Select Committee on Science and Technology First Report


CHAPTER 3: UNDERSTANDING THE AGEING PROCESS

Introduction

3.1.  The timeliness of our inquiry derives not only from the dramatically changing demography, reviewed in Chapter 2, but also from recent advances in the biological understanding of the ageing process. Scientific research on ageing, including research within the UK, has revealed significant new insights into how and why we age, and what might be done to improve the prospects for healthy ageing. This research is overturning many aspects of what might be termed the "traditional" view of ageing. It is also helping us to understand why, contrary to previous expectation, human life expectancy is continuing to increase.

3.2.  In this chapter we consider the natural ageing processes, and in the following chapter those diseases which are particularly prevalent in old age. Not everyone agrees that there is a clear distinction between the two, or that it is helpful to attempt to draw such a distinction. For the reasons given later in this chapter[28] we believe that, at least for the purposes of this report, such a distinction is useful.

The Ageing Process

3.3.  From a biological perspective, ageing is commonly defined in terms of what it does to an organism's vitality and prospects for further survival. Typically, biological gerontologists—those who study the biological mechanisms of ageing—define ageing as "a progressive, generalized impairment of function resulting in a loss of adaptive response to stress and an increasing probability of death".[29] For humans, the underlying pattern of increase in mortality rates shown by the exponential curve in Figure 3, demonstrates that once a person attains adulthood, the annual risk of dying approximately doubles with every 8 additional years that pass.

3.4.  Perhaps the first lesson to draw from these figures is that the common public perception of ageing as something which afflicts only older people, and those approaching old age, is a fallacy. Ageing begins at birth. The increase in the rate of ageing begins at puberty. If this were more widely understood, two consequences might follow. First, if younger people understood that they too are members of a cohort which is ageing at a progressively faster rate, this might have an impact on their frequently ageist attitude to older people. The second consequence is that this younger cohort might learn earlier what can be done—and what they can do—to promote good health and slow the ageing process.

3.5.  Not all creatures age. There are some animals, such as the freshwater Hydra, for which the mortality rate does not increase with the passage of time. Thus, ageing is not an absolute biological necessity. As for why species like our own are subject to the inevitability of ageing, the commonly held view has been that ageing is, in effect, biologically programmed by some inner mechanism that imposes a strict upper limit to the lifespan. Were this view to prove

FIGURE 3

Changes in Mortality Rates

Deaths per thousand population per year, by age and sex. The lower graph shows the same figures plotted on a logarithmic scale. This highlights the fact that for both sexes mortality rates increase exponentially, following the minimum which occurs around the age of puberty and a brief period of excess mortality from accidental causes occurring during young adulthood (ages 18-26).







correct, there would be little that could be done to modify the ageing process, unless some means could be found to alter the mechanisms programming our death.

3.6.  However, the traditional view that the ageing process is actively programmed by some kind of self-destruct mechanism has been abandoned by most biological gerontologists in favour of the idea that ageing is caused by a gradual build-up of subtle faults in the cells and organs of our bodies. This revised view has opened many new possibilities for research that can improve the prospects for healthy ageing. As will be described later, it also provides important new insights into the relationship between ageing and disease. Equally importantly, it challenges the widespread fatalism that tends to prejudice our ideas about growing old. To some extent the view that deterioration with age is inevitable seems to be a self-fulfilling prophecy. We were told:

  "Surprisingly, the age-related decline in physical fitness appears to be more related to expectation than to biology. As we age, we expect to be less fit, so we exercise less, worry less about weight gain, and attempt less demanding roles."[30]

OUR SEMINAR

3.7.  We began our inquiry with a seminar held on 14 September 2004 and attended by a number of distinguished participants. A full note of the proceedings is in Appendix 4.

3.8.  Professor Kirkwood explained that life expectancy was influenced by a number of factors. Genetic heritability accounted for about 25% of the differences between individuals, with longevity tending to run in families and monozygotic twins having lifespans more similar to each other than dizygotic twins. However, the ageing process was not itself genetically programmed—there are no genes for ageing—but was caused by an accumulation of cellular defects resulting from random molecular damage, with genes influencing cellular repair. Other factors affecting ageing were nutrition, lifestyle and environment, each of which has the potential to modify the rate of accumulation of damage by influencing the body's exposure to intrinsic or extrinsic sources of molecular damage, or by acting upon the body's natural mechanisms for maintenance and repair. These non-genetic factors were in turn amenable to influence by socio-economic factors, as could be seen from variations in life span recorded by different local authorities. In a similar way, the concept of ageing as damage allows the continuing increases in LE to be explained, if the improving conditions within many present-day societies mean that our bodies are accumulating damage more slowly.

3.9.  Professor Steve Jackson, from the Gurdon Institute, Cambridge University, addressed the role of damage in ageing further when he considered what ageing was; why and how we aged; whether we could slow down or prevent ageing.

3.10.  The symptoms of ageing are a matter of common observation. They consist, among other things, of a loss of vigour; in skin, a loss of the subcutaneous fat cell layer leading to loss of suppleness and wrinkling; connective tissue changes; greying hair and loss of hair; impairment of the senses; osteoporosis; and cardiovascular and neurological degeneration. The underlying changes are cellular damage leading to impaired cell function; accumulated tissue and organ damage leading to dysfunction; and the loss of ability for tissue renewal. What we call "ageing" is the intrinsic accumulation of such damage.

3.11.  Many matters will influence longevity, but essentially the reason we have not evolved to live longer is that evolution acts to maximise reproductive success, rather than longevity. There is little selective pressure to evolve genes which might allow an individual to live significantly longer than it was likely to survive in the wild, where death usually occurs from accidental causes long before ageing becomes apparent. On the contrary, evolution will select genetic factors which increase reproductive fitness even though this may well cause accelerated ageing.

3.12.  Oxidative stress[31] is a major factor causing ageing, and a major target for oxidative damage is DNA. Laboratory animals bred through artificial selection to live longer are those which are more resistant to biochemical stresses such as oxidative stress. The reason calorie restriction tends to enhance the life-span of many organisms is related to its effects on oxidative metabolism and stress-resistance.

3.13.  Most human cells can divide only a limited number of times, and when they reach the end of their replication capacity, they enter into senescence. There is evidence that cell senescence also takes place during the ageing of a person. Telomeres, the protective structures at the ends of chromosomes (sometimes likened to the plastic tips that prevent a shoelace from unravelling), shorten over time as a result of oxidative stress. Telomeres in cells thus provide a mechanism to limit cell division: when the telomeres became too short, senescence is induced. There are strong links between telomere shortening and DNA damage. Another link to DNA damage is Werner's syndrome, an autosomal recessive disorder which leads to death in the fourth to sixth decade of life.

3.14.  As well as the limitation on cell division capacity, many human cells, such as brain or muscle cells, are essentially post-mitotic (that is, they have attained a specialised state that is unlikely or unable to undergo further division). In these types of cells ageing and death tend to occur not through telomere shortening but through the build up of other types of fault, such as abnormal, damaged proteins. When a cell does not divide, its capacity to clear damage is mainly dependent on turnover ("garbage" disposal and recycling processes), and these appear to become gradually overwhelmed.

3.15.  The impressions we gained about the basic biology of ageing during our seminar were borne out during subsequent examination of detailed scientific aspects of ageing, which included a visit to the United States National Institute on Aging.[32] It was clear that in terms of understanding how and why we age, there is a broad consensus among biological gerontologists. However, it was also clear that this is relatively new science being conducted by a number of researchers which is small when compared with more established fields such as cancer or cardiovascular disease. When looking beyond the present areas of knowledge, there is a vast amount yet to be discovered. Not least of the difficulties is the integration of the many different factors and mechanisms that impact upon the ageing process.

Implications of the scientific understanding of ageing

3.16.  The implications of the realisation that ageing is caused by lifelong accumulation of molecular and cellular damage, rather than by some rigid inner "clock", are profound. In particular it can be seen, first that the ageing process is more malleable than has been generally appreciated, and secondly that the mechanisms governing health in old age are at work throughout life. This view also has implications for concepts of "normal" ageing and for the perceived value of trying to draw clear scientific distinctions between intrinsic ageing and age-related diseases. We consider this question later in this chapter.[33]

3.17.  Intrinsic malleability of the ageing process is evident in the changes that are continuing to occur in LE, long after the major gains that were brought about from the control of infectious diseases (particularly those which killed the young during the 19th and first half of the 20th centuries) were essentially complete. What is driving the current increase in LE is a decline in death rates among older people, including the oldest old (those over 85 years). It is perhaps an unreliable commonplace to observe that "70 is the new 50", but we are all aware that, on average, today's cohorts of older people are different from their predecessors. It is this apparent malleability of the ageing process that gives scientific basis to the hope expressed in Chapter 2, that it may be possible to reduce the expectation of unhealthy years of life, even while LE itself is increasing.

3.18.  The importance of recognising that ageing begins in youth cannot be overstated. Indeed, from what we are learning about the underlying mechanisms of ageing, the build up of molecular and cellular damage probably starts in utero. The evidence that genetic factors account for just 25% of human longevity suggests that much can be gained from targeting the non-genetic factors such as nutrition, lifestyle and environment as early as possible.

3.19.  It is as yet unclear how far the intrinsic malleability of the ageing process can be exploited. This is a matter for future research. In order to slow the accumulation of molecular and cellular damage that underpins the ageing, the immediate targets are those that are already known to affect damage and repair, while it is in principle possible that future interventions using drugs or stem cells might open new avenues. This plainly raises the question whether extending the human life-span would in fact be beneficial for the individual, and desirable for the individual or for society as a whole. These are not matters we have considered; to do so would have unacceptably broadened the scope of our inquiry. We do however note that, in marked contrast to the perennial fascination of the media with the idea that science might discover the secret of eternal youth, none of those we have consulted suggested that an aim of scientific research should be to seek to extend the human life-span (as opposed to eliminating factors which shorten it). Indeed, among the many experts on diseases and disabilities of ageing to whom we have listened, there have been few who have even referred to the possible benefits of stem cell therapies. These therapies are frequently promoted as having the potential to treat and even cure age-related pathology; we suspect that realistic progress down this route is as yet uncertain and at best some way off.

Factors that promote good health and slow the ageing process

3.20.  Age Concern England summarised what appears to be a consensus view when they told us that the factors that promote good health and slow the ageing process are—

We consider each of these factors in turn.

PHYSICAL ACTIVITY

3.21.  Those of our witnesses who addressed this were unanimous in believing that physical activity is a key to predicting independence and mortality in later life. Disability and infirmity may be largely the result of disuse of muscle rather than the inevitable process of ageing.[35] The Royal College of Physicians of Edinburgh agreed: "Physical activity is the major modifiable influence on health in old age."[36] The Royal Society of Edinburgh explained that "exercise can positively affect peak bone mass in children and adolescents, has been shown to help maintain or even modestly increase bone density in adulthood, and can assist in minimizing age related bone loss in older adults."[37]

3.22.  After age 40 we lose muscle mass at about one to 2% per year. A comparison of athletes and non­athletes in their 70s shows that their rate of loss is the same, but the athletes start from a higher standard. The rate of muscle loss can be influenced by strengthening exercise programmes. A three­month exercise programme can rejuvenate muscle mass by a 15­year equivalent. By starting early enough it is possible to raise the threshold at which we can influence those inevitable age­related changes (Q 346).[38] Recent evidence has shown that community-based exercise training programmes for healthy older people can have profound effects in reversing muscle wasting and the accompanying functional deficit.[39] Lost fitness can be regained with regular activity even in extreme old age.[40]

3.23.  It comes as no surprise to find strong evidence that dog ownership leads to substantial increases in physical exercise. A study of new pet-owners in 1990 found that new dog-owners "displayed a dramatic increase in the number/duration of walks taken after the first month, and this increase was maintained both to six months and to ten months". At the end of the study, dog-owners reported that increased exercise was one of the most important differences made to them, second only to increased companionship and affection.[41]

3.24.  Two cautionary notes need to be sounded when advocating the benefits of exercise. First, although the beneficial effects of exercise are clear, there may be adverse effects, particularly on the joints, of too much physical wear; these effects can be mitigated by choosing which kinds of exercise to undertake and by taking appropriate precautions, such as wearing suitable shoes for running. Second, extreme exercise such as is undertaken by world class athletes appears sometimes to accelerate age-related degeneration of muscle cells, probably through over-use. However for most of us, even though exercise temporarily increases metabolic rate and thereby the potential to suffer oxidative damage, this appears to be more than compensated by stimulating the body's repair and antioxidant defence systems.

3.25.  Local authorities can do much to help people of all ages, including older people, to benefit from exercise. Facilities for cycling are often poor or non-existent; sometimes even walking is a perilous activity. Local authorities should aim to improve facilities for exercise; they should make it their business to inform older people about these facilities; they should encourage them to use these facilities; and they should ensure that adequate transport is available.

3.26.  In the longer term, it is plain that increase in exercise during the school years will have a beneficial effect throughout life, and that the benefits will be particularly felt in old age. It is therefore a matter of concern to us that more is not being done to reverse the selling off of school playing fields and the consequent reduction in school sports. Since October 1998, when section 77 of the School Standards and Framework Act 1998 came into force, such sales have required the consent of the Secretary of State for Education. However, since that consent is withheld only in a very small proportion of cases,[42] this has slowed but not halted the sale of playing fields. In August 2004 the then Secretary of State stated that the rules were being tightened up, and that the sale of a playing field "must be an absolute last resort". We hope that future figures will bear this out.

3.27.  DCMS figures show that in 2002 only 25% of 5-16 year olds spent "a minimum of two hours each week on high quality PE and school sport".[43] By July 2004 this proportion had risen to 62%. This trend is in the right direction, but must be continued if we are not to have a generation which, because it had in its youth limited opportunities for physical activity, will as it grows older be increasingly at risk of disability and infirmity. The White Paper Choosing Health, published in November 2004, states that the national target is to increase this figure from 62% to 75% in 2006 and to 85% in 2008.[44] If these targets are achieved, that will be a very welcome development. But considerably more than two hours a week is needed to make a real difference; we would like to see a further target for a substantial increase in this minimal time.

3.28.  Exercise at all ages is one of the most effective ways to counter the adverse effects of ageing on functional capacity. The Government should publish plans showing how they intend to promote, in schools and elsewhere, the benefits of exercise as a factor contributing to improved health at all ages.

3.29.  Consent for the disposal of playing fields must be refused unless the facilities lost are to be replaced by sports or exercise facilities which are as good or better.

NUTRITION

3.30.  There is very considerable evidence that health in old age is greatly influenced by nutrition earlier in life, in childhood, and even before birth (QQ 90-91).[45] Since nutrition provides the essential raw materials of life, it is unsurprising that foods can both promote and retard the accumulation of cellular and molecular damage. "Bad" foods include those containing saturated fats, those with a high sugar intake, and substances which may cause DNA damage (it should be noted that some natural substances, including plant materials, can damage DNA, probably as part of the plant's defences). "Good" foods include fruits and vegetables and those containing natural antioxidants, such as fish oils.

3.31.  Dr van der Ouderaa explained this further:

"There is very strong data from epidemiology and in particular the excellent EPIC-Norfolk study by the University of Cambridge which shows that high fruit and vegetable nutrition reduced the prevalence of disease by up to 50% for cardiovascular disease and a similar percentage for mortality in the period of eight years that the two studies were done ... However, on the other extreme, if you have someone who chain smokes, has a sedentary life and has high stress shift work, then a couple of pieces of broccoli and two oranges are not going to save this person."(Q 89)

3.32.  In order to achieve maximum benefit from healthy nutrition, good habits should be established as early as possible. There is currently considerable concern about the long-term health effects of poor nutrition among school children, with the associated increase in obesity. What is less well understood is that poor nutrition also contributes to an acceleration of features of the underlying ageing process, leading to an increased risk of diabetes, cardiovascular disease and stroke in later life. This can also be caused by insufficient or inadequate nutrition in utero (Q 90).

3.33.  Professor Elizabeth Kay, who gave evidence to us on behalf of the British Dental Association, explained that nutrition has a double effect on oral health. A person's life time nutrition affects how oral health turns out when they are elderly; it is mostly exposure to sugar and exposure to fluoride that will affect the amount of dental decay in later years. That dental decay will in turn affect whether they have teeth in later years, and loss of a significant number of teeth affects what they are able to eat. Specifically, it reduces the amount of fruit, vegetables and vitamin C they consume, with all the knock-on effects that that may have (Q 89). "In terms of nutrition in oral health there are two things: decrease sugar intake, and have the optimum level of fluoride intake." (Q 111)

3.34.  The White Paper Choosing Health devotes a chapter to this problem. It states, and we agree, that "it is not for Government to dictate to [people] what they can and cannot consume". The central message is that there is no lack of information about what food is healthy, but that "messages about health are sometimes inconsistent or uncoordinated and out of step with the way people actually live their lives". The paper sees the Government's role as "to help information providers to give factual information that is up to date and accurate". It states that the Government "will press vigorously both before and during the UK presidency of the EU in 2005 to simplify nutrition labelling and make it mandatory on packaged foods". The Government "intends to discuss with the food industry how they might contribute to funding national campaigns to promote positive health information and education".[46]

3.35.  We very much welcome and support the approach taken in the White Paper. It is perhaps natural that, at a time of great concern about childhood obesity and the lifestyles of younger people, this chapter is addressed mainly to the needs of the young. It is not only children, however, who have unhealthy diets. Older people too have problems which include inadequate knowledge of appropriate diets, and affordability and availability of healthy foods. They have particular problems with labelling which is not only uninformative, but often in such minute print that it is for practical purposes illegible. We believe that the approach proposed by the Government should not concentrate on the young to the exclusion of the old. The presentation of labelling is as important as its content.

3.36.  Nutrition and oral health have major impacts on health throughout the lifespan. Since a person's health in old age reflects molecular and cellular damage that accumulates throughout life, and since nutrition affects the accumulation of such damage (adversely in the case of poor nutrition, beneficially in the case of good nutrition), the links between healthy eating and healthy ageing need to be better understood and communicated to the public.

3.37.  We welcome and commend the approach of the White Paper Choosing Health, and the importance it attaches to the provision of information about healthy nutrition. We recommend that this approach should be extended to cover the specific problems of older people.

ABSENCE OF RISK FACTORS: SMOKING, AND DRINKING TO EXCESS

3.38.  Damage to cells and molecules within the body can be accelerated, sometimes dramatically, by exposure to specific agents, such as tobacco smoke, drugs and excess alcohol. The adverse effects of tobacco smoke are very well known and almost certainly include acceleration of ageing. "Healthy ageing starts with smoking cessation" (Q 125);[47] cigarette smoking "is almost certainly a risk factor for dementia" (Q 327).[48] Maternal smoking is linked to the capacity to transport calcium across the placenta and the foetus and subsequently the infant's capacity to grow, which may also have long-term effects with implications for healthy ageing (Q 51).[49] Relatively little is known as yet about the specific adverse effects of drug abuse and binge drinking on the damage that underlies ageing; however, we would be surprised if such effects are absent.

HAVING A SOCIAL ROLE AND FUNCTION

3.39.  Long-term population-based studies show that social and productive activities are as important as physical activity in reducing the likelihood of illness and institutionalisation. The mechanisms for these effects are unclear. It is very possible that physical activity is a pre-condition for participation in many social activities, or that it may derive in part from the incidental social and purposeful activity involved. Physical activity may in itself reflect social competence and being in control of one's life. Whatever the mechanism, the two factors are clearly related to better health and the delay of onset of illness.[50]

3.40.  It also appears to be the case that, leaving aside the effects of all the factors we have listed above, people with higher social status have better health and longer lives than those of lower status: the social gradient, as it has been called by Professor Sir Michael Marmot, Professor of Epidemiology and Public Health at University College London. Professor Marmot has carried out a number of Whitehall studies which show that the most junior civil servants—clerks and messengers—are significantly more likely to suffer from coronary heart disease and other diseases of old age than senior civil servants. Low status leads to stress; the more one is in control of the situation, the higher on the social ladder one goes, the better one's health is likely to be.[51]

GENERAL WELL-BEING

3.41.  The factors we have listed above will all contribute to the promotion of good health and to slowing the ageing process from the earliest years into old age. There are other factors which, though not unimportant when a person is younger, play a major part in promoting health and longevity in later years. Prominent among these are good housing in a safe and pleasant neighbourhood, and the other environmental matters we mention in Chapter 5. Neighbourhood issues such as crime and antisocial behaviour (or the fear of them), or environmental concerns such as poor paving and litter which can lead to falls, can prevent older people from leaving their houses. This reduces opportunities for social interaction with family and friends, and this in turn can impact on mental and physical health.

3.42.  We note that the Wanless Report shares our view as to the importance of promoting those matters which can improve health:

"Better public health measures could significantly affect the demand for health care. A number of respondents emphasised that, while much of the beneficial impact might occur beyond the end of the 20-year period, that should not prevent action being taken in the short term ... Others said that investment in changing people's behaviour now, such as cutting out smoking, improving diet and encouraging more exercise, could significantly improve the populations' health status."[52]

Variability and diversity

INDIVIDUALITY OF THE AGEING PROCESS

3.43.  In our seminar, Professor Kirkwood drew attention to a curious feature of the ageing process, namely the individuality of how it affects us. We know that one day we will die, but we generally have little advance warning of how long we will live or what we will die from. We have seen that genes, nutrition, lifestyle and socioeconomic factors all play a part, but in addition to these there is a significant degree of variability in the ageing process. As Professor  Kirkwood showed, this variability is seen even within populations of genetically identical animals raised under conditions of extreme uniformity. To some extent such variability is inevitable, given that ageing is driven ultimately by the accumulation of damage, which will not follow an identical course even in identical twins.

3.44.  Recognising the individuality of ageing is important at many levels. The general deterioration of the human body with age, and the consequent increase of frailty, is well documented. However, the extent and underlying causes of individuality are less well known. Box 3 gives the findings of the 2002 English Longitudinal Study of Ageing (ELSA).

BOX 3

Variations in Physical Impairment

There is considerable variation in the level of physical impairment between age groups. The prevalence of reported physical functional limitation is surprisingly high at the youngest end of the sample, with 43% of respondents in their 50s reporting difficulty with mobility, and 13% reporting difficulty with a basic activity of daily life (self-care). At the same time, most (58%) of the respondents in their 80s and older report no difficulties with basic activities of daily life, and 17% report no difficulty with mobility functions

The variation in the level of impairment by occupational class is also considerable. Respondents with routine and manual occupations report up to twice as many difficulties with physical function as those with managerial or professional occupations. This occupational class disability gap is equivalent to the disability gap between age groups 10-15 years or more apart

Walking speed slows dramatically with age. Only around one in forty people aged between 60 and 64 walk more slowly than 0.4 metres/second, compared with one in five at age 80 and over. This deterioration in walking speed is more marked in women than in men.[53]


3.45.  The current publicly accepted view is undoubtedly that deterioration over time is inevitable, and that it is only the rate of deterioration which differs between individuals. For example, hearing impairment has long been viewed as an inevitable consequence of growing old, not only among the medical profession but also by the man in the street, so that very often people do not complain about it as much as they should as they grow older (Q 342).[54] The same applies to incontinence, a disabling and distressing condition which, according to Help the Aged,[55] is suffered by 6 million people of all ages in the UK.

3.46.  Measuring individual differences in ageing rate remains an important challenge, for which there is as yet no entirely satisfactory solution. We talk about people being "old before their time", and we envy those who, though in their eighties, not only enter the London Marathon, but finish it. These are extreme examples, but the fact remains that their bodies have aged at different rates—sometimes startlingly different. If we want to be able to understand the factors that affect ageing rate, we need better tools to measure individual differences in this rate. The measurements provided by such procedures are often described as "biomarkers" of ageing. They are particularly important if we want to measure the impact of interventions that might slow ageing rates without having to wait decades to determine their effectiveness. A biomarker provides an indication of a person's biological age (that is, how far, in bodily terms, they are on the journey from birth to death), as distinct from chronological age which merely measures the number of years they have lived.

3.47.  In the light of improved knowledge of underlying biological mechanisms and the need to measure the efficacy of interventions aimed at improving healthy ageing, we recommend that specific attention be given to funding research on biomarkers of ageing.

DISTINCTIONS IN THE AGEING PROCESS BETWEEN THE SEXES

3.48.  If evidence were needed that the ageing processes in men and women are different, it is provided by the statistics set out in Chapter 2 and by the mortality data shown in Figure 3. These reveal the markedly higher life expectancy of women, with lower age-specific mortality at all ages, but also their greater unhealthy life expectancy. There has been much speculation about the underlying causes for the difference in LE between men and women. Some argue that the difference is behavioural, and that as women increasingly adopt work and lifestyle patterns similar to those of men, the difference will diminish. However, in animal studies it has been shown that cells from female rats are intrinsically better protected against oxidative stress than cells from male rats, suggesting that the difference may be more biological. Biological differences between the sexes that impact on ageing, such as the difference in antioxidant protection, appear to be regulated at least partly by sex hormones. For example, there is some evidence from animal studies (and even some for humans) that male castration reduces or eliminates the lifespan difference between the sexes.

DISTINCTIONS BETWEEN SOCIAL GROUPS

3.49.  We explained in paragraph 2.10 the contribution made by differences in social class to the very marked differences in life expectancy between local authority areas which in some cases are separated by no more than a few miles. Commonly assigned reasons for this are, as we have explained,[56] poor nutrition and smoking (including of the mother during pregnancy), but also sub-standard housing, child poverty, and teenage pregnancies. All of these are factors which will increase the risk of ill-health and disease, not just in old age, but throughout the lifespan; and they are all factors which were considered by Sir Donald Acheson in his 1998 report on Health Inequalities.[57] General ill-health is outside our remit, but ill-health in early life will of course adversely affect health in old age. To this extent therefore we have included it in our deliberations. We agree with Professor Christopher Phillipson that there are great differences in the quality of life people will achieve in old age, and that this cannot be resolved when people are already old (Q 33).

3.50.  Social advantages do sometimes have attendant disadvantages. A recent study[58] has shown that, while there appears to be no difference in bone mass between children from different social classes, those from Social Class I are, by age 10, on average 1.5cm taller and 1kg lighter than those from Social Class V. Their bones therefore tend to be longer and more slender, and this appears to make them more vulnerable to fractures or osteoporosis in later life.

DISTINCTIONS BETWEEN ETHNIC GROUPS

3.51.  We explained in the previous chapter that the difficulties involved in attempting to isolate the individual factors which contribute to a lower life expectancy among lower social groups are even more acute in the case of ethnic minorities. It nevertheless appears that on all health indicators, Pakistani and Bangladeshi elders and, to a lesser extent, Indian and Black Caribbean elders, are more likely to report ill-health, and that the ethnic differences remain even after allowance has been made for differences in material resources.[59]

3.52.  The underlying biological reasons for ageing do not appear to differ between different ethnic groups. Thus, "a recent Canadian study showed that, although the prevalence of heart disease varied greatly in the 52 countries examined, the actual causes of disease (e.g. hypertension, diabetes, smoking, alcohol, abnormal lipids) did not differ."[60]

3.53.  We also received evidence from the Policy Research Institute on Ageing and Ethnicity (PRIAE), which seeks to improve the health and quality of life of black and minority ethnic (BME) elders at national and European level.[61] From this evidence it is clear that the incidence of hypertension is higher among middle-aged South Asians and African Caribbeans than among the overall population; yet while there is a substantially higher incidence of CHD among South Asians, the incidence among African Caribbeans is lower than the national average. It is however not easy to determine to what extent this is influenced by factors such as diet, lifestyle and socio-economic circumstances, and what contribution is made by genuine ethnic and genetic differences. But these differences undoubtedly exist. Dr Frans van der Ouderaa told us that if one compared three ethnic groups—the Chinese, the Indian and the Malays—in Singapore, it appeared that in a high stress urbanised environment Asian Indians became diabetic about fifteen years before the Chinese and about ten years before the Malays (Q 132). There is some indication that populations may become adapted to prevailing nutritional patterns and that if these patterns are altered, either through changing economic circumstances or through migration, this may have important effects on health.[62]

3.54.  Since submitting their evidence to us, PRIAE published in December 2004 their report of a study into Minority Elder Care in ten European countries. This includes statistics showing marked differences in the incidence of a range of medical problems among black and minority ethnic elders in the UK.

TABLE 4

Medical Problems of Black and Minority Ethnic Elders



The relationship between ageing and disease

3.55.  A question of immense significance is the distinction between the natural ageing processes, and those diseases which are particularly prevalent in old age. The Medical Research Council (MRC), the Department of Health (DoH) and the Wellcome Trust all told us that they directed most of their attention within the field towards diseases and disabilities, with relatively little focus on the ageing process itself. In contrast, the Biotechnology and Biological Sciences Research Council (BBSRC) focused on underpinning mechanisms of ageing and not directly on diseases.

3.56.  Within the United States, we heard from the National Institute on Aging that they drew a distinction between the two areas, but found funding research into specific diseases much easier; much of their research was therefore disease-related. On the other hand the Ellison Medical Foundation, a private foundation investing $20 million annually on ageing, concentrated more on basic research. Dr Richard Sprott, the Executive Director of the Foundation, told us he felt that the funding of research was too much orientated towards research into diseases, to the exclusion of the basic underlying science.

3.57.  Although we could understand the reasons why different organisations should focus more on ageing or on disease, we quickly discovered that the distinction is not always a clear one. Professor Cyrus Cooper, who gave evidence to us on behalf of the National Osteoporosis Society and the Arthritis Research Campaign, explained that this was particularly true in the rheumatological arena. Bone mineral density and the thickness of the cartilage of the joint changed with age, leading to an increasing risk of the likelihood of the adverse health event: fractures and osteoporosis, joint pain, disability and osteoarthritis. The original approaches to definition simply picked the threshold at which it was felt that the risk of disease became unacceptably high, and set the definition at that point. Definitions were now more sophisticated, but there was still no very clear distinction between gradual deterioration with age, and the stage at which it was appropriate to say that a person was suffering from a disease (Q 47).

3.58.  Furthermore, it may sometimes be difficult and unhelpful to distinguish between age-related diseases and the deterioration which results from them. It seems to us that whilst specific diseases and disabilities are the manifestations of growing older, there are underlying basic processes that inevitably age us which are to be found in the mechanisms contributing to the accumulation of molecular and cellular damage. In the words of Professor Linda Partridge, Weldon Professor of Biometry, University College London, "what we are looking at is an underlying process of progressive loss of function that leads to increasing vulnerability to various diseases… there is an underlying ageing process that can affect all these diseases simultaneously" (Q 387).

3.59.  However in the majority of fields, witnesses thought that a helpful distinction could be drawn. The Royal College of Physicians of Edinburgh agreed that "the crucial distinction between the effects of age alone and the effects of disease require[s] to be reinforced in the minds of both the lay public and health professionals".[63]

3.60.  Professor Clive Ballard, Director of Research at the Alzheimer's Society, supported this view:

  "It is not ageing itself that causes the problems but the diseases that become more common with ageing. If you look at the age of a particular population then the risk of particular conditions will be higher, but that is because the underlying factors that contribute to these conditions become higher rather than that age itself causes problems per se." (Q 308)

3.61.  Dr van der Ouderaa said: "I think it is helpful to discriminate between age related diseases and ageing as separate processes from a communication point of view." However, he qualified this by going on to say: "I think a lot of the etiological factors are actually quite similar"(Q 123). Professor Mathers agreed and added: "I tend to think of the ageing process as a process in which our ability to cope with perturbations of the norm become more and more difficult. The ability to maintain homeostasis, if you like, becomes more difficult so we need to be able to defend that state, and ageing is a way in which we begin to lose that ability." (Q 124)

3.62.  There does seem to be a widely held perception of such a distinction, which has implications both for finding the path to scientific understanding and for attitudes. For example, in the case of cardiovascular disease, if it proves possible to prevent atherosclerosis (hardening of the arteries) from occurring, the age-related increase in heart disease and stroke will be greatly reduced. Whether this will entirely eliminate circulatory problems that develop with age is less certain, however, and it may be that in order to prevent atherosclerosis we will need to understand why older arteries are intrinsically more vulnerable to atherosclerosis that young ones.

3.63.  In terms of attitude, diseases are regarded as being susceptible of a cure, and deserving of sympathy. Ageing is thought of as the general lot of mankind, and as something which must be endured. This affects public attitudes—it is much easier to raise funds for research on specific diseases—and it also affects the attitudes of professionals. For many doctors, whose motivation is to cure disease, we suspect that ageing too often has undertones of failure.

3.64.  We believe that there are three reasons to be cautious about accepting too readily a distinction between ageing and disease. First, for most age-related diseases, age itself is the single largest risk factor, so to try to research the disease without also addressing the underlying process of ageing seems ill-advised. It may simply be impossible to combat the one without the other.

3.65.  The view that ageing is driven by an accumulation of cellular and molecular damage is not very different from the view of the mechanisms responsible for most if not all age-related diseases, so there is great potential for specific age-related diseases to share common causative mechanisms not only with ageing itself but also with other age-related diseases.

3.66.  Finally, attempts to maintain a distinction between ageing and disease are likely to work to the disadvantage of those who are not "fortunate" enough to have a clearly recognised disease and who "merely" suffer from the multiple conditions that tend to afflict older people.

3.67.  Most of the research on ageing and health within the UK is focused on specific diseases and medical conditions for which age is the single largest risk factor. However, there is little research on underpinning mechanisms of such diseases which may be linked to basic processes of ageing. The Department of Health and other medical research funders, including the major charities, should develop and implement strategies to address links between ageing and disease.

3.68.  In this chapter, we have considered the intrinsic processes of ageing. In the following chapter we explore more closely age-related diseases and disorders.


28   Paragraphs 3.54 to end. Back

29   Professor John Maynard Smith, The Causes of Ageing, Proceedings of the Royal Society, 1962. Back

30   QinetiQ, from research on service personnel, p 381. Back

31   Oxidative stress is caused by highly reactive molecules called "reactive oxygen species", (ROS) popularly known as "free radicals". ROS are formed chiefly as by-products of the cell's requirement for oxygen, which is used to generate the chemical energy needed to power bodily functions. ROS can damage any structure within the cell, whether proteins, membranes, chromosomal DNA, mitochondrial DNA or telomeres. Back

32   A full account of this visit is at Appendix 5. Back

33   Paragraphs 3.55 to end. Back

34   p 274. Back

35   Age Concern, p 274. Back

36   p 392. Back

37   p 390. Back

38   From the evidence of Professor Rose Anne Kenny, Professor of Geriatric Medicine in the University of Newcastle-upon-Tyne, p 178. Back

39   Biosciences Federation, p 330. Back

40   Royal College of Physicians of Edinburgh, p 393. Back

41   J.A. Serpell, Beneficial aspects of pet ownership on some aspects of human health and behaviour, Journal of the Royal Society of Medicine, 84: 717-720, 1991. Back

42   The National Playing Fields Association stated in Fields Focus, Spring 2003, that of the disposals of school playing fields scrutinised by the Secretary of State between October 1998 and December 2002, over 97% had been approved. Back

43   DCMS Autumn Performance Report, January 2004, Cm 6095. Back

44   Cm 6374, chapter 3, paragraph 70. Back

45   From the evidence of Professor John Mathers on behalf of the British Nutrition Foundation and of Dr  Frans van der Ouderaa, Vice-President, Corporate Research, Unilever plc, p 40. Back

46   Cm 6374, Chapter 2, paragraphs 7, 11, 19, 23 and 43. In 2004 the Government spent £7 million on food campaigns; in 2003 the food industry spent £743 million on advertising food, soft drinks and chain restaurants. Back

47   From the evidence of Dr Frans van der Ouderaa, p 48; and see also paragraphs 3. Back

48   From the evidence of Professor Carol Brayne, Professor of Public Health Medicine, Cambridge, p 170. Back

49   From the evidence of Professor Cyrus Cooper, Professor of Rheumatology, University of Southampton, p30. Back

50   Age Concern England, p 274. Back

51   Michael Marmot, Status Syndrome, published by Bloomsbury, June 2004. Back

52   Final Report of the Review by Derek Wanless, Securing our Future Health: Taking a Long-Term View, April 2002, paragraph 1.27. Back

53   ELSA, summary of chapter 7. 0.4 metres/second is less than 1 mph. Back

54   From the evidence of Professor Karen Steel, Principal Investigator, Wellcome Trust Sanger Institute,
p  177. 
Back

55   p 280. Back

56   Paragraphs 3.30 and 3.38. Back

57   Sir Donald Acheson, Independent Inquiry into Inequalities in Health, part 1 (The Stationery Office, 1998). Back

58   By Dr Emma Clark, based on the Avon Longitudinal Study of Parents and Children. Back

59   Maria Evandrou, Ethnic Inequalities in Health in Later Life, Health Statistics Quarterly 08, Winter 2000. Back

60   Academy of Medical Sciences, p 193. Back

61   p 372. Back

62   Bateson et al, Developmental Plasticity and Human Health, Nature 430, 22 July 2004. Back

63   p 392. Back


 
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