus. Some took the Bosnerupian - and essentially more optimistic - view that economic resources had a tendency to grow faster than population did. In a Lecture presented at the University of Oxford in 1828, Nassau Senior argued that if what he termed savage nations were in “a state of habitual poverty and occasional

famine” this was due to their inability to develop their productive resources rather than an excess in the growth of their population. If they had but scanty populations, he argued, this was because their means of subsistence were even

scantier. In contrast in every 'civilized' country he found that “there is now less poverty than is universal in a savage state.” and he took the presence of this higher standard of living as testimony to the fact that “the means of subsistence have a greater tendency to increase than the population” (Senior, 1831: 47-48).



Archibald Alison also came to a similar conclusion, arguing that “the rapidity of increase in poulation is in the inverse ratio of the means which are afforded of maintaining a family in comfort and independence: it is greatest when these means are the least, and least when they are the greatest” (Alison, 1840, Vol. 1: 112).





One noteworthy point in both the Malthusian and non-Malthusian accounts is that it was consumption aspirations which played a key role in the explanation. There was however one subtle but important difference between the two views. On the Malthusian account it is the desire to maintain consumption which drives the preventive checks, whereas Senior, Alison, and others believed that consumption aspirations increased rapidly with economic growth, and that it is the desire to keep raising consumption which produces the fertility restraint. Indeed so closely did they believe that delayed marriage was tied to consumption aspirations that they postulated that economic expansion would ultimately lead to the increased postponement of marriage and a reduction in the rate of population increase. In this sense they are undoubtedly 'modern', and in some sense their work foreshadows the recent 'second transition' literature.



In truth the core idea that consumption aspirations increased with economic resources preceded both Malthus and his contemporary critics. Adam Ferguson writing in 1767 had already advanced the modern idea that what is necessary in life is vague and relative. According to Ferguson what is necessary “is one thing in the opinion of the savage; another in that of the polished citizen: it has a reference to the fancy, and to the habits of living” (Ferguson, 1980/1767: 142).



Ferguson went on to argue that there is apparently no limit to the expansion of consumption aspirations. “No ultimate remedy is applied to this evil, by merely accumulating wealth; for rare and costly materials, whatever these are, continue to be sought; and if silks and pearl are made common, men will begin to covet some new decorations, which the wealthy alone

can procure. If they are indulged in their humour, their demands are repeated: For it is the continual increase of riches, not any measure attained, that keeps the craving imagination at ease” (Ferguson, 1980/1767: 143).





Later Archibald Alison was even to offer an intergenerational mechanism for increasing artificial wants. According to Alison “each succeeding generation is bred up in the habits of indulgence to which the preceding one only attained by the result of many years of successful exertion. The parent who has raised himself from the middling to the higher ranks of life, or from the lower to the middling by a laborious industry, communicates to his children the habits and the wants to which he latterly succeeded. The gratifications which were considered as the highest objects of ambition, or the last step of luxury during the best years of his life, are regarded as mere necessaries by his posterity” (Alison, 1840, Vol. 1: 104).



This is, of course, is precisely that ideational mechanism which now plays such a central role in modern models of fertility decline which regularly refer to the way in which aspirations incorporated in such notions as 'ideal family size' tend to evolve with time and across generations (Lutz et al, 2006, Watkins 1990).



Ferguson argued in the eighteenth century that “while arts improve, and riches increase; while the possession of individuals, or their prospects of gain, come up to their opinion of what is required to settle a family, they enter on its cares with alacrity. But when the possession, however redundant, falls short of the standard, and a fortune supposed sufficient for marriage is attained with difficulty, population is checked, or begins to decline.” (Ferguson, 1980/1767: 142-143).



This is, in essence, the cohort theory of fertility change which has sometimes been offered to explain the transition to below replacement fertility. (Easterlin, 1987, Macunovich, 2000). Alison went even further, writing that the increase in artificial wants was the “great and important change” that provided the “principal counterpoise which Nature has provided to the principle of population. The indulgence of artificial wants is incompatible with a rapid increase of the human species. If the labourer finds himself burdened early in life with a wife and children, he must forego many enjoyments which otherwise would be within his reach…Strong as the principle of population is, experience proves that these prudential considerations, when suffered to develop themselves, are still stronger, and are perfectly sufficient to restrain the rate of human increase” (Alison, 1840, Vol. 1: 109-110).



Awareness of the existence and extension of this deferment process was in fact so general that Richard Jones felt the confidence to write that “this self-restraint is so far exercised that there is no record of the customary age of marriage having at any time, in any country, coincided with the age of puberty. Its strength increases, and its sphere of operation enlarges, with the advance of civilization” (Jones, 1859: 245).





The European Marriage Pattern and The Historical Record





Now according to Clark the European marriage pattern exhibited four main features (Clark, 2005):



1. A late average age of first marriage. Typically between 24 and 26 for women.



2. No control of fertility within marriage.



3. Large numbers of women never married. Typically 10-25 percent, but in some populations and periods the percent unmarried was even higher.



4. Low illegitimacy rates. Typically less than 6 percent of all births were illegitimate, even though the majority of women of reproductive age were unmarried. Illegitimacy rates were as low as 1.5 percent in England in some decades of the seventeenth century. French illegitimacy rates were probably even lower.



These four features are important, and their association not merely incidental, since age at first marriage, use of contraception, marriage and illegitimacy rates may be considered as key indicators, one whose movement tends to define the dynamic evolution of any given fertility regime whatsoever.





Clearly embarking on a marriage and establishing a home constitutes a key life course event in any society, and one which is often fraught with difficulty. In this sense early modern Europe is no exception requiring as it does the resources to establish and maintain a separate household (and this would of course be a by-product of the various European family and kinship systems which were in operation, Voland, 2000), and the resulting age at first marriage for women seems to have been typically comparatively late, normally averaging around 25. In fact a substantial proportion of women never actually married (Flinn, 1981, Livi-Bacci, 2000), and, as a consequence, although fertility was high within marriage, the total fertility rate (TFR) was only a relatively modest four to five births per woman (Livi-Bacci, 2000). In England, for example, the mean age at first marriage for women in the mid seventeenth century was 25.9 years and 17.5% of women never married.



Obviously there were considerable differences between social classes here, while rich (and often aristocratic) families reduced their fertility earlier, and often more markedly, than the rest of the population (Livi Bacci, 1986) this was a reversal of an earlier historic trend. During most of the pre-modern period there was a strong correlation between wealth, probability of marriage, younger age at marriage, and completed fertility (Voland, 2000). However, restricted inheritance and the desire to concentrate wealth limited the reproductive value of noninheriting sons and daughters. Thus, as we enter the modern period and as life expectancy improved and economic structures became saturated, resource holding groups began to delay marriage into the late 30s and early 40s for men and mid-20s for women (Szreter and Garrett, 2000; Voland, 2000).Generally, wealth brought a higher probability of marriage at a younger age, to a younger spouse, and more children. However,

as environments became more saturated, and local resource competition among siblings differentially affected resource-holding families, as opposed to day laborers, in a way which increased the likelihood of dispersal of later-born children (Clarke and Low, 1992; Towner, 1999, 2001; Voland and Dunbar, 1997) since the benefits to resource holders of having an above average number of children was increasingly offset by a more and more intense sibling competition for access to inheritance (Voland, 2000). One extreme example of this kind of parental manipulation of offspring marital opportunities was polyandry, in which a male sibship jointly marries a single woman in order to avoid division of property and labor among competing households of wives and children of brothers (Crook and Crook, 1988; Haddix, 2001).





The other interesting detail about the European marriage pattern is the degree of variability which it exhibited. In England, for example, during the seventeenth century limitations on fertility turned out to be so severe that population even began to fall. In the mid-eighteenth century, average age at first marriage fell, and continued to fall, dropping more or less consistently from a seventeenth century high of 25.9 to a low-point of 23.4 by the end of the first half of the 19th century. Over the same time scale the percentage of women never marrying fell to around 7 percent, while the illegitimacy rate (despite the much smaller fraction of the female population at risk of having an illegitimate child) rose from 1.5% to 6%. (Clark, 2005)



A comparable state of affairs to that which existed in England was also to be found in the Verviers region of what is now Belgium, where the average age at first marriage in 1650-59 was 25.3 for women. This rose to 27.5 by 1700-9, before falling again to 25.9 during the years 1730-39. (Alter, 1988, Desama, 1985).



Such changes, while apparently small, actually have quite profound effects on achieved fertility outcomes. At the 1660 low-point, for example, each woman in England had an average of only 1.9 surviving offspring (a figure which seems almost contemporary), by 1815 this figure had risen to 3 children per woman. The consequence was, of course, that during the years of the Industrial Revolution population rose rapidly in England, from 6.7 m. in 1770 to 17.7 m. in 1850, with the increase being partially a product of the fact that the drop in marriage age meant more children being born and being born earlier in the life course. Of course, at the same time morbidity was falling and life expectancy rising, and this was the other component driving the increase in population size. Thus, other things being equal, what can be seen here is that in the area of demography from small changes big things do grow.



Outside of Europe data on mortality or fertility are, unfortunately, only occasionally available for most countries before the World War II era (Preston, 1980), but what little information we do have suggests that the European experience is not a-typical.



Lee and Cambell (1996), for example, show how in Liaoning, China, during the late eighteenth and early nineteenth centuries, despite high marriage rates, within-marriage fertility was only at two thirds of the level found in pre-industrial Western Europe (also see Lee and Feng, 1999 and Cambell, Feng and Lee 2002). They also found that it took longer after marriage for the first child to be born than it did in Europe, and that women terminated their child-bearing earlier. It is not known with any degree of confidence why fertility within marriage in Liaoning was so low, but as in pre-Industrial western Europe there is no clear indication of contraceptive use, and the most likely explanation is the existence of social customs that resulted in and sustained lower fertility levels.



On the other hand recent anthropological research tends to suggest that most pre-agricultural societies limit fertility in a variety of ways. The numbers of births recorded in the few remaining contemporary hunter-gatherer societies, for example, are far below the limits of what is biologically possible, and,indeed, often not dissimilar to those found in pre-industrial Europe. (Ellison, 2001, Kramer and Boon, 2002).





As has been suggested already,prior to the agricultural revolution it is possible to argue that, via the processes which have come to be known as 'natural fertility' (Henry, 1961), human fertility was homeostatically regulated. Such 'natural fertility' was effectively regulated by a combination of fluctuating first-birth-ages and changes in the distribution of births, and these were regulated by a combination of taboos and social practices and by changes in nutrition and other environmentally related factors. That such mechanisms exist in human populations is hardly surprising since virtually all complex organisms exhibit some sort of flexibility in both age-at-first-reproduction and fertility rates. Natural selection it seems has resulted in the appearance of physiological and psychological mechanisms by which both organisms and individuals adjust fertility onset and fertility rates in relation to changing environmental conditions. (Kaplan& Gangestad, 2004 ).



In the case of pre-agricultural hunter-gatherer society this regulation seems to have been achieved by means of a variety of reproductive strategies - such as, for example, extended lactation, or nutritionally and activity driven fluctuating age at menarche - many of which have the characteristic of being biological responses to a constantly changing external environment (Ellison, 2001). Put in other words such mechanisms might well be described as 'natures contraceptives'.





The view that foragers limit fertility so as to maintains their populations in dynamic equilibrium with available resources has become common currency among anthropologists since the 1970s (Dumond 1975; Hayden 1972, 1986).



One source of critique for the standard 'natural fertility view' originates in the work of Hill and Hurtado and their pithy observation that ‘No natural fertility population yet observed is characterized by zero growth, as would be required over much of our species’ history’ (Hill and Hurtado, 1996: 471). Following this work there has been a greater appreciation of the fact that individual energetic efficiency in resource acquisition and production, rather than total productivity rates or the carrying capacity of the environment, may well play the critical part in determining reproduction rates (Belovsky 1988; Hawkes and O’Connell 1992; Winterhalder et al. 1988). Also the idea that human population history has been characterized not by a series of stepped dynamic equilibria but rather a saw-tooth pattern of periods of rapid growth interrupted by infrequent but serious crashes has become increasingly recognized as an alternative explanation for near-zero growth through much of human prehistory.(Blurton-Jones et al. 1999; Boone and Kessler 1999; Hill and Hurtado 1996: 471–2; Keckler 1997).





In any environment in which humans find themselves, there is typically a wide array of animal and plant food items that could be successfully captured, collected, processed and eaten. And yet, rarely is it the case that human populations capture, collect and consume everything that available. In some contexts, human foragers tend to ignore small mammals, reptiles and birds, while, in others, such prey are pursued and consumed. Plants foods that are relatively time-consuming to collect and process, such as acorns or other seeds, are ignored by some foragers, and routinely collected, processed and consumed by others. The question thus arises as to what kinds of factors actually affect how humans choose which food items to pursue, process and consume?



In an important and systematic study of pre-modern fertility patterns, Campbell and Wood elaborate a cross-cultural tabulation of total fertility rates (TFRs) for 70 forager, horticultural, and intensive agricultural societies basing themselves on the contemporary ethnographic record. Their findings show that there is very little significant difference in TFRs across subsistence regimes (Campbell and Wood, 1988). Hewlett carried out a similar analysis of 40 mobile and sedentary foragers and pastoralists. He found the existence of slightly higher fertility rates among pastoralists, although the difference was not significant (Hewlett, 1991).



Bentley et al. subsequently published an extensive critique and re-evaluation of the Campbell and Wood study, presenting their owncross-cultural comparison of 57 forager, horticultural, and intensive agricultural groups. Using a subset of the Campbell and Wood sample, excluding non-independent cases (ethnic groups that were closely related) and populations with high levels of sterility, they found that intensive agriculturalists had significantly higher fertility rates (Bentley et al 1993b).



Although pre-transitional fertility was often higher in the agricultural societies of the third-world in the twentieth century than it was in the earlier European case, its levels were normally far below the hypothetical biological upper limit for a population, which is normally thought to be around 15 to 17 births per woman (Bongaarts, 1978).



The consensus view amongst economists (see eg Kremer 1993) that, on an aggregate level, population growth has been globally slow over the past millennium is almost certainly correct. This slow growth has, however, also been characterised by a puzzling phenomenon of large and significant variance from the mean, with large swings about the growth path being evident - examples of this would be the stagnation in the fourteenth and seventeenth centuries and a more rapid growth rate in the fifteenth and eighteenth centuries. While exchanges of disease (and techniques for treating them) through exploration and trade may have played some role in this, and variability in relations between pathogens and their human hosts may form another part of the picture (Fridlizius 1984; Perrenoud 1984), global climatic change was possibly at the end of the day the principal driving force (Galloway, 1988, 1987, 1986).





What is the Demographic Transition?







The expression 'demographic transition' has been used here extensively, and a number of stylised characteristics have even been offered, but perhaps it is worth looking just a little bit more closely at this concept, its origins, its history and its current useage. The concept is of course a familiar and widely used one. Perhaps it has become just a little too familiar, producing the sort of familarity that breeds if not contempt then at least a 'taking for granted' of the kind which should make us wary, especially when, as will be explained in more detail below, some of its underlying assumptions are being subjected to be continuous questioning and revision. The concept itself may well, in fact, turn out to be something of a "false friend".



The body of theory which undelies our modern concept of the demographic transition was first advanced by Warren S. Thompson’s in a now classic work , "Population" (Thompson, 1929). Thompson in the now time-honoured fashion broke the process of demographic change down into evolutionary stages according to the various levels levels of the birth, death and natural growth rates. Following Thompson's lead the 'theory proper' was subsequently elaborated by a group of Princeton-based researchers - Kinslay Davis, Frank Notestein and Irene Taeuber - in the years immediately after WWII (Davis, 1945, Notestein, 1945, Taeuber, 1945). The theory was really a huge generalisation based on earlier studies they had carried out of mortality and fertility declines, as such it was clearly a product of its times, and of the data which was then available. In particular this meant the Swedish data, which was among the first to be systematically compiled, and which was to mark the schematisation of the transition from the very start.



Taking Sweden as its prototype, the theory attempted to explain the mortality and fertility changes which accompanied the revolution in living standards and social conditions which followed from the agricultural and industrial revolutions of the late eighteenth and early nineteenth century. As has been repeatedly mentioned thought about the transition itself seems from the very begining characterised by an obsession with breaking it down into phases. In what could fairly be called the moden 'authorised version' the phasal structure is essentially presented by Ronald Lee in the following way:



"The classic demographic transition starts with mortality decline, followed after a time by reduced fertility, leading to an interval of first increased and then decreased population growth and, finally, population aging" (Lee, 2003).



This is a pretty normal typology, encapsulating as it does:



i) A pre-transition 'Malthusian' regime



ii) A mortality decline phase



iii) A reduced fertility phase (itself subdivided into (a) an accelerating population growth sub-phase and (b) a decelerating population growth sub-phase



iv) An ageing phase



As we have already noted, population ageing must start from the moment the fertility decline begins. There are however other problems and many of these have long been known. Lee himself draws our attention to the existence of cases in which fertility declined before mortality, most notably the United States and France, while, as mentioned above, in the UK case fertility rose at the same time as mortality declined. As a consequence of the appearance of such anomolies the theory has, over the years, been subjected to considerable criticism. (See Chesnais 1992 for a good summary of the waxings-and-wanings of the theory across time).



Some critics have even gone so far as to suggest that the demographic transition cannot really be characterised as a theory at all (in any meaningful sense of the term) , and would better be seen as a useful rule-of-thumb generalisation. The prestigous Italian demographer Massimo Livi-Bacci once famoulsy proposed that "we should just destroy all this nonsense of transition theory" (cited in Coale 1994). The essential grounds for much of the criticism has been the discovery through subsequent research that the transition itself has, as mentioned above, followed quite different patterns in different places. In fairness to the original Princeton researchers it should be pointed out here that the real fertility-decline part of the transition only began in earnest in the third world with the arrival of the 1960s, while good collection and analysis of much of the European data only took place in the 1970s and 80s. The failure of the transition to materialise in the third world did, of course lead to ridicule being heaped - often most unjustifiably - on the heads of many demographers. Robert Fogel has recently humourously speculated that the hand of some malevelolent deity or other may be at work since there is a clear rule that demographers run out of patience after about 20 years, if what they theorize would happen doesn't happen, and the deity intervenes so that the expected event - in this case the fertility decline - arrives since it was just about the same time as leading demographers began saying the theory of the demographic transition was dead, that the fertility rate in third world countries, including amongst them many Islamic countries, began to decline rapidly (Fogel, 2005).



As suggested above, one problem case for the theory was immediately presented by France, since the French data show that while mortality began to fall in the early nineteenth century just as it did in Sweden, birth rates commenced a long and steady decline at more or less the same time (and here the difference with the Swedish case couldn't be clearer). Consequently what the earlier theorists had called the second and third phases of the transition coincided. Indeed, no substantial population growth corresponding to that which occured in Sweden took place in France. In England, on the other hand, where mortality likewise began to fall early in the nineteenth century, birth rates were actually rising at the same time (Schofield 1984). England therefore experienced a period of extremely high population growth throughout the 19th century.



As has been indicated above, in order to believe in the explanatory value of the original version of the demographic transition theory it is also important to believe in the idea that in the agrarian society preceding the demographic transition, mortality was always at a high level even if varing substantially from year to year. It is, however, precisely this assumption that has provided a second important difficulty for the original version of the theory. The essential idea was that during the so-called 'Malthusian Regime' mortality was high due to a combination of low living-standards (as population tested the limits of agricultural technology) and recurrent epidemics.



However many historical observers soon started to note that death rates in pre-industrial Europe fluctuated widely across decades and across the centuries. Now as long as the theory was based primarily on the Swedish population data (originating in the mid-eighteenth century) the pre-industrial high-mortality data seemed relatively secure. This situation, however was to change as scholars started to realise that before the mid-eighteenth century the European mortality level was far from stable. Patterns of fluctuating mortality had been demonstrated by a number of scholars, but normally only for individual parishes or institutions, or for regions like southern Sweden (Bengtsson and Oeppen 1993) or northern Italy (Galloway 1994). What really put the cat among the pidgeons for the classical version of transition theory was the surfacing the data on English population dynamics (basically these started arriving from the early 1980s onwards) producing a discrepancy which it was impossible to ignore. In particular Wrigley and Schofield - in a study of population in England from the 1540s to the 1870s - found the existence of a markedly different state of affairs to that which would have been anticpated by the standard theory.(Wrigley and Schofield 1981).



Wrigley and Schofield’s classical data provide evidence which is not entirely consistent with a straightforward working of the original Malthusian mechanism. For quite long periods, notably the early 17th century and in the 19th century, there is - in contradiction with what the Malthusian model would anticipate - a simultaneous increase in both population and the real wages. As a consequence there does not appear to be any strong Malthusian type link between mortality and the standard of living in England at this time, and death rates seem to vary in a way which is hard to correlate precisely with the movement of real wages.



The Swedish demographer Bo Malmberg, after an in-depth examination of Wrigley and Schofield’s data, discovered that during the whole period between 1541 and 1871 the English population underwent several cycles of age structure change. Correlating these changes in age structure with the real wage index it became evident to Malmberg that real wages were high when there were large increases in the 30-64 age group. (Malmberg and Sommestad, 2000) He also found a negative correlation between the share of young adults and the real wage. In addition he found these correlations to be valid across the entire 1541 to 1871 period.



Much as Malmberg's work may throw light on what was actually driving the movements in real wages, the mortality problem would appear to be a much more serious one, since if mortality fluctuations cannot be neatly tied down to changes in living standards then this presents real problem for traditional transition theory, since part of the causal mechanism it seems to rely on is called into question.



It is hard here to overstate the importance of the English population studies in initiating the subsequent re-consideration of transition theory, since what these studies did was reinforce the idea that the norms and institutions regulating birth rates, in both the long and the short run, were sensitive to movements in economic indicators, with the important proviso that they did this in a rather surprising way since, it turned out, it was marriage and not mortality which was the principal regulating factor: when times get harder fewer people would get married, producing a simultaneous rise in the marriage age, and a simaltaneous decline in the fertility rate (the 'guilty party' being the now notorious 'tempo effect', which was only really 'discovered and analysed' by Bongaarts and Feeney at the end of the twentieth century, Bongaarts and Feeney 1998).



Thus the work of Wrigley and Scofield was path-breaking in the sense that their results represented a frontal challenge to two of the basic assumptions contained in the original formulation of demographic transition theory. In the first place mortality levels were not high and stable, and in the second it was births, not deaths, which were influenced by the longer-term movements in the economy. Subsequent Swedish studies, which were conducted in the light of the earlier English work, re-examined demographic and economic co-variance in eighteenth century Sweden and came up with results which pointed in a similar direction to the English ones (Fridlizius 1984). Births and marriages were found to be considerably more sensitive to changes in the economy, both long- and short-term, than mortality (Bengtsson 1993, Galloway 1988), and population changes seemed more influenced by economic developments than by social norms.





As I say above, following the initial mortality decline all societies are effectively ageing, the ageing is continuous, and at the present time it is hard to identify a natural barrier to this process. In this sense the transition doesn't really seem to have an 'end state', and thus can hardly be called a transition, since the word transition seems to imply something. If there is in fact a transition it is one from a society homeostatically balanced around high mortality to one which is pivoted around low and steadily declining mortality.



Having said this, and in fairness to Lee, what may be meant by ageing is a society with a comparatively high proportion of dependent elderly. On this view the initial mortality decline creates a dependency ratio which is considerably higher than that in the earlier agricultural society. This 'imbalance' takes many years to correct as fertility rates remain high and societies slowly recover the earlier ratios. But equilibrium is not recovered, and dependency ratios once more start to rise, this time amongst the elderly population. So this is what many may mean by ageing societies: societies where elderly dependency ratios rise (and continue to increase) above a certain notional level.



This way of looking at things has a certain validity, but it does beg one very important - indeed possibly critical from a policy perspective - question: just what do we mean by 'old'. The expression, like the terms modern and post-modern is a deceptive one, since it gives the impression of veing carved eternally in time, when in fact it is, of course, an extraordinarily relative one. To give one illustrative example, one populist Turkish politician got himself elected on a promise to introduce male pensions from the age of 43 and female ones from the age of 39 (something which, of course, resulted in the worst pension's crisis in history). He presumeably thought that 43 was 'old' and those who voted him into power evidently agreed. What we consider to be old is a socially defined (and hence relative) concept. It will hold different values at different times, and as life expectancy reaches ever higher limits we can expect our definition to adjust accordingly. This topic however, will have to await a later stage in the argument to receive the elaboration which it deserves. Simply consider this a foretaste.



Whatever the ultimate verdict on the validity of the phases schema, it should be noted that societies which enter the transition later tend to pass through it at an ever increasing rate. This if we take the mortality decline component we can see that gains in life expectancy have occured in the twentieth century in developing countries at rates which are rapidly by historical standards. In India, life expectancy rose from around 24 years in 1920 to 62 years today (a gain of 0.48 years per calendar year over 80 years), while in China, life expectancy rose from 41 in 1950–1955 to 70 in 1995–1999, (a gain of 0.65 years per year over 45 years.(Lee 2003) Fertility transitions since World War II have typically been more rapid than those for the developed countries, with fertility reaching replacement in 20 to 30 years after onset for those countries that have now completed the transition. Fertility transitions in east Asia have been particularly early and rapid, while those in south Asia and Latin America have been slower in starting but now seem to be accelerating (Casterline, 2001, United Nations Population Division, 2003).

Cohort-Based Mortality

As has been outlined in the previous section, belief in the explanatory value of the traditional version of the demographic transition theory hinged, in part,on the idea that in the agrarian society which preceded the transition mortality was always and everywhere at a relatively high level, even if did, as a matter of fact, vary not insubstantially from one year to another. It is, however, precisely this assumption that has furnished one of the most important difficulties for the original version of the theory, since historical observers have long been able to confirm the proposition that death rates in pre-industrial Europe fluctuated widely from one decade to another over a time-span of centuries.





The McKeown Hypothesis





Awareness of this reality lead researchers to begin to explore a variety of issues associated with the social and medical determinants of health, and to examine how these might impact on mortality. The standard account of the 'great mortality decline' which accompanied the transition can in many ways be traced back to the work of Thomas McKeown (1976, 1979). McKeown argued that economic growth and better nutrition were the fundamental causes of the remarkable improvements in population health which were seen in Western Europe from the late 18th century onwards. His criticism of earlier views was based on a study of cause-specific mortality in England and Wales from 1838 to 1947, where he found 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 a wider group of countries and argued that, contrary to what was at the time the received opinion, medical advances had little direct influence on health before the breakthrough which followed the generalised use of sulphonamides and antibiotics in the 1930s and 40s. According to McKeon, up to this time the only disease that active medical treatment had been able to cure was diphtheria, and this even this was achieved via the use of an antitoxin whose existence itself only dated back to around 1900. Thus only a very small part of the pre-twentieth century mortality decline could , on McKeon's account, be credited to active medical intervention, and even where medical advance was pertinent - as in the case of the diphtheria antitoxin - it could hardly claim to have played a significant part in the mortality conquest, since the disease was in fact already in remission by the time the antitoxin was developed and widely available.



Addressing the earlier part of the mortality decline - from the late 18th to the mid 19th centuries - McKeown made the seemingly valid point that medical influence on one of the key 'killer diseases', smallpox, was not essentially attributable to modern medicine since vaccination (despite being available from the end of the eighteenth century) was not widely used in England until after 1840 when it became freely available at public expense. Gunnar Fridlizius has also drawn similar conclusions regarding the evolution of the decline in Sweden (Fridlizius 1984).



According to McKeown, while an 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, a change which must surely have reduced the incidence of waterborne infections. Since changes in mortality from intestinal infections constituted only a small part of the general mortality decline prior to 1870 the general reduction must have been in large part due to factors other than improved personal hygiene and equally those public health measures which were introduced must have had little impact on the great mortality decline prior to 1870 and only a partial effect thereafter.



In fact long before the time of McKeown researchers had been aware of the existence of apparently 'spontaneous' changes in mortality, and of the changes in population size that these seemed to produce (Helleiner,1957, Chambers, 1972, Fridlizius, 1984, Schofield,1984). In particular Helleiner argued, based on Western European data, that population sizes had fluctuated substantially with a marked increase occuring from the mid-eleventh century until the late thirteenth century and then again from the mid-fifteenth century to the end of the sixteenth century.



The population growth which occured in the eighteenth century was therefore not unique, except insofar as mortality started its decline from a higher level and then continued for longer than it had done previously. McKeown's argument is essentially that since the eighteenth century decline forms an initial (integrated) part of what was later to become the great decline, it is not plausible simply to view it as being a spontaneous decline, one which was due, for example, to a remittance in the virulence of pathogens. McKeown's strong argument seemed to lie in the fact that once started this decline then continued across the entirety of the two following centuries. In explaining the decline McKeown himself focused on the role played by nutrition, and argued that the nutritional improvement determined not only declining impact of infectious diseases from 1848 onwards, but also the initial phase of the decline which began in the late 18th century.



His intransigence over the idea of a common nutritional causal component, and his consequent 'condensation' of what some consider to be two phenomena into one is really the by-product of his laudable desire to find a single common explanation for the entire process of the great mortality decline.





Inflamation, and the Thrifty Phenotype Hypothesis



The Mckeown thesis, however, has not worn well with time (see, for example, Emily Grundy's review: The McKeown debate: time for burial, Grundy, 2005) and ideas which were to seriously challenge what had to all intent and purpose had become the "Mckeown consensus" were not long in appearing. The death knell was perhaps first tolled among what might seem a rather surprising congregation: the practitioners of modern epidemiology. In his seminal work "Mothers, Babies, and Disease in Later Life" (Barker, 1994), the epidemiologist David Barker brought together under one roof what was at the time a growing body of medical evidence which drew attention the apparent importance of fetal nutrition in the subsequent health of the mature adult. The "Barker hypothesis" - which is sometimes referred to as the "womb with a view" hypothesis (Deaton, 2005) - is essentially constituted by the idea that events in the womb have long-lasting effects on health throughout the entire lifespan, and especially effects on health outcomes that only express themselves later in the life course. More technically put, nutritional insults in utero, which prevent the foetus developing to its full potential, or which produce an adaptation ill suited to the external environment which the individual will ultimately encounter, may cause a selective abandonment of function, an abandonment which disfavors or disables precisely those features in the organism whose primary function is to prevent disease in late life beyond the normal reproductive span. While the hypothesis itself is still somewhat controvesial, evidence in support of it has been mounting in recent years.



In this context Gabrielle Dobblhammer and James Vaupel (Dobblhammer and Vaupel 2000, Dobblhammer, 2002), for example, have shown that life expectancy at 50 varies seasonally depending on the month of birth. According to their findings, in the northern hemisphere, 50 year olds in the cohorts studied who were born in the months of October and November (to mothers who perhaps had had better access to cheap and plentiful fresh fruits, vegetables, and eggs through most of their pregnancy) could expect to live about three-quarters of a year longer than those born in the spring.



In the southern hemisphere, the same seasonal pattern was found to occur, although with a six-month shift in the timing of the effect, while those born in the Northern hemisphere who die in the South (European immigrants to Australia, for example) continue to display the Northern pattern.



Other similar evidence comes from the Dutch famine of 1943, follow-up studies on which seem to support the claim that nutritional deficits in pregnancy have long-term consequences for, for example, obesity, with deficits in the first trimester of pregnancy predicting later adiposity, and deficits in the third trimester inhibiting it. There have even been findings which relate subsequent behavioural disorders and schizophrenia to early prenatal nutrition in this context.(Susser and Lin, 1992, Neugebauer, Hoek, Ravelli et al, 1998, 1999, Rosebooma, 2000, Susser, 1999, van der Zee, 1998).



Indeed, explosions of obesity and associated diseases (adult-onset diabetes, heart disease, and so on) have often been found to come come close on the heels of a loosening of nutritional constraints, when those whose parents were undernourished, who were themselves undernourished in utero, move into an environment in which food is plentiful and heavy manual work is no longer the norm. One study found, for example, that in the black township of Khayelitsha near Cape Town in South Africa, more than a half of the adult women had body-mass indexes above 30 (Case and Deaton, 2005).





One clear implication of the Barker hypothesis is that the health of the adult may be a function of birth timing: the when of birth. This has given rise to what has come to be called cohort analysis in epidemiological research, a line of investigation which attempts to explore how disease incidence and life expectancy vary across cohorts in differing (and especially extreme) environmental settings.





The Cohort Thesis and the Great Mortality Decline





As has been said, what later became known as 'the great mortality decline' began in Western and Northern Europe around the middle of the eighteenth century (in some cases possibly a little earlier), levelled off slightly in the mid-nineteenth century, and then continued an inexorable downward course. During this time life expectancy at birth rose from around 35 years to more than 70. In several countries the increase in life expectancy was, indeed, truly spectacular: For the earliest cohorts to have been systematically studied - Sweden 1751, France 1806, England 1841, and Switzerland 1876 - cohort life expectancy at birth was initially very low: 34 years in Sweden, 38 years in France, 42 years in England, and 45 years in Switzerland. By the 1899 cohort, however, life expectancy had jumped to 55 years in Sweden, 56 years in Switzerland, 53 years in England, and 50 years in France.



In these initial (prototypical) European cases mortality began to decline somewhere between 50 and 150 years before the arrival of the industrial revolution in each country and in any event significantly before living standards started their long monotonic upward movement. Also life expectancy normally tended to start to rise some 100 to 150 years before marital fertility started its long-term decline. It should be noted that there are important exceptions to this 'rule'. In England the decline in death rates started around the same time as the initiation of the industrial revolution, during, as it happened, a time of falling real wages, while in France, fertility started declining at about the same time as mortality did, and both of these changes again took place well before living standards started to improve. This having been said, it is noteworthy how the timing of the great mortality decline was strikingly similar across the countries of Western and Northern Europe despite the not insignificant differences in their respective levels of economic and social development. It was also often surprisingly simultaneous in different regions of the same country despite again the large differences in the internal economic development of the countries concerned. (Bengtsson, 2001).



Initially the decline was characterised by a dramatic and sustained decline in infant and child mortality, however later in the nineteenth century improvements in adult mortality also began to occur. Adult and old age mortality had in fact started to decline slowly right from the beginning of the nineteenth century, and possibly even earlier for England. But this decline became much 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 then slowed for adults and the elderly around 1950 but from the 1970s onwards it has once more continued apace (Crimmins and Finch, 2006).



In the context of the 'great mortality decline' when we talk about cohort-based health factors what we are normally talking about are factors which affect only certain generational groups, factors which may nonetheless may have longlasting effects on the lifetime health of those groups themselves.



In fact in terms of the great mortality decline 'cohort analysis' is essentially concerned with with two factors, improvements in nutrition and living conditions during the pre-birth foetal period and in early childhood, and the disease environment present during pregnancy and the early life years of a child. Both of these factors may, through their subsequent impact on health, be associated with longer term changes in life expectancy.



As suggested above, in the literature it is possible to identify two types of cohort-related explanations for the great mortality decline:



(1) increased nutritional intake during the foetal stage and/or early years of life, and

(2) decreased 'effort' during the foetal stage or early childhood being required to fight disease either on the part of the mother or of the child, or both.



In each case these factors operate not only through their impact on short term mortality but through their longer run effects on the health of the individual. One possible mechanism for this process may be via the imact of early life events on the rate of growth of the individual and how this affects long run health. (Mangel and Munch, 2005, Gluckman, Hanson and Spencer, 2005, Metcalfe and Monaghan, 2003). Certainly laboratory studies on rodents have found that severe caloric restriction retards growth (resulting in a small bodied adult) but also lengthens lifespan, which might be thought to suggest that fast growth can have negative impacts on subsequent mortality and lifespan (Rollo, 2002; Metcalfe and Monaghan, 2003). Calorie restriction of rats at young ages has also been found to have a tendancy to slow down growth rates and to lead to short adult stature, even when food becomes abundant later in the juvenile period (Shanley and Kirkwood, 2000).



Epidemiologists and demographers of an earlier generation, and who studied the modern mortality decline during the 1920s and 30s, were already aware of this 'early life history' possibility (Derrick 1927, Kermack et al 1934). They noticed that mortality for children declined much earlier than mortality for adults, and that each succeeding generation seemed to carry with it the same relative mortality from childhood though to old age. Distinguishing here between what are called period and what we have termed cohort effects, if period effects (that is environmentally significant imacts on health like more clement weather, or better nutrition, or rising living standards, operating across a given time period) were the dominant factor in the decline, then the heath consequences of these effects should be found to be evenly distributed between both young and old. If, however, this change is found to be asymmetric with one group showing a different pattern from the other, then there are arguably reasonable prima facie grounds for suspecting that cohort factors may be at work, and this in fact was the conclusion these early researchers began to draw.



In more recent times studies have continued to confirm the impact of cohort membership on health and mortality. Sam Preston and Etienne van de Walle , for example, in their study of urban France, and Gunnar Fridlizius, who examined the Swedish case, found such effects to be significant (Preston and van de Walle, 1978, Fridlizius, 1989). But in the realm of modern economic theory, and in it's interaction with economic history, there can be little doubt that if there has been one scholar who has done than any other to advance our understanding of how the cohort hypothesis might play a central role not only in epidemiological research, but also in our understanding of the process of modern economic growth, it has been Robert Fogel (Fogel, 1993, 1996, 2004).





In support of his thesis that cohort factors play a decisive role in the process of long term improvement in life expectancy Fogel used final heights as a proxy measure of net nutrition and health during childhood. Height is seen by Fogel as a cohort related measure of health, while weight and body mass index are seen as life-period measures (Fogel, 1996). On the Fogel account, individuals who, as a consequence of having had well-nourished and healthy mothers, were well nourished during the foetal stage experience lower death-risk during infancy. If they are well nourished and healthy their cells and organs develop better, they attain a greater height and tend to have a longer life.



Since here it is net and not gross nutrition that determines health and height, there is no direct link between gross nutrition during childhood, or GDP, and heights. This is because improvements in health and height may be the result of either better nutrition, or of reduced claims on health due to the impact of disease, or, of course, of both of these. Thus a decline in the prevalence of smallpox, for example, has a positive effect on heights and on the length of the life span, everything else being equal. One problem that immediately presents itself in this line of research is how to evaluate the extent to which the improvement in height and health is due to diet, as opposed to being due to lower claims from disease. Calculating diets for pre-modern populations is a difficult task (Fogel,1996), and it is even more difficult to calculate disease claims. Still, historical records do show similarities between trends in height and GDP (Fogel 1994, 1996), which suggested to Fogel at least that the trend in disease claims may have been been of lesser importance.



Now if Fogel is right here, then one important immediate consequence, and one that is central to his entire argument, is the absence of any single determinate equilibrium between food supply, population heights and population numbers: the relationship is characterised, in fact, by the esistence of multiple equilibria (Fogel 1994). Undernourishment, whether a result of low or badly-composed food intake, or a consequence of an increased disease claim, may rather lead to a stunting of height or weight and a higher incidence of illness, disease and mortality in later life as opposed to any notable increase in direct and immediate mortality. The one-to-one relationship (or period link) between economic output and mortality is thus much weaker than Malthus appears to have believed, at least on Fogel's account.





Now body size has received a good deal of attention in life history analysis (Roff, 1992, Stearns, 1992), and between species, body size is found to correlate with a number of life history traits, including mortality rates. In general large species, including humans, tend to have lower mortality rates and longer lifespans (Harvey and Zammuto, 1985; Gaillard et al., 1989). As a large bodied mammal, we have relatively low mortality and relatively long lives (though our lifespan seems to be proportionately longer than would be predicted by referring to our body size alone: Hill and Kaplan, 1999; Hill et al., 2001). Within species however the relationship between size and mortality is less clear-cut, since large size may offer some advantages, such as protection from predators, but these advantages do not come without cost, since, for example, there are greater nutrient requirements involved in maintaining a large body (Blanckenhorn, 2000). One complicating factor, as we have noted, is the speed of growth experienced during childhood, which is correlated with final adult height but may also have implications for mortality in adulthood.





The relationship between adult size (height) and mortality in humans has been extensively studied. Changes in height have been shown to correlate with mortality trends in both the US and the UK, with life expectancy appearing to rise with average height (Floud et al., 1990; Fogel, 1993), and being taller has been found to correlate with a lower mortality rate (Marmot et al., 1984; Waaler, 1984), but the situation may not be as straightforward as it appears to be. There is evidence that while the incidence of some causes of death, such as cardio-vascular and respiratory disease, are inversely related to height; others, such as reproductive cancers, increase in frequency with height (Barker et al., 1990; Leon et al., 1995; Smith et al., 2000; Song et al., 2003). There is therefore some debate as to whether being taller is as beneficial as it is sometimes thought to be (Samaras et al., 2003).



It is also not clear what the exact relationship is between measures of body condition and mortality. As in the case of height, there has been a good deal of research has into how exactly BMI interacts with mortality. The relationship is normally thought to be non-linear (Wienpahl et al., 1990; Rissanen et al., 1991; Laara and Rantakallio, 1996; Yuan et al., 1998; Engeland et al., 2003; Kuriyama et al., 2004). Individuals with low BMI experience high mortality rates, but those with high BMI do too.





Being short, on the other hand may also be considered to be an indicator of early life conditions, however when it comes to analysis, correlations are one thing, and explanatory mechanisms another. In this context indirect support for a modified variant of the Fogel hypothesis has come more recently from the work of Caleb Finch and Eileen Crimmins (Finch and Cribbins, 2004a, Crimmins and Finch, 2006). Finch and Crimmins advance the general proposition that a 'cohort morbidity phenotype' may serve as a representative of the inflammatory processes (disease claims) that persist from early age into adult life. Specifically Finch and Crimmins propose the hypothesis that decreased inflammation experienced during early life, which is associated with improved infant and child health, led directly to the subsequent decrease in morbidity and mortality resulting from chronic conditions found in old age. They point out that, for example, later life risk of heart attack and stroke is known to be correlated with serum levels of inflammatory proteins such as C-reactive protein (CRP). At the individual level, CRP levels are also correlated with the number of seropositivities to common pathogens, a relationship which tends to indicate a history of prior infections. Furthermore, drugs with anti-inflammatory properties (nonsteroidal anti-inflammatory drugs, statins etc) have been found to reduce the risk of vascular events and even possibly Alzheimer's disease. This kind of evidence may be read as implying the existence of links between levels of inflammation and major chronic conditions which are important in old age, and thus between exposure to infectious disease in early life and health in old age.



Now if we seek to apply these known correlations to the course of the great mortality decline, the early Swedish example assumes,due to its systematic character, considerable importance, and it is hardly surprising that Finch and Crimmins have recourse to the detailed, micro-level, work of Bengtsson and Lindström, as well as other earlier work based on aggregate data conducted in a UK context by William Kermack and the pioneering work (again using aggregated data) of HB Jones for Sweden (Bengtsson and Lindström, 2003, Kermack et al, 1934, Jones, 1956).



So, using the longer data series that is available today for Sweden (infant mortality data was not available to Jones for cohorts which had been born before 1895) Finch and Crimmins have updated Jones’ earlier work, detailing age-specific mortality rates for five birth cohorts in the years between 1751 and 1940. They find that mortality at any given age across the lifespan drops steadily across successive cohorts. Cohorts with lower young-age mortality also have lower mortality at any given age in later life, and this is entirely consistent with an earlier (and very interesting) Jones hypothesis to the effect that “the physiological age of each new generation is remaining more youthful at the same chronological age”.



As Finch and Crimmins emphasise the historical demography of Sweden offers an unparralled possibility of deriving unique mortality profiles across the entire life span, starting with the years immediately prior to the industrial revolution (when mortality was, of course, high) and following each cohort across the entire life course from birth to old age. Taking this data as their starting point they proceed to examine age-specific mortality trajectories for Sweden from 1751 right through to 1940, and find that the data offer support to the hypothesis that old-age mortality declined in a cohort and not a period fashion across all ages. In so doing they develop two points which were essentially already hinted at in the earlier work of Kermack et al. and Jones:



(i) that the historical mortality decline among the old and young begins in the same cohort, and



(ii) that infant mortality has a stronger relationship to later-life mortality than does mortality in subsequent childhood years.



They also conclude that declines in mortality after age 70 tend to lag about 70 years behind those for infants. When they relate childhood mortality to later-age mortality for Swedish birth cohorts born in the 177-year period from 1751 to 1927, they find strong relationships between rates of childhood mortality and mortality for cohort survivors in old age, indeed they found that most of the identified variance in cohort mortality was explicable in terms of mortality before the age of 10. Moreover, they also found that the annualized effect of each childhood year on old-age mortality was three times as great for infant mortality as it was for mortality in subsequent childhood years.



Based on this study of the Swedish data they go on to argue that the inflammatory-infection and Barker fetal-nutrition hypotheses may be seen not as competing but rather as complementary hypotheses, in that they jointly link the two mechanisms of morbidity between early and later life. As they argue, even well-fed babies are vulnerable to rampant infections, and infections alone can cause malnutrition and later dietary deficiencies. Childhood diarrheas, for example, impair cardiac muscle synthesis, and this could underlie the associations which have been found between infant diarrhea and later cardiovascular disease . As they suggest slowed infant growth under the Barker hypothesis could in part be consequent to infections that cause inflammatory responses as well as impairing nutrient absorption.



In a similar vein Bengtsson and Lindstrom, using longitudinal data, and following individual cases rather than relying on grouped aggregate data - a limitation which had characterised the earlier work of Kermack, Fridlizius, and others - have studied historical Swedish cohorts to test both the nutritional and the inflammation hypotheses. They did this by examining the effects of food prices and the disease load at the time of birth on subsequent old age mortality during the years 1766–1894. They conclude that the level of infection among infants was a stronger influence than food availability on later-life mortality and life expectancy. In particular they identify problems leading to the impairment of the respiratory mechanism as the principal source of this influence. (Bengtsson and Lindström, 2000, 2003)



Barbi and Vaupel - in a rejoinder to Finch and Crimmins (Barbi and Vaupel, 2004) - have objected to their findings on the ground that the most recent analyses of mortality patterns over age and time have revealed that period effects are generally more important than cohort ones in explaining mortality decline at the older ages and that, in fact contemporary demographic and epidemiological studies tend to suggest that the cohort effect is at best modest.. In defence of their position they cite, for example, the Danish twin studies which indicate that less than 10% of the variation in how long these twins live is attributable to variation in shared health conditions early in life ( McGue et al, 1993, Herskind et al, 1996). In particular they point out that, in developed countries at least, progress in reducing old-age mortality accelerated around 1950 and accelerated even further around 1970, doing so simultaneously at all older ages.



Finch and Cribbins (2004b) have responded to this by pointing out that since their analysis explicitly excludes modern birth cohorts, members of which have benefited from immunizations and the use of antibiotics, many of the points made by Barbi and Vaupel have limited validity in the context of their argument. They specifically hypothesize that inflammation associated with vascular disease and cancer (the incidence of which is attenuated by modern drugs with anti-inflammatory activities) is the strongest connective link between early and later cohort mortality and that such cohort inflammatory mechanisms are most active when mortality from infections is high. As childhood infection has decreased due to immunization, public health advances, and the use of antibiotics, early inflammatory exposure has had much less impact on cohort old-age mortality for the modern cohorts.



What we seem to have here are two interrelated, but distinct phenomena, the pre-1950 cohort-related effects of decreased childhood inflammation on average life expectancies, and the post 1950 improvement in mortality

rates at the older ages. At this level the arguments of Finch & Crimmins and Barbi & Vaupel are entirely compatible, with the former having a high degree of relevance to the pre-1950 situation, and the latter to the post 1950 one.Now analytically these processes are really quite distinct, as is the economic interpretation which can be given to each of them. Basically, following Finch and Crimmins, we might say that a predominance of cohort influences characterise the first stage, whilst (following Vaupel) period (or environmental and health care) influences characterise the

second one. It also raises the rather interesting point about whether Jones, when he observed that "the physiological age of each new generation is remaining more youthful at the same chronological age" may not have been looking at cohorts which came from the first stage of mortality decline, and not cohorts which form part of the elderly expectancy improvement we are currently seeing. If this is so the implications will be important.



As indicated above the age-specific mortality trajectories from 1751 to 1940 used in the Finch and Cribbins work strongly suggest that old-age mortality declined in a cohort, and not a period, fashion. The mortality trends at age 70 in any given calendar year, or the period mortality trend in old age, do not resemble the trend for the younger age groups. In fact they find that, following an initial rise after 1751, mortality declines first became significant in the Swedish 1791 cohort, and this at both the young and the older ages for that cohort. Period mortality, on the other hand, first declined significantly among the old in the years from 1861 to 1870, years, of course, which correspond to the very cohort in which the onset of the decline was first observed. Again, generally speaking child mortality trends correlate less with old-age mortality trends in the same year (period effect) than with mortality trends seven decades later (Finch and Crimmins, 2004b).



Barbi and Vaupel's critique has not, however, been completely barren, and it has forced Finch and Crimmins to sharpen and clarify their argument considerably. Hence, in a second, and subsequent, work on the same core topic (Crimmins and Finch, 2006) , where they extend their analysis to France, England and Switzerland, they are at pains to point out that they:



"focus exclusively on cohorts born before the 20th century, when levels of infection were high, but before smoking, a major inflammatory stimulus, became popular. Most importantly, these cohorts entered adulthood before general childhood immunizations and before antibiotics. The inflammatory mechanisms that we describe can only work when mortality from infection is high; once childhood infection is low, it can no longer be a factor in explaining old-age

trends."



In fact in their second paper Crimmins and Finch produce some really intriguing cohort-relative life-expectancy data. For the earliest cohorts they study (Sweden 1751, France 1806, England 1841, and Switzerland 1876) cohort life expectancy at birth was low: 34 years in Sweden, 38 years in France, 42 years in England, and 45 years in Switzerland. By the time we get to the 1899 cohort, however, life expectancy has jumped to 55 years in Sweden, 56 years in Switzerland, 53 years in England, and 50 years in France. In both cases the comparatively low life expectancies imply that all the cohorts (both the earlier and the later ones) were exposed to the then highly prevalent infections.



Confirmation of these Crimmins and Finch findings comes in more recent work from Tommy Bengsston (in association this time with Göran Broström). Bengtsson and Broström once more develop a methodology to try to test whether or not events which occur during the subsequent life course may mediate the effects of early-life factors on later life mortality, and in particular whether the degree of access to land in adult life plays any kind of role (Bengtsson and Broström, 2006). Bengtsson and Broström find no support for the null hypothesis that the influence of disease load in the first year of life is not permanent throughout life but is moderated by an individual’s socioeconomic condition later in life (and more specifically at age 50 years). They find that those who (according to the land-wealth criteria they use) could be considered economically unsuccessful by the time they reached 50 did not suffer more from the damage caused by the first year of life disease load than those who had done relatively well (economically speaking) and who had attained or retained access to land. They also find that those who were exposed to a heavy disease load in the first year of life, and who survived to be 50, had an estimated remaining median life expectancy of about two years less than those who were born in years with low to moderately high infant mortality: This is indeed an intersting finding as it makes exposure to infection during the birth year a more important determinant of later life health than sex or socio-economic status.





Similar results showing links between early infections and late-life health have also been found in the case of Union Army veterans in the United States using data from the current Health and Retirement sample (Costa, 2000).



As Crimmins and Finch also point out , maternal infections, including influenza, malaria, and tuberculosis, were common in Europe and the United States well into the 20th century (Riley, 2001). Babies of mothers with infections are known to reveal elevated inflammatory markers and retarded uterine growth (Moorman et al, 1999) and Crimmins and Finch even specualte that suboptimal adult female health may transgenerationally transmit the imprints of infections and inflammation as well as malnutrition while increasing the risk of smaller babies with lowered resistance to environmental pathogens. This additional path is not developed in the Barker hypothesis and is consistent with observations that improved infant mortality lags a generation behind the decline in adult mortality (Kermack et al, 1934).



Now at this point the argument becomes truly interesting. Fogel himself has recently proposed that a ‘‘techno-physiological revolution’’ increased energy available for growth and improved resistance to infection through a dual mechanism which both improved food production and at the same time lead to higher incomes which enabling an ongoing revolution in living conditions (Fogel, 2004). The Fogel hypothesis has been thought to present the difficulty that increases in height did not always follow increases in income and nutrition; and certainly not in the way his theory would anticipate. Height has even been found to have decreased during some periods of improving income in early industrial cities (Flood et al, 1990). However modifying (or blending) the Fogel hypothesis with the work of Crimmins and Finch it can be argued that a decrease in infections and ensuing inflammation had the potential to increase height independently of improved food intake, thus making the joint hypothesis far more compatible with the observed evidence.



Also, as Hillard Kaplan would argue, 'Life is an energy harvesting process'. More specifically this process is characterised by a series of trade-offs, of which the most important are those between growth, maintenance and reproduction. Since energy used for one purpose cannot be used for another (the ‘principal of allocation’), much of what has come to be known as life history theory is concerned with the functioning and impact of such energetic trade-offs. As Kaplan says:



"Organisms capture energy (resources) from the environment. Their capture rate (or income) determines their energy budget. At any point in time, they can "spend" income on three different activities. Through growth, organisms can increase their energy capture rates in the future, thus increasing their future fertility. For this reason, organisms typically have a juvenile phase in which fertility is zero until they reach a size at which some allocation to reproduction

increases fitness more than growth. Through maintainance, organisms repair somatic tissue, allocate energy to immune function, engage in further energy production, and so on. Through reproduction, organisms replicate genes. How organisms solve this energetic tradeoff shapes their life histories."

(Kaplan and Gangestad, 2004)



Mixing this further with an old idea of Lionel Robbins that 'economics is the science which studies human behavior as a relationship between given ends and scarce means which have alternative uses.' we can begin to see just how such trade-offs may have important implications.



Bengtsson and Broström, for example, find that:



"Children born in years with very high disease load, face more than 90 percent higher mortality than the others after controlling for all the covariates included in the model"



Well lets think about this for a moment, and lets think about it in the context of the behavioural relationship between scarce means and conflicting demands, in the context of Kaplans trichotomy between growth, reproduction and maintenance and lets go back in order to do so to Vaupel's original objection to Finch and Crimmins. Which was

that:



"while Finch and Crimmins hypothesize that decreased inflammation during early life has led directly to a decrease in morbidity and mortality resulting from chronic conditions in old age.......demographic and epidemiological studies suggest that the effect is modest".



Well, as we have noted, this leads Finch and Crimmins to respond to Vaupel with a much sharper version of their argument. In particular the qualify their argument by stating:



"Our analysis excludes modern birth cohorts, individuals of which have benefited from immunizations and the use of antibiotics....(while)...The comment by Barbi and Vaupel incorrectly implies that death rates among the elderly in developed countries declined only after 1950.....As childhood infection decreases because of immunization, public

health advances, and antibiotics, the early inflammatory exposure has much less impact on cohort old-age mortality."



So what we have here are two interrelated, but distinct phenomena, the pre-1950 cohort-related effects of decreased childhood inflammation on average life expectancies, and the post 1950 improvement in mortality levels in the older ages.



Crimmins and Finch in fact clearly spell this in their 2006 PNAS piece:



"We focus exclusively on cohorts born before the 20th century, when levels of infection were high, but before smoking, a major inflammatory stimulus, became popular. Most importantly, these cohorts entered adulthood before general childhood immunizations and before antibiotics. The inflammatory mechanisms that we describe can only work when mortality from infection is high; once childhood infection is low, it can no longer be a factor in explaining old-age trends."





So inflammation is largely a pre-1950 issue (in the Swedish, but not of course, in the current developing world, context) and this is where things get, frankly interesting, especially if we think about Bengsston's finding that children born in years with a low disease load experience around 10% of the mortality exposure of children born in the high disease load years.



These (low disease load) children, not only survive in greater numbers, they also live longer, healthier (and hence logically more productive) lives. Now lets think of this in terms of Kaplan's tripartite trade off. And in terms of economics. And in terms of his embodied capital model.



Firstly the low disease-load years mean the mums need to invest less energy in reproduction, since more children survive. That immediately frees off more energy for growth and maintenance. But, since the children are healthier there is less expenditure on maintenance, or, what amounts to the same thing, the investment in maintenance is more

cost effective.



Then there is growth, and let's think here in terms of economic growth, since as Xavi Sala i Martin nicely points out:



"The relation between most measures of human capital and economic growth is weak. Some measures of health, however, (such as life expectancy) are robustly correlated with growth" (Sala i Martin, 2002)



Now, if we go back to Kaplan we should easily be able to see why this relation between growth and "growth" (which was also to some extent evident to Fogel) should be so.



Kaplan estimates that no child in any society is ever really self-sufficient till the age of around 20. Now in the low disease-load years, getting the individual child to 20, not only involves less maintenance energy, it also produces an individual with say 35 productive years out in front of them instead of. say, none, or at least considerably less than 35. The productive impact of this has to be enormous. Of course this productive impact can only be realised within a technological and institutional context that makes such realisation possible, but in the presence of this we seem to have here a huge increasing-returns type mechanism which can help explain why demographic processes are much more important to economic development and growth than has been hitherto modelled.



This also has very important implications for those contemporary societies where diahorrea and malaria etc are still huge killers, and might give us some indication of how societies which are still caught in this health trap will be able to grow once they break out. The finding is also important since it indicates that such a demographic 'dividend' is only possible in the cases of societies where child-health related inflammation is still an issue, and thus tells us

relatively little about the economic outloook for those societies where the major increases in life expectancy come from improving the outlook in the older age groups.





Is There An End State?



The sum total of everything which has gone before is that the fall in mortality which preceded the industrial revolution may be much better seen not as the start of something new, but as the end of something old. There was, of course, something new to follow (in the shape of better public hygiene, and later imporved medical intervention), but that something "new" did not come onstream until well into the nineteenth century, when general improvements in conditions of life, in the form of better diet, better housing, improved hygiene, better child care and better sanitary systems in the towns, effectively prevented a posterior mortality increase, an increase which had unfailingly taken place following all earlier periods of enduring mortality reductions.



This leads us to one rather obvious and uncomfortable conclusion: all those economic growth models which have predicated the rise of the modern 'growth era' on a fall in mortality consequent to the technology revolution which accompanied the industrial one may in fact have the causal arrows pointing the wrong way.





In the account of Galor and Weil (2000), for example, growing population, through its assumed effect on the growth rate of skill-biased technological progress, causes the rate of return to human capital accumulation to increase. This ultimately leads to sustained growth in per capita income. Jones (1999), argues that increasing returns to accumulable factors (usable knowledge and labour) cause growth rates of population and technological progress to accelerate over time, and eventually, it is this which permits an escape from the Malthusian stagnation. The reality, as we have seen, is more complex, and both the 'weakly-Malthusian' initial state, and the low-fertility, increasing-life-expectancy end state seem to be full of surprises both interms of their implications for the initial demographic transition theory, and for the economic growth theory explanations which have rested on it.





As I have already emphasised, following the initial mortality decline which marks the onset of the transition all societies are effectively ageing. This ageing is a continuous process, and at the present time it is hard to identify an indestructible natural barrier which stands in its way. In this sense the transition doesn't really seem to have an 'end state', and thus can hardly be called a transition, since the word transition seems to imply a movement from something to something. If, in fact, there is a transition it is one from a society homeostatically balanced around high mortality to one which is pivoted around declining fertility, declining mortality, and ever-increasing life expectancy. As Lutz emphasises we don't yet know if there is any lower bound to fertility, and as Vaupel suggests there is now no good reason to assume that life expectancy has any natural upper limit..



Having said all this, and in fairness to Ronald Lee and others who use the expression, what may be meant by the process of 'population ageing' may well be a society with a comparatively high proportion of dependent elderly, as indicated by a conventionally determined life-course anchor point, such as the retirement age.Following the Lee account the initial mortality decline creates a child dependency ratio which is considerably higher than that in the earlier agricultural society. This 'imbalance' takes many years to correct as fertility rates remain high and societies slowly recover the earlier ratios. But equilibrium is not restored, and, after an initial 'sweet demographic period' (which may, as we have seen really be a 'sweet immuniological period', dependency ratios once more start to rise, only this time the rise is amongst the elderly population. This transition is rooted in the structure of the human life history and its mortality representation, with the disease load being attacked asymmetrically, initially in the earlier years, then in the later ones.In fact, what many authors may mean when they talk of ageing societies are societies where elderly dependency ratios rise (and continue to increase) above a certain notional level, and this dependency increase is, in the longer run of things, simply the historical footprint and shadow of the earlier, initial, mortality decline (in other words what we may have is one single 'great mortality decline', or transition, otherwise known as the rectangularisation of human mortality).



The traditional demographic transition way of looking at the mortality decline does, of course, have a certain validity, but it does beg one very important - indeed possibly from a policy perspective critical - question: just what do we mean by 'old'. This expression, like similar socially relative terms - 'modern' and`post-modern' would be good examples - is a deceptive one, since it gives the impression of being carved eternally in time, when in fact it is, of course, extraordinarily relative to our life course and our life history evolution.. To give a simple illustrative example, a populist Turkish politician famously got himself elected during the early 1990s on the promise of introducing comprehensive male pensions starting at the age of 43, with female entitlement starting at the even more 'tender' age of 39 (a policy decision which, of course, resulted in one of the worst pension's crises in world history). The politician in question presumeably considered that the age of 43 was 'old', and those who voted him into power evidently agreed with him. The point really is that what we consider to be old is a socially defined (and hence relative) concept. It will hold different values at different times. In the Turkey of the 1990s life expectancy was not especially high when compared with that which which may now be anticipated in contemporary developed societies, an indeed similar, if not so spectacular, examples of the Turkish definition are to be found littered around the history of the third world. They correspond to an earlier, and rapidly transforming, shape associated with the population pyramids.



However as modern life expectancy breaches ever higher limits we can expect our definition of 'old' to increasingly adjust itself upwards accordingly, and in general we should probably keep our fingers crossed that Jones was right when he surmised - back in 1956 - that “the physiological age of each new generation is remaining more youthful at the same chronological age”.



Whatever the ultimate verdict on the validity or utility of the transition phases schema, we should not leave the topic without noting one last thing: those societies which enter their transition process later tend to pass through it at an ever increasing rate. In the case of the mortality decline component of the transition we can see that gains in life expectancy occured in the twentieth century in developing countries at rates which were very rapid by historical standards. In India, life expectancy rose from around 24 in 1920 to the contemporary level of 62 (a gain of 0.48 years per calendar year over 80 the 80 years in question), while in China, life expectancy rose from 41 in 1950–1955 to 70 in 1995–1999, (a gain of 0.65 years per year over 45 years.(Lee 2003) (Find some other data here, this is less than useless as an illusrtation, to myself, Edward). Like wise fertility transitions since World War II have typically been more rapid than those which occured in the nineteenth century, with fertility reaching replacement level in 20 to 30 years post onset, and then continuing to fall steadily, and apparently inexorably, in the direction of lowest-low fertility.. Fertility transitions in East Asia were particularly early and notably rapid, while those in South Asia and Latin America were slower in starting but now seem to be accelerating very rapidly (Casterline, 2001, United Nations Population Division, 2003).







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