
Contents
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The ageing person The ageing person
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Changes not due to ageing Changes not due to ageing
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Changes due to ageing Changes due to ageing
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Ageing and senescence Ageing and senescence
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Further reading Further reading
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Theories of ageing Theories of ageing
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Oxidative damage Oxidative damage
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Abnormal control of cell mitosis Abnormal control of cell mitosis
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Protein modification Protein modification
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Wear and tear Wear and tear
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Ageing and evolution Ageing and evolution
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Demographics: life expectancy Demographics: life expectancy
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Individualized life expectancy estimates Individualized life expectancy estimates
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Demographics: population age structure Demographics: population age structure
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Fertility Fertility
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Deaths and cause of death Deaths and cause of death
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Population ‘pyramids’ Population ‘pyramids’
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Demographics: ageing and illness Demographics: ageing and illness
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Healthy life expectancy and prevalence of morbidity Healthy life expectancy and prevalence of morbidity
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Social impact of ageing population Social impact of ageing population
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Further reading Further reading
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Illness in older people Illness in older people
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Features of illness in older people Features of illness in older people
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Investigating older people Investigating older people
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Treating disease in older people Treating disease in older people
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Cite
The ageing person
There are many differences between old and young people. In only some cases are these changes due to true ageing, ie due to changes in the characteristic(s) compared with when the person was young.
Changes not due to ageing
Selective survival. Genetic, psychological, lifestyle, and environmental factors influence survival, and certain characteristics will therefore be over-represented in older people
Differential challenge. Systems and services (health, finance, transport, retail) are often designed and managed in ways that make them more accessible to young people. The greater challenge presented to older people has manifold effects (eg impaired access to health services)
Cohort effects. Societies change, and during the twentieth century, change has been rapid in most cases. Young and old have therefore been exposed to very different physical, social, and cultural environments
Changes due to ageing
Primary ageing. Usually due to interactions between genetic (intrinsic, ‘nature’) and environmental (extrinsic, ‘nurture’) factors. Examples include lung cancer in susceptible individuals who smoke, hypertension in susceptible individuals with high salt intake, and diabetes in those with a ‘thrifty genotype’ who adopt a more profligate lifestyle
Additionally there are genes which influence more general, cellular ageing processes. Only now are specific genetic disease susceptibilities being identified, offering the potential to intervene early and to modify risk
Secondary ageing. Adaptation to changes of primary ageing. These are commonly behavioural, eg reduction or cessation of driving as reaction times increase
Ageing and senescence
Differences between old and young people are thus heterogeneous, and individual effects may be viewed as:
Beneficial (eg increased experiential learning, increased peak bone mineral density (reflecting the active youth of older people))
Neutral (eg greying of hair, pastime preferences)
Disadvantageous (eg decreased reaction time, development of hypertension)
However, the bulk of changes, especially in late middle and older age, are detrimental, especially in meeting pathological and environmental challenges. This loss of adaptability results from homeostatic mechanisms that are less prompt, less precise, and less potent than they once were. The result is death rates that increase exponentially with age, from a nadir around age 12. In very old age (80–100 years), some tailing off of the rate of increase is seen, perhaps due to selective survival, but the increase continues nonetheless.
Further reading
Theories of ageing
With few exceptions, all animals age, manifesting as increased mortality and a finite lifespan. Theories of ageing abound, and over 300 diverse theories exist. Few stand up to careful scrutiny, and none has been confirmed as definitely playing a major role. Four examples follow.
Oxidative damage
Reactive oxygen species fail to be mopped up by antioxidative defences and damage key molecules, including DNA. Damage builds up until key metabolic processes are impaired and cells die.
Despite evidence from in vitro and epidemiological studies supporting beneficial effects of antioxidants (eg vitamins C and E), clinical trial results have been disappointing.
Abnormal control of cell mitosis
For most cell lines, the number of times that cell division can occur is limited (the ‘Hayflick limit’). Senescent cells may predominate in tissues without significant replicative potential such as cornea and skin. The number of past divisions may be ‘memorized’ by a functional ‘clock’—DNA repeat sequences (telomeres) shorten until further division ceases.
In other cells, division may continue uncontrolled, resulting in hyperplasia and pathologies as diverse as atherosclerosis and prostatic hyperplasia.
Protein modification
Changes include oxidation, phosphorylation, and glycation (non-enzymatic addition of sugars). Complex glycosylated molecules are the final result of multiple sugar–protein interactions, resulting in a structurally and functionally abnormal protein molecule.
Wear and tear
There is no doubt that physical damage plays a part in ageing of some structures, especially skin, bone, and teeth, but this is far from a universal explanation of ageing.
Ageing and evolution
In many cases, theories are consistent with the view that ageing is a by-product of genetic selection: favoured genes are those that enhance reproductive fitness in earlier life but which may have later detrimental effects. For example, a gene that enhances oxidative phosphorylation may increase a mammal's speed or stamina, while increasing the cumulative burden of oxidative damage that usually manifests much later.
Many genes appear to influence ageing; in concert with differential environmental exposures, these result in extreme phenotypic heterogeneity, ie people age at different rates and in different ways.
Demographics: life expectancy
Life expectancy (average age at death) in the developed world has been rising since accurate records began and continues to rise linearly
Lifespan (maximum possible attainable age) is thought to be around 120 years. It is determined by human biology and has not changed
Population ageing is not just a minor statistical observation but a dramatic change that is easily observed in only a few generations
In 2002, life expectancy at birth for women born in the UK was 81 years, and 76 years for men
This contrasts with 49 and 45 years, respectively, at the end of the nineteenth century
Although worldwide rises in life expectancy at birth are mainly explained by reductions in perinatal mortality, there is also a clear prolongation of later life in the UK as shown by calculations of life expectancy at 50 or 65 (see Fig. 1.1)
Between 1981 and 2002, life expectancy at age 50 increased by 4.5 years for men and 3 years for women
While projections suggest this trend will continue, it is possible that the modern epidemic of obesity might slow or reverse this

Individualized life expectancy estimates
Simple analysis of population statistics reveals that mean male life expectancy is 76 years. However, this is not helpful when counselling an 80 year old. Table 1.1 demonstrates that as a person gets older their individual life expectancy actually increases. This has relevance in deciding on healthcare interventions.
Age at time of estimate . | Median years left to live . | That is, death at age . |
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40 | 36.5 | 76.5 |
60 | 17.9 | 77.9 |
80 | 5.6 | 85.6 |
90 | 2.8 | 92.8 |
Age at time of estimate . | Median years left to live . | That is, death at age . |
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40 | 36.5 | 76.5 |
60 | 17.9 | 77.9 |
80 | 5.6 | 85.6 |
90 | 2.8 | 92.8 |
More accurate individualized estimates should take into account sex, previous and current health, longevity of direct relatives, as well as social and ethnic group.
Demographics: population age structure
Fertility
Fertility is defined as the number of live births per adult female. It is currently around 1.9 in the UK. If this rate were maintained, then in the long term population would fall unless ‘topped up’ by net immigration. In contrast during the ‘baby boom’ years of the 1950s, fertility rates reached almost 3. This bulge in the population pyramid will reach old age in 2010–2030, increasing the burden on health and social services.
Deaths and cause of death
The driver of mortality decline has changed over the twentieth century, from reductions in infant/child mortality to reductions in old age mortality.
Infant mortality accounted for 25% of deaths in 1901, but had fallen to 4% of deaths by 1950. Currently over 96% of deaths occur >45 years
Deaths at age 75 and over comprised 12% of all deaths in 1901, 39% in 1951, and 65% in 2001
The most common cause of death in people aged 50–64 is cancer (lung in men, breast cancer in women); 39% of male and 53% of female deaths are due to cancer. Over the age of 65, circulatory diseases (heart attacks and stroke) are the most common cause of death. Pneumonia as a cause of death also increases with age to account for 1 in 10 among those aged 85 and over.
All these statistics rely on the accuracy of death certification (see Documentation after death’, p. 648) which is likely to reduce with increasing age.
Population ‘pyramids’
These demonstrate the age/sex structure of different populations. The shape is determined by fertility and death rates. ‘Pyramids’ from developing nations (and the UK in the past) have a wide base (high fertility but also high death rates, especially in childhood) and triangular tops (very small numbers of older people). In the developed world the shape has become more squared off (see Fig. 1.2) with some countries having an inverted pyramidal shape—people in their middle years outnumber younger people—as fertility declines below replacement values for prolonged periods.


Demographics: ageing and illness
Healthy life expectancy and prevalence of morbidity
Healthy life expectancy is that expected to be spent in good or fairly good health. As total life expectancy rises it is better for society and the individual to spend as much of this extended life in good health as possible.
It is not known whether ‘compression of morbidity’—where illness and disability is squeezed into shorter periods at the end of life—can be achieved. Trends in data from USA suggest that compression of morbidity is occurring, but challenges to public health are different in the UK. Obesity and lack of exercise may negate diminishing morbidity from infectious diseases; as more people survive vascular deaths they might develop dementia (and other old age-associated diseases). The jury is still out; some data gathered in the UK using self-rated health measures show that in 1981 the expected time lived in poor health was 6.5 years (men) and 10.1 years (women); by 2001 this was 8.6 and 10.7 years.
Social impact of ageing population
Those >80 are the fastest growing age group in UK. Currently around a quarter of the population is >60 years old but by 2030 this will rise to a third. Governments can encourage migration (economic migrants are mostly young) and extend working lives (eg increase pensionable age for women) but these will have little effect on the overall shift. The impact of this demographic shift on society's attitudes and economies is huge. Examples include:
Financing pensions and health services—in most countries these are financed on a ‘pay-as-you-go’ system, so will have to be paid for by a smaller workforce. This will inevitably mean greater levels of taxation for those in work or a reduction in the state pension. Unless private pension investment (which works on an ‘insurance’ system of personal savings) improves there is a risk that many pensioners will continue to live in relative poverty
Healthcare and disability services—the prevalence and degree of disability increases with age. American Medicare calculations show that more than a quarter of healthcare expenditure is on the last year of a person's life, with half of that during the last 60 days
Families are more likely to be supporting older members
Retired people comprise a growing market and companies/industries that accommodate the needs/wishes of older people will flourish
Transport, housing, and infrastructure must be built or adapted
Political power of older people (the ‘grey lobby’ in America) will grow
How can success be defined, ie towards what aim should public health and clinical medicine be striving? The following definitions are to some extent stereotypical and culture-sensitive. More flexible definitions would acknowledge individual preferences.
Successful ageing. Without overt disease, with good physical and cognitive function, a high level of independence and active engagement with broader society. Usually ended by a peaceful death without a prolonged dying phase
Unsuccessful ageing. Accelerated by overt disease, leading to frailty, poor functional status, a high level of dependence, social and societal withdrawal, and a more prolonged dying phase where life quality may be judged unacceptable
Further reading
Illness in older people
One of the paradoxes of medical care of the older person is that the frequency of some presentations (‘off legs’, delirium . . .) and of some diagnoses (infection, dehydration . . .) encourages the belief that medical management is straightforward, and that investigation and treatment may satisfactorily be inexpensive and low skill (and thus intellectually unrewarding for the staff involved).
However, the objective reality is the reverse. Diagnosis is frequently more challenging, and the therapeutic pathway less clear and more littered with obstacles. However, choose the right path, and the results (both patient-centred and societal (costs of care etc.)) are substantial.
Features of illness in older people
Present atypically and non-specifically
Cause greater morbidity and mortality
May progress much more rapidly—a few hours delay in diagnosis of a septic syndrome is much more likely to be fatal
Health, social, and financial sequelae. Failures of treatment may have long-term wide-ranging effects (eg nursing home fees >£800/week)
Co-pathology is common. For example, in the older patient with pneumonia and recent atypical chest pain, make sure myocardial infarction (MI) is excluded (sepsis precipitates a hyperdynamic, hypercoagulable state, increasing the risk of acute coronary syndromes; and a proportion of atypical pain is cardiac in origin)
Lack of physiological reserve. If physiological function is ‘borderline’ (in terms of impacting lifestyle, or precipitating symptoms), minor deterioration may lead to significant disability. Therefore, apparently minor improvements may disproportionately reduce disability. Identification and correction of several minor disorders may yield dramatic benefits
Investigating older people
Investigative procedures may be less well tolerated by older people. Thus the investigative pathway is more complex, with decision-making dependent on clinical presentation, sensitivity and specificity of test, side effects and discomfort of the test, hazards of ‘blind’ treatment or ‘watchful waiting’ and of course the wishes of the patient
Consider the significance of positive results. Fever of unknown cause is a common presentation, and urinalysis a mandatory investigation. But what proportion of healthy, community-dwelling, older women have asymptomatic bacteriuria and a positive dipstick? (A: around 30%, depending on sample characteristics). Therefore in what proportion of older people presenting with fever and a positive dipstick is urinary tract infection (UTI) the significant pathology? (A: much less than 100%)
The practical consequence of this is the under-treatment of non-urinary sepsis.
Treating disease in older people
When treating disease in older people, they:
May benefit more than younger people from ‘invasive’ treatments—eg thrombolysis. On a superficial level, think ‘which is more important—saving 10% of the left ventricle (LV) of a patient with an ejection fraction (EF) of 60% (perhaps a healthy 50 year old) or of a patient with an EF of 30% (perhaps, an 80 year old with heart failure)?’. Note that the significant criterion here is more the LVEF than the age, the principle being that infarcting a poor LV may cause long-term distress, morbidity, and mortality, whereas infarcting a part of a healthy myocardium may be without sequelae
May benefit less than younger people. Life expectancy and the balance of risks and benefits must be considered in decision-making. For example, the priority is unlikely to be control of hypertension in a frail 95 year old who is prone to falls
May have more side effects to therapies. In coronary care: β-blockade, aspirin, angiotensin-converting enzyme (ACE) inhibitors, thrombolysis and heparin may all have a greater life (and quality-of-life)-saving effect in older patients. Studies show these agents are underused in MI patients of all ages, but much more so in the elderly population. The frequency of side effects (bradycardia and block, profound hypotension, renal impairment and bleeding) is greater in older people, although a significant net benefit remains
May respond to treatment less immediately. Convalescence is slower, and the doctor may not see the eventual outcome of his/her work (the patient having been transferred to rehabilitation, for example)
The natural history of many acute illnesses is recovery independent of medical intervention, particularly in the young. Beware false attributions and denials of benefit:
The older person frequently benefits from therapy, unwitnessed by medical staff
The younger person recovers independent of medical efforts, though his/her recovery is falsely attributed to those interventions (by staff and patient)
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