Network for Studies on Pensions, Aging and Retirement

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1 Netspar Panel Papers Johan Mackenbach, Wilma Nusselder, Suzanne Polinder and Anton Kunst Compression of morbidity: a promising approach to alleviate the societal consequences of population aging?

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3 Johan Mackenbach, Wilma Nusselder, Suzanne Polinder and Anton Kunst Compression of morbidity: a promising approach to alleviate the societal consequences of population aging? panel paper 7

4 Network for Studies on Pensions, Aging and Retirement Colophon Panel Papers is a publication of Netspar June 2008 Editorial Board Henk Don (Chairman) - Erasmus University Rotterdam Jan Marc Berk Dutch Central bank (DNB) Bernard ter Haar Ministry of Finance Jan Koeman Ministry of Social Affairs and Employability Peter Kooreman - Tilburg University Niels Kortleve - PGGM Albert Mentink - AEGON Joos Nijtmans - Interpolis Alwin Oerlemans - Cordares Rick van der Ploeg - Oxford University Hens Steehouwer - ORTEC Tom Steenkamp - APG Marno Verbeek - Erasmus University Rotterdam Design Bladvulling, Tilburg Printing Printing Office Tilburg University Editorial address Netspar Tilburg University PO Box LE Tilburg Phone info@netspar.nl No reproduction of any part of this publication may take place without permission of the authors.

5 contents Preface 7 Executive summary 9 1. Introduction Conceptual progress and empirical trends since Fries Potential impact of lifestyle modification Policy recommendations 32 Illustrations 35 References 45 Summary of discussion 49

6 Johan Mackenbach, Wilma Nusselder, Suzanne Polinder and Anton Kunst Department of Public Health, Erasmus MC

7 7 preface Netspar stimulates debate and fundamental research in the field of pensions, aging and retirement. The aging of the population is front-page news, as many baby boomers are now moving into retirement. More generally, people live longer and in better health while at the same time families choose to have fewer children. Although the aging of the population often gets negative attention, with bleak pictures painted of the doubling of the ratio of the number of people aged 65 and older to the number of the working population during the next decades, it must, at the same time, be a boon to society that so many people are living longer and healthier lives. Can the falling number of working young afford to pay the pensions for a growing number of pensioners? Do people have to work a longer working week and postpone retirement? Or should the pensions be cut or the premiums paid by the working population be raised to afford social security for a growing group of pensioners? Should people be encouraged to take more responsibility for their own pension? What is the changing role of employers associations and trade unions in the organization of pensions? Can and are people prepared to undertake investment for their own pension, or are they happy to leave this to the pension funds? Who takes responsibility for the pension funds? How can a transparent and level playing field for pension funds and insurance companies be ensured? How should an acceptable trade-off be struck between social goals such as solidarity between young and old, or rich and poor, and individual freedom? But most important of all: how can the benefits of living longer and healthier be harnessed for a happier and more prosperous society? The Netspar Panel Papers aim to meet the demand for understanding the ever-expanding academic literature on the consequences of aging populations. They also aim to help give a better scientific underpinning of policy advice. They attempt to provide a survey of the latest and most relevant research, try to explain this in a non-technical manner and outline the implications for policy questions faced by Netspar s partners.

8 8 Let there be no mistake. In many ways, formulating such a position paper is a tougher task than writing an academic paper or an op-ed piece. The authors have benefited from the comments of the Editorial Board on various drafts and also from the discussions during the presentation of their paper at a Netspar Panel Meeting. I hope the result helps reaching Netspar s aim to stimulate social innovation in addressing the challenges and opportunities raised by aging in an efficient and equitable manner and in an international setting. Henk Don Chairman of the Netspar Editorial Board

9 9 executive summary The twentieth century rise in life expectancy is one of the great successes of public health, but has also contributed importantly to the aging of western populations. Aging poses great challenges to the modern welfare state, and there is an urgent need for strategies to be developed that will help to alleviate the societal consequences of population aging. This paper focuses on one promising approach: achieving a compression of morbidity, i.e. a reduction of the number of years spent in ill health. For a given level of life expectancy, a compression of morbidity into a smaller number of years at the end of life would enable people to stay at work for a longer period of time, and also to care for themselves at advanced ages. The concept of compression of morbidity was introduced in 1980 by the American gerontologist James Fries. He saw viable opportunities for reducing the number of years spent in ill health, because he thought that it was unlikely that life expectancy would continue to increase, whereas he saw no barriers to further increasing the age at which people contract their first disease or disability (e.g. by lifestyle modification). Recent developments have proven him both right and wrong. Empirical studies of trends in disability and the number of years spent with disability suggest that a compression of disability has indeed occurred in a number of countries, including the United States and the Netherlands. This occurred despite a further and rapid increase of life expectancy at birth, and probably not as a result of favorable lifestyle developments but of better treatment and rehabilitation. It is not yet clear why this has occurred in some countries but not in others, and further study will help us to identify the crucial factors in achieving a compression of morbidity. Can lifestyle modification produce a compression of morbidity? This paper analyses the data from the famous Framingham study, which suggests that some changes (e.g. reduction of obesity and hypertension) are likely to lead to a compression of morbidity due to cardiovascular diseases, while other changes (e.g. reduction of smoking and physical

10 10 inactivity) are likely to be neutral with regard to compression. One finding is that while an appropriate mix of lifestyle interventions may indeed help to achieve compression while further increasing life expectancy, further study is needed to determine the right amounts of the ingredients of the mix. The paper concludes that compression of morbidity is a promising approach to alleviate the societal consequences of aging, but that it is currently unclear how it can best be achieved. Lifestyle modifications do not always seem to be effective in achieving compression of morbidity while increasing life expectancy. Other methods (e.g. better treatment and rehabilitation to prevent morbidity from carrying over into disability) should therefore also be considered.

11 compression of morbidity: a promising approach to alleviate the societal consequences of population aging? Introduction 1.1 Staircases of life and other conventional representations of old-age infirmity The twentieth century rise in life expectancy is one of the great successes of public health, but has also contributed importantly to the aging of western populations. Aging poses great challenges to the modern welfare state, not only by threatening the sustainability of pension systems but also by inducing a greater demand for social services, including healthcare. Although several factors underlie the increase in healthcare costs, aging is an important driver of this increase in the long run (43, 59). There is an urgent need for developing strategies that help to alleviate the societal consequences of the aging of populations. Unfortunately, the ill health that tends to accompany aging is often seen as an immutable factor. If the association between age and ill health is immutable, then population aging will inevitably lead to higher rates of morbidity, disability, and demand for healthcare and other social services. Is this, however, an immutable factor? Previous generations certainly thought that it was, as illustrated by so-called staircases of life (illustration 1). These representations of aging and its consequences were popular in the 18th century, and are based on the idea that man is at the height of his powers at the age of 50, and that beyond that age decline is inevitable until disability and finally death occur. Some evidence suggests, however, that many manifestations of ill health at advanced ages are amenable to intervention (e.g. prevention by lifestyle modification), early detection, treatment or rehabilitation. Not only mortality can be postponed (as reflected in the increase of

12 12 panel paper 7 life expectancy at birth); other manifestations of ill health may also be postponed as well. If that is true, then some of the societal consequences of aging might also be more manageable than previously thought. Whereas population aging is inevitable, its consequences may not be inevitable to the same extent. If the manifestations of ill health that usually accompany aging can be postponed to higher ages, then it becomes easier to continue working, to care for oneself and to continue providing informal care to other people. How can this be achieved? 1.2 James Fries and his syllogism The amenability of the health consequences of aging was first clearly proposed by the American gerontologist James Fries, in his highly cited paper, Aging, natural death, and the compression of morbidity, published in the New England Journal of Medicine in 1980 (11). His paper provides a more optimistic view of aging than most people had at that time. His reasoning can best be summarized as based on a logical syllogism: the human lifespan is fixed (and average life expectancy is rapidly approaching this limit); the age at first infirmity (functional impairment due to ill health) will increase; the average duration of infirmity will therefore inevitably decrease. The first two parts of this syllogism (from which the third should logically follow) are based on a number of empirical observations and theoretical insights. Like many other scientists, Fries believed that the human lifespan is fixed, in the sense that there is a genetically endowed limit to the life of the human species. There is no major disagreement among scientists on whether this is true the disagreement starts when it comes to deciding at what age this limit may lie, or whether there is a possibility for medical technology to even change this limit. Fries thought that there must be some immutable upper limit, and, more importantly, that average life expectancy is already rapidly approaching its biological limit. One of his main arguments was that increases in life expectancy during the 20th century mainly reflected declines in mortality at younger ages, and that declines in mortality at

13 COMPRESSION OF MORBIDITY 13 older ages have been much less clear. This has led to a rectangularization of the survival curves of many human populations (i.e. a change in the shape of the curve of survival by age, during which the first part becomes more and more horizontal (because at younger ages almost no one dies), and the second part becomes more and more vertical (because beyond a certain age mortality rates increase rapidly)). Fries maintained that this rectangularization is likely to increase in strength over time, reflecting the natural tendency of biological organisms to wear out and die off. His view that we are already near to the end-point in this development is based on an analysis of historical developments in remaining life expectancy at higher ages in the United States. Extrapolating these developments, Fries concluded that, ultimately, survival curves would stabilize around a mean age at death of 85 years. After making his argument for the first part of his syllogism, Fries then began to provide arguments for the second part. Fries thought that the age at first infirmity (or disability) was likely to increase further and further, because he already saw declines of the frequency of some chronic diseases in the United States around that time (e.g. in cardiovascular disease). More importantly, he saw a great potential for further reduction of morbidity, particularly by lifestyle improvement, because many of the risk factors for these chronic illnesses were already known, and seemed to be amenable to intervention. If the average age of death does not increase much further, while the average age at first disease or disability continues to rise, then a reduction of the number of life-years spent with morbidity or disability is inevitable. This is what Fries meant by compression of morbidity (illustration 2). The term compression of morbidity complements terms that have become commonplace in later literature, such as healthy life expectancy and disability-adjusted life expectancy (47). Whereas all measures are used to add information on morbidity to information on length of life, they emphasize different things. Measures such as healthy life expectancy focus on good health, rather than on morbidity. They express the extent to which people can expect to live a long and healthy life. These terms are especially useful in assessing people s health-related quality of life, and act as key outcome measures to policies that ultimately aim to improve the health of populations. Measures and concepts such as

14 14 panel paper 7 compression of morbidity look at morbidity instead of positive health. They focus on the burden of disease and disability that people experience across their life course and that can be quantified in terms of life expectancy with disability or related measures. These measures are particularly useful in expressing the adverse impacts of disease and disability on people s lives, including their use of healthcare. These measures are used to assess how much the demand for healthcare might increase in conjunction with population aging. Fries concept of compression of morbidity focuses specifically on the important relationship between the burden of morbidity and proximity of death. If, as Fries envisaged, death would be preceded by increasingly shorter periods of disease and disability, then the burden of morbidity would decrease. 1.3 Central role of lifestyle factors in this reasoning Lifestyle factors, and lifestyle modification, played a central role in Fries reasoning. This reflected the fact that modern disease patterns are strongly influenced by determinants that are linked with (seemingly) voluntary behavior, such as exposure to tobacco smoke, consumption of diary fat, and lack of physical exercise. Historically, the seminal paper of Fries should be seen against the background of the epidemiological transition (38, 58). This medical variant of the demographic transition describes a transition from a health situation dominated by infectious diseases, to one dominated by man-made and degenerative diseases. In the decades before 1980, this transition had been achieved in many high-income countries, but had left mixed feelings about the benefits to population health. Although people lived longer, they also frequently suffered from chronic diseases. Many of these chronic diseases were seen to be man-made because of their association with lifestyle factors, as in the case of several cancers (related to smoking, sunlight exposure, reproductive factors, etc.) and cardiovascular diseases (related to smoking, consumption of dietary fat and sodium, sedentary behavior, etc.). One of the clearest examples, of course, is smoking. The history of cigarette smoking can be described in terms of some sort of an epidemic that follows a more or less similar trajectory in many countries (illustration 3). The rise and fall of smoking is roughly mirrored by the rise and fall of mortality from several diseases, including ischemic heart disease, and, with some delay, lung cancer (26).

15 COMPRESSION OF MORBIDITY 15 Around 1980, this fall had not yet occurred, and a further improvement of population health clearly required effective intervention on these lifestyle factors. Fries then argued that this would not only decrease the incidence and prevalence of many chronic diseases, but would also lead to a compression of morbidity. While it is fairly clear that lifestyle modification can delay the age at first disease, and the age at death, it is not immediately clear, however, whether lifestyle modification can also be expected to lead to a compression of morbidity. If not only the age at onset increases, but also the age at death, then the time spent with morbidity will not always be smaller, but can be the same or may even increase (36). Fries predictions were based on theoretical arguments, not on empirical observations. For example, it has never been established whether the epidemiological transition was actually accompanied by some sort of an expansion of morbidity, as one would perhaps predict on the basis of Fries reasoning. Also, studies of the effects of interventions against lifestyle factors have only looked at the effects on the incidence of disease or death, and have never demonstrated that these interventions lead to a compression of morbidity. 1.4 Main purpose of this paper This paper has three main objectives: to provide an overview of the conceptual and empirical progress in this field of research since Fries seminal paper; to provide a quantitative estimate of the potential impact of lifestyle modification on the number of years lived in ill health; to discuss the implications of these findings for policy.

16 16 panel paper 7 2. Conceptual progress and empirical trends since Fries 2.1 Better conceptual distinctions and indicators Shortly after Fries paper, Manton formulated the hypothesis of dynamic equilibrium (28). He stated that increased survival would produce an increase in years with morbidity, but that years with severe levels of morbidity would be relatively constant because the rate of progression of chronic diseases would be reduced. This hypothesis stipulated that a distinction should be made between the onset of diseases, their progression, and the effects of disease processes in terms of disability and other general health indicators, and that morbidity and mortality do not change independently. Soon afterwards, the burgeoning literature demonstrated that various measures of morbidity and disability showed different trends over time and different relationships with age (48). New theories and empirical findings thus stressed the need for refined measurement of disease processes and outcomes. Important developments were then made, particularly with regard to the measurement of disability (56). Disability is regarded as a general health outcome with particular relevance for elderly populations, who are primarily concerned with functioning well and maintaining independence in their daily life. At the conceptual level, distinctions have been made among different aspects of disability, which have come to be known as a disablement process that consists of a set of interrelated layers. A main distinction was made between functional limitations (related to problems of functioning at the physical level) and activity restriction (problems with the functioning of the person in society). Building on this basic conceptual framework, further distinctions have been made according to type of impairment (e.g. sensory vs. mobility impairments) and severity levels (e.g. mild vs. severe disability). Important developments were also made regarding the reversibility of disability. Disability was traditionally thought to be a permanent loss in functioning (i.e. irreversible). Since it is now widely acknowledged that disability can both increase and decrease over time, disability is nowadays seen as a dynamic process rather than a permanent state (35). At the empirical level, new indicators have been developed to assess the disability status of elderly people. Gerontology research began increasingly to use performance-based measures (e.g. to assess objectively the level of functioning of individuals (32)). In population

17 COMPRESSION OF MORBIDITY 17 surveys, however, it has become widely accepted to assess the disability status of respondents by means of questionnaires. It has been agreed that a single question could be used to assess overall disability status, such as the recently recommended question, For at least the last six months, have you been limited because of a health problem in activities people usually do? Yes, strongly limited / yes, limited / no, not limited (46). In addition, batteries of questions have been developed for a more comprehensive assessment of disability status. Examples of such item lists are the questions in the Dutch POLS surveys on functional limitations and on restrictions in ADL, respectively ( Unfortunately, the items included differ greatly between surveys from different countries, thus hampering international comparisons and overviews. Efforts have been made, however, to harmonize the measurement of disability (e.g. through development of standard lists for use within the EU (46)). More recent studies on the compression of morbidity have moved from generic health outcomes such as disability to disease-specific morbidity. These studies aim to assess the prevalence of specific diseases in relationship to population aging and the increasing length of life (9). In such analysis, a key outcome of interest is the number of years lived with and without the specific disease of interest, both in the total population and at specific ages. While most studies of this type have focused on cardiovascular morbidity (see section 3 of this paper), a few have focused on others diseases, such as diabetes (20). A main challenge in this area was to establish a link between studies on disease-specific morbidity and studies on general health outcomes, such as disability. A bridge has been built from both sides. On the one side, studies focusing on specific diseases have applied newly developed disability weights to express the effect of disease prevalence on general health, and to be able to make comparisons among diseases with regards to their effect on population health (6, 52). On the other side, studies focusing on disability have developed methods to attribute disability prevalence to specific diseases, similar to the well-known attribution of mortality to causes of death. For example, Nusselder et al. developed a regression-based methodology for determining the contribution of specific diseases to (time trends or population variations in) the occurrence of disability among elderly populations (34). Studies on the effects of increasing life expectancy have not only considered health outcomes (such as morbidity and disability), but

18 18 panel paper 7 also evaluated the consequences for healthcare utilization and costs. New methods have been developed and applied in order to estimate healthcare costs according to age, sex and disease group. These estimates have made it possible to assess the effects of population aging on total healthcare costs in the Netherlands (31). An important insight from these assessments is that age patterns and time trends in healthcare costs do not run parallel to those in morbidity (44). Age-related increases in healthcare costs are larger than those for morbidity, implying that the aging of the population may lead to a stronger rise in healthcare costs than may morbidity and disability. 2.2 Development of population health models Since Fries seminal paper, new techniques to assess compression of morbidity in aging populations have been developed and applied in studies both in the Netherlands and abroad. During the 1980s, the interrelationship between mortality and morbidity was studied mainly by means of the Sullivan life table (30, 47). This technique obtained information on age-specific mortality rates from one source (mostly mortality registries), and information on the age-specific prevalence of disability from other sources (mostly cross-sectional health interview surveys). As the Sullivan table could easily be applied wherever such data were available, researchers from many countries have increasingly used this technique to study mortality in relationship to morbidity. Issues related to the compression or expansion of morbidity were addressed using life-table measures such as expectancy of life in poor health and life expectancy with disability (LwD). Increasingly, however, it was recognized that the Sullivan method was far from perfect. The basic problem with this method is that information on mortality and morbidity were derived from different sources whereas, in reality, these two health outcomes are closely related. Failure to take account of this intimate association led to unexpected effects. For example, in the early 1990s, Barendregt et al. noted that this technique would yield biased estimates of LwD in situations of rapid change (1). This bias was related to the fundamental problem that the Sullivan method mixes information on transitions (mortality) with information on states (disability prevalence). To address this problem, researchers applied new methods, aiming to study morbidity and mortality as the joint outcomes of the same set of

19 COMPRESSION OF MORBIDITY 19 underlying transitions (47). In recent years, the most commonly applied method has been the multi-state life table (49). The core structure of the multi-state model is illustrated in illustration 4. When applied to disability, the multi-state life table distinguishes between a non-disabled state and one or more disabled states. Transitions between these states are modeled using empirical estimates of age-specific disability incidence rates and recovery rates. In addition, transition from these different states to the state of death is modeled using state-specific mortality rates. From these underlying transitions, the multi-state life table derives a consistent set of age-specific estimates of disability prevalence, total mortality, and life expectancy with and without disability. Thanks to the widespread application of multi-state models, it is now generally recognized that morbidity and mortality do not change independently (36). Changes with regard to some of the transition rates are necessarily accompanied by changes in both disability prevalence and overall levels of mortality. It is particularly important to assess the effects of changes in incidence rates, because these are most sensitive to changes in environmental conditions, lifestyles and preventive policies. A decline in incidence would, ceteris paribus, lead to a decline in both disability prevalence and overall mortality rates, and to a compression of morbidity. However, when in addition also state-specific mortality rates decline, it is much harder to achieve a compression of morbidity. Multi-state life-table analyses also demonstrated the potential role of changes in recovery from disability. Not only lower incidence rates but also higher recovery rates potentially produce a compression of morbidity. The main virtue of multi-state life tables has been to demonstrate these mechanisms and to quantify their effects in specific cases, such as the evaluation of preventive policies. Important for application in specific cases is to have valid and precise empirical estimates of the transition rates. In case of disability, these estimates have to be derived from longitudinal studies with repeated measurement of disability. During the mid 1990s, such data became available from a number of Dutch epidemiological studies, including the GLOBE, ERGO and LASA studies (15, 35, 54). New longitudinal data sets also became available for the 2000s, thanks also to the linkage of date registries at Statistics Netherlands. At European levels, longitudinal datasets have become available from surveys that cover large population samples and include different EU member states, including

20 20 panel paper 7 the Netherlands. An early example from the 1990s is the ECHP (51), while a recent example is the SHARE panel survey (21). Whereas many studies have used the multi-state life table to study the interrelationship between mortality and disability, others have used the same modeling technique to study the dynamics of specific diseases. Multi-state models have been developed for several diseases, including diabetes, heart disease, stroke, COPD and some cancer sites (47). Disease-specific models have the advantage that they can be based on disease incidence data available from epidemiological registries or from longitudinal epidemiological studies. In addition, transition rates could be modeled in relationship to well-known disease-specific risk factors, such as smoking and obesity. These models have been used to model the effect of changes in these risk factors on disease-specific outcomes under conditions of increasing life expectancy. An example of such analyses appears in section 3 of this paper. Other extensions to the multi-state life table are illustrated by the Chronic Disease Model of the RIVM (7), which models several diseases simultaneously, while taking into account interrelationships between diseases such as diabetes and heart disease. In addition, the RIVM model is a dynamic model that follows the development of a population by calendar time. This feature, which is also applied in models such as Prevent (3), makes it possible to assess the development over time of both mortality and morbidity within real-life cohorts. This is especially important for cohorts such as the baby boom cohort, which will comprise a large part of the Dutch elderly population between about 2010 and Development of mortality since Fries Since Fries paper, many studies have noted that mortality trends in highincome countries have continued to decline at a steady rate during the late 20th century. In most countries, the increase in life expectancy has been much stronger than Fries anticipated. Since 1980, the life expectancy at birth in many Northern and Western European countries has increased by more than two years per decade. Eastern European countries are lagging behind the trends in the West, although countries such as the Czech Republic seem to have started catching up (2). Outside Europe, trends broadly similar to those in Northern and Western Europe have been observed in the US, Canada, Australia and New Zealand. The most spectacular increase has been observed in Japan, where life expectancy

21 COMPRESSION OF MORBIDITY 21 among women rose to a record height of 85 years in the period (37). It is important to note, in light of Fries hypothesis, that substantial mortality declines have been observed not only for middle-aged populations, but also for the elderly populations, and even the oldest of the old (i.e. 85 years and over). With regard to the latter, mortality rates in Northern and Western European countries have shown substantial declines since 1950, with rates of decline exceeding 1 percent per year, especially for women (19). Important variations in the rate of decline were observed between countries and periods, however, with even some periods of stagnation in some Northern and Western European countries. The most recent examples are the stagnation in the decline in old-age mortality in the Netherlands since 1980, which was paralleled by a similar stagnation in Denmark and Norway. Mortality in these countries, however, started to decline again in the 1990s or the 2000s (19). The evidence from recent trends in old-age mortality suggests that Northern and Western Europe are far from approaching a limit to life expectancy at about 85 years (16). In most countries, first of all, there has been no deceleration in the mortality decline in recent years even though female life expectancies are exceeding 80 years. Second, mortality declines are not smaller in populations with the highest life expectancy. For example, in France and Sweden, where life expectancies are relatively high for women and men, respectively, old-age mortality has continued to decline at a steady pace. Thus, periods of stagnation of mortality decline, such as in the Netherlands in the 1980s and 1990s, cannot be taken as evidence that limits to life expectancy were close to being reached. This stagnation is likely to be related to temporal factors such as the smoking epidemic, which especially affected Dutch men born at the turn of the 20th century (18). The generalized mortality decline that has been observed in most European countries seems to be closely related to the unprecedented social and economic progress in Europe since the late 19th century (17). General socioeconomic development has far-reaching benefits for birth cohorts throughout their lifetime. Birth cohorts with a relatively favorable mortality level at younger ages also have relatively low mortality at higher ages. This suggests that mortality decline is embedded in factors that start at middle age or even earlier. Given this positive association, it is important to observe that also in the Netherlands, mortality rates began again

22 22 panel paper 7 to decline among younger generations (such as those who attained their 60th birthday by the year 2000). It suggests that further declines may occur in the future, when these cohorts will live into old age in decades to come(16). Fries hypothesized a rectangularization of the survival curve (i.e. a decline in the standard deviation in the age distribution of deaths around an average of about 85 years (11)). There is some evidence for a verticalization of the age distribution of deaths in a number of countries during the second half of the 20th century. In the Netherlands, for example, the number of deaths that occurred within the ten-year interval around the modal age at death increased from 25 percent in 1950 to almost 35 percent in 2000 (45). The increase is modest, however, and implies that also in recent years there is a substantial dispersion of deaths across the age range. In addition, the standard deviation in the age distribution of deaths has remained constant since the 1990s. Illustration 5 shows trends in the age distribution of deaths at ages 60 years and over in the Netherlands. The modal age at death increased substantially between 1970 and 2005: from 76 to 81 years for men, and from 82 to 88 years for women. The standard deviation changed only marginally between and 2005, even though the peak number of deaths is slightly higher in 2005 than it was before. An upward shift of the age distribution of deaths has also been observed in other countries, such as Japan (4). To conclude, there is no consistent evidence for Fries expectation that survival curves would become more rectangular and that mortality would be compressed at an age of about 85 years. The modal age of death has increased at a steady rate in most countries and has surpassed the age of 85 years. In addition, the standard deviation in age of death has remained substantial, and has not decreased in recent years in some countries. This removes some of the conditions that Fries postulated for a compression of morbidity to occur. 2.4 Development of morbidity since Fries Whereas the study of secular trends in mortality has a long tradition, the study of trends in morbidity has a shorter history. As of 2008, however, trends in morbidity, especially in disability prevalence, have been studied in a large number of countries. Many of these studies are from the US. This section summarizes the results of studies on disability, drawing heavily

23 COMPRESSION OF MORBIDITY 23 on a recent review carried out by Muth et al. (33), whose conclusions are similar to those of a recent review performed by the OECD (24). Note, first of all, that it is much more difficult to determine trends in disability than to determine trends in mortality. Disability studies must cope with problems involving the comparability over time of disability measures. Moreover, many interview surveys feature rather small samples of elderly respondents, exclude institutionalized people, and have considerable non-response (or attrition) rates. In addition, the time period covered by two consecutive surveys is often relatively short (less than ten years), and secular change in this period may be too small to be determined with precision. As a result, the results for disability that are summarized below have a much higher degree of uncertainty than those for mortality. The general impression from the several studies that have been done is that age-specific rates of disability prevalence generally declined during the 1980s and 1990s. As Muth et al. conclude: The review of the trends in disability showed that there was a common improvement in health of the older populations for most countries in terms of disability over the 1980s and 1990s (33). The results presented in the literature, however, are inconsistent. Many studies found evidence of increasing disability rates or at least no support for declining rates. While such inconsistencies may in part be related to the data problems listed above, some of these may reflect true variations between study populations or disability indicators. Trends may have differed between countries. Declining rates of disability among elderly people have consistently been observed in most studies from the US. In contrast, for some other countries, the available evidence suggests an increase in disability prevalence. Limited but consistent evidence for deterioration in rates exists for Sweden and Canada. In addition to variations between countries, trends in disability may vary over time. For example, a US study suggested a relatively slow decline in disability prevalence in the 1980s followed by a much larger decline during the 1990s (10, 53). A parallel change was observed in Finland, where disability prevalence was found to increase slightly in the 1980s and to decrease during the 1990s (57). These results suggest that, as with mortality, periods with declining rates may be interspersed with periods of stagnation or even increasing disability prevalence. For the Netherlands, the available evidence is less consistent, but still suggests a decline in the prevalence of several types of disability or

24 24 panel paper 7 functional limitations. Illustration 6 shows trends in mobility limitations for the Netherlands. The prevalence of such limitations among elderly populations (65 years and over) decreased from about 33% in the early 1990s towards about 25% in the early 2000s (13). Positive trends were also observed on the basis of data of the LASA study, where improvements in mobility were demonstrated not only on the basis of respondents self reports but also using performance tests (13). Similar improvements were observed with regards to functional limitations in sight or in hearing, but not as consistently with regards to ADL disability. In many studies, the observed trends vary according to the disability measure that is applied. In Dutch studies, for example, trends in disability have generally been favorable for severe or moderate levels of disability, but not for mild levels of disability (41). This finding supports the hypothesis, derived from the Manton hypothesis of a dynamic equilibrium, that a compression of severe levels of disability could occur simultaneously with an expansion of mild levels of disability (28). However, despite the support from some Dutch studies, there is no consistent support from the recent international literature for the hypothesis of a dynamic equilibrium. For the debate on compression of morbidity, it is important to translate trends in disability rates into trends in life expectancy measures. Especially important are trends in the life expectancy with disability (LwD), as an increase in LwD directly implies an expansion of disability, while decreasing LwD implies compression. LwD measures have been applied in only a few Dutch trend studies, including a series of studies by Perenboom et al. (41). According to the latter studies, mild LwD increased between 1989 and 2000 both among men (from 3.7 to 6.2 years) and among women (from 3.6 to 5.0 years), while severe LwD decreased. More recent estimates, however, showed that the gain in disability-free life expectancy exceeded the gain in total life expectancy, indicating that a compression of morbidity occurs (42). Declines in disability have been found to occur together with stable levels of disease prevalence. Thus, despite an about-constant prevalence of chronic diseases among elderly populations, their levels of disability tended to decrease (48). The explanations for these diverging trends are as yet unclear. The burden of disability may be determined not only by the simple prevalence of chronic diseases, but also by the extent to which individual cases of disease lead to disability. Advances in curative and

25 COMPRESSION OF MORBIDITY 25 rehabilitative care, and the widespread availability of assistive devices are likely to have reduced the impact of some diseases on disability. Alternative explanations include changes in the perception and reporting of disability, and changes in the living conditions of disabled people (13, 48). To conclude, the evidence emerging from the international literature provides meager support for an expansion of disability. Instead, the results of many studies, particularly those of the US, support a more positive view, while Dutch studies tend to support Manton s hypothesis of dynamic equilibrium. However, discrepancies between study results seem to indicate a need for greater caution. Therefore, as an OECD study concludes on the basis of current evidence, it would not be prudent for policymakers to count on future reductions in the prevalence of severe disability among elderly people to offset completely the rising demand for long-term care that will result from population aging (24).

26 26 panel paper 7 3. Potential impact of lifestyle modification 3.1 Introduction to the study Cardiovascular disease is the number one cause of mortality and morbidity in the world (25, 29). Advancing age is a major risk factor for cardiovascular disease, and population aging will therefore have a major impact on the prevalence of cardiovascular disease. The risk of developing cardiovascular disease, however, also depends strongly on the presence of modifiable risk factors such as smoking, hypertension, physical inactivity and being overweight/obesity. Reducing the exposure to these risk factors therefore holds great potential for reducing the burden of cardiovascular disease, or for reducing the increase in the burden of cardiovascular disease, which can be expected on the basis of population aging. While it is likely that reducing exposure to these risk factors will lead to a reduction in the incidence of cardiovascular disease, and to a reduction in the number of deaths from cardiovascular disease, it is currently unknown whether this will also lead to a reduction in the number of years spent with cardiovascular disease. This is not immediately obvious, because this will depend on the balance between the two primary effects: the postponement of the average age of cardiovascular disease incidence, and the postponement of the average age of death. Analyzing the conditions for compression of cardiovascular disease morbidity provides an excellent opportunity to shed more light on the general conditions for compression of morbidity, because of existing knowledge about risk factors, and because of good data availability. We therefore decided to carry out an in-depth analysis of the effects of risk-factor modification on compression of cardiovascular disease morbidity. For details we refer to a series of recent publications. This analysis used data of the Framingham Heart Study to assess the effects of four cardiovascular disease risk factors (smoking, hypertension, physical activity and overweight/obesity) in 50-year-old persons. The Framingham Heart Study is a widely known epidemiological study that provides high quality data collected among a sample of more than 5000 individuals living in Framingham (Massachusetts) around 1950 (20). Data covering a similarly long follow-up period (almost 50 years) are not available for the Netherlands. Like every other advantage, this one also has a mirroring disadvantage: the data are to some extent historical in nature. Because they cover several decades of follow-up, they can therefore no

27 COMPRESSION OF MORBIDITY 27 longer be assumed to accurately reflect the current situation with regard to, e.g., amenability of the health risks of obesity to prevention and treatment. We analyzed these data to estimate the effect of each risk factor on three transition rates incidence of cardiovascular disease (CVD), risk of dying among those having cardiovascular disease, and risk of dying among those not having cardiovascular disease. These are the three transition rates needed to construct multi-state life tables, which were then used to calculate years of life with and without cardiovascular disease, and to estimate the impact of risk-factor modification on these outcomes. Illustration 7 provides greater detail about data and methods of this comparative analysis of four risk factors. Analyses for some of the individual risk factors have been reported previously, and we refer readers to these previous reports for further details about data and methods (8, 9, 27, 39, 40). 3.2 Results Illustration 8 presents the results of the analysis of the effect of each risk factor on all three of the transition rates. The three transition rates have been abbreviated No CVD to CVD (i.e. incidence of cardiovascular disease), No CVD to Death (i.e. risk of dying among those not having cardiovascular disease), and CVD to Death (i.e. risk of dying among those having cardiovascular disease). The results are presented in the form of Rate Ratios (i.e. the transition rate among those exposed to the risk factor, divided by the transition rate among those not exposed to the risk factor). For the first risk factor, smoking (illustration 8a), the main results are that current smokers have elevated rates of all three transitions but the highest Rate Ratio is seen for the risk of dying among those not having cardiovascular disease. This can be interpreted as follows. Smoking increases not only the risk of dying from cardiovascular disease (through an increased incidence of cardiovascular disease, plus an increased risk of dying among those having cardiovascular disease), but also the risk of dying from many other diseases (e.g. several cancers, chronic obstructive pulmonary disease). For hypertension (illustration 8b), a completely different pattern is seen. The main effect is on the transition from No CVD to CVD : people with hypertension have substantially elevated incidence rates of cardio-

28 28 panel paper 7 vascular disease. Hypertension doesn t increase the risk of dying for either those with cardiovascular disease, or those not having cardiovascular disease. As compared with smoking, the risk factor of hypertension thus has a relatively stronger effect on cardiovascular morbidity than on cardiovascular mortality. For physical activity (illustration 8c), the effects are similar to those seen for smoking. All three of the transition rates are elevated for those with low physical activity. For overweight/obesity (illustration 8d), the effects are similar to those seen for hypertension. The main effects are seen for the transition from No CVD to CVD. In conclusion, being a current smoker, hypertensive, physically inactive or overweight are all associated with higher risks of developing cardiovascular disease. The risk of dying among those with or without cardiovascular disease, however, is only affected by smoking and physical inactivity. We now proceed to the results of the second step in the analysis: the calculation of life expectancy with and without CVD by level of exposure to the four risk factors (illustration 9). These results can be seen from two perspectives. When one compares the exposed with the unexposed (by going from left to right), one sees an indication of the impact of current exposure on years of life with and without cardiovascular disease. When one compares the unexposed with the exposed (by going from right to left), one sees an indication of the impact of reducing exposure on years of life with and without cardiovascular disease. The results for smoking (illustration 9a) suggest that current smokers not only have lower total life expectancies, but also lower expectancies of life without cardiovascular disease. The number of years lived with cardiovascular disease is no different between current smokers and never smokers. In other words, elimination of smoking is likely to lead to higher total life expectancy and higher expectancy of life without cardiovascular disease, without affecting the number of years lived with cardiovascular disease. The above results contrast sharply with those for hypertension (illustration 9b). People with hypertension have lower total life expectancies, lower expectancies of life without cardiovascular disease and higher numbers of years lived with cardiovascular disease. This suggests that elimination of (the effects of) hypertension will lead to higher total life expectancy, higher expectancy of life without cardiovascular disease, and